tag:blogger.com,1999:blog-3250055980807139362024-03-24T23:09:43.864-07:00Renal Cancer BlogThis Blog is just a collection of snippets of information that will help in deciding what to ACTUALLY DO. This is the good mixed up with the bad. Brainstorming and inspirational ...
=== DON'T BELIEVE THE HYPE ===Unknownnoreply@blogger.comBlogger166125tag:blogger.com,1999:blog-325005598080713936.post-16194401384838383472011-11-28T17:14:00.001-08:002011-11-28T17:14:53.131-08:00MRI - Fast t2 sequences explained<br>Imaging of the urinary tract: the role of CT and MRI<br><br><br>Melanie P. Hiornscorresponding author<br>Great Ormond Street Hospital for Children - Radiology Department, Great Ormond Street, London, WC1N 3JH UK<br>Melanie P. Hiorns, Email: hiornm XatX <a href="http://gosh.nhs.uk" target="_blank">gosh.nhs.uk</a>. corresponding author<br> Received March 9, 2010; Revised August 4, 2010; Accepted August 4, 2010.<br><br><br><br>Abstract<br>Computed tomography (CT) and magnetic resonance imaging (MRI) are increasingly valuable tools for assessing the urinary tract in adults and children. However, their imaging capabilities, while overlapping in some respects, should be considered as complementary, as each technique offers specific advantages and disadvantages both in actual inherent qualities of the technique and in specific patients and with a specific diagnostic question. The use of CT and MRI should therefore be tailored to the patient and the clinical question. For the scope of this article, the advantages and disadvantages of these techniques in children will be considered; different considerations will apply in adult practice.<br> Keywords: Magnetic resonance imaging, Computed tomography, Ultrasonography, Child, Kidney, Urinary tract, Diagnostic imaging<br><br><br><br>Introduction<br>Computed tomography (CT) was invented by Sir Godfrey Hounsfield and was introduced into medical practice in 1973 [1–3]. The technique relies on the original theory that one can determine what is inside a box by taking X-ray "readings" at all angles around the object (tomograms). A computer then takes input from the X-rays at various angles to create an image of the object in slices, hence the name computed tomography. CT is therefore an X-ray technique and uses ionizing radiation. X-rays (whether conventional, plain radiographs or CT) give pictorial information on the density of an object or material. A CT image is therefore a pictorial demonstration of all the densities in the object, with high-density material (bone, calcium, metalwork) being represented as white and low-density materials being dark grey or black (air, fat). Their density can be measured in Hounsfield units (HU), and this can give the radiologist important information about the type of material (or tissue). Water is used as the reference point and has a value of between –7 and +7 HU (typically 0 HU), bone and other calcification will be of higher density (?500 HU), fat will be of lower density (–25 to –250 HU), and soft tissues are in the range +10 to +60 HU.<br> Modern CT scanners are very fast and can scan the abdomen and pelvis in typically 5–7 s once the planning view (the 'scout' or 'scanogram') has been set up. This has great advantages in children, as for the most part, children will not need to have a general anesthetic to ensure they keep still. Babies can undergo "feed and wrap" and will generally sleep through the scan; toddlers and preschool children can be scanned with encouragement and caregiver support (or occasionally with mild sedation), and older children are easily able to tolerate the short scan times. Modern scanners typically have a slice thickness of <1 mm (0.6–0.75 mm) depending on the manufacturer. This allows for very detailed information that can be reconstructed in other planes, such as sagittal and coronal projections, which are often very helpful to the physician in understanding the image. Three dimensional (3D) images can also be produced in postprocessing, allowing rotating visualization of any part of the image that is required. CT provides a high spatial resolution image (the ability to distinguish two structures an arbitrarily small distance from each other as separate) with low noise, giving exquisite anatomical depiction, but it cannot give as much information with respect to processes within different tissues types, such as inflammation or necrosis, unless these are quite pronounced. The use of intravenously administered contrast medium helps in this respect and would be given routinely unless the main clinical question was regarding calcification or high-density objects (such as when looking for renal calculi). There is almost no indication in children for doing both pre- and postcontrast scans as part of the same examination. The only occasion for routinely performing a precontrast (unenhanced) scan is when evaluating calculi, and if the examination is solely for that purpose, then there is no indication to routinely perform a postcontrast scan as well. Conversely, if there is no diagnostic concern regarding calculi, then only a postcontrast scan should be performed, as there is so little additional diagnostic yield (if any) from doing both a pre- and postcontrast scan, and the significant radiation dose from the additional precontrast scan cannot be justified. All patients should be asked for any history of contrast allergy (or other severe allergies) before contrast is given intravenously (IV). Contrast is always most safely administered in the setting of good effective volume and hydration. Moreover, in the setting of a depressed glomerular filtration rate (GFR), consideration should be given to both hydration and alkalinization and, in some instances, there may be a role for the use of postcontrast dialysis. Planning for imaging children with depressed GFR is best accomplished in a multidisciplinary fashion, with input from both radiologist and nephrologist. Intravenously administered contrast must not be given in severe renal failure unless the patient will subsequently be dialyzed. In mild renal failure, a risk assessment (based on the potential benefit of the examination) must be performed by the clinician, and the patient must be well hydrated beforehand. CT is a high-radiation-dose technique and as such is used much more cautiously and infrequently in children than in adults, with children being many times more biosensitive to radiation than adults. Background radiation is typically 2–3 mSv per year, and a CT scan of the abdomen and pelvis is approximately 2–6 mSv, or the equivalent of 200–300 chest X-rays. Much effort is being made by pediatric radiologists to reduce radiation doses in children, especially in CT imaging, and information regarding this can be found at <a href="http://www.pedrad.org/associations/5364/ig/" target="_blank">http://www.pedrad.org/associations/5364/ig/</a>. Consideration should be given to performing specialized imaging studies that are elective in nature in facilities with pediatric expertise and pediatric imaging protocols, if these are available.<br> Magnetic resonance imaging (MRI) provides much greater contrast between different soft tissues [4] than does CT, as it relies on obtaining a radiofrequency (RF) signal from alignment and subsequent relaxation of protons in hydrogen atoms in water in the body. Soft tissue throughout the body will have varying water contents depending on cell types and the processes going on in and around those cells (e.g. normal different tissues, inflammation, tumor, infection, etc). An MR scanner uses a powerful magnetic field to align the nuclear magnetization of protons of hydrogen atoms in water (intra- and extracellular), and RF fields are then applied to alter the alignment of this magnetization, causing hydrogen nuclei to produce a rotating magnetic field that is detectable by the scanner. When RF fields are reversed, the protons relax to their normal state and give off a tiny RF signal that is detected by the scanner and is used to construct the image. Different tissues return to their equilibrium state at different rates. By changing the parameters of the scan, this effect is used to create an image that depicts the different tissues by showing the contrast between them. In a typical MRI scan, several different pulse sequences are performed to best exploit the different signals between tissues and give the most information. The main advantage of MRI over CT is that it gives far better contrast resolution (the ability to distinguish the differences between two arbitrarily similar but not identical tissues) and thus its ability to demonstrate changes between normal and pathological tissues. A sequence may last between a few seconds to several minutes, with most routine sequences lasting 1–3 min. Between five and ten sequences would usually be performed. MRI can produce images in any plane desired, and this is achieved by the radiographer or technician when setting up scan parameters. Sequences can be selected specifically to demonstrate particular qualities of tissues, such as water content. For example, with particular values of the echo time (TE) and the repetition time (TR), which are basic parameters of image acquisition, a sequence may take on the property of T2 weighting. On a T2-weighted scan, water- and fluid-containing tissues are bright (most modern T2 sequences are actually fast T2 sequences), and fat-containing tissues are dark. The reverse is true for T1-weighted images. Damaged tissue tends to develop edema, which makes a T2-weighted sequence sensitive for pathology and generally able to distinguish pathologic tissue from normal tissue. Heavily T2-weighted sequences are especially useful in the urinary tract, as water-containing structures are bright white, such as the collecting system and the bladder.<br> MRI contrast agents are frequently used. Most common of these is gadolinium, which is given intravenously. These agents work by shortening the T1 or T2 relaxation time of protons nearby. Reduction of T1 relaxation time results in a hypersignal with a reduced T2 relaxation time, thus reducing both T2 and T2* signals. Gadolinium is therefore of most benefit in T1-based sequences. A rare but severe complication of gadolinium use is nephrogenic systemic fibrosis (NSF), which causes fibrosis in various tissues and organs. Patients with poor renal function are considered a greater risk of NSF, and therefore, gadolinium contrast agents must only be used with caution in these patients. As a result, gadolinium-containing contrast is now considered contraindicated in patients with an estimated GFR <60 ml/min and especially <30 ml/min [5]. Depressed GFR encompasses both acute and chronic kidney injury. As such, individuals with transient renal dysfunction should also be considered at risk, even though their usual GFR may be normal.<br> MRI scans will usually take 30–45 min and therefore generally require a general anesthetic in children from approximately 1–6 or 7 years of age. Older children are usually able to cooperate, but if they are unable to remain still and limit any movement for this length of time, they may also require a general anesthetic. Younger children (<12 months) may undergo feed and wrap or sedation. Further details of the practical aspects are covered in the pediatric MRI literature [6–8] (Table 1).<br> <br>Table 1<br><br>Comparison of advantages and disadvantages between computed tomography (CT) and magnetic resonance (MR) imaging modalities<br><br><font size="2"><br></font><table cellpadding="2" cellspacing="3" frame="hsides" rules="groups"> <thead><tr><th><font size="2">CT</font></th><th><font size="2">MR</font></th></tr></thead><tbody><tr><td align="left"><font size="2">Uses ionizing radiation, high-dose procedure</font></td><td><font size="2">Uses magnetic resonance, no ionizing radiation</font></td> </tr><tr><td align="left"><font size="2">Excellent spatial resolution</font></td><td><font size="2">Excellent contrast resolution</font></td></tr><tr><td align="left"><font size="2">Actual scanning time measured in seconds (typically <10 s)</font></td> <td><font size="2">Actual scanning time measured in minutes (typically 45 min)</font></td></tr><tr><td align="left"><font size="2">Rarely requires general anesthetic in children</font></td><td><font size="2">Frequently requires general anesthetic in children, depending on age</font></td> </tr><tr><td align="left"><font size="2">Excellent at showing calcification</font></td><td><font size="2">Poor at showing calcification (signal void)</font></td></tr><tr><td align="left"><font size="2">Poor at showing edema or pathological changes in specific tissue types</font></td> <td><font size="2">Excellent at showing edema and pathological changes in specific tissue types</font></td></tr><tr><td align="left"><font size="2">Usually requires intravenous contrast (unless looking for calcification when not required)</font></td> <td><font size="2">Usually requires intravenous administration of contrast (but certain sequences can be tailored if this is contraindicated)</font></td></tr><tr><td align="left"><font size="2">No known risk of nephrogenic systemic fibrosis (NSF)</font></td> <td><font size="2">Risk of NSF (rare, but renal patients believed to be at increased risk)</font></td></tr><tr><td align="left"><font size="2">Widely available</font></td><td><font size="2">Less widely available, especially for children</font></td> </tr><tr><td align="left"><font size="2">Less expensive</font></td><td><font size="2">Expensive</font></td></tr><tr><td align="left"><font size="2">Usually available as an emergency imaging technique</font></td><td><font size="2">Not routinely available as an emergency technique</font></td> </tr><tr><td align="left"><font size="2">No significant contraindications</font></td><td><font size="2">Contraindicated in patients with any internal ferrous objects (pacemakers, defibrillators, recent orthopedic metalware, other implanted metallic devices, metallic foreign bodies)</font></td></tr><tr><td align="left"><font size="2">Open-style scanners</font></td><td><font size="2">Generally quite enclosed scanners – risk of claustrophobia</font></td></tr><tr><td align="left"> <font size="2">Can only scan in one plane (but can do reconstructed images later)</font></td><td><font size="2">Can scan in any plane</font></td></tr><tr><td align="left"><font size="2">Few artefacts</font></td><td><font size="2">Prone to artefacts depending on sequence type (especially motion artifact)</font></td> </tr></tbody></table><font size="2"><br></font><br><br><br>Imaging the urinary tract – which modality to use for first-line examination?<br> <br>In imaging the urinary tract in children, the modality of choice for the initial examination will almost universally be ultrasound (US). US is inexpensive, immediate, painless, requires no sedation or anesthetic, is widely available, and is radiation free. In children, the urinary tract is easily visualized, as usually children have less body fat than adults, and the kidneys and bladder are relatively superficial structures. Children should be scanned both supine and prone, and the posterior approach (with the child lying prone) often gives the best anatomical detail of the kidneys. US can be used to scan in any plane at the discretion of the operator, and whereas the technique is entirely operator dependent, most centers have staff with a high level of skill. In most pediatric centers, it is considered completely unacceptable to proceed to CT or MRI in routine practice unless US had already been performed and had been unable to fully answer the diagnostic question. Acute multiorgan trauma would be the main exception to this. It is common practice in adult medicine to perform a CT scan of the abdomen and pelvis as the first-line examination for renal colic. In children, the first-line examination, even in renal colic, should ideally be US (on radiation dose risk vs. benefit considerations), recognizing that a few children will still need to proceed to CT. However, there is some variation in this practice between North America and Europe and on the availability of US expertise out of hours. Renal colic in children is much less common than in adults, even in children with known stone disease, and their stones pass more readily. US can show renal calculi with exquisite detail, demonstrating stones down to approximately 1–2 mm in diameter, and is also highly sensitive in the bladder. It is less sensitive, however, in the ureters, which may be obscured by bowel and other pelvic structures, so in the context of a normal US and ongoing clinical features suggestive of calculi (colicky pain, hematuria, known existing stone disease), CT may still be indicated. There is further discussion of this topic in the section "Calcification in the urinary tract". US is the first-choice examination for all other pathologies relating to the kidney and urinary tract.<br> <br><br><br>The use of CT and MR for specific clinical indications<br>Congenital conditions<br>In pediatric practice, many congenital conditions of the urinary tract are demonstrated in utero on antenatal scans, whereas some are only detected in infancy or later due to subsequent complications. Ninety percent of fetal kidneys can be identified by 17–20 weeks of gestation and 95% by 22 weeks. Both antenatally and postnatally, US remains the examination of choice in demonstrating kidney and urinary tract anatomy. Structural urinary tract anomalies include renal dysplasia, renal hypoplasia, renal aplasia, multicystic dysplastic kidney, pelviureteric junction obstruction, duplication anomalies, fusion anomalies, renal ectopia, ureteroceles, cystic kidney diseases, and posterior urethral valves. All of these may be demonstrated by US, with additional information being acquired in some cases by other modalities (such as nuclear medicine imaging or fluoroscopy). MRI may subsequently be useful in these patients, as illustrated in Fig. 1 for cystic disease, either in the further workup following US [7, 9] when the clinical question has not been resolved, or when the child presents with (or has) complications that remain unexplained by US or require further delineation [10–12]. Heavily T2-weighted sequences (water-based sequences) are very useful in demonstrating dilatation of the urinary tract secondary to congenital anomalies, such as duplex kidneys with dilated moieties and occult moieties in a previously undiagnosed duplex kidney [13] (Fig. 2), and for demonstrating the exact anatomy of fusion anomalies, such as a crossed, fused, ectopic kidney and horseshoe kidney [4, 6].<br> <br><br><img alt="http://www.ncbi.nlm.nih.gov/corecgi/tileshop/tileshop.fcgi?p=PMC3&id=616652&s=23&r=1&c=1" src="http://www.ncbi.nlm.nih.gov/corecgi/tileshop/tileshop.fcgi?p=PMC3&id=616652&s=23&r=1&c=1"><br> <br><br>Fig. 1<br>Magnetic resonance image: coronal T2 sequence in a 6-month-old girl with autosomal dominant polycystic kidney disease showing multiples high-signal cysts throughout both kidneys<br><br><br><img alt="http://www.ncbi.nlm.nih.gov/corecgi/tileshop/tileshop.fcgi?p=PMC3&id=616656&s=23&r=1&c=1" src="http://www.ncbi.nlm.nih.gov/corecgi/tileshop/tileshop.fcgi?p=PMC3&id=616656&s=23&r=1&c=1"><br> <br> Fig. 2<br>Magnetic resonance imaging: an unexpected right-sided duplex kidney in a 7-month-old girl whose anatomy could not be delineated by ultrasound, with a tiny lower moiety that is almost hidden by the dilated upper moiety (arrow)<br> <br><br><br> CT arteriography (CTA) is sometimes performed in instances of known horseshoe kidney when surgery is being planned. This is to optimally delineate the multiple vessels that often supply these kidneys before surgery is undertaken. Pelviureteric junction obstruction can usually be diagnosed adequately on US, but a crossing vessel may be demonstrated by MRI (Fig. 3) [14], which cannot be visualized by US; in very gross hydronephrosis, MRI may give a better demonstration of the anatomy (Fig. 4).<br> <br><br><a href="http://www.ncbi.nlm.nih.gov/corecgi/tileshop/tileshop.fcgi?p=PMC3&id=616660&s=23&r=1&c=1" target="_blank">http://www.ncbi.nlm.nih.gov/corecgi/tileshop/tileshop.fcgi?p=PMC3&id=616660&s=23&r=1&c=1</a><br> <br><br>Fig. 3<br>Magnetic resonance imaging: a 9-year-old boy with right-sided flank pain with a reconstructed postcontrast image showing an inferior pole "crossing" vessel (artery) (arrow) causing right-sided hydronephrosis<br> <br><br><a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2991216/bin/467_2010_1645_Fig4_HTML.jpg" target="_blank">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2991216/bin/467_2010_1645_Fig4_HTML.jpg</a><br><br>Fig. 4<br> Magnetic resonance imaging: T2-weighted sequence demonstrating the extent of bilateral pelviureteric junction obstruction, nondilation of ureters, and normal bladder, confirming the obstruction to be at the renal pelvis on both sides<br> <br><br>Very complex urogenital anomalies, such as cloacal anomalies in female patients, are usually imaged by US and fluoroscopy in the first instance, but further cross-sectional imaging is invariably required. MRI may offer satisfactory depiction of the anatomy, but frequently, the workup has to occur very soon after birth so that an intermediate management plan can be made before definite surgery can be performed when the infant is older. In this situation, MRI is rarely able to offer sufficient spatial resolution to allow full understanding of the anatomy in these very small patients. In a few very select cases, CT, with a combined distal loopogram and micturating cystogram performed at the time of the scan, as well as contrast intravenously with the scan delayed to excretory phase, can offer exceptional 3D visualization of the entire urogenital tract (Fig. 5). There is little value in a conventional CT alone in these cases, and the routine use of CT is absolutely not advocated.<br> Fig. 5<br> <br>Fig. 5<br>Computed tomography: Reconstructed 3D images showing the complicated anatomy of the urogenital tract in a 3-month-old girl with a cloacal anomaly; the entire urogenital system is demonstrated in one study<br> Infection<br>Most commonly, infection of the lower urinary tract presents clinically and is treated empirically. However, in a few more complicated cases, US will be performed to look for complications, such as abscess formation or pyelonephritis, within the kidneys and for the presence of underlying contributory factors, such as stone disease or previously undiagnosed structural anomalies. In most instances, US is able to resolve these clinical issues and is clearly the modality of choice for assessing infection (both in the acute stage and at follow-up). If US cannot answer the diagnostic question, further cross-sectional imaging may sometimes be useful. In the acute setting, with a very ill patient and suspected sepsis related to the urinary tract, CT may add further information regarding, for example, abscess rupture or retroperitoneal fluid (or pus) collections (Fig. 6). CT is useful in showing calcification and extrarenal complications in xanthogranulomatous pyelonephritis, if this has not already been confirmed by US. MRI may be of value after the acute episode for demonstrating underlying structural anomalies if these have not been determined by US.<br> Fig. 6<br> <br>Fig. 6<br>Computed tomography: a 15-year-old girl with chronic renal failure on peritoneal dialysis with recent onset of abdominal pain and signs of sepsis. The shriveled right kidney (arrow) is the expected size of both kidneys, but the left kidney shows acute (more ...)<br> Trauma<br>In the acute setting of trauma in children, US is once again the first-line technique in the emergency room. US can quickly demonstrate whether the kidney is still vascularized, if there is physical damage (fracture, laceration, avulsion) of the kidney, and provide some information regarding surrounding complications. If the trauma is believed to be confined solely to the kidney and the child is stable, it may not be necessary to proceed to any further immediate imaging. However, it is frequently the case that these patients have been involved in a complex trauma, and as such, multiple injuries may have occurred. In most cases, major renal injuries are associated with injuries to other major organs, and renal trauma occurs in 8–10% of patients with significant blunt or penetrating abdominal trauma [15, 16]. In this instance, CT is usually performed straight from the emergency room. CT will demonstrate direct trauma to the kidney and to any other intra-abdominal organs and may show retroperitoneal injuries or complications better than US [17]. Typical findings include contusions (shown as ill-defined or sometimes sharply marginated areas of reduced enhancement and excretion), nonexpanding subcapsular hematomas (appearing as a hyperattenuating fluid collection between the renal parenchyma and the renal capsule, at times deforming the underlying kidney), perinephric hematomas (an ill-defined, hyperattenuating fluid collection located between the Gerota fascia and the renal parenchyma), renal lacerations (jagged or linear parenchymal disruptions that can contain fresh or clotted blood), renal lacerations with collecting system involvement (which frequently produce extravasation of urine or contrast agent), and renal segmental infarction appearing as well-delineated, linear or wedge-shaped, often multifocal and nonenhancing areas that extend through the parenchyma in a radial or segmental orientation. Thrombosis, dissection, and laceration of segmental renal arteries are primary causes of segmental infarctions, and such infarctions are frequently associated with other renal injuries. Severe injuries include a shattered or devascularized kidney (which appears nonenhancing, with CTA showing a blind-ending renal artery), ureteropelvic junction (UPJ) avulsions, and complete laceration or thrombosis of the main renal artery or vein. CT of the urinary tract should usually be obtained in severe pelvic trauma prior to surgery. MRI has no indication in the acute setting of trauma. Very occasionally, it may have some value in the follow-up of renal trauma, but in children, this would usually be by US.<br> Vascular<br>Both CT and MRI can give excellent information with respect to normal vascular supply to the kidneys and wider urinary tract and in the context of vasculopathies. US would be the first-line investigation, but if anatomical delineation is required – for example, for surgical planning – then CT or MRI can be performed at the surgeon's and radiologist's discretion. CT will give better spatial resolution with the CT scan being performed in the arterial phase and allows 3D reconstruction of the vascular tree but at a considerable radiation dose. The clinician must be sure that sufficient information cannot be obtained by another method before proceeding. MRI is increasingly able to offer detailed vascular information with no radiation dose, and this should be considered as an entirely viable alternative in cooperative children (Fig. 7). At the time of writing this article, conventional angiography remained the gold standard for demonstrating subtle abnormalities in the renal vasculature, but it is both invasive and carries a relatively high radiation dose. However, in the diagnosis of subtle renal artery stenosis, for small arteriovenous malformations of the kidney, and for tiny aneurysms such as in polyarteritis nodosa or Wegner's granulomatosis, it is still the investigation of choice. It is no longer indicated in the diagnosis or workup of renal tumors prior to surgery.<br> Fig. 7<br> <br>Fig. 7<br>Magnetic resonance imaging: gadolinium-enhanced MR angiography demonstrating arterial anatomy in an 11-year-old girl with a known horseshoe kidney<br>MRI plays an important role in the workup of children waiting for renal transplant. Whereas initial assessment of their native vessels [aorta, inferior vena cava (IVC), iliac and femoral vessels] may be by US, proceeding to MRI may be necessary if the US is technically inadequate (due to the presence of bowel gas or other structures) or if it is indeterminate. Conventionally, gadolinium contrast agents have been given to best illustrate the vessels, but in patients who are known to be in renal failure (hence the need for transplant), gadolinium is no longer given due to the risk of NSF. In these patients, MR angiography (MRA) is still achieved using tailored sequences [true fast imaging with steady-state precession (FISP) and time-of-flight (TOF) sequences], which obviate the need for intravenously administered contrast. It is also helpful in patients who have had renal transplant and in whom the anatomy may be difficult to demonstrate by US.<br> Calcification in the urinary tract<br>Stone disease and calcification relating to the urinary tract in children deserves special mention, as its imaging management differs to that in adults. US is a highly effective imaging tool when looking for calcification (nephrocalcinosis) and calculi within the kidney. Subtle nephrocalcinosis may be demonstrated by using a high-resolution probe when it has not been demonstrated by a conventional linear probe, and the pediatric sonographer should always use both techniques if nephrocalcinosis is being sought. There is no indication to use CT or MRI when diagnosing nephrocalcinosis in children unless there is a specific concern regarding the additional presence of calculi, which may be difficult to delineate by US in the presence of particularly florid nephrocalcinosis.<br> Children's smaller body habitus allows good visualization of even tiny calculi within the collecting system, parenchyma, and bladder. If the ureters are dilated, US may also show calculi in the upper and lower third of the ureter but remains consistently poor at demonstrating calculi in the middle third of the ureter. In a select group of patients, it may be appropriate to proceed to CT, but CT should not be routine imaging for stone disease children. It is, however, highly sensitive (97%) and specific (96%) for urinary tract calculi and is undoubtedly an excellent technique in this respect [18]. Children who may benefit from CT include those with a high body mass index (BMI) in whom US cannot sufficiently penetrate soft tissues for adequate visualization, those in whom US is not tolerated, children with severe scoliosis in whom there is not a suitable acoustic window to access the kidneys, children who continue to have symptoms of stone disease in which no calculi have been demonstrated by repeated US, and children in whom a history of stone disease is known but symptoms are out of proportion to US findings. It must be remembered that many children will have recurrent calculi, and it is therefore highly undesirable to perform a high radiation dose examination on every occasion for an underlying benign condition with a normal life expectancy. If CT is requested, it should be performed with a low-dose technique and without intravenously administered contrast (which would obscure any calcific focus) [19, 20].<br> Neoplastic<br>Many tumors may involve the urinary tract depending on the organ of origin and the age of the child. Renal malignancies represent about 6% of cancer diagnoses in children <15 years of age. Wilms tumor is by far the most common of the renal tumors, representing approximately 95% of cases overall and 96% in children <5 years (Fig. 8).<br> Fig. 8<br> <br>Fig. 8<br>Computed tomography showing the extent of a large, left-sided Wilms tumor in a 2-year-old girl with thrombus extending the full length of the inferior vena cava (IVC) and into the right atrium (between arrows)<br> In all instances, the first imaging should be by US, which can confirm the presence of the mass and can usually (but not always) determine the organ of origin. However, further cross-sectional imaging is indicated for further anatomical delineation, information on tissues characteristics, and to establish staging. In centers with pediatric MRI, this is absolutely the imaging modality of choice: it provides a wealth of information regarding the tumor itself, provides a base-line for follow-up (thus avoiding repeated CTs), and can provide accurate staging. Sequences will typically include T1- and T2-weighted sequences, short-tau inversion recovery (STIR) sequences, apparent diffusion coefficient (ADC) sequences, and postgadolinium contrast-enhanced 3D fast low-angle shot (FLASH) sequences in a combination of axial and coronal planes. ADC sequences are relatively new in abdominal imaging (but have been used extensively in the brain for some time). These sequences give information about how easily water can diffuse in and between cells; thus, a tumor with densely packed cells will return low signal intensity and will appear dark on this MRI sequence. If it, or a part of it, is undergoing necrosis, it will return a higher (whiter) signal intensity. This is especially useful when monitoring a tumor to assess its response to treatment such as chemotherapy and to follow-up for recurrence. MRI can give information as to IVC and renal vein patency (Fig. 8) if this has not already been determined with certainty by US. Detailed MRA may also be performed, if necessary, to allow surgical planning. In centers with no access to MRI, then CT still provides good information, recognizing that it cannot supply tissue-specific information as MRI and that it incurs a heavy radiation burden. Follow-up of treated tumors should be by US where possible, although many cancer protocols determine that MRI (or CT) should be performed at specifically determined intervals.<br> Renal functional MRI<br>US, CT, and MRI all provide good anatomic images [21] of the kidney and urinary tract, but MRI (both in adults and children) has developed very rapidly over recent years and has great potential in the near future to change the way the urinary tract is imaged after the initial US. Uniquely, MRI can also give functional information on the kidneys [4, 22], unlike the other cross-sectional modalities. Traditionally, nuclear medicine studies have been employed for this purpose, but they give poor spatial resolution and provide only relative information rather than absolute values with respect to renal function. MRI is therefore alone in being able to give both anatomical and functional information. Functional renal imaging techniques such as contrast-enhanced MR renography [23, 24], and unenhanced techniques such as diffusion-weighted imaging (DWI) and blood-oxygen-level-dependent (BOLD) imaging, have shown considerable promise in evaluating renal function in health and disease. Whereas this is a relatively new area in clinical terms, it is rapidly advancing and crossing over from being a research technique to offering a real clinical alternative to existing techniques for assessing renal function [25]. Technically, it is no different performing this in children than in adults, but – as with all MRI in children – the rate-limiting step for the technique is the child's ability to remain completely still through a long scan without the need for general anesthesia. It is likely, therefore, that it will be incorporated into the repertoire of renal imaging for older children in the reasonably near future but probably not for younger children unless there is a very specific indication.<br> <br> Contrast-enhanced MR renography:<br> The basis of the technique relies on dynamic contrast enhancement of the kidneys using MRI to monitor transit of contrast material, typically a gadolinium chelate, through the renal cortex, the medulla, and the collecting system. Most gadolinium contrast agents are cleared by glomerular filtration and pass through capillaries and renal tubules, causing renal tissue signal intensity to increase. By analyzing renal tissue enhancement as a function of time, clinically important single-kidney parameters such as renal blood flow [24], GFR, and cortical and medullary blood volumes can be determined and can be plotted graphically to generate various functional parameter curves. Split renal function can be calculated [25]. Current indications in adult imaging include functional imaging in renal artery stenosis and assessing potential allograft dysfunction in the early postoperative period, potentially avoiding the need for biopsy to distinguish between acute tubular necrosis and acute rejection. It should be noted that as this technique relies on administration of gadolinium as a contrast agent, it is not suitable for patients with renal failure, due to the risk of NSF.<br> Diffusion-weighted MRI:<br> DWI has traditionally been used in imaging stroke victims, as it is very sensitive in detecting acute ischemia. The ADC calculation can be used in vivo for quantifying the combined effects of capillary perfusion and diffusion. This technique was referred to above in tumor assessment; however, it also has applications in assessing renal insufficiency with studies showing good correlation between GFR and ADC values, highlighting the potential role for evaluating renal dysfunction in native kidneys. DWI also appears to have a future role in renal allograft evaluation and renal artery stenosis.<br> Blood-oxygen-level-dependent (BOLD) MRI:<br> BOLD MRI can be used for noninvasive but direct measurement of renal oxygenation [26]. It exploits the paramagnetic effect of deoxyhemoglobin for acquisition of images sensitive to local oxygen concentration. Again, it has application in the context of renal artery stenosis and renal allograft dysfunction but also in diabetic nephropathy<br> <br><br><br>Conclusion<br>Imaging of the urinary tract in children relies on US as the first-line imaging modality; however, MRI has an invaluable role to play, with CT playing a lesser part. Considerations specific to children revolve around radiation dose issues with CT and the need (or not) for a general anesthetic in MRI. It is crucial that the clinical question is clearly established and the study chosen is tailored to the specific child after discussion between the clinician and the radiologist. MRI is the technique of choice for imaging tumors and congenital anomalies when these cannot be satisfactorily delineated by US, and it should generally be regarded as an excellent advanced problem-solving technique. CT is indicated in multisystem trauma and in some children with renal calculi. Functional MRI is rapidly developing in the adult world, and some applications are becoming relevant in children. Center-specific expertise may lead to a certain study being performed in one setting versus a different study in another. This factor may be an important consideration in choosing which modality is appropriate. For elective imaging, referral of the patient to a center with pediatric expertise for superior study should be considered, if it is a realistic option. Ultimately, it is the collaboration between the nephrologist and the radiologist that will lead to the best imaging modality for each patient.<br> <br><br><br>Self-assessment questions<br>(Answers appear following the reference list)<br><br> Which examination has the highest sensitivity for detecting renal-tract calculi in children?<br> CT with contrast enhancement<br> CT without contrast enhancement<br> CT with contrast enhancement and delayed images to show the level of obstruction<br> MRI using a T1-weighted sequence<br> US in the hands of an experienced operator who is aware of the clinical history<br> Which patient cannot have an MRI examination?<br> A child with claustrophobia<br> A child with end-stage renal failure in whom gadolinium is therefore contraindicated<br> A baby 5 days old who is on a ventilator<br> A child who had a CT the previous day<br> A child with a pacemaker<br> Which series has the highest radiation dose?<br> Enhanced CT of the abdomen and pelvis with a delayed series<br> Enhanced CT of the abdomen and pelvis without a delayed series<br> MRI with T1, T2, post-gadolinium TI and ADC sequences, in coronal and axial planes, of the abdomen and pelvis, with a delayed series<br> Unenhanced CT of the abdomen only, followed up by unenhanced CT of the abdomen (only) 4 weeks later<br> MRI of the abdomen and pelvis followed up by CT of the abdomen and pelvis 6 weeks later<br> Which of the following is poorly demonstrated on MRI?<br> Urine<br> Blood<br> Calcium<br> Renal medulla<br> Renal cortex<br> Regarding NSF, which of the following is false?<br> NSF does not occur in healthy patients with normal renal function<br> The risk of NSF is increased in patients with a low GFR<br> The relationship between NSF and MRI contrast agents has only been recognized in the last 5 years<br> The risk of NSF is not reduced by dialysis<br> All types of gadolinium contrast agents pose a similar risk of NSF in patient with renal failure<br> <br>Footnotes<br>Answers<br>1. b. CT without contrast enhancement has the highest sensitivity for detecting calculi but carries a heavy radiation dose penalty. It is therefore NOT the first examination of choice in children. US should always be used in the first instance, and CT only when there is still diagnostic difficultly. Contrast may obscure the presence of stones, as it is also of high density (white).<br> 2. e. A pacemaker is generally considered an absolute contraindication to MRI, as it may become deprogrammed or pulse erratically in the strong magnetic field. (In absolutely exceptional cases, a clinical decision can be made to turn some pacemakers off or turn them to fixed-pulse mode). A child with claustrophobia may have MRI under sedation or general anesthetic if clinically indicated. Modern sequences often obviate the need for gadolinium in patients with end-stage renal failure. The age of the patient and the previous imaging history would not affect the clinical decision to request MRI.<br> 3. a. This series involves scanning through the abdomen and pelvis on two occasions. The absence or presence of intravenously administered contrast agent makes no difference to radiation dose. MRI does not involve radiation.<br> 4. c. Calcium (such as in renal calculi) contains no water and therefore does not have protons that are easily influenced by magnetic fields, and as such, it returns almost no signal (signal void) on all sequences and is difficult to detect.<br> 5. e. Not all gadolinium contrast agents are the same. Omniscan and Magnevist are thought to pose increased risk due to the chelate to which the gadolinium is attached, with these compounds being more likely to release free gadolinium ions into the body. Dotarem is currently considered to be the least likely agent to allow release of free gadolinium ions.<br> <br><br><br>References<br>1. Ambrose J, Hounsfield G. Computerized transverse axial tomography. Br J Radiol. 1973;46:148–149. doi: 10.1259/0007-1285-46-552-1023. [PubMed] [Cross Ref]<br>2. Hounsfield GN. Computerized transverse axial scanning (tomography). 1. Description of system. Br J Radiol. 1973;46:1016–1022. doi: 10.1259/0007-1285-46-552-1016. [PubMed] [Cross Ref]<br> 3. Hounsfield GN. Computed medical imaging. Science. 1980;210:22–28. doi: 10.1126/science.6997993. [PubMed] [Cross Ref]<br>4. Grattan-Smith JD, Jones RA. MR urography in children. Pediatr Radiol. 2006;36:1229–1132. doi: 10.1007/s00247-006-0222-2. [Cross Ref]<br> 5. Kanal E, Barkovich AJ, Bell C, Borgstede JP, Bradley WG, Jr, Froelich JW, Gilk T, Gimbel JR, Gosbee J, Kuhni-Kaminski E, Lester JW, Jr, Nyenhuis J, Parag Y, Schaefer DJ, Sebek-Scoumis EA, Weinreb J, Zaremba LA, Wilcox P, Lucey L, Sass N. ACR guidance document for safe MR practices: 2007. AJR Am J Roentgenol. 2007;188:1447–1474. doi: 10.2214/AJR.06.1616. [PubMed] [Cross Ref]<br> 6. Grattan-Smith JD, Little SB, Jones RA. MR urography in children: how we do it. Pediatr Radiol. 2008;38(Suppl 1):S3–S17. doi: 10.1007/s00247-007-0618-7. [PubMed] [Cross Ref]<br>7. Grattan-Smith JD, Jones RA. Magnetic resonance urography in children. Magn Reson Imaging Clin N Am. 2008;16:515–531. doi: 10.1016/j.mric.2008.04.002. [PubMed] [Cross Ref]<br> 8. Grattan-Smith JD. MR urography: anatomy and physiology. Pediatr Radiol. 2008;38(Suppl 2):S275–S280. doi: 10.1007/s00247-008-0793-1. [PubMed] [Cross Ref]<br>9. Grattan-Smith JD, Jones RA. MR urography: technique and results for the evaluation of urinary obstruction in the pediatric population. Magn Reson Imaging Clin N Am. 2008;16:643–660. doi: 10.1016/j.mric.2008.07.003. [PubMed] [Cross Ref]<br> 10. Greenbaum LA. Renal dysplasia and MRI: a clinician's perspective. Pediatr Radiol. 2008;38(Suppl 1):S70–S75. doi: 10.1007/s00247-007-0586-y. [PubMed] [Cross Ref]<br>11. Little SB, Jones RA, Grattan-Smith JD. Evaluation of UPJ obstruction before and after pyeloplasty using MR urography. Pediatr Radiol. 2008;38(Suppl 1):S106–S124. doi: 10.1007/s00247-007-0669-9. [PubMed] [Cross Ref]<br> 12. Cerwinka WH, Damien Grattan-Smith J, Kirsch AJ (2008) Magnetic resonance urography in pediatric urology. J Pediatr Urol 4:74–82, quiz 82-83.<br>13. Lipson JA, Coakley FV, Baskin LS, Yeh BM. Subtle renal duplication as an unrecognized cause of childhood incontinence: diagnosis by magnetic resonance urography. J Pediatr Urol. 2008;4:398–400. doi: 10.1016/j.jpurol.2008.01.213. [PMC free article] [PubMed] [Cross Ref]<br> 14. Calder AD, Hiorns MP, Abhyankar A, Mushtaq I, Olsen OE. Contrast-enhanced magnetic resonance angiography for the detection of crossing renal vessels in children with symptomatic ureteropelvic junction obstruction: comparison with operative findings. Pediatr Radiol. 2007;37:356–361. doi: 10.1007/s00247-007-0416-2. [PubMed] [Cross Ref]<br> 15. Kawashima A, Sandler CM, Corl FM, West OC, Tamm EP, Fishman EK, Goldman SM. Imaging of renal trauma: a comprehensive review. Radiographics. 2001;21:557–574. [PubMed]<br>16. McAninch J. Renal injuries. In: Gillenwater J, Grayhack J, Howards S, Duckett J, editors. Adult and pediatric urologyMosby. Mo: St Louis; 1996. pp. 539–553.<br> 17. Lee YJ, Oh SN, Rha SE, Byun JY. Renal trauma. Radiol Clin North Am. 2007;45:581–592. doi: 10.1016/j.rcl.2007.04.004. [PubMed] [Cross Ref]<br>18. Smith RC, Verga M, McCarthy S, Rosenfield AT. Diagnosis of acute flank pain: value of unenhanced helical CT. AJR Am J Roentgenol. 1996;166:97–101. [PubMed]<br> 19. Kalra MK, Maher MM, D'Souza RV, Rizzo S, Halpern EF, Blake MA, Saini S. Detection of urinary tract stones at low-radiation-dose CT with z-axis automatic tube current modulation: phantom and clinical studies. Radiology. 2005;235:523–529. doi: 10.1148/radiol.2352040331. [PubMed] [Cross Ref]<br> 20. Memarsadeghi M, Heinz-Peer G, Helbich TH, Schaefer-Prokop C, Kramer G, Scharitzer M, Prokop M. Unenhanced multi-detector row CT in patients suspected of having urinary stone disease: effect of section width on diagnosis. Radiology. 2005;235:530–536. doi: 10.1148/radiol.2352040448. [PubMed] [Cross Ref]<br> 21. Kirsch AJ, Grattan-Smith JD, Molitierno JA., Jr The role of magnetic resonance imaging in pediatric urology. Curr Opin Urol. 2006;16:283–290. doi: 10.1097/01.mou.0000232051.66718.34. [PubMed] [Cross Ref]<br>22. Rohrschneider WK, Haufe S, Clorius JH, Troger J. MR to assess renal function in children. Eur Radiol. 2003;13:1033–1045. doi: 10.1007/s00330-003-2005-6. [PubMed] [Cross Ref]<br> 23. Jones RA, Schmotzer B, Little SB, Grattan-Smith JD. MRU post-processing. Pediatr Radiol. 2008;38(Suppl 1):S18–S27. doi: 10.1007/s00247-007-0616-9. [PubMed] [Cross Ref]<br>24. Martin DR, Sharma P, Salman K, Jones RA, Grattan-Smith JD, Mao H, Lauenstein TC, Burrow BK, Tudorascu DL, Votaw JR. Individual kidney blood flow measured with contrast-enhanced first-pass perfusion MR imaging. Radiology. 2008;246:241–248. [PubMed]<br> 25. Chandarana H, Lee VS. Renal functional MRI: Are we ready for clinical application? AJR Am J Roentgenol. 2009;192:1550–1557. doi: 10.2214/AJR.09.2390. [PubMed] [Cross Ref]<br>26. Hofmann L, Simon-Zoula S, Nowak A, Giger A, Vock P, Boesch C, Frey FJ, Vogt B. BOLD-MRI for the assessment of renal oxygenation in humans: acute effect of nephrotoxic xenobiotics. Kidney Int. 2006;70:144–150. doi: 10.1038/sj.ki.5000418. [PubMed] [Cross Ref]<br> <br><br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-46924868462172334542011-11-27T15:22:00.000-08:002011-11-27T15:23:12.747-08:00research kidney<br><div class="gmail_quote">XGP is a rare form of chronic pyelonephritis and probably represents<br> an abnormal immune response to bacterial infection.<br> <br> <br> <br> urinary tract obstruction -- nephrolithiasis<br> <br> <br> xanthogranulomatoese Pyelonephritis<br> xanthogranulomatous Pyelonephritis<br> <a href="http://en.wikipedia.org/wiki/Xanthogranulomatous_pyelonephritis" target="_blank">http://en.wikipedia.org/wiki/Xanthogranulomatous_pyelonephritis</a><br> <br> <a href="http://www.ncbi.nlm.nih.gov/pubmed/19114330" target="_blank">http://www.ncbi.nlm.nih.gov/pubmed/19114330</a><br> Xanthogranulomatous pyelonephritis successfully treated with antibiotics only.<br> <br> <a href="http://www.patient.co.uk/doctor/Pyelonephritis.htm" target="_blank">http://www.patient.co.uk/doctor/Pyelonephritis.htm</a><br> <br> <a href="http://www.google.de/search?q=antibiotica+Pyelonephritis" target="_blank">http://www.google.de/search?q=antibiotica+Pyelonephritis</a><br> <br> Ciprofloxacin is a broad-spectrum antibiotic that is active against<br> both Gram-positive and Gram-negative bacteria<br> <br> <br> Urine typically contains both leukocytes and bacteria. The pH is often<br> basic because Proteus mirabilis is a urease-producing organism. The<br> erythrocyte sedimentation rate is frequently elevated.<br> <br> <br> XGP and renal cell carcinoma have even been observed in the same specimen.<br> <br> <br> interesting reading<br> <a href="http://ndt.oxfordjournals.org/content/22/11/3344.full" target="_blank">http://ndt.oxfordjournals.org/content/22/11/3344.full</a><br> XGP typically presents with non-specific symptoms [5] and laboratory<br> abnormalities [6] including leucocytosis, increased blood urea<br> nitrogen and creatinine levels. Typical features that may be found on<br> CT scan include enlarged kidneys with multiple low-density areas<br> associated with hydronephrosis, and indications of perirenal<br> extension. In native kidneys, the cases with diffuse XGP require total<br> nephrectomy. Partial nephrectomy or medical therapy with antibiotics<br> could be considered for focal disease.<br> <br> <br> <a href="http://en.wikipedia.org/wiki/Malakoplakia" target="_blank">http://en.wikipedia.org/wiki/Malakoplakia</a> >> antibiotics<br> <a href="http://de.wikipedia.org/wiki/Malakoplakie" target="_blank">http://de.wikipedia.org/wiki/Malakoplakie</a><br> <br> <br> <br> Bei der akuten Pyelonephritis ist die Antibiotikagabe über mindestens<br> 10 Tage[11] zwingend erforderlich. Schwere Infektionen sollten mit<br> Fluorchinolonen, z. B. Ciprofloxacin, oder mit<br> Breitspektrum-Cephalosporinen, auch in Kombination mit<br> Aminoglykosiden, behandelt werden.[11] Zur Anwendung kommen außerdem<br> Amoxicillin, Piperacillin mit Tazobactam, sowie Imipenem. Wenn möglich<br> erfolgt die Therapie nach Erreger- und Resistenzbestimmung.<br> <br> Die perorale Gabe ist zu bevorzugen, wenn es der klinische Zustand des<br> Patienten erlaubt. In einer Studie mit 141 Patienten war die<br> intravenöse Gabe von Ciprofloxacin der oralen nicht überlegen<br> </div><br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-52950414185554799152011-08-25T03:37:00.001-07:002011-08-25T03:37:42.763-07:00GMO Killer T-Cells FEVER -Leukemia Cure<br>TWO ARTICLES ON A RECENT CANCER TREATMENT BREAKTHROUGH<br><br><br><i>Genetically engineered cell offers possible cancer-killing breakthrough</i><br><font size="1">Published: Thursday, Aug. 11, 2011 3:29 p.m. MDT<br>By Lois M. Collins, Deseret News</font><br> <br>Research that changes a type of white blood cell so it's a weapon against cancer cells is being hailed by experts as a potential breakthrough in cancer research.<br><br>Scientists at the University of Pennsylvania turned T cells into cancer cell killers in a common type of leukemia using genetic engineering. Experts say it may be possible to engineer T cells to kill other types of cancer, including blood, breast and colon, as well.<br> <br>The research, part of a very small clinical trial involving just three patients who had advanced cases of the chronic lymphocytic leukemia, is published online this week in the New England Journal of Medicine and also in Science Translational Medicine.<br> <br>Two of the patients have been cancer-free for more than a year, while the other experienced improvements. The plan now, given such promising results, is to expand the trial and treat other patients, then follow them to see long-term effects, the researchers said. They also hope to test it in other, perhaps more aggressive cancers.<br> <br>"This is a huge accomplishment — huge," Dr. Lee M. Nadler, dean for clinical and translational research at Harvard Medical School, told the Los Angeles Times. Nadler is credited with finding the molecule on cancer cells that the genetically engineered T cells attack.<br> <br>The researchers said they added instructions to a virus for creating a molecule that binds to leukemia cells and tells the T cells to destroy them. In the clinical trial, they drew blood from the three patients who had chronic lymphocytic leukemia, infected the T cells with the virus and reinjected the blood back into the patients. The engineered T cells multiplied rapidly and killed the cancer cells, then remained for months. "They even produced dormant 'memory' T cells that might spring back to life if the cancer was to return," wrote the Times' Eryn Brown.<br> <br>A CBS/Associated Press story said the therapy "resulted in armies of serial killer cells that targeted and destroyed cancer cells, even new cancer cells as they emerged. T cells typically attack viruses that way," but it noted study author <br> <br><img alt="http://www.stopovariancancer.com/gifs/carl_june.jpg" src="http://www.stopovariancancer.com/gifs/carl_june.jpg"><br><br>Dr. Carl June, professor of pathology and laboratory medicine at the University of Pennsylvania, said it's the first time it has been turned against cancer.<br> <br>The study describes what happened after the engineered T cells were reinjected in the patient. After 13 days, "the patient began having chills and low-grade fevers associated with grade 2 fatigue. Over the next five days, the chills intensified and his temperature escalated to 102.5 degrees," they wrote, noting he suffered a variety of miserable digestive symptoms, including nausea and diarrhea. But within slightly more than three weeks of having the modified cells reintroduced, "there was no evidence of (the leukemia) in the bone marrow." Ten months out, when the study was written, that patient remained cancer free.<br> <br>The researcher believe that each engineered T cell killed 1,000 cancer cells or more. They noted that the engineered cells remained for six months at high levels in the blood and bone marrow and while there they continued to express the chimeric antigen receptor.<br> <br>Bone marrow transplants have been the best hope for patients suffering from chronic lymphocytic leukemia and have been the only hope for an actual cure. But the side effects have been potentially serious, even fatal, including infections and liver and lung damage. About 20 percent of those who receive such a transplant may die of complications of those side effects, rather than the leukemia that was being treated.<br> <br>Dr. David Porter, director of the blood and marrow transplant program at the Hospital of the University of Pennsylvania and a study co-author, told the Los Angeles Times that earlier efforts to modify T cells have been disappointing. It was different this time because the researchers added more instructions to the virus telling the cells to "multiply, survive and attack more aggressively."<br> <br>The National Cancer Institute describes leukemia as "cancer that starts in blood-forming tissue such as the bone marrow and causes large numbers of blood cells to be produced and enter the bloodstream." It says 44,000 new cases are diagnosed each year and about 22,000 people die from the disease. The institute also offers an online guide to the disease and its treatments.<br> <br>The Mayo Clinic says that the form of leukemia called chronic lymphocytic leukemia affects a group of white blood cells called lymphocytes, which help the body fight infection.<br><br>One of the patients, who asked not to be identified, issued a statement through the university. He said chemotherapy worked for years, but it stopped. Now, he wrote, "I'm healthy and still in remission. I know this may not be a permanent condition, but I decided to declare victory and assume that I had won."<br> <br><br><img alt="http://www.genetherapyreview.com/images/stories/lentiviral_vector.png" src="http://www.genetherapyreview.com/images/stories/lentiviral_vector.png"><br><br><br>Genetically Modified "Serial Killer" T Cells Obliterate Tumors in Patients with Chronic Lymphocytic Leukemia, Penn Researchers Report<br> <br>(PHILADELPHIA) -- In a cancer treatment breakthrough 20 years in the making, researchers from the University of Pennsylvania's Abramson Cancer Center and Perelman School of Medicine have shown sustained remissions of up to a year among a small group of advanced chronic lymphocytic leukemia (CLL) patients treated with genetically engineered versions of their own T cells. The protocol, which involves removing patients' cells and modifying them in Penn's vaccine production facility, then infusing the new cells back into the patient's body following chemotherapy, provides a tumor-attack roadmap for the treatment of other cancers including those of the lung and ovaries and myeloma and melanoma. The findings, published simultaneously today in the New England Journal of Medicine and Science Translational Medicine, are the first demonstration of the use of gene transfer therapy to create "serial killer" T cells aimed at cancerous tumors.<br> <br>"Within three weeks, the tumors had been blown away, in a way that was much more violent than we ever expected," said senior author Carl June, MD, director of Translational Research and a professor of Pathology and Laboratory Medicine in the Abramson Cancer Center, who led the work. "It worked much better than we thought it would."<br> <br>The results of the pilot trial of three patients are a stark contrast to existing therapies for CLL. The patients involved in the new study had few other treatment options. The only potential curative therapy would have involved a bone marrow transplant, a procedure which requires a lengthy hospitalization and carries at least a 20 percent mortality risk -- and even then offers only about a 50 percent chance of a cure, at best.<br> <br>"Most of what I do is treat patients with no other options, with a very, very risky therapy with the intent to cure them," says co-principal investigator David Porter, MD, professor of Medicine and director of Blood and Marrow Transplantation. "This approach has the potential to do the same thing, but in a safer manner."<br> <br>Secret Ingredients<br><br>June thinks there were several "secret ingredients" that made the difference between the lackluster results that have been seen in previous trials with modified T cells and the remarkable responses seen in the current trial. The details of the new cancer immunotherapy are detailed in Science Translational Medicine.<br> <br>After removing the patients' cells, the team reprogrammed them to attack tumor cells by genetically modifying them using a lentivirus vector. The vector encodes an antibody-like protein, called a chimeric antigen receptor (CAR), which is expressed on the surface of the T cells and designed to bind to a protein called CD19.<br> <br>Once the T cells start expressing the CAR, they focus all of their killing activity on cells that express CD19, which includes CLL tumor cells and normal B cells. All of the other cells in the patient that do not express CD19 are ignored by the modified T cells, which limits side effects typically experienced during standard therapies.<br> <br>The team engineered a signaling molecule into the part of the CAR that resides inside the cell. When it binds to CD19, initiating the cancer-cell death, it also tells the cell to produce cytokines that trigger other T cells to multiply -- building a bigger and bigger army until all the target cells in the tumor are destroyed.<br> <br>Serial Killers<br>"We saw at least a 1000-fold increase in the number of modified T cells in each of the patients. Drugs don't do that," June says. "In addition to an extensive capacity for self-replication, the infused T cells are serial killers. On average, each infused T cell led to the killing of thousands of tumor cells – and overall, destroyed at least two pounds of tumor in each patient."<br> <br>The importance of the T cell self-replication is illustrated in the New England Journal of Medicine paper, which describes the response of one patient, a 64-year old man. Prior to his T cell treatment, his blood and marrow were replete with tumor cells. For the first two weeks after treatment, nothing seemed to change. Then on day 14, the patient began experiencing chills, nausea, and increasing fever, among other symptoms. Tests during that time showed an enormous increase in the number of T cells in his blood that led to a tumor lysis syndrome, which occurs when a large number of cancer cells die all at once.<br> <br>By day 28, the patient had recovered from the tumor lysis syndrome –– and his blood and marrow showed no evidence of leukemia.<br><br>"This massive killing of tumor is a direct proof of principle of the concept," Porter says.<br> <br>The Penn team pioneered the use of the HIV-derived vector in a clinical trial in 2003 in which they treated HIV patients with an antisense version of the virus. That trial demonstrated the safety of the lentiviral vector used in the present work.<br> <br>The cell culture methods used in this trial reawaken T cells that have been suppressed by the leukemia and stimulate the generation of so-called "memory" T cells, which the team hopes will provide ongoing protection against recurrence. Although long-term viability of the treatment is unknown, the doctors have found evidence that months after infusion, the new cells had multiplied and were capable of continuing their seek-and-destroy mission against cancerous cells throughout the patients' bodies.<br> <br>Moving forward, the team plans to test the same CD19 CAR construct in patients with other types of CD19-positive tumors, including non-Hodgkin's lymphoma and acute lymphocytic leukemia. They also plan to study the approach in pediatric leukemia patients who have failed standard therapy. Additionally, the team has engineered a CAR vector that binds to mesothelin, a protein expressed on the surface of mesothelioma cancer cells, as well as on ovarian and pancreatic cancer cells.<br> <br>In addition to June and Porter, co-authors on the NEJM paper include Bruce Levine, Michael Kalos, and Adam Bagg, all from Penn Medicine. Michael Kalos and Bruce Levine are co-first authors on the Science Translational Medicine paper. Other co-authors include June, Porter, Sharyn Katz and Adam Bagg from Penn and Stephan Grupp the Children's Hospital of Philadelphia.<br> <br>The work was supported by the Alliance for Cancer Gene Therapy, a foundation started by Penn graduates Barbara and Edward Netter, to promote gene therapy research to treat cancer, and the Leukemia & Lymphoma Society.<br> <br> <br><br>###<br><br>Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $4 billion enterprise.<br> <br>Penn's Perelman School of Medicine is currently ranked #2 in U.S. News & World Report's survey of research-oriented medical schools and among the top 10 schools for primary care. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $507.6 million awarded in the 2010 fiscal year.<br> <br>The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania -- recognized as one of the nation's top 10 hospitals by U.S. News & World Report; Penn Presbyterian Medical Center; and Pennsylvania Hospital – the nation's first hospital, founded in 1751. Penn Medicine also includes additional patient care facilities and services throughout the Philadelphia region.<br> <br>PennMedicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2010, Penn Medicine provided $788 million to benefit our community.<br><br>Penn Medicine, Philadelphia, PA 800-789-PENN © 2011, The Trustees of the University of Pennsylvania<br> <br>Media Contact Holly Auer O: <a href="tel:215-349-5659" value="+12153495659" target="_blank">215-349-5659</a> C: <a href="tel:215-200-2313" value="+12152002313" target="_blank">215-200-2313</a><br><br>Department of Communications (Media Relations) P: <a href="tel:%28215%29%20662-2560" value="+12156622560" target="_blank">(215) 662-2560</a> F: <a href="tel:%28215%29%20349-8312" value="+12153498312" target="_blank">(215) 349-8312</a><br> <br>For the General Public <a href="tel:1-800-789-7366" value="+18007897366" target="_blank">1-800-789-7366</a> <a href="http://pennmedicine.org" target="_blank">pennmedicine.org</a> Contact upenn<br> <br><br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-81463896000717424622011-07-30T03:30:00.001-07:002011-07-30T03:30:53.997-07:00CancerWife had 15 injections of Coley's toxins but then the blog stopped<img alt="http://physpharm.ohsu.edu/faculty/PKCore/12x32vials.jpg" src="http://physpharm.ohsu.edu/faculty/PKCore/12x32vials.jpg"><img alt="http://www.placidway.com/images/679/OOH1_pic.jpg" src="http://www.placidway.com/images/679/OOH1_pic.jpg" height="160" width="200"><br> 1.5ml vial with coley's toxins <br><br><br><br><b>CancerWife had 15 injections of Coley's toxins </b><br>from 9 August 2010 to 9 September 2010<br>at <br>Oasis of Hope Hospital Paseo Playas No.19. Playas de Tijuana (aka Contreras Clinic)<br> in Mexico, $8000 or more<br><br style="color: rgb(153, 153, 153);"><font style="color: rgb(153, 153, 153);" size="1">This is a record of the blogreport until CancerHusband's blog stopped... <br></font><font style="color: rgb(153, 153, 153);" size="1">They got coley's toxins supply and now are doing it at home by themselves for no money ... and have to keep quite about it because of doctors, pharma FDA mafia.<br> </font><a style="color: rgb(153, 153, 153);" href="http://www.google.com/search?q=cancerwife.com" target="_blank">http://www.google.com/search?q=cancerwife.com</a><br> <br><img alt="http://images.wikia.com/diabetesindogs/images/4/44/3_10.JPG" src="http://images.wikia.com/diabetesindogs/images/4/44/3_10.JPG" height="120" width="596"><br> 0.3ml syringe (originally for diabetes) -- cancerwife did not use a syringe but used a drip, a port, an infusion<br> <br><br>The standard protocol starting <b>dose recommended is 0.001ml</b><br><br><br>First injection. (INFUSION actually)<br><br><b>== DOSE 0.0005ml ==<br></b><br>Coley's Toxins IV #1 - Our adventure begins <br> Submitted by CancerHusband on Mon, 08/09/2010 - 21:20 <br> <br>We had brought a large body-sized far-infrared heating pad to warm her, as well as smaller one for her chest. I kept her under blankets and turned up the room thermostat to 80F. We did this to take the edge of the chills and shakes, as well as to reduce energy requirements by the body to raise core temperature.<br> <br>1.5 hours after infusion, she began experiencing chills. We cranked up the heat, in order to fend off more extreme chills and the shakes. That worked very well. Shortly after cranking up the heat, her chills all but disappeared. Then, 45 minutes after onset of chills, her temperature reached 102.1F.<br> <br>So then, it seems that our very first infusion, at 1/2 the typical starting dose managed to induce fever! The actual time above 102.5F was probably not more than 15 minutes. So, it wasn't a very strong response, but a good response nevertheless.<br> <br>Some observations:<br><br> Her pulse peaked at 117<br> Her face was flush red<br> Her minimum blood pressure was a drop to 102/54 about an hour before the chills happened (during the pre-warming phase)<br> She felt some bone pain in the hip and some soreness in the back. These were very minor.<br> <br>Generally, we felt that our very first Coleys went as well as one could ask for. We achieved fever in the target range and there were no complications! Overall, the entire fever process took about 6 hours, after which she felt 100% back to normal.<br> <br><b>== DOSE 0.0005ml ==<br></b><br>Coley's Toxins IV #2 - Substantial fever attained! <br>Submitted by CancerHusband on Wed, 08/11/2010 - 21:46 <br><br>Today, we stuck with the same 0.0005mL CFIV dosage. We expected that there may not be any fever today because we're using the same dosage as past Monday's. If you remember, Monday's fever broke past the 102.5F barrier for only 15 minutes. Furthermore, the body is supposed to get more tolerant to Coleys so one would expect a lower fever than expected this time.<br> <br>However.... to our pleasant surprise, today's fever was a robust one. Chills began almost like clockwork at 1 hour after start of infusion (this is what the MBVax documentation also says).<br><br>Her temperature hit 102.5F at 45 minutes after onset of chills. Thereafter, the fever was long and robust. In all, it stayed above 102.5F for a full 2.5 hours. Furthermore, it stayed above 103F for over an hour, reaching a peak of 103.5F.<br> <br>One unexpected side effect today was she experienced a few minutes shortness of breath. We notified the nurse just in case. The nurse seemed to have seen this before and immediately hooked up an oxygen cannula, running at 1.5 LPM.<br> <br>Generally, we observed that she sweated quite intensely today. This may have been due to the more aggressive pre-warming (higher heat pad settings, higher room thermostat setting, more blankets). To compensate, I made sure that she consumed more oral electrolytes.<br> <br>So, it would seem that more aggressive pre-warming may potentially have contributed to a more intense generation of fever? An alternate explanation is she wasn't feeling very strong before commencing Monday's first dosage. Perhaps that would be a more apt explanation for today's higher fever (with same dosage).<br> <br>Summary: Today's was an extremely successful fever. However, we're curious why it was better than Monday's despite staying at the same dose level.<br><br><b>== DOSE 0.0005ml ==<br></b><br>Coley's Toxins IV #3 - Learning to avoid dehydration during pre-heating <br> Submitted by CancerHusband on Fri, 08/13/2010 - 21:16 <br><br>Looking back at today's treatment, we concluded that we have been too aggressive with the heating pads. In our enthusiasm to avoid the chills and shakes that Coley's induces, we've been aggressively pre-heating her to the extent that she began sweating profusely even before the fever started.<br> <br>This inadvertently led to significant dehydration, which manifested as flushing of face, low blood pressure (as low as 108/43), and requiring oxygen to alleviate shortness of breath.<br><br>The doctor had her feet raised and ordered an IV drip of Hartmann Solution to counter the dehydration and hypotension.<br> <br>She eventually stabilized and the blood pressure rose. Shortly thereafter, she was able to achieve a fever. However, the fever stayed mainly between 101 and 102F. There were only 2 extremely transient peaks where her temperature managed to exceed the 102.5F target threshold. These peaks lasted for a few minutes, dropping thereafter.<br> <br>It is our conclusion that the significant dehydration probably robbed her body of the necessary energy to mount a proper fever response today. The 2 transient peaks were indicative of her body trying to raise temperature but "running out of steam".<br> <br>After her fever peaked and died down, she was, as before, able to get up and enjoy a meal. Her appetite was good and she felt normal, except for being a little tired (The picture below is of her enjoying her post-fever dinner).<br> <br>For the next Coley's, we plan to alter strategy and go easier with the pre-heating. It'll be interesting to see if that doesn't prematurely tire her body out as much, and therefore help her achieve a higher fever.<br> <br><br><b>== DOSE 0.0005ml ==<br></b><br>Coley's Toxins IV #4 - On the right track <br>Submitted by CancerHusband on Mon, 08/16/2010 - 21:15 <br><br>She was rather tired over the weekend. The Issels doctors prescribed IV protein + Magnesium to replenish her (a CBC done on Saturday morning showed that her protein levels had dropped to 5.8 g/dL (normal minimum being 6.0). The doctor had already predicted it may happen before the CBC was done. The doctor said that drops in protein levels may happen when you have fevers. This, by the way, is one of the advantages of doing Coleys at a place that has a long legacy of doing immunotherapy.<br> <br>Anyway, the doctors think that her tiredness on Sunday was probably due to her body replenishing after the draining fevers. We decided then to stick with the same CFIV dosage (0.0005mL) and see what temperature she'll achieve with less aggressive pre-heating.<br> <br>As usual, we had our breakfast from 830-930am. However, after last week's experiences, we concluded there was no way that the Coley Fluid infusion would begin on time at around 11am (The MBVax protocol calls for 2 hours of no food prior to start of IV). Thus, I advised her to eat a good breakfast, knowing that she'll have no lunch.<br> <br>As it turns out, today's Coley's began even later. By the time we got the diluted solution hooked up to her PICC port, it was about 2:00pm. By that time, it was 5 hours after breakfast and she was already getting hungry. I started her on the oral electrolytes to keep her energy up (there's a good amount of sugar in there).<br> <br>As planned, we kept the heat pad on a lower setting and modulated other variables such as the number of blankets and room thermostat. Our guiding principle was to keep her warm but avoid making her sweat.<br><br>Things went slow and there was no indication of chills or fever for quite a while. But about 2 hours after infusion start, her hands began to feel tingly and she felt some light chills. This seemed to be a delayed response as compared to previous weeks, but nevertheless a response. At 4:30pm her temperature broke through to 102.7F and stayed above 102.5 until 6:00pm. As we had hoped for, she experienced no dehydration, no major drop in blood pressure, no need for oxygen, no flushing of the face. We were ecstatic. Furthermore, she only needed to drink a little over 2 cups of the oral electrolyte formula (as opposed to 6 cups last Friday).<br> <br>Overall, today's fever was a successful one. 1 1/2 hours above 102.5, with a peak of 102.9F. Not a very high fever, but still a good one. One should also note that the fever was significantly higher than last Friday's treatment, although at the same CFIV dose level. This further corroborates our thinking that dehydration robs the body of energy to mount a good fever.<br> <br>As aforementioned, there were few unpleasant side effects, the primary one being tiredness and fatigue. The main thing though is it seems we've figured out a very important guideline - which is to avoid sweat (and consequently dehydration) during pre-heating.<br> <br><b>== DOSE 0.00075mL ==<br></b><br>Coley's Toxins IV #5 - First dose increase (to 0.00075mL) <br>Submitted by CancerHusband on Wed, 08/18/2010 - 17:06 <br><br>Today, we increased the dosage from 0.0005mL by 50% to 0.00075mL. Those of you familiar with the MBVax protocol will note that this is still less than the typical starting dose of 0.001mL. The reason why we're treading cautiously is from previous experience with various drugs and chemo. She just tends to react quite strongly to typical dosages (even those adjusted for body weight).<br> <br>Coley Fluid infusion started at 12:30pm. The first sign of chills occurred about 45 minutes later. By 3:15pm, her temperature broke through to 102.6F. It stayed there for a little over an hour. The highest point being 102.7F.<br> <br>Compared to Monday's fever, this one was a tad lower (Monday's highest was 102.9, with 1.5 hours above 102.5 threshold). This may indicate a need to increase the dosage to 0.001ml next.<br><br>Also, a new development today was her pulse rate reached a peak of 130 (10 points higher than Monday's highest). This is a first. I notified the nurse who contacted the doctor. The doctor didn't seem concerned but ordered IV hydration. I'm guessing the doctor thinks the elevated pulse is probably due to dehyration.<br> <br>Overall, she felt pretty good throughout the fever. The primary symptom, again, was fatigue. Again, she had some slight coughing (coming from the diaphragm). The doctor said that it's most likely due to inflammation caused by the fever.<br> <br>Even though she felt pretty good throughout the fever, she was quite tired out at the end of the day. Not enough energy to go down to dinner so I brought food up from the cafeteria. We'll see how she feels tomorrow.<br> <br><b>== DOSE 0.00075mL ==<br></b><br>Coley's Toxins IV #6 - Looks like it's time to increase dosage more aggressively <br>Submitted by CancerHusband on Fri, 08/20/2010 - 17:26 <br><br>Today, it took almost 2 hours before there was any rise in temperature at all. However, she eventually developed fever, although it was clear that the temperature rise was not as fast and as high as previous treatments. She also experienced some light chills at that time.<br> <br>Three hours after infusion start, she reached 102.6F. This lasted for barely an hour. Also, her peak was 102.7F. She also tolerated the fever very easily and didn't feel much discomfort, except for the fatigue that's always most prominent during fever peak.<br> <br>As in the past 2 treatments, we kept the heating pads to a minimum and avoided making her sweat before onset of chills of fever. We also observed that she began to sweat during the cool-down phase of the fever (consistent with the MBVax protocol documentation).<br> <br>As before, the side effects experienced during the fever were<br><br> chills (kept to a minimum using heat pads & blankets)<br> achy feeling in hips downwards (intensity 2 out of 10)<br> minor one-sided headache (2 out of 10)<br> dry cough especially when lying on the side<br><br>All the above side effects disappeared after the fever subsided. We also observed something interesting (but not surprising). During the chill phase, if she turned on her side, the shoulder not in contact with the heating pad would start to feel the chills. This would be immediately mitigated by lying on her back against the heating pad.<br> <br>Again, this fever seemed to be lesser in intensity and duration. By 5 hours after start of infusion, she was all ready to head down for dinner (she never gets to eat lunch during the days when she gets Coleys, mainly to avoid nausea during the fever). She even felt strong enough to take a shower before heading down to the cafeteria for dinner.<br> <br><b><span style="color:rgb(204, 0, 0)">Next week, we are considering increasing the dose to 0.002ml. We feel that the increase from 0.0005 -> 0.00075 didn't do all that much, and hence, a further increase to 0.001 may not be all that meaningful.</span></b><br style="color:rgb(204, 0, 0)"> <br>===== The wife reports on how it feels =======<br><br>Coley's Toxins Weeks 1 & 2<br>Submitted by CancerWife on Sun, 08/22/2010 - 22:37<br><br>We had heard and read much about Coley's Toxins and its potential side effects, and now I was to experience it. We want to share my experience with others: how Coley's Toxins actually makes one feel - both immediately during and after treatment. The past two weeks have been like a long experiment. We recorded every sensation I felt during and after the Coley's treatment. Constant temperature, oxygen, pulse and blood pressure measurements gave us more clues on how to ameliorate the side effects.<br> I am following MBVax's protocol (<a href="http://www.mbvax.com" target="_blank">www.mbvax.com</a>), which calls for intravenous administration and dose escalation to achieve fevers between 102.5-106F. The frequency of administration is five times for the first 6 weeks, then three times a week for 3 weeks, then two times a week for 6 months or more. I am aiming to do Coley's for a total of six months for maximum effectiveness.<br> During the first two weeks of Coley's Toxins treatment, I have been receiving intravenous infusions on Mon, Wed and Fri.<br>(unusable pixelated picture of a a [sic ]vial of Coley's Toxins (not MBVAX vial!) - red because of the Serratia marcescens bacteria)<br> <br>Prewarming<br>One of the common side effects of Coley's Toxins is chills and shakes. A way to minimize the shakes and chills is to prewarm the patient before the infusion of Coley's Toxins. This raises the body temperature so the body does not need to shake and generate chills to warm the body up as it responds to the Coley's.<br> Every time before the administration of Coley's, I lie in bed with blankets over me, and a full-body heat pad underneath. I only turn on the heat pad if I don't feel warm enough. After a few times of Coley's, we realized that it is best *not* to sweat before I reach a temperature above 102.5F. Somehow the sweat drains energy from me, making it difficult for me to hit the high temperatures.<br> <br>Chills<br>Of the six times that I've had Coley's so far, I have not experienced any shakes. This may be because I am prewarmed, so the body does not need to shake to raise the temperature. I have felt chills though. It feels like a cool breeze along my back. Sometimes it is on one side of my back, going from the top to bottom, or sometimes it goes from left to right, and sometimes it radiates from the center of the back outwards.<br> Once I feel a chill, I immediately turn on the full-body heat pad. The warmth minimizes the chills. I usually feel 5-10 chills before it stops.<br>Sometimes during the chills, my bones feel achy.<br><br>Fever<br>Once the chills stop, my temperature starts to climb. During this time, I feel hot and fatigued. Usually the volume of my voice decreases, and I feel like keeping my eyes closed. I try to stay warm but not to a point where I am sweating.<br> I also keep on sipping electrolytes. MBVax recommends making your own electrolytes with sugar, salt and water, as the store bought ones have too much sugar. The amount of electrolyte I need seems to correlate with how much I've sweat.<br> I have felt headaches during the fever phase. Usually it's only on one side of the head - a dull headache. It usually goes away by the end of the fever and after I take more oral electrolytes.<br><br>Flush phase<br>It's been quite consistent that when I feel I cannot take the heat anymore and throw away the blankets, that is usually when my temperature starts to decrease. I also feel much warmer and start to sweat more.<br> <br>After the fever<br>When my temperature drops to 100-101, I usually feel well enough to eat dinner with a good appetite (see picture below - my dinner after the fever). I don't eat during the fever, so I skip lunch. I am usually a bit fatigued, and my bones feel achy and tired.<br> The next day I usually feel 100% back to normal. A few times I felt flushed and hot, but that only lasted about 10 mins or so.<br>An interesting thing is that if I get Coley's on Friday, I feel totally fine on Saturday, but I start to feel a bit fatigued and my bones ache a bit on Sunday.<br> <br>===== END wife report =======<br><br><br><b>== DOSE 0.002ml ==<br></b><br>Coley's Toxins IV #7 - A long but sub-optimal fever DOSE 0.002ml<br>Submitted by CancerHusband on Mon, 08/23/2010 - 22:24 <br><br>Today's fever was uneventful but interesting. We went with an increased dose of 0.002ml thinking that an increase from 0.00075ml to 0.001ml wouldn't do much. We were right.<br> <br>The chills began 1 hour after infusion start like clockwork. However, 3 hours after infusion start, her temperature was still 101.2F. It became apparent that today's was not going to a very high fever.<br><br>The fever stayed mostly between 101 and 102F for a good 3 hours. It briefly touched 102.5F but only for a few minutes.<br> <br>In general, she was pretty fatigued for the duration of the fever. All other symptoms were consistent with previous fevers - bone pain in the hips, tingling in the fingers, very slight chills (with heating pad), one sided headache, elevated pulse. These were all minor and they all resolved quickly as the fever subsided. However, the fatigue seemed to linger a little longer than usual.<br> <br>The lingering fatigue might be explained by her anemia. Her Hemoglobin, MCV and MCH were low even before we started on Coley's. The MBVax protocol explains that Coley's may cause anemia itself due to competition in the bone marrow for increased white cell production. Furthermore, it seems that fever itself can lead to a drop in iron levels. Well, today, we got the results of her CBC and Serum Iron test done last Saturday.<br> <br> Her iron levels are 33 ug/dL (normal being 50-180).<br> Hemoglobin has improved a little to 10.8 (from 10.1)<br> MCV declined slightly from 73 -> 72<br> MCH declined slightly from 24 -> 23.9<br> RDW is high at 18.7<br> <br>It looks as like this is likely iron deficiency anemia. However, the Issels program does not recommend iron supplementation (iron through food is OK). Nevertheless, we have ordered Floradix iron supplements from the US via mail and hope that it'll make it to the hospital in a couple of days. Strictly speaking, we're not on the Issels treatment plan, but rather, we're following the MBVax protocol. And that protocol does call for Iron supplementation.<br> <br>I also wonder if this anemia would compromise her body's capability to achieve higher fevers. Regardless, we will try to fix this and hope it'll resolve soon.<br><br>On a separate positive note, her total WBC is still at 7500/mm3 (if you remember, it doubled from 4000 to 8000 after the first 3 fevers. It has never been this high, ever, since chemo). In addition, a new development is her lymphocyte count is now at 2000/mm3. This is a first ever since chemo. Her highest has been around 1000/mm3 for the past 2 years since radiation and chemo.<br> <br>Well, it looks like we'll have to increase dosage again the next time.<br><br><b>== DOSE 0.002ml ==<br></b><br>Coley's Toxins IV #8 - Another sub-optimal fever at 0.002mL<br>Submitted by CancerHusband on Wed, 08/25/2010 - 23:00 <br> <br>After some deliberation, we decided not to increase the dose level. Instead, we wanted to see if a higher fever could be obtained by increasing external heat instead. After all, we felt that the previous fever (#7) was quite a good one, despite the sub-optimal temperature. It's duration was long and she was quite fatigued after that fever.<br> <br>Well, as it turns out, increasing the external heat did not lead to a higher fever. Instead, she again developed a fever mainly between 100-101F. This was noticeably lower and of shorter duration than the previous one. She also tolerated it easier and was less fatigued. She did experience some chills but very light ones and very short. She had bone aches from the hip down to the legs.<br> <br>Our conclusion: increasing external heat did not seem to substantially affect her ability to achieve higher fever. It's clear that we need to escalate dosage.<br><br><br><b>== DOSE 0.003ml ==<br></b><br>Coley's Toxins IV #9 - A better fever but could be higher. A lingering (but very infrequent) cough.<br> Submitted by CancerHusband on Sat, 08/28/2010 - 16:37 <br><br>Today we increased dosage again to 0.003ml. The fever was uneventful and predictable. It was somewhat better than the last one. However, it wasn't as high as we'd hoped for. The peak was a tad below the desired 102.5F threshold. So we'll need to increase again next Monday.<br> <br>Well, so far, it looks like her Coley fevers are becoming quite predictable and boring -- and that's the way we like it. It'll be interesting though to see if we're able to reach the higher temperatures - and to see how how she tolerates them.<br> <br>Again, the side effects have been quite minimal. The fatigue, increased heart rate, bone aches that occur during the fever all disappear as the fever subsides. And they are very minor to start with.<br><br>The only side effect that seems to somewhat linger on after fevers are gone are a slight cough. It's very infrequent -- we're talking maybe 20 coughs over the entire day.<br> <br>The doctors think this could be due to general inflammation that Coley's induces. The worse case scenario would be the cough is caused by potential lung tumor(s). Our last scan on June 7th showed two tiny 2mm and 3mm nodules that are suspicious. They were too small to biopsy. Sarcomas can grow very fast. Thus, there's always the possibility that if those were tumors, they may have grown large enough to be symptomatic.<br> <br>Even so, the cough may not be a bad thing. It could signify the vaccine having positive effect on potential tumors. There's a clear correlation between the frequency & intensity of coughs and the fevers. Coughing is more frequent during fevers - and more so during the fever peak. Regardless, let's hope the cough is due to something else.<br> <br><br><br>===== The wife reports on how it feels =======<br><br>Coley's Toxins Week 3<br>Submitted by CancerWife on Sun, 08/29/2010 - 10:02 <br><br>This week I had two increases in dosage - to 0.002mL and 0.003mL. Neither dosages gave me sustained fever above 102.5F. Most likely I'm developing some tolerance, so there will be more dose escalation next week.<br> <br>We learned this week that if I don't sweat much during the fever, I feel more fatigued after the fever ends. This happened on Coley's #7 - I had to rest my head on the dining table during dinner time that night! Thus, for Coley's #8 and #9, we cranked up the heat pad when my fever started to subside. This caused me to sweat more and I had more energy after the fever ended.<br> <br>Another thing we noticed is my hands have gotten darker. (No, I have not been tanning here in Tijuana :-)) The only other time this happened was during chemotherapy, when I received doxorubicin and ifosfamide. It is a normal side effect of the chemo. It could be that somehow Coley's is causing side effects from chemo to reoccur. Reactivation of "old injuries" has been observed in other patients receiving Coley's.<br> <br>===== END wife report =======<br><br><br><b>== DOSE 0.004ml ==<br></b><br>Coley's Toxins IV #10 - Still not good enough<br>Submitted by CancerHusband on Mon, 08/30/2010 - 20:43 <br><br>Today's dosage was again an increase to 0.004ml. This was because last Friday's fever wasn't very high and maxed out at 102.4F for a short duration.<br> <br>Today's was even lower. It maxed out at 101.9F and for not very long either. I would estimate that the average fever was about 101F. It wasn't very difficult to tolerate and recovery as the fever subsided was very quick.<br> <br>So it seems clear that her body is developing resistance to the toxins. Let's hope that dose escalation will be able to break this. We will ask the doctors if it would be appropriate to skip the next dose level and go straight to 0.006ml.<br> <br><br><b>== DOSE 0.006ml ==<br></b><br>Coley's Toxins IV #11 - Breaking tolerance<br>Submitted by CancerHusband on Tue, 08/31/2010 - 21:53 <br><br>Today, we increased the dosage from 0.004ml -> 0.006ml. We did this because it was becoming apparent that her body is developing tolerance to Coley's Toxins. We felt that increasing to 0.005 wouldn't do too much based on previous fever curves.<br> <br>Increasing to 0.006ml was probably the right choice. We clearly noticed that today's chills were much more apparent (even with the heat pad). This was more in line with the robust fever from IV#2. Also, the chills occurred about 45min-1 hour after infusion start. This was followed by rise in body temperature shortly after. In contrast, fevers 8, 9 and 10 were slow to happen.<br> <br>Today's peak was 102.7F. This is above the 102.5F threshold. We were happy about that. However, one interesting thing we noticed is that it dropped off rather quickly (in comparison to robust fever #2).<br><br>I wonder what it'll take to re-create a sustained fever. Do we merely need to hit a high enough dose? Or could it be that her body has become more efficient at neutralizing the Toxins? Hmm...<br> <br><br><b>== DOSE 0.009ml ==<br></b><br>Coley's Toxins IV #12 - 104 Fahrenheit<br>Submitted by CancerHusband on Thu, 09/02/2010 - 17:38 <br><br>Today, we decided to be a little daring and upped the dosage from 0.006ml -> 0.009ml (a factor of 50%). We decided to do this based on her response from fever #11 where we increased from 0.004->0.006ml. That 50% increase resulted in a clearly better fever, but still not quite high enough.<br> <br>We got the go ahead from the doctors here. The fever was a little slow to start. Normally, the stronger fevers seemed to manifest chills 1 hour after infusion start. This one was later at almost 2 hours.<br><br>The historical records really are true - that robust fevers are clearly associated with more intense chills. Today's chills didn't last that long -- only about 30 minutes. However, it was clear that they were more intense compared to previous ones. Similarly, fever#2 resulted in intense chills as well. Today's chills were continuous and occurred in many places - in her shoulders, arms, legs -- and a new location -- behind her head! I suppose the pillow under her head prevented the heating pad from warming up that area. Nonetheless, it was interesting to that this is the first time chills have occurred there.<br> <br>Once the chills subsided, her temperature began to rapidly rise. It reached 103.4F about 15 minutes after the chills subsided. Shortly thereafter, it peaked at 104F. This is the first time it's hit that high.<br> <br> Interestingly, her fever didn't sustain at high levels for long. As in fever#11, it began to drop quite soon after peaking. Nevertheless, it was still a good, robust fever, reaching the highest peak ever.<br><br><br> Other observations:<br> <br> The past 2 fevers have not resulted in much aching in her long bones and hips. This occurred quite noticeably in earlier fevers. If those aches were indicative of bone marrow growth, it would be interesting to see how her WBC counts this Saturday are.<br> As before, she began coughing 30 mins after infusion of Coley's started. This time, the coughing was more frequent. Not more intense, just more frequent. Her temperature was normal at that time, but her face looked a little flush/red. Later on, during the post-chills phase when her temperature began to rise, I noticed that her cough also became quite frequent. Subsequently, it diminished as her fever decreased.<br> <br>Note:<br><br> We just spoke with another patient here at the Issels ward. She received Coley's subcutaneously into her arm. She developed a fever of 104F (40C) for 5 hours! Boy, was that a major fever! After the fever broke, she had profuse sweating. The interesting point is that other Issels patients have also reported very long lasting fevers, 8 hours or more in some cases, that had to be stopped with Tylenol. That may be an advantage of subcutaneous administration (the downside being pain at injection site along with possibly unreliable development of fevers due to variable amount of Toxins entering the bloodstream?).<br> <br><br><b>== DOSE 0.009ml ==<br></b><br>Coley's Toxins IV #13 - Revamped fever charts. Figuring out the dry cough.<br>Submitted by CancerHusband on Sat, 09/04/2010 - 16:31<br><br>I've programmed a chart that's hopefully easier for folks to see how the Coley's Toxins fevers progress over time. I did it mainly for ourselves to be able to visualize how a given fever compares with the prior one - and also how it compares with the "best" fever thus far. The best one she's had is fever #2. It was long and protracted, and she stayed well above 102.5F for a good 2.5 hours.<br> <br>Now, back to today's fever. Since the prior fever was a good one that reached 104F, we chose to stay at the same dose level. That's what the MBVax protocol calls for.<br><br>Chills<br><br>The chills took a while to develop - but they did come eventually. The chills were frequent but very gentle this time. Mainly a light cool sensation on the back, arms, back of head. Remember now - she has a full body far-infrared heating pad along with blankets and a second chest heating pad. These are turned on and put in place right from the start, before the chills. Again, the purpose is to ward off violent chills and shakes which happen when the body resets it desired temperature point upwards and tries to generate internal heat.<br> <br>The gentle chills foretold of a lesser fever. Still, she managed to hit 103.1F (39.5C). In all, I estimate that she stayed above 102.2F (39C) for a good 1.5 hours. The plot of this fever (#13) versus the prior one shows a more or less similar curve, except with a lower peak. This indicates her body is beginning to develop tolerance to this dose level (hence the lower peak). We will need to think about whether to increase dosage for next Monday.<br> <br>Figuring out the cough<br><br>For today's infusion, we worked with the doctor here at Issels and decided to eliminate their pre-infusion vitamins and minerals (all prior Coley's infusions were preceded by an IV infusion of B vitamins and minerals to strengthen the body. This was mixed into 500ml saline). For today, all that was given was 250ml of pure saline. The reason we did this was to see if the pre-infusion was contributing to the dry cough that happens each time she gets Coleys.<br> <br>The doctor also listened carefully to her lungs before infusion, and during the fever, when the cough started up. Here's what we found:<br><br> Her lungs sounded very clear before infusion (when there was no cough)<br> During this fever, the cough was noticeably less than the prior fever (#12). Three differences in today's fever are<br> Smaller volume of infused liquid (250ml versus 500ml)<br> No B vitamins + multi-minerals<br> No Coley's dose increase (hence a less intense reaction than #12)<br> During the fever cough, the doc listened again very carefully and noted the following:<br> When breathing normally, her lungs sound clear -- i.e. no evidence of general bronchial constriction that may be indicative of allergic reaction due to Coleys.<br> However, when coughing, it does sound like a "wheeze" (only during the cough).<br><br>The doc suggests one possibility is a small tumor that might be pressing on a nerve. Coley's causes tumors to inflame. This might be an explanation for why the cough comes during infusions. The doc didn't think it was a pleural cough. The doc said that a pleural cough would be triggered when one breathes in deeply -- and would manifest in a sharp spasm/pain in the sides. (In her case, she does cough whenever she breathes in deeply, but there are no sharp pains).<br> <br>Is the dry cough due to general inflammation?<br><br>Another possibility that we're pondering is general inflammation caused by Coley's. We've been observing minor but noticeable aches and pains here and there - like on a finger tip, behind the knee cap, in the hip. These generally occur during the peak of the fever.<br> <br>We can't help but to make an association with an episode 2 years ago when she was given a single shot of Depot Lupron before chemotherapy. This led to all sorts of pains and aches on her chest, ribs, jaw, scalp, shoulder... and it also caused a dry cough. All our doctors and oncologists were totally stumped. CT scan, X-ray, nuclear perfusion tests, blood tests were negative. The ER doc suggested that her cough could be caused by inflammation in the pleura surrounding the lungs. In the end, we did a little experiment, based on the hunch that what we were seeing was generalized systemic inflammation. So she took a single dose of ibuprofen, and that IMMEDIATELY killed the cough and aches and pains. It was like magic - really. Coleys almost definitely causes temporary inflammation. So, you can see why we might believe that the dry cough, aches and pains that we're seeing are due to a generalized inflammatory process.<br> <br><br>===== The wife reports on how it feels =======<br><br>Post-fever appetite: Coley's #13<br>Submitted by CancerWife on Sat, 09/04/2010 - 21:32 <br><br>During my Coley's treatments, I eat breakfast around 8:30am, skip lunch, then I eat dinner after the fever subsides. Today I decided to eat some fruit during the fever, as I was getting quite hungry. I had a plum, then a banana. That wasn't quite enough for me, so after the fever came down, I went down to the cafeteria and asked for a snack. I had two pieces of cake (healthy cake with nuts and fruit) and a cup of apple juice.<br> <br>Then came dinner time. We went out to a nearby restaurant with other patients. I had a bowl of tortilla soup (with avocado, homemade cheese, tortilla strips) and ostrich steak. The ostrich tastes like very lean beef. I've been low in iron, so I've ordered ostrich a few times already. I had room even after that! So, I ended the meal with a large piece of carrot cake. After all that eating, I wasn't even stuffed!<br> <br>I'm in awe that I have very good appetite each time after Coley's. It's such a stark contrast to the time when I had chemo (doxorubicin and ifosfamide). My appetite got worse and worse with each round of chemo, and my weight kept on dropping. With Coley's, I have no problems eating dinner afterwards, and as you can see for today, I can eat quite a large meal!<br> <br>===== END wife report =======<br><br><br><b>== DOSE 0.009ml (+) ==<br></b><br>Coley's Toxins IV #14 - Another good fever.<br>Submitted by CancerHusband on Mon, 09/06/2010 - 20:08 <br><br>Today's fever was another good one. She stayed above 102.2F for a good 2 hours.<br> <br>The fever curve was quite similar to fever #2. The maximum temperature was 103.6F (39.8C). However, you'll notice that it took a little longer to reach its peak. However, once reached, it seemed to stay up there a little longer than recent fevers.<br> <br>Observations for today's fever:<br><br> Chills lasted for about 20 minutes but were very mild<br> The dry cough was even less than fever #13. It occurred only when she would lay on her side. And even so, they were sparse. Could it be that it's resolving??<br> She had some numbness and sensitivity in her left hand today -- more so than previous fevers.<br> She had a dull headache (mainly center front) and also a transient sharp pain in the back of her head (left side). These are were quite minor (in terms of intensity).<br> <br>Other than that, I would classify today's a robust fever, with weak chills. Lasted on the longer side at relatively high temperatures.<br><br>OK to eat during fever?<br><br>The MBVax protocol warns not to eat before Coley's, as well as during the chill phase. I need to check again, but my impression was not to eat during fever as well. It would make sense too, since digestion would probably be impaired during fever.<br> <br>Well, today we decided to experiment a bit. Whenever she gets Coley's, she doesn't get to eat lunch. And today's Coley's started dripping at around 12:45pm. So, by 4:00pm, she was pretty hungry. Thus, even though she had just reached a high temperature of 103.6F (today's peak), I decided to let her eat a little fruit. We went slow and she had no problems. No nausea. Eventually, she probably ate a full cup of fruit (grapes, canteloupe, papaya). Later on, I gave her a cookie to eat as well.<br> <br>Interesting observation regarding dilution<br><br>Coley's Toxins has to be diluted before being administered intravenously. Today, the Coley's Toxins vial was almost empty. It probably had 0.2ml left, of which 0.1ml was removed, and then diluted. We noticed that it seems a little darker red (more concentrated). This could happen if the vial is not shaken thoroughly each time before extraction. This would result in the remnant solution becoming more and more concentrated. Therefore, even though we kept at 0.009ml, we probably got more than that today.<br> <br>Possible reactivation of old injuries by Coley's Toxins<br><br>We've heard from MBVax that they've observed Coley's reactivating "old injuries". Secondly, the doctors here at Issels believe that Coley's mobilizes toxins and possibly any remnant chemo from the body. They believe it is very important to have a good sweat during/after Coley's (in order to get rid of these toxins).<br> <br>Well today, we observed something reminiscent of a side effect from chemo 2 years ago. Chemo caused callouses to develop on her fingers, and also some skin peeling. Today, before Coley's started, she observed some of that on her left thumb. She doesn't think it's due to soap because it's only on the left thumb and not on any of the other fingers. A few hours after the fever, she observed little bumps on the thumb. These are all pretty minor, but still noteworthy.<br> <br><br>Postponed until tomorrow<br>Submitted by CancerHusband on Wed, 09/08/2010 - 18:21 <br><br>Early this morning, she woke up with a slight burning sensation across the upper middle area of her chest. Later on, she felt a slight heavyness in her chest. It would eventually get better by evening time.<br> <br>The doctors listened carefully to her lungs. They said her lungs sounded clear.<br><br>One possibility is she might be fighting off an upper respiratory infection. It's been going around here in the small ward where we are. There are no open windows here so it's hard to get real fresh air.<br> <br>Our standard protocol when we see the first signs of an upper respiratory infection -- and which has worked very well for us the past 2 years -- is to immediately supplement with the following for no more than 3 days:<br> <br> High dose Vitamin D3 - 90,000IU / day for 3 days max<br> Sambucol (Black Elderberry extract) - 2-3 Tbsp / day (better than Tamiflu)<br> Lactoferrin (between 500mg - 1000mg, twice daily)<br><br>Generally, we try to minimize supplements during Coley's. One can do as much research as possible and choose supplements that may be complementary to Coley's. However, there's always a risk of negative interaction. For example, taking high dose fish oil is anti-inflammatory and there is the risk of muting the immune response (which we don't want with Coley's!!). Likewise, there is the theoretical risk for Vitamin D3, Curcumin, and maybe even EGCG. These are all based on our own research trolling through pubmed research articles. Therefore, we intend to take the above supplements only for 3 days maximum.<br> <br>We'll see how she fares tomorrow. We agree with the doctors that it makes sense to postpone Coley's and re-evaluate come tomorrow.<br><br><br><b>== DOSE 0.012ml ==<br></b><br>Coley's Toxins IV #15 - A good fever given the circumstances<br> Submitted by CancerHusband on Thu, 09/09/2010 - 21:25 <br><br>This morning, she woke up and felt good enough to to Coley's. There wasn't any "slight burning sensation" in the chest. Neither was there any noticeable heavyness. However, she did have some light yellow phlegm that had to be cleared with some difficulty. So we're thinking that the symptoms she felt yesterday were the beginnings of an upper respiratory infection after all. Perhaps our standard high dose Vitamin D3 - Sambucol - Lactoferrin mix nipped it in the bud, as it has done so reliably for the past 2 years. Only time will tell.<br> <br>As usual, she received an infusion of saline + B vitamins + multi-minerals. She's received this with almost every Coley fever. This is standard operating procedure at Issels. The actual Coley's was infused beginning at 1pm. It's now 7pm and she's finally gotten up and gone to wash up.<br> <br>Mild chills<br><br>She experienced fleeting chills 1 hour post infusion start. Then, nothing for a while until about 2.5 hours post infusion start. The second occurrence of chills ended up being only about 15 minutes. As usual, they were mild, which we assume is due to our pre-warming with the far infra red pad.<br> <br>Even milder cough<br><br>If you remember, the last Coley's was characterized by a rather mild cough. We were wondering/hoping then that her fever associated cough was beginning to resolve. Well, today's cough was even milder. When coughed only a few times the entire day. There were no spontaneous coughs. They had to be triggered with deep breathing. This happened only after the fever peaked.<br> <br>Fever strength and duration<br><br>The fever peak wasn't very high. But we're not too surprised. We did increase dosage to 0.012ml. We did so because we feel that the previous dosage of 0.009ml was in actuality higher due to the more concentrated remnant fluid left at the bottom of the vial. So, we wanted to stay at the "same dosage" as before. And we took a best guess and estimated it to be 0.012ml, not daring to go higher.<br> <br>Today's fever peaked at 102.7F. It hovered above the lower threshold of 102.5F for just about an hour and 20 minutes. So, while it wasn't a very high fever, it was a relatively protracted one.<br><br>Overall, we were both quite pleased with today's fever given that she was a bit under the weather to start with. An interesting observation:- after the fever, she observed that her lungs felt clearer -- perhaps the fever helped smack down any upper respiratory tract infection! ..... we'll see.....<br> <br><br>Back home for the weekend. A four day break.<br>Submitted by CancerHusband on Sun, 09/12/2010 - 11:32 <br><br>We're back home for the weekend. She just had a routine Chest CT done and we're waiting for the film lab to burn the disk. As a result of our little haitus, it'll be 4 days break in between Coley's Toxins treatments (we'll resume Coley's next Tuesday).<br> <br>The MBVax protocol talks about loss of tolerance to Coley's Toxins. Patients who stop Coley's for more than a week are supposed to go back to the beginning and start at 0.001ml all over. Ours will be 4 days - not quite 1 week. We might consider reducing dosage. We'll have to discuss this with the Issels doctors.<br> <br>Well one thing's for sure, we're enjoying the food back home and eating as much as we can! (The food at Oasis is really quite good, but it's primarily vegetarian)<br><br><br>An unexpected delay in treatment<br> Submitted by CancerHusband on Tue, 09/14/2010 - 18:56 <br><br>Sunday night, she suddenly came down with spontaneous shaking chills and high fevers - three of them in the ensuing 24 hours. Her highest registered temperature was 105.6.<br> <br>After the first fever subsided, we thought it was most likely some viral infection that was resolving. However, when the second one hit, we cancelled the flight back down to San Diego (no way she could walk with the severe chills). We waited for the chills to subside and the fever to spike.<br> <br>The second fever seemed to resolve after some time. I wanted to take her to the urgent care clinic but she wanted to have a meal. After the meal, the chills hit yet again, and her temperature spiked again.<br><br>We took her to the Stanford University ER where they did blood cultures, X-rays, urine samples. They administered broad spectrum IV antibiotics empirically, as there was no obvious infection (no flu like symptoms, no burning during urination, no diarrhea etc).<br> <br>For many hours the ER doctors had no clear idea what could be causing the fevers. I had to explain to about 6 different physicians our adventures for the past 5 weeks in Mexico.<br><br>After about 14 hours, they found evidence of bacterial contamination in her PICC line. They removed the line and sent it for further analysis, hoping to isolate the primary bacterial strain. By that time, she was already beginning to feel much better.<br> <br>It may take a few days (or more) to take care of this infection. This will cause a delay in her treatment. We won't be going back down to Mexico until this is completely taken care of. Sorry.... but there'll be no Coley's fever graphs until then ....<br> <br>Delay in Coley's while waiting for Graves' to subside<br>Submitted by CancerHusband on Sat, 11/27/2010 - 14:23 <br><br>We're still waiting to resume Coley's. Unfortunately, there's been a resurgence of her Graves' disease (which started in April 2010). One of the symptoms that we have to be careful about is the elevated heart rate due to Graves'. We're trying to get that under control before considering resuming Coley's.<br> <br>There's the possibility that Coley's caused her Graves' disease to re-surge. However, there are other potential causes including the Pseudomonas sepsis itself, or a recent bad allergic reaction triggered by her PICC dressing.<br> <br>Our best guess is that she may have had Graves since 2008 (or at least some tendency towards autoimmunity). Why do we think this? Mainly because she experienced a major unexplained bout of systemic inflammation from a single dose of Lupron in 2008, and then half-side body numbness after a single Pneumovax shot in mid 2009. These occurrences were unexplainable and self-limiting. A neurologist-oncologist we consulted with at Stanford concurred with us that the Pneumovax reaction was most likely an autoimmune attack on the nervous system.<br> <br>There are also historical references to Coley's being used to ameliorate autoimmune diseases such as rheumatoid arthritis. Obviously, we hope that Coley's was not the cause of the Graves' resurgence. Regardless, we will have to proceed carefully in the future to ensure that it does not exacerbate Graves' too much.<br> <br><br>END<br><br><br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-8821358346704567772011-07-30T00:02:00.000-07:002011-07-30T00:03:10.859-07:00Chemotherapy drug in combination with Coley's Toxins<br>A very advanced breast cancer patient (liver and bone metastases) received epirubicin 20mg a week, plus Coleys.<br>"The results can only be described as amazing" <br><br><br><br>Epirubicin is an anthracycline drug used for chemotherapy. It is marketed by Pfizer under the trade name Ellence in the US and Pharmorubicin or Epirubicin Ebewe elsewhere.<br> <br>Similarly to other anthracyclines, epirubicin acts by intercalating DNA strands. Intercalation results in complex formation which inhibits DNA and RNA synthesis. It also triggers DNA cleavage by topoisomerase II, resulting in mechanisms that lead to cell death. Binding to cell membranes and plasma proteins may be involved in the compound's cytotoxic effects. Epirubicin also generates free radicals that cause cell and DNA damage.<br> <br>Epirubicin is favoured over doxorubicin, the most popular anthracycline, in some chemotherapy regimens as it appears to cause fewer side-effects. Epirubicin has a different spatial orientation of the hydroxyl group at the 4' carbon of the sugar, which may account for its faster elimination and reduced toxicity. Epirubicin is primarily used against breast and ovarian cancer, gastric cancer, lung cancer, and lymphomas.<br> <br>Development history<br><br>The first trial of epirubicin in humans was published in 1980. Upjohn applied for approval by the U.S. Food and Drug Administration (FDA) in node-positive breast cancer in 1984, but was turned down because of lack of data. It appears to have been licensed for use in Europe from around this time however. In 1999 Pharmacia (who had by then merged with Upjohn) received FDA approval for the use of epirubicin as a component of adjuvant therapy in node-positive patients.<br> <br>Patent protection for epirubicin expired in August 2007.<br><br><br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-35754348623024103602011-07-25T08:41:00.000-07:002011-07-25T08:42:03.822-07:00Afinitor used for Kidney (Renal) Cancer - Old info?Chemotherapy Drugs Afinitor ($3500 us dollars per 30 day treatmenet<p>Afinitor is used in the treatment of advanced renal cell cancer, after<br>sunitinib and sorafenib failure. (sunitinib is one of the most<br>expensive drugs widely marketed)<br>.<br>no wonder they do not want Coley's toxins (Coley's fluid, MBV mixed<br>bacterial vaccine) to be on the market, because it costs VERY little.<br>see this video <a href="http://www.youtube.com/watch?v=w9wNHw3FCmc">http://www.youtube.com/watch?v=w9wNHw3FCmc</a> extraordinary!!!<p>Full text<p>Generic Name: Everolimus<p>Afinitor is the trade name for the generic name drug everolimus. In<br>some cases, health care professionals may use the generic name<br>everolimus when referring to the trade drug name Afinitor.<p>Drug Type:<p>Afinitor is a targeted therapy and is classified as an mTOR inhibitor.<p>What Afinitor Is Used For:<p>Afinitor is used in the treatment of advanced renal cell cancer, after<br>sunitinib (see below) and sorafenib failure.<p>Note: If a drug has been approved for one use, physicians may elect to<br>use this same drug for other problems if they believe it may be<br>helpful.<p>How Afinitor Is Given:<p> Afinitor is given as a tablet by mouth.<br> Take at the same time each day, may be taken with or without food.<br> Swallow whole with a glass of water, do not chew or crush tablets.<br> Avoid contact with or exposure to crushed or broken tablets.<br> There are 2 tablet strengths<br> 5mg tablet; white to slightly yellow, elongated tablet with a<br>bevelled edge and no score, engraved with "5" on one side and "NVR" on<br>the other<br> 10mg tablet; white to slightly yellow, elongated tablet with a<br>bevelled edge and no score, engraved with "UHE" on one side and "NVR"<br>on the other.<br> The amount of Afinitor that you will receive will be prescribed by<br>your doctor based on established dosing guidelines.<p>Afinitor Side effects:<p>Important things to remember about the side effects of Afinitor:<p> You will not get all of the Afinitor side effects mentioned below.<br> Afinitor side effects are often predictable in terms of their<br>onset, duration, and severity.<br> Afinitor side effects are almost always reversible and will go<br>away after therapy is complete.<br> Afinitor side effects are quite manageable. There are many options<br>to minimize or prevent them.<p>The following side effects are common (occurring in greater than 30%)<br>for patients taking Afinitor:<p> Low red blood cell count(anemia)<br> Increased blood cholesterol level<br> Increased blood trigylceride level<br> Increased creatinine<br> Mouth sores<br> low phosphorus level<br> Infection<br> Weakness<br> Diarrhea<br> Cough<p>These are less common (occurring in 10-29%) side effects for patients<br>receiving everolimus:<p> Rash<br> Low blood counts. Your white blood cells and platelets may<br>temporarily decrease. This can put you at increased risk for<br>infectionand/or bleeding.<br> Nausea, vomiting<br> Increased liver enzymes<br> Swelling<br> Poor appetite<br> Shortness of breath<br> Fever<br> Fatigue<br> Headache<br> Nosebleeds<br> Itching<br> Lung problems<br> Dry skin<p>This list includes common and less common side effects for those<br>taking Afinitor. Side effects that are very rare -- occurring in less<br>than about 10 percent of patients -- are not listed here. But you<br>should always inform your health care provider if you experience any<br>unusual symptoms.<p>When To Contact Your Doctor or Health Care Provider:<p>Contact your health care provider immediately, day or night, if you<br>should experience any of the following symptoms:<p> Fever of 100.5º F (38º C) or higher, chills (possible signs of infection)<p>The following symptoms require medical attention, but are not an<br>emergency. Contact your health care provider within 24 hours of<br>noticing any of the following:<p> Nausea (interferes with ability to eat and unrelieved with<br>prescribed medication)<br> Vomiting (vomiting more than 4-5 times in a 24 hour period)<br> Diarrhea (4-6 episodes in a 24-hour period)<br> Unusual bleeding or bruising<br> Black or tarry stools, or blood in your stools<br> Blood in the urine<br> Pain or burning with urination<br> Extreme fatigue (unable to carry on self-care activities)<br> Mouth sores (painful redness, swelling or ulcers)<p>Always inform your health care provider if you experience any unusual symptoms.<p>Precautions While Taking Afinitor:<p> Before starting Afinitor treatment, make sure you tell your doctor<br>about any other medications you are taking (including prescription,<br>over-the-counter, vitamins, herbal remedies, etc.).<br> Do not receive any kind of immunization or vaccination without<br>your doctor's approval while taking Afinitor.<br> Inform your health care professional if you are pregnant or may be<br>pregnant prior to starting this treatment. Pregnancy category D<br>(Afinitor may be hazardous to the fetus. Women who are pregnant or<br>become pregnant must be advised of the potential hazard to the fetus.)<br> For both men and women: Do not conceive a child (get pregnant)<br>while taking Afinitor. Barrier methods of contraception, such as<br>condoms, are recommended. Discuss with your doctor when you may safely<br>become pregnant or conceive a child after therapy.<br> Do not breast feed while taking this medication.<p>Self-care Tips While Taking Afinitor:<p> Drink at least two to three quarts of fluid every 24 hours, unless<br>you are instructed otherwise.<br> You may be at risk of infection so try to avoid crowds or people<br>with colds, and report fever or any other signs of infection<br>immediately to your health care provider.<br> Wash your hands often.<br> To help treat/prevent mouth sores, use a soft toothbrush, and<br>rinse three times a day with 1 teaspoon of baking soda mixed with 8<br>ounces of water.<br> Use an electric razor and a soft toothbrush to minimize bleeding.<br> Avoid contact sports or activities that could cause injury.<br> To reduce nausea, take anti-nausea medications as prescribed by<br>your doctor, and eat small, frequent meals.<br> Avoid sun exposure. Wear SPF 15 (or higher) sunblock and<br>protective clothing.<br> In general, drinking alcoholic beverages should be kept to a<br>minimum or avoided completely. You should discuss this with your<br>doctor.<br> Get plenty of rest.<br> Maintain good nutrition.<br> If you experience symptoms or side effects, be sure to discuss<br>them with your health care team. They can prescribe medications and/or<br>offer other suggestions that are effective in managing such problems.<p>Monitoring and Testing While Taking Afinitor:<p>You will be checked regularly by your doctor while you are taking<br>Afinitor, to monitor side effects and check your response to therapy.<br>Periodic blood work will be obtained to monitor your complete blood<br>count (CBC) as well as the function of other organs (such as your<br>kidneys and liver) will also be ordered by your doctor.<p>How Afinitor Works:<p>Targeted therapy is the result of about 100 years of research<br>dedicated to understanding the differences between cancer cells and<br>normal cells. To date, cancer treatment has focused primarily on<br>killing rapidly dividing cells because one feature of cancer cells is<br>that they divide rapidly. Unfortunately, some of our normal cells<br>divide rapidly too, causing multiple side effects.<p>Targeted therapy is about identifying other features of cancer cells.<br>Scientists look for specific differences in the cancer cells and the<br>normal cells. This information is used to create a targeted therapy<br>to attack the cancer cells without damaging the normal cells, thus<br>leading to fewer side effects. Each type of targeted therapy works a<br>little bit differently but all interfere with the ability of the<br>cancer cell to grow, divide, repair and/or communicate with other<br>cells.<p>There are different types of targeted therapies, defined in three<br>broad categories. Some targeted therapies focus on the internal<br>components and function of the cancer cell. The targeted therapies<br>use small molecules that can get into the cell and disrupt the<br>function of the cells, causing them to die. There are several types<br>of targeted therapy that focus on the inner parts of the cells.<br>Other targeted therapies target receptors that are on the outside of<br>the cell. Antiangiogenesis inhibitors target the blood vessels that<br>supply oxygen to the cells, ultimately causing the cells to starve.<p>Researchers agree that targeted therapies are not a replacement for<br>traditional therapies. They may best be used in combination with<br>traditional therapies. More research is needed to identify which<br>cancers may be best treated with targeted therapies and to identify<br>additional targets for more types of cancer.<p>Afinitor is an inhibitor of mTOR. mTOR inibition blocks the<br>translation of genes that regulate cancer cell proliferation. It also<br>results in reduced levels of certain cell growth factors involved in<br>the development of new blood vessels, such as vascular endothelial<br>growth factor (VEGF).<p>Note: We strongly encourage you to talk with your health care<br>professional about your specific medical condition and treatments. The<br>information contained in this website is meant to be helpful and<br>educational, but is not a substitute for medical advice.<p><br>SUNITINIB<br>is one of the most expensive drugs widely marketed.<br>Doctors and editorials have criticized the high cost, for a drug that<br>doesn't cure cancer but only prolongs life.<p><p><br>Sunitinib (marketed as Sutent by Pfizer, and previously known as<br>SU11248) is an oral, small-molecule, multi-targeted receptor tyrosine<br>kinase (RTK) inhibitor that was approved by the FDA for the treatment<br>of renal cell carcinoma (RCC) and imatinib-resistant gastrointestinal<br>stromal tumor (GIST) on January 26, 2006. Sunitinib was the first<br>cancer drug simultaneously approved for two different indications<p><br>Renal cell carcinoma<p>Sunitinib is approved for treatment of metastatic RCC. Other<br>therapeutic options in this setting are sorafenib (Nexavar),<br>temsirolimus (Torisel), interleukin-2 (Proleukin), everolimus<br>(Affinitor), and bevacizumab (Avastin).<p>RCC is generally resistant to chemotherapy or radiation. Prior to<br>RTKs, metastatic disease could only be treated with the cytokines<br>interferon alpha (IFNα) or Interleukin 2 (IL-2). However, these agents<br>demonstrated low rates of efficacy (5%-20%).<p>In a phase 3 study, median progression-free survival was significantly<br>longer in the sunitinib group (11 months) than in the interferon alfa<br>group (5 months), hazard ratio 0.42.[6][11] In the secondary<br>endpoints, 28% of had significant tumor shrinkage with sunitinib<br>compared to 5% with IFNα. Patients receiving sunitinib had a better<br>quality of life than IFNα.<p>At ASCO 2008, Dr Robert Figlin presented updated data from the final<br>study analysis, including overall survival. The primary endpoint of<br>median progression-free survival (PFS) remained superior with<br>sunitinib: 11 months versus 5 months for IFNα, P<.000001. Objective<br>response rate also remained superior: 39-47% for sunitinib versus<br>8-12% with IFNα, P<.000001.[12][13]<p>Sunitinib was associated with somewhat longer overall survival,<br>although this was not statistically significant.<p> Median OS was 26 months with sunitinib vs 22 months for IFNα<br>regardless of stratification (P-value ranges from .051 to .0132,<br>depending on statistical analysis).<br> The first analysis includes 25 patients initially randomized to<br>IFNα who crossed over to sunitinib therapy, which may have confounded<br>the results; in an exploratory analysis that excluded these patients,<br>the difference becomes more robust: 26 vs 20 months, P=.0081.<br> Patients in the study were allowed to receive other therapies once<br>they had progressed on their study treatment. For a "pure" analysis of<br>the difference between the two agents, an analysis was done using only<br>patients who did not receive any post-study treatment. This analysis<br>demonstrated the greatest advantage for sunitinib: 28 months vs 14<br>months for IFNα, P=.0033. The number of patients in this analysis was<br>small and this does not reflect actual clinical practice and is<br>therefore not meaningful.<br> Also worth noting in this presentation was the fact that the<br>updated percentage of patients that had to discontinue sunitinib due<br>to adverse events was 19%. This is a clinically meaningful number.<p>This was the largest comparative trial in RCC to date, and sunitinib<br>is the first agent to demonstrate an overall survival longer than 2<br>years in these patients.<p>Hypertension was found to be a biomarker of efficacy in patients with<br>metastatic renal cell carcinoma treated with sunitinib.[14] Patients<br>with mRCC and sunitinib-induced hypertension had better outcomes than<br>those without treatment-induced HTN (objective response rate: 54.8% vs<br>8.7%; median PFS: 12.5 months, 95% confidence interval [CI] = 10.9 to<br>13.7 vs 2.5 months, 95% CI = 2.3 to 3.8 months; and OS: 30.9 months,<br>95% CI = 27.9 to 33.7 vs 7.2 months, 95% CI = 5.6 to 10.7 months; P <<br>.001 for all).<br>[edit] Other solid tumors<p>The efficacy of sunitinib is currently being evaluated in a broad<br>range of solid tumors, including breast, lung, thyroid and colorectal<br>cancers. Early studies have shown single-agent efficacy in a number of<br>different areas. Sunitinib blocks the tyrosine kinase activities of<br>KIT, PDGFR, VEGFR2 and other tyrosine kinases that are involved in the<br>development of tumours.<p> A Phase II study in previously-treated patients with metastatic<br>breast cancer found that sunitinib "has significant single agent<br>activity" [15]<br> A Phase II study of refractory non-small-cell lung cancer found<br>that "Sunitinib has provocative single-agent activity in previously<br>treated pts with recurrent and advanced NSCLC, with the level of<br>activity similar to currently approved agents." [16]<br> In a Phase II study of patients with nonresectable neuroendocrine<br>tumors (NET), 91% of patients responded to sunitinib (9% partial<br>response + 82% stable disease) [17]<p>Unsuccessful trials<p>Between April 2009 and May 2011 Pfizer has reported unsuccessful<br>late-stage trials in breast cancer, metastatic colorectal cancer,<br>advanced non-small-cell lung cancer, and castration-resistant prostate<br>cancer.[18]<br>History<p>The drug was discovered at SUGEN a biotechnology company which<br>pioneered protein kinase inhibitors. It was the third in a series of<br>compounds including SU5416 (Semaxanib) and SU6668. The concept was of<br>a ATP analogue that would compete with ATP for binding to the<br>catalytic site of receptor tyrosine kinases.[citation needed] This<br>concept led to the invention of many small-molecule tyrosine kinase<br>inhibitors including Gleevec, Sutent, Tarceva and many other cancer<br>drugs.Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-20045303202645570232011-07-19T06:36:00.001-07:002011-07-19T06:36:42.146-07:00Liege XGP xgpnFrench text, English google Translation<br><a href="http://www.urofrance.org/fileadmin/documents/data/PU/2001/PU-2001-00111274/TEXF-PU-2001-00111274.PDF">http://www.urofrance.org/fileadmin/documents/data/PU/2001/PU-2001-00111274/TEXF-PU-2001-00111274.PDF</a><br> <br> Mots-clés : Rein, pyélonéphrite, xanthogranulomateuse, biopsie percutanée, traitement médical.<br><br> O. Reul et coll., Progrès en Urologie (2001), 11, 1274-1276<br><br> CAS CLINIQUE Progrès en Urologie (2001), 11, 1274-1276<br> <br> Pyélonéphrite xanthogranulomateuse pseudotumorale : diagnostic<br> par la biopsie percutanée et succès du traitement conservateur<br><br> Olivier REUL (1), David WALTREGNY (1), Jacques BOVERIE (2), Jean de LEVAL (1),<br> Robert ANDRIANNE (1)<br><br> (1) Service d'Urologie, (2) Service d'Imagerie Médicale, Centre Hospitalier Universitaire du Sart-Tilman, Liège, Belgique<br><br>Manuscrit reçu : avril 2001, accepté : juin 2001.<br>Adresse pour correspondance : Dr. O. Reul, Service d'Urologie, Université de<br> Liège, Bloc central, 1, Sart-Tilman, 4000 Liège, Belgique.<br>e-mail : <a href="mailto:olivierreul@hotmail.com">olivierreul@hotmail.com</a><br><br> RESUME<br><br> La pyélonéphrite xanthogranulomateuse est une forme<br> inhabituelle d'infection rénale dont le diagnostic est<br> souvent méconnu avant l'intervention chirurgicale.<br> Nous rapportons le cas d'une jeune fille âgée de 19<br> ans qui présentait une masse rénale pseudotumorale. Le<br> diagnostic de pyélonéphrite xanthogranulomateuse<br> focale a été suspecté par les caractéristiques de la<br> masse aux différents examens d'imagerie médicale et<br> confirmé par l'analyse histologique d'un fragment<br> prélevé par une biopsie percutanée échoguidée. La<br> guérison a été obtenue avec un traitement<br> antibiotique.<br><br> Une exploration exhaustive comprenant une biopsie<br> rénale devrait être réalisée afin de poser le<br> diagnostic de pyélonéphrite xanthogranulomateuse avant<br> tout geste chirurgical. Nous préconisons le traitement<br> antibiotique comme traitement de première intention de<br> la pyélonéphrite xanthogranulomateuse focale.<br><br><br> OBSERVATION<br><br>Une jeune fille âgée de 19 ans a été adressée à notre<br> hôpital pour des douleurs lombaires droites<br>importantes, permanentes, présentes depuis 3 semaines<br>et en aggravation depuis 3 jours. Lors de son<br>admission, la patiente était apyrétique et ne signalait<br>aucun symptôme urinaire. Elle n'avait pas d'antécédents<br> d'infection urinaire ou de lithiase. L'examen clinique<br>était sans particularité hormis un point douloureux<br>costo-musculaire droit. Il n'y avait pas<br>d'organomégalie ni de contact lombaire au palper<br>bimanuel. Sur le plan biologique, il n'y avait pas<br> d'anomalie à l'exception d'une élévation de la CRP à<br>49 mg/l. La leucocytose était de 9780/mm3 dont 64% de<br>neutrophiles et l'hémoglobine est de 12.3g/dl. La<br>fonction rénale était conservée avec une urémie de 0.2<br> g/l et une créatinémie de 8 mg/l. La culture urinaire<br>était stérile.<br><br>L'échographie rénale a objectivé une masse hétérogène<br>de 5 cm de diamètre au pôle inférieur du rein droit<br>tandis que le rein gauche avait un aspect normal. La<br> tomodensitométrie abdominale a confirmé la présence<br>d'une lésion de 5 cm à zone centrale hétérogène et<br>hypodense entourée d'une coque rehaussée par<br>l'injection de produit de contraste (Figure 1) Une<br>seconde lésion de 1 x 1,2 cm de mêmes caractéristiques<br> densitométriques était visible à la partie antérieure<br>du pôle inférieur du rein droit. A l'artériographie<br>rénale sélective, la lésion était hypovascularisée avec<br>étirement des vaisseaux en périphérie sans<br> caractéristique de vascularisation anarchique<br>tumorale (Figure 4)<br><br>L'urographie intraveineuse puis la pyélographie<br>rétrograde, l'UIV étant insuffisante, ont révélé un<br>syndrome de masse avec refoulement des tiges<br> calicielles inférieures. <br> <br>Nous avons réalisé deux biopsies percutanées de la<br>lésion la plus volumineuse sous guidage<br>échographique. L'analyse anatomo-pathologique a<br>révélé un envahissement du parenchyme rénal par un<br> infiltrat inflammatoire chronique formé de<br>macrophages d'aspect spumeux associés à des monocytes,<br>lymphocytes et de la fibrose. Cet aspect était<br>compatible avec le diagnostic de pyélonéphrite<br>xanthogranulomateuse. La culture de la deuxième biopsie<br> était posi- tive pour des E. Coli, sensibles aux<br>quinolones. La patiente a été traitée pendant cinq<br>semaines par de la ciprofloxacine per os à raison de<br>250 mg 2 fois par j o u r. Une réduction<br>considérable du volume de la masse a été<br> observée à l'examen tomodensitométrique réalisé<br>après un mois de traitement (Figure 2) Trois mois<br>plus tard, la tomodensitométrie a révélé <br>des zones cicatricielles au niveau des sites des deux<br>lésions initiales (Figure 3). Durant les douze mois<br> suivants, aucune récidive n 'a ét é const atée.<br>L'échographie, à un an, était normale<br><br> DISCUSSION<br><br>La pyélonéphrite xanthogranulomateuse est une forme de<br>suppuration rénale chronique survenant à tout âge, le<br> plus souvent après 40 ans et touchant trois fois plus<br>fréquemment les femmes que les hommes. La forme focale<br>est de diagnostic difficile car elle est so confondue<br>avec un processus néoplasique. L'étiopathogénie de<br> la pyélonéphrite xanthogranulomateuse n'est pas connue<br>avec certitude mais plusieurs facteurs étiologiques<br>ont été incriminés dont l'obstruction de la voie<br>excrétrice (lithiase, sténose, tumeur, …), l'infection<br> urinaire récidivante plus ou moins décapitée par les<br>antibiothérapies et les déficits immunitaires [5] Aucun<br>des ces facteurs n'est présent dans notre observation.<br><br>Les patients souffrant de pyélonéphrite<br> xanthogranulomateuse focale présentent classiquement<br>une douleur intermittente du flanc, de la fièvre,<br>des frissons ou une altération de l'état général avec<br>perte de poids. La symptomatologie dure<br>habituellement depuis plusieurs semaines avant que le<br> diagnostic ne soit posé.<br><br>Sur le plan biologique, on note des signes d'infection<br>avec élévation des tests inflammatoires (C reactive<br>protein, vitesse de sédimentation, fibrinogène) et <br>hyperleucocytose. La culture urinaire est stérile dans<br> 50 % des cas de pyélonéphrite xanthogranulomateuse<br>mais la culture du tissu rénal est presque toujours posi-scan.<br>tive, comme dans notre observation. Les bactéries les <br>plus souvent en causes sont le Proteus Mirabilis et .<br> l'E.Coli. <br><br>La pyélonéphrite xanthogranulomateuse focale doit<br>être suspectée à l'examen tomodensitométrique qui<br>révèle classiquement une masse hétérogène centrée sur<br>une tige calicielle et faiblement rehaussée en<br> périphérie par le produit de contraste [7]. L'absence<br>de lymphonoeuds pathologiques, de thrombus veineux ou<br>de métastases sont des signes importants pour orienter<br>le diagnostic. L'échographie rénale, l'urographie<br> intraveineuse et la pyélographie rétrograde révèlent un<br>syndrome de masse aspécifique. Même si la<br>tomodensitométrie abdominale et l'artériographie ont<br>permis de suspecter fortement la nature inflammatoire<br>et non tumorale des lésions rénales dans le cas<br> présenté, ces deux examens ne peuvent pas exclure<br>formellement le diagnostic de lésion néoplasique.<br>Nous avons donc opté pour la biopsie percutanée de la<br>masse rénale, ce ut. Assist. qui a permis de confirmer<br> le diagnostic de pyélonéphrite xanthogranulomateuse.<br><br><br>Le traitement habituel de la pyélonéphrite<br>xanthogranulomat euse focale est malheureusement<br>souvent la néphrectomie totale ou partielle [3]. Cette<br> approche thérapeutique est attribuable à un diagnostic<br>préopératoire rarement correct ement posé [4]. Le<br>trait ement conservateur de la pyélonéphrite<br>xanthogranulomat euse pseudotumorale par une<br>antibiothérapie seule est donc une exception, avec de<br> rares cas décrits dans la littérature [1, 2, 6]<br>Pour ces cas décrits comme dans le nôtre, le<br>traitement médical s'est avéré efficace avec une<br>résolution complète des lésions rénales. n.<br><br>Nous pensons donc qu'une exploration exhaustive suivie<br> d'une biopsie percutanée pourrait être réalisée afin de<br>poser le diagnostic de pyélonéphrite<br>xanthogranulomateuse focale avant tout geste<br>chirurgical. De plus, la culture des biopsies rénales<br>permet d'identifier les micro-organismes en cause et<br> d'adapter le traitement en fonction de l'antibiogramme.<br>Nous suggérons l'utilisation du traitement antibiotique<br>comme traitement de première intention de la<br>pyélonéphrite xanthogranulomateuse focale à condition<br> qu il n'y ait pas de pathologie obstructive sousjacente <br>telle qu'une lithiase ou une lésion des voies<br>excrétrices. <br><br><br> REFERENCES<br><br> 1. AIZAWA T., KURATA M., OHKUBO Y. A case of xanthogranulo-<br> matous pyelonephritis followed by computed tomographic<br> Hinyokika Kiyo, 1998, 44, 729-732.<br> 2 . BROWN P.S. Jr, DODSON M ., WEINTRUB P. S<br> Xanthogranulomatous pyelonephritis: report of nonsur-<br> gical management of a case and review of the literature. Clin. Infe<br> Dis., 1996, 22, 308-314.<br> <br> 3. CHUANG C.K., LAI M.K., CHANG P.L.,HUANG M.H., CHU <br> S.H., WU C.J., WU H.R. Xanthogranulomatous pyelonephritis<br> experience in 36 cases. J. Urol., 1992, 147, 333-336. <br> <br> 4. EASTHAM J., AHLERING T., SKINNER E. Xanthogranulomatous<br> p yelonephritis: clin ical findings and surgical considerations .<br> Urology, 1994, 43, 295-299.<br> <br> 5. MALEK R.S., ELDER J.S. Xanthogranulomatous pyelonephritis: A<br> critical analysis of 26 cases and of the literature. J. Urol., 1977<br> 589-593.<br> <br> 6. MOLLIER S., DESCOTES J.L., PASQUIER D., COQUILLAT P.,<br> MICHEL A., DALSOGLIO S., RAMBEAUD J.J. Pseudoneoplastic <br> xanthogranulomatous pyelonephritis. A typical clinical presentation<br> but unusual diagnosis and treatment. Eur . Urol., 1995, 27, 170-173.<br> <br> 7. SHAH M., HAAGA J.R. Focal xanthogranulomatous pyelonephritis <br> simulating a renal tumor: CT characteristics. J. Comp<br> Tomogr., 1989, 13, 712-713. <br> <br> ____________________ <br> SUMMARY <br> <br> Pseudo-tumoral xanthogranulomatous pyelonephritis : dia-<br> gnosis by percutaneous biopsy and success of conservatory <br> treatment.<br> Focal xanthogranulomatous pyelonephritis is an unusual form<br> of chronic renal infection that is difficult to diagnose prior to <br> surgery. We report on a 19-year-old woman who presented with<br> a renal mass that mimicked malignancy. The diagnosis of focal <br> xanthogranulomatous pyelonephritis was first suspected by<br> radiological findings and further confirmed by histopathologic<br> examination of percutaneous biopsy specimens of the lesio<br> Successful treatment of the patient was achieved with antibiotic<br> therapy alone. Maximal efforts, including percutaneous rena<br> biopsy, should be made to establish the diagnosis of focal xan - <br> thogranulomatous pyelonephritis before a therapeutic decision <br> is reached. We recommend the use of antibiotics as a first-line <br> treatment for patients with focal xanthogranulomatous pyelone -<br> phritis. <br> <br> Key-words : Kidney, pyelonephritis, xanthogranulomatous, per - <br> cutaneous biopsy, antibiotics.<br><br><br><br>Figure 2. Après un mois de traitement, diminution importante<br>de la taille des lésions en tomodensitométrie abdominale<br> <br><br>Figure 4. Masse hypovascularisée avec étirement des <br>vaisseaux en périphérie à l'artériographie rénale sélective.<br><br><br>Figure 3. Aspect cicatriciel au contrôle tomodensitométrique<br>après 4 mois.<br><br> <br><br>GOOGLE TRANSLATION ENGLISH<br><br>SUMMARY<br><br> Xanthogranulomatous pyelonephritis is a form<br> unusual kidney infection whose diagnosis is<br> often unrecognized before surgery.<br> We report the case of a girl aged 19<br> years who had a renal mass pseudotumoral. The<br> diagnosis of xanthogranulomatous pyelonephritis<br> lens was suspected by the characteristics of the<br> mass to different medical imaging and<br> confirmed by histological analysis of a fragment<br> collected by ultrasound-guided percutaneous biopsy. The<br> cure was obtained with treatment<br> antibiotic.<br><br> An exhaustive exploration including biopsy<br> impairment should be conducted to ask the<br> before diagnosis of xanthogranulomatous pyelonephritis<br> any surgical procedure. We recommend treatment<br> antibiotic as first line treatment of<br> Focal xanthogranulomatous pyelonephritis.<br><br><br> OBSERVATION<br><br>A girl aged 19 was sent to our<br>hospital for back pain right<br> significant, permanent, present for 3 weeks<br>and worse for 3 days. During his<br>admission, the patient was afebrile and reported no<br>urinary symptoms. She had no history<br>urinary tract infection or stones. Clinical examination<br> was unremarkable except for a sore point<br>costo-muscular right. There was no<br>of organomegaly or contact palpate lumbar<br>bimanual. Biologically, there was no<br>abnormality except for elevation of CRP<br>49 mg / l. The WBC was 9780/mm3 with 64%<br> neutrophils and hemoglobin is 12.3g/dl. The<br>renal function was preserved with a blood urea of ??0.2<br>g / l and a creatinine of 8 mg / l. Urine culture<br>was sterile.<br><br>Renal ultrasound has objectified a heterogeneous mass<br> 5 cm in diameter at the lower pole of right kidney<br>while the left kidney had a normal appearance. The<br>abdominal CT scan confirmed the presence<br>a lesion of 5 cm central area and heterogeneous<br>hypodense surrounded by a shell enhanced by<br> injection of contrast (Figure 1) A<br>second lesion of 1 x 1.2 cm with the same characteristics<br>densitometric was visible at the anterior<br>the lower pole of the right kidney. A arteriography<br>selective kidney, the lesion was hypovascularisée with<br> stretching of the vessels in the periphery without<br>characteristic of chaotic vasculature<br>tumor (Figure 4)<br><br>Intravenous urography and pyelography<br>retrograde, IVU is insufficient, revealed a<br>syndrome with mass repression stems<br> caliceal below.<br> <br>We performed two percutaneous biopsies of<br>the most voluminous lesion-guided<br>ultrasound. The pathologic analysis was<br>revealed invasion of the renal parenchyma by a<br>chronic inflammatory infiltrate composed of<br> foamy macrophages aspect associated with monocytes,<br>lymphocytes and fibrosis. This aspect was<br>compatible with the diagnosis of pyelonephritis<br>xanthogranulomatous. The culture of the second biopsy<br>was posi-tive for E. Coli sensitive to<br> quinolones. The patient was treated for five<br>weeks of ciprofloxacin orally at a rate of<br>250 mg two times a j o u r. A reduction<br>in the volume of the mass was<br>observed in the CT scan performed<br>After one month of treatment (Figure 2) Three months<br> later, CT revealed<br>scarred areas at the sites of two<br>initial lesions (Figure 3). During the twelve months<br>following no recurrence n 'a and e const ATEE.<br>The ultrasound at one year, was normal<br><br> DISCUSSION<br> <br>Xanthogranulomatous pyelonephritis is a form of<br>chronic renal suppuration occur at any age,<br>usually after 40 years and three times more<br>common in women than men. Form focal<br>is difficult to diagnose because it is so confused<br> with a neoplastic process. The etiopathogenesis of<br>Xanthogranulomatous pyelonephritis is not known<br>with certainty, but several causal factors<br>which have been implicated tract obstruction<br>excretory (stones, stricture, tumor, ...), infection<br> recurrent urinary tract more or less decapitated by<br>antibiotics and immune disorders [5] No<br>of these factors is present in our observation.<br><br>Patients with pyelonephritis<br>Focal xanthogranulomatous conventionally<br> intermittent flank pain, fever,<br>chills or impairment of general health with<br>weight loss. The symptoms lasted<br>usually for several weeks before the<br>diagnosis is made.<br><br>Biologically, there are signs of infection<br> Elevated inflammatory tests (C reactive<br>protein, sedimentation rate, fibrinogen) and<br>leukocytosis. The urine culture is sterile<br>50% of cases of xanthogranulomatous pyelonephritis<br>but the culture of kidney tissue is almost always positive scan.<br> tive, as in our observation. The bacteria<br>most frequently involved are Proteus Mirabilis and.<br>E. Coli.<br><br>Focal xanthogranulomatous pyelonephritis should<br>be suspected that the CT scan<br>typically shows a heterogeneous mass centered<br> stem and calyx slightly enhanced by<br>periphery by the contrast [7]. The absence<br>lymphonoeuds of pathological thrombus or venous<br>metastases are important signs to guide<br>diagnosis. Renal ultrasound, urography<br> Intravenous pyelography and retrograde reveal a<br>Mass nonspecific syndrome. Although<br>abdominal CT scan and arteriography have<br>allowed to suspect strongly inflammatory<br>and non-tumor kidney damage in the case<br> presented, these two tests can not exclude<br>formal diagnosis of neoplastic lesions.<br>So we opted for percutaneous biopsy of<br>renal mass, it ut. Assist. which confirmed<br>the diagnosis of xanthogranulomatous pyelonephritis.<br> <br><br>The usual treatment of pyelonephritis<br>Focal xanthogranulomatous euse is unfortunately<br>often the total or partial nephrectomy [3]. This<br>therapeutic approach is due to a diagnosis<br>Correct preoperative rarely posed no way [4]. The<br> Conservative in no way related pyelonephritis<br>Xanthogranulomatous euse pseudotumoral by<br>antibiotic therapy alone is an exception, with<br>rare cases described in the literature [1, 2, 6]<br>For these cases described as in ours,<br> Medical treatment was effective with<br>complete resolution of renal injury. n.<br><br>We therefore followed an exhaustive exploration<br>a percutaneous biopsy may be performed to<br>the diagnosis of pyelonephritis<br>Focal xanthogranulomatous before any action<br> surgery. In addition, the culture of renal biopsies<br>to identify the microorganisms involved and<br>to adapt the treatment according to the antibiogram.<br>We suggest the use of antibiotics<br>as first-line treatment of<br> Focal xanthogranulomatous pyelonephritis provided<br>that there is no patho-logy obstructive sub-<br>predicate such as stones or injury tract<br>excretory.<br><br>GOOGLE TRANSLATION TO GERMAN<br><br><br>ZUSAMMENFASSUNG<br> <br> Xanthogranulomatöse Pyelonephritis ist eine Form<br> ungewöhnliche Nierenentzündung, deren Diagnose<br> oft unerkannt vor der Operation.<br> Wir berichten über den Fall eines Mädchens im Alter von 19<br> Jahren, die eine renale Masse pseudotumoral hatte. Die<br> Diagnose xanthogranulomatöse Pyelonephritis<br> Objektiv wurde von den Eigenschaften der Verdacht<br> Masse zu verschiedenen Bereichen medizinische Bildgebung und<br> bestätigt durch histologische Analyse eines Fragments<br> gesammelt durch Ultraschall-gesteuerte perkutane Biopsie. Die<br> Heilung wurde mit der Behandlung erhalten<br> Antibiotikum.<br><br> Eine erschöpfende Untersuchung einschließlich Biopsie<br> Beeinträchtigungen sollten durchgeführt, um die fragen<br> vor der Diagnose des xanthogranulomatöse Pyelonephritis<br> jedem chirurgischen Eingriff. Wir empfehlen die Behandlung<br> Antibiotika als First-Line Behandlung von<br> Focal xanthogranulomatöse Pyelonephritis.<br><br><br> BEOBACHTUNG<br><br>Ein Mädchen im Alter von 19 wurde gesendet<br>Krankenhaus für Rückenschmerzen rechts<br>signifikante, dauerhafte Geschenk für 3 Wochen<br>und schlimmer noch für 3 Tage. Während seiner<br>Aufnahme war der Patient fieberfrei und berichteten keine<br> Beschwerden beim Wasserlassen. Sie hatte keine Geschichte<br>Harnwegsinfektion oder Steine. Die klinische Untersuchung<br>war bis auf einen wunden Punkt unauffällig<br>costo-muskulösen rechten Seite. Es gab keine<br>von Organomegalie oder kontaktieren Sie tasten Lendenwirbelsäule<br> bimanuelle. Biologisch, gab es keine<br>Anomalie mit Ausnahme Höhe von CRP<br>49 mg / l. Der WBC war 9780/mm3 mit 64%<br>Neutrophilen und Hämoglobin 12.3g/dl. Die<br>Nierenfunktion wurde mit einem Blut-Harnstoff von 0,2 erhalten<br> g / l und einem Kreatinin von 8 mg / l. Urinkultur<br>war steril.<br><br>Renal Ultraschall hat eine heterogene Masse objektiviert<br>5 cm im Durchmesser am unteren Pol der rechten Niere<br>während die linke Niere hatte eine normale Erscheinung. Die<br> Bauch-CT bestätigte die Anwesenheit<br>eine Läsion von 5 cm zentralen Bereich und heterogenen<br>hypodense von einer Hülle umgeben, verstärkt durch<br>Injektion von Kontrastmittel (Abbildung 1) A<br>zweite Läsion von 1 x 1,2 cm mit den gleichen Eigenschaften<br> densitometrische wurde an der vorderen sichtbaren<br>den unteren Pol der rechten Niere. Eine Arteriographie<br>selektive Niere, wurde die Läsion hypovascularisée mit<br>Dehnung der Gefäße in der Peripherie ohne<br>Merkmal der chaotischen Gefäßsystem<br> Tumor (Abbildung 4)<br><br>Intravenöse Urographie und Pyelographie<br>retrograde, IVU ist unzureichend, ergab eine<br>Syndrom mit Masse Repression beruht<br>caliceal unten.<br> <br>Wir führten zwei perkutanen Biopsien<br> die umfangreichste Läsion-guided<br>Ultraschall. Die pathologische Analyse wurde<br>zeigte Invasion des Nierenparenchyms durch eine<br>chronisch-entzündliche des Infiltrat<br>schaumigen Makrophagen Aspekt mit Monozyten assoziiert,<br> Lymphozyten und Fibrose. Dieser Aspekt wurde<br>kompatibel mit der Diagnose Pyelonephritis<br>xanthogranulomatöse. Die Kultur der zweiten Biopsie<br>war positiv für E. Coli sensibel auf<br>Chinolone. Der Patient wurde für fünf behandelt<br> Wochen Ciprofloxacin oral mit einer Geschwindigkeit von<br>250 mg zweimal j o u r. Eine Reduktion<br>in das Volumen der Masse<br>beobachtet in den CT-Scan durchgeführt<br>Nach einem Monat der Behandlung (Abbildung 2) Drei Monate<br> später enthüllte CT<br>vernarbten Bereiche an den Standorten von zwei<br>ersten Läsionen (Abbildung 3). Während der 12 Monate<br>folgenden kein Rezidiv n 'a und e const ATEE.<br>Der Ultraschall nach einem Jahr wurde der Normalwert<br> <br> DISKUSSION<br><br>Xanthogranulomatöse Pyelonephritis ist eine Form der<br>chronischer Niereninsuffizienz Eiterung in jedem Alter,<br>in der Regel nach 40 Jahren und drei Mal mehr<br>bei Frauen häufiger als Männer. Form Mittelpunkt<br> ist schwer zu diagnostizieren, weil sie so verwirrt ist<br>mit einer neoplastischen Prozess. Die Ätiopathogenese der<br>Xanthogranulomatöse Pyelonephritis ist nicht bekannt,<br>mit Sicherheit, aber mehrere ursächliche Faktoren<br> die wurden Obstruktion verwickelt<br>Ausscheidungsorgane (Steine, Strikturen, Tumor, ...), Infektion<br>rezidivierenden Harnwegsinfektionen mehr oder weniger geköpft durch<br>Antibiotika und Immunstörungen [5] Keine<br>dieser Faktoren ist in unserer Beobachtung.<br> <br>Patienten mit Pyelonephritis<br>Focal xanthogranulomatöse konventionell<br>intermittierende Flankenschmerzen, Fieber,<br>Schüttelfrost oder Beeinträchtigung der allgemeinen Gesundheit mit<br>Gewichtsverlust. Die Symptome dauerten<br> in der Regel mehrere Wochen vor dem<br>Diagnose gestellt wird.<br><br>Biologisch gibt es Anzeichen einer Infektion<br>Erhöhte entzündliche Tests (C-reaktives<br>Protein, Blutsenkungsgeschwindigkeit, Fibrinogen) und<br>Leukozytose. Der Urin ist steril Kultur<br> 50% der Fälle von xanthogranulomatöse Pyelonephritis<br>aber die Kultur des Nierengewebes ist fast immer positiv zu scannen.<br>TIVE, wie in unserer Beobachtung. Die Bakterien<br>Am häufigsten betroffen sind Proteus mirabilis und.<br> E. Coli.<br><br>Focal xanthogranulomatöse Pyelonephritis sollte<br>werden vermutet, dass die CT-Scan<br>zeigt typischerweise eine heterogene Masse zentrierte<br>Stamm und Kelch leicht durch verstärkte<br>Peripherie durch den Kontrast [7]. Das Fehlen<br> lymphonoeuds von pathologischen Thrombus oder venösen<br>Metastasen sind wichtige Zeichen zu führen<br>Diagnose. Renal Ultraschall, Urographie<br>Intravenöse Pyelographie und retrograde zeigen eine<br>Messe unspezifischen Syndrom. Obwohl<br> Bauch-CT und Angiographie haben<br>darf vermuten, stark entzündliche<br>und Nicht-Tumor Nierenschäden bei<br>präsentiert, können diese beiden Tests nicht ausschließen,<br>formale Diagnose neoplastischer Läsionen.<br>So entschieden wir uns für eine perkutane Biopsie<br> Nieren-Masse, es ut. Assist. die bestätigt<br>die Diagnose von xanthogranulomatöse Pyelonephritis.<br><br><br>Die übliche Behandlung der Pyelonephritis<br>Focal xanthogranulomatöse euse ist leider<br>oft die vollständige oder partielle Nephrektomie [3]. Dieser<br> therapeutische Ansatz beruht auf einer Diagnose<br>Korrekte präoperative selten gestellt keiner Weise [4]. Die<br>Konservative in keiner Weise im Zusammenhang Pyelonephritis<br>Xanthogranulomatöse euse pseudotumoral durch<br> Antibiotika-Therapie allein ist eine Ausnahme, mit<br>seltenen Fällen in der Literatur [1, 2, 6] beschrieben<br>Für diese Fälle als in unseren beschrieben,<br>Ärztliche Behandlung wirksam war mit<br>eine vollständige Rückbildung der Nierenschädigung. n.<br> <br>Deshalb folgte eine erschöpfende Untersuchung<br>eine perkutane Biopsie kann durchgeführt werden<br>die Diagnose der Pyelonephritis<br>Focal xanthogranulomatöse vor jeglicher Aktion<br>Chirurgie. Darüber hinaus die Kultur des Nierenbiopsien<br> zur Identifizierung der Mikroorganismen beteiligt und<br>die Behandlung nach dem Antibiogramm anzupassen.<br>Wir empfehlen den Einsatz von Antibiotika<br>als First-Line-Behandlung von<br>Focal xanthogranulomatöse Pyelonephritis vorgesehen<br> dass es keine patho-logie obstruktive sub-<br>Prädikat wie Steine ??oder Verletzungen Darm-Trakt<br>Ausscheidungsorgane. <br><br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-69243405853042474132011-07-18T01:34:00.000-07:002011-07-18T01:35:08.969-07:00Vaccineurin also a GDR Product<p class="mobile-photo"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgK3ddmm_dwUmRI0z1uJGtIHXzDDMkQkiuzgQwA6VoTUu2TFLGm1GNOGhNk79SD3bAh4kv6FOsTQ_JFgUGxJjgn5vnYUuqG5wtKZUgoawGuaiuyambXb9zbx6eOp-bnUixLtVc96MKED3_J/s1600/saechsischesSERUMwerk-708970.jpg"><img src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgK3ddmm_dwUmRI0z1uJGtIHXzDDMkQkiuzgQwA6VoTUu2TFLGm1GNOGhNk79SD3bAh4kv6FOsTQ_JFgUGxJjgn5vnYUuqG5wtKZUgoawGuaiuyambXb9zbx6eOp-bnUixLtVc96MKED3_J/s320/saechsischesSERUMwerk-708970.jpg" border="0" alt="" id="BLOGGER_PHOTO_ID_5630608106702666914" /></a></p><h2></h2>As it turns out, the East Germans (DDR) made Vaccineurin, too. It seems to have been used for psychiatry as well.<br>When Suedmedica in Munich stopped production of coley's toxins-type vaccineurin, the sächsiche serumwerke did too.<br> Maybe both were taken over by Glaxo smith kline?<br><br>Much good research on vaccines must have been undertaken in Dresden. Below is a german story,<br>and a google translation in english<br><br>In Dresden 1911 much money was spent on a ferment-technique to identify cancer. Who knows what that was?<br> Please leave a comment!!<br><br><br><img alt="http://www.dhm.de/gos-cgi-bin/jpeglogoneu?ak601/ak601286" src="http://www.dhm.de/gos-cgi-bin/jpeglogoneu?ak601/ak601286"><br><br>Verpackung des Vaccineurin II-Serums mit Gebrauchsanweisung<br> <br>Datensatz GOS-Nr. AK601285<br>Inventarnr. HI 72/132.22<br>Alltagskultur I: Gesundheitswesen > Medizin > Impfstoff > Vaccineurin B<br><br>Verpackung des Vaccineurin B-Serums<br><br>Datierung: von 1961 bis 1969<br> Werkstatt: Sächsisches Serumwerk KG, Dresden<br>Entstehungsort: Dresden<br>Entstehungsland: Deutschland<br>[historisch: Deutsche Demokratische Republik]<br>________________________________<br>Maße: 1,5 cm (Höhe), 7 cm (Breite), 8,6 cm (Länge)<br> Material/Technik: Papier : Pappe / gestanzt, gepresst<br>________________________________<br>Schlagworte: Arzneimittel · Verpackung · Gesundheitswesen · Medizin · DDR-Produkt ·<br><br><img alt="http://www.dhm.de/gos-cgi-bin/jpeglogoneu?ak601/ak601282" src="http://www.dhm.de/gos-cgi-bin/jpeglogoneu?ak601/ak601282"><br> <br><h2><strong>Vaccineurin I</strong></h2><br><img alt="http://www.dhm.de/gos-cgi-bin/jpeglogoneu?ak601/ak601283" src="http://www.dhm.de/gos-cgi-bin/jpeglogoneu?ak601/ak601283"><br><br>Vaccineurin 1/15<br><br><img alt="http://www.dhm.de/gos-cgi-bin/jpeglogoneu?ak601/ak601285" src="http://www.dhm.de/gos-cgi-bin/jpeglogoneu?ak601/ak601285"><br> Vaccineurin B<br><br><br><img alt="http://www.dhm.de/gos-cgi-bin/jpeglogoneu?ak601/ak601284" src="http://www.dhm.de/gos-cgi-bin/jpeglogoneu?ak601/ak601284"><br><br><span class="st"><em>Febrivaccin</em> Serie II zur Fiebertherapie von 1961 bis 1969<br> <br></span>2008 Das Sächsische Serumwerk Dresden bekommt einen neuen Namen: GlaxoSmithKline Biologicals<br>1991 Übernahme vom SSW durch SmithKline Beecham <span class="st">Zirkusstraße 40, D- 01069 Dresden</span><br> In den Jahren 1909 bis 1910 erfolgte der Aufbau des Sächsischen Serumwerkes und Institutes für Bakteriotherapie auf der Löbtauer Str.45<br> Die dabei erzielten Gewinne ermöglichten die kostspieligen Untersuchungen zur Herstellung eines<br>Karzinomserums für die <b>fermentative Erkennung von Krebserkrankungen</b>.<br>Für diesen Zweck inve- stierte das Serumwerk etwa 100.000 Goldmark.<br> <br><img alt="http://u.jimdo.com/www25/o/se6e58aea4731bd32/img/i071af5ecb6c12486/1279796545/std/image.jpg" src="http://u.jimdo.com/www25/o/se6e58aea4731bd32/img/i071af5ecb6c12486/1279796545/std/image.jpg" height="279" width="382"><br> <br><br>Sächsisches Serumwerk Dresden um 1915<br><br><a href="http://lingner-archiv.jimdo.com/lingner-biographie/s%C3%A4chs-serumwerk/">http://lingner-archiv.jimdo.com/lingner-biographie/s%C3%A4chs-serumwerk/</a><br><br> Sächsisches Serumwerk<br> <br>Es waren vor allem der Botaniker und Pflanzenphysiologe Ferdinand Julius Cohn (1828-1898) und Robert Koch (1843-1910), die die wissenschaftliche Bakteriologie in Deutschland begründeten. Beschäftigte sich die bakteriologische Forschung in ihrer frühen Entwicklungsphase insbesondere mit den Möglichkeiten des Erregernachweises, so wuchs in den achtziger Jahren des 19. Jahrhunderts das Interesse an spezifischen Bakteriengiften und vom Körper gebildeten Antitoxinen. 1890 konnte der Koch-Schüler und -Mitarbeiter Emil von Behring (1854-1917) durch Immunisierungs- versuche an Tieren die Bildung von Antitoxinen belegen. Es gelang ihm in den neunziger Jahren, ein Diphtherieserum (ein Antitoxinkonzentrat gegen Diphtheriebakterien) zu entwickeln und erstmalig diphtheriekranke Kinder erfolgreich zu behandeln. Damit war der Anfang der serumtherapeutischen Ära gemacht, und es entwickelte sich in der Folgezeit die Blutserumtherapie. Lingner war von der Möglichkeit, Bakterien mit ihren "eigenen Waffen" zu bezwingen, begeistert und plante schon frühzeitig die Herstellung von entsprechenden Substanzen. Hueppe berichtete, dass die Einführung des Diphtherieserums durch von Behring (dieser hatte dafür 1901 den Nobelpreis erhalten) Lingner zur Aufnahme der Se- rumherstellung veranlasste. 1902 erwarb Lingner von dem bekannten Münchner Bakteriologen Prof. Rudolph Emmerich (geb. 1852) das Verfahren zur Herstellung von Pyocyanase. Dieses von Pyocyaneus-Kulturen gebildete bakteriolytische Enzym fand als Heilmittel gegen Diphtherie, Blutvergiftung, Milzbrand, Soor und Genickstarre Verwendung.<br> <br>1903 begründete Lingner im Dresdner Chemischen Laboratorium Lingner die Bakteriologische Abteilung zur Herstellung von Pyocyanase. Diese Abteilung auf der Nossener Str.2/4 wurde von Dr. L. Lange geleitet. Hier erfolgte auch die Fertigung von Modellen, Moulagen und Bakterienkulturen für die Ausstellung "Volkskrankheiten und ihre Bekämpfung" 1903 in Dresden. Somit war auch der Vorläufer der späteren Lehrmittelwerkstätten des Deutschen Hygiene-Museums begründet. 1904 wurde die Bakteriologische Abteilung nach der Kaitzer Straße 22, I. Etage, verlegt und in Folge als Bakteriologisches Institut bezeichnet. Das Institut besaß unter anderem technische Einrichtungen zur Herstellung von Pyocyanase. In Kulturkolben erfolgte die Anzüchtung von Pyocyaneus-Kulturen, die das bakteriolytische Enzym bilden. Durch Filtration und Eindampfung im Vakuum wurde die Enzymlösung auf 1/10 ihres Volumens konzentriert. Mittels eines Elektromotors erfolgte die Herstellung der dazu erforderlichen luftleeren Flaschen. Im Juni 1906 verließ Dr. Lange das Institut und erhielt 1907 eine Privat-Dozentur an der Kgl. Sächs. Technischen Hochschule in Dresden. Um 1912 wurde Prof. Lange als Oberregierungsrat an das Reichs- gesundheitsamt Berlin berufen. Nach dem Ausscheiden von Lange über- nahm der Apotheker Glaser, ehemaliger Mitarbeiter von Prof. Emmerich, die Leitung des Bakteriologischen Institutes. Neben Glaser waren zwei Che- miker und zwei Diener im Institut beschäftigt. Inwieweit die Pyocyanase als pharmazeutisches Produkt verkauft bzw. in der Kinderklinik mit Säuglingsheim zur Anwendung gelangte, konnte nicht ermittelt werden. Auch fehlen Belege über eine mögliche Zusammenarbeit zwischen dem Bakteriologischen Institut und der Zentralstelle für Zahnhygiene. Letztere Ein- richtung befand sich von 1904-1906 im Erdgeschoss der Kaitzer Straße 22. Carl Roese, ihr Leiter, war vor seiner Berufung nach Dresden ebenfalls bei Prof. Emmerich in München bakteriologisch tätig. Das Bakteriologische Institut wurde 1908 in die erweiterte Fabrik auf der Nossener Str.2/4 verlegt. Für die weitere Entwicklung des Bakteriologischen Institutes bis zur Gründung des Sächsischen Serumwerkes waren die sich entwickelnden Kontakte zum Hygiene Institut der Universität Bern und dem Schweizer Serum- und Impfinstitut Bern entscheidend. Über das Zustandekommen dieser Beziehung lassen sich folgende Vermutungen anstellen: Zur Vorbereitung der Ausstellung "Volkskrankheiten und ihre Bekämpfung" 1903 begründete Lingner ein Ehrenkomitee, in dem unter anderem Prof. Richard Pfeiffer (1858- 1945), der Entdecker des Influenza-Bazillus und Bakteriolysins von Choleravibrionen, mitarbeitete. Über Pfeiffer könnte Lange, der wissenschaft- liche Betreuer der Ausstellung und Leiter der Bakteriologischen Abteilung, Verbindung zum Direktor des Hygiene Institutes der Universität Bern, Prof. Wilhelm Kolle (1868-1935), aufgenommen haben. Professor Pfeiffer arbeitete jahrelang mit Professor Kolle über Grundlagen der Immunität bei Cholera- und Typhusinfektionen zusammen. Auch ein unvermittelter Besuch Lingners am Hygiene Institut der Universität Bern scheint denkbar, da er in Vorbereitung seiner Ausstellung 1903 mehrere Universitätsinstitute besuchte, um sich insbesondere Sammlungen von Bakterienreinkulturen anzusehen.<br> <br>Prof. Kolle fungierte als Wissenschaftlicher Leiter des 1898 in Bern gegründeten Schweizer Serum- und Impfinstitutes. Ein Protokoll der Aufsichtsratssitzung des Schweizer Serum- und Impfinstitutes vom 9. Januar 1909 beleuchtet die Zusammenarbeit mit Lingner [158]. Demnach vermittelte Prof. Kolle die Kontakte zwischen Lingner und dem Schweizer In- stitut. Auf Betreiben Kolles wurden seit Oktober 1908 Vgeführt, die im Januar 1909 zum Abschluss kamen. Danach verpflichtete sich das Schweizer Serum- und Impfinstitut zur Unterstützung beim Aufbau des Sächsischen Serumwerkes und zur Überlassung von Absatzmärkten. Als Leiter des zu gründenden Sächsischen Serumwerkes wurde Privatdozent Dr. Otto Heller eingesetzt. Heller habilitierte sich als Privatdozent und war am Berner Universitäts-Institut für Infektionskrankheiten unter Kolle tätig. Zu seinen Forschungsthemen zählte der Versuch zur Herstellung eines nichtinfektiösen Impfstoffes gegen Tollwut [193]. Prof. Kolle versicherte gegenüber dem Schweizer Serumwerk, die wissenschaftliche Oberleitung in Dresden für mindestens drei Jahre zu führen. Lingner verpflichtete sich zur Zahlung von jährlich zehn Prozent des Reingewinns (Minimum: 8.000 Mark) für zehn Jahre an das Schweizer Serumwerk. Zusätzlich hatte Lingner eine Pauschalabfindung von 50.000 Mark zu zahlen. Davon erhielt Kolle zweimal 6.000 Mark und vom Reingewinnanteil 3.000 Mark pro Tätigkeitsjahr.<br> <br>Nach Vertragsabschluß wurde Lingner Aufsichtsratsmitglied im Schweizer Serum- und Impfinstitut Bern. Er gewährte dem Schweizer Institut eine Anleihe von 5.000 Franken, Zeitpunkt und Grund sind unbekannt [41]. Im Februar 1909 teilte Lingner dem Ministerium des Innern mit, dass er beabsichtigt, auf der Löbtauer Straße 45 "Einrichtungen für die Fabrikation und den Vertrieb von Heilsera zu treffen". Zu diesem Zwecke mietete er von der Aktienbierbrauerei Gambrinus entsprechende Gebäude. Unter Hellers Leitung entstanden Räume für die Verwaltung, Laboratorien, Ställe für 30 Pferde zur Serumgewinnung und Kühl-, Aufbewahrungs-, Ab- füll- und Verpackungsräume.<br> <br>In den Jahren 1909 bis 1910 erfolgte der Aufbau des Sächsischen Serumwerkes und Institutes für Bakteriotherapie auf der Löbtauer Str.45. Daneben bemühte sich Lingner, die formellen Genehmigungen für die geplante Serumherstellung zu beschaffen. Neben dem Innenministerium, der Kreishauptmannschaft Dresden und der Medizinalpolizei mußte das Gewerbeamt tätig werden.<br> <br>1910 zeigte Lingner dem Gewerbeamt Dresden die Absicht zur Eröff- nung des Sächsischen Serumwerkes und Institutes für Bakteriotherapie an. Mit Schreiben des Gewebeamtes vom 19.Juli 1910 erhält Lingner letztendlich die Erlaubnis "...zur Herstellung und Vertrieb der Heilseris". Am 17. Oktober 1911 wurde das Sächsische Serumwerk und Institut für Bakterio- therapie als GmbH im Handelsregister beim Amtsgericht Dresden registriert. Das Direktorat wurde mit Otto Heller besetzt und die Herren Bethke und Reichelt zu Geschäftsführern ernannt, auch war Georg Seiring an der Leitung des Unternehmens beteiligt. Lingner hielt als Vorsitzenderer des Aufsichtsrates maßgebliche Gesellschaftsanteile. Erste Erfolge erzielte das Sächsische Serumwerk mit der umfassenden Bereitstellung von Seren und Impfstoffen gegen Cholera und Typhus im ersten Balkan- krieg 1912/13. Die dabei erzielten Gewinne ermöglichten die kost- spieligen Untersuchungen zur Herstellung eines Karzinomserums für die fermentative Erkennung von Krebserkrankungen. Für diesen Zweck inve- stierte das Serumwerk etwa 100.000 Goldmark. Ab 1912 führte eine bakte- riologisch-serologische Untersuchungsstelle im Serumwerk unter anderem die Wassermann ́sche Reaktion zur Syphilisdiagnostik durch.<br> <br>Der erste Weltkrieg setzte diesen intensiven Forschungen jedoch vor- erst ein Ende, da an der Front ein großer Bedarf an Tetanusserum zu decken war. Auch wurden Seren gegen Diphtherie, Ruhr, Cholera, Gasbrand und Strepto- und Pneumokokken sowie Pest benötigt und hergestellt. Seiring beschreibt die Situation wie folgt: "Der Krieg brachte aber wieder andere Aufgaben. Man hatte allgemein mit einer kurzen Kriegsdauer gerechnet und deshalb für eine längere Zeit nicht vorgesorgt. Das Sanitätswesen war am meisten im Rückstand. So fehlte u.a. Tetanus-Serum fast vollständig. Ich übernahm die betriebliche Leitung des Sächsischen Serumwerkes und ließ sofort 200 Pferde impfen, die wir von der Heeresleitung zur Verfügung gestellt bekamen, um tunlichst schnell das wichtige Serum zu beschaffen. Zusätzlich zur eigenen Produktion erwarb das Sächsische Serumwerk im Auftrag der deutschen Heeresverwaltung Seren im Ausland, dabei könnte Lingner seine Beziehungen zum Schweizer Serum- und Impfinstitut genutzt haben. Nach dem ersten Weltkrieg arbeitete das Sächsische Serumwerk vorrangig auf dem Gebiet<br> <br>der Syphilisbekämpfung, der Proteinkörper-Therapie und der Tu- berkulosebekämpfung. Nach Lingners Tod wurde entsprechend der testamentarischen Verfügung den Angestellten und Arbeitern des Sächsischen Serumwerkes eine einmalige Geldzuwendung in der Gesamthöhe von etwa 6.700 Mark ausgezahlt. Lingners Gesellschaftsanteile konnten im Fe- bruar 1917 mit einem Gewinn von 30.000 Mark verkauft werden. Nach der Umwandlung zur Aktiengesellschaft 1922 wurde im Sinne Lingners ein Vertreter der Landesregierung Sachsens in den Aufsichtsrat delegiert, um die Interessen der Allgemeinheit für die Bekämpfung der Volkskrankheiten zu sichern. Die Beziehungen zum Schweizer Serum- und Impfinstitut blieben durch die Berufung seines Direktors, Paul Gardinaux, in den Aufsichtsrat des Sächsischen Serumwerkes bestehen.<br> <br>google translation<br><br><br>Saxon Serum Plant<br><br>It was primarily a botanist and plant physiologist Ferdinand Julius Cohn (1828-1898) and Robert Koch (1843-1910) who founded the scientific bacteriology in Germany. Employees in the bacteriological research in its early development stage, particularly with the possibilities of pathogen detection, it grew in the eighties of the 19th Century, interest in specific bacterial toxins and antitoxins made by the body. 1890, the cooking school staff and Emil von Behring (1854-1917) supported by immunization experiments in animals, the formation of antitoxins. He succeeded in the nineties to develop a diphtheria serum (an anti-toxin concentrate against diphtheria bacteria) and to treat children suffering from diphtheria for the first time successfully. Thus the beginning of the therapeutic serum era was made, and it developed in the period following the serum therapy. Lingner was the possibility of bacteria with their own "weapons" to defeat, thrilled and planned early on the production of corresponding substances. Hueppe reported that the introduction of the diphtheria serum from Behring (this had it received the 1901 Nobel Prize) Lingner to accommodate the production of serum induced. Lingner 1902 acquired by the famous Munich bacteriologist Professor Rudolph Emmerich (born 1852), the process for the production of pyocyanase. This formed by pyocyaneus cultures bacteriolytic enzyme found as a remedy for diphtheria, blood poisoning, anthrax, thrush and use a stiff neck.<br> <br>Founded in 1903 Lingner Lingner Dresdner chemical laboratory for the production of the Bacteriological Department pyocyanase. This department on the Nossener Str.2 / 4 was directed by Dr. L. Lange. This was also the production of models, plaster casts, and bacteria cultures for the exhibition "common diseases and their control" in 1903 in Dresden. Consequently, the precursor of the later teaching aid workshops of the German Hygiene Museum was founded. In 1904, the Bacteriological Department after 22 Kaitzer street, I. floor was laid, and named in sequence as the Bacteriological Institute. The Institute had among other technical equipment for the manufacture of pyocyanase. In culture flasks was the cultivation of pyocyaneus cultures that make up the bacteriolytic enzyme. By filtration and evaporation in vacuum, the enzyme solution to 1 / 10 of their volume was concentrated. By an electric motor was required to manufacture the vacuum bottles. In June 1906, Dr. Long left the institute in 1907 and received a private teacher at the Kgl. Saxon. Technische Hochschule in Dresden. By 1912 Professor Lange was appointed as a senior executive officer of the Reich Health Office in Berlin. Following the departure of Long took over the pharmacist Glaser, former co-worker of Prof. Emmerich, head of the Bacteriological Institute. Glaser next two chemists and two servants were employed at the Institute. The extent to which pyocyanase as a pharmaceutical product sold in the children's hospital or home for use with infants arrived, could not be determined. Also, evidence is lacking on possible cooperation between the Bacteriological Institute and the Centre for dental hygiene. The latter facility was located on the ground floor of 1904-1906 Kaitzer 22nd Street Carl Roese, its director was, before his appointment to Dresden with Prof. Emmerich also bacteriologically active in Munich. The Bacteriological Institute was expanded in 1908 moved the factory to the Nossener Str.2 / 4. For the further development of the Bacteriological Institute until the founding of the Saxon Serumwerk the developing contacts with the Hygiene Institute of the University of Bern and the Swiss Serum and Vaccine Institute Berne were crucial. About the genesis of this relationship can employ the following assumptions: The preparation of the exhibition "common diseases and their control" in 1903 founded Lingner an honorary committee, which included Prof. Richard Pfeiffer (1858 - 1945), who discovered the influenza bacillus and bacteriolysine of collaborated cholera. About Pfeiffer might Lange, the scientific supervisor of the exhibition and director of the Department of Bacteriology, connect to the director of the Hygiene Institute of the University of Bern, Prof. Wilhelm Kolle (1868-1935), was added. Professor Pfeiffer worked together for years with Professor Kolle on the fundamentals of immunity in cholera and typhoid. Even a sudden visit Lingner the Institute of Hygiene, University of Bern seems conceivable, since he visited in preparation for his 1903 exhibition several university institutes, in particular, to collections of pure cultures of bacteria to be considered.<br> <br>Prof. colleagues acted as Scientific Director of the established in 1898 in Bern, Swiss Serum and Vaccine Institute. A log of the Supervisory Board meeting of the Swiss Serum and Vaccine Institute, 9 January 1909 highlights the cooperation with Lingner [158]. Therefore mediated contacts between colleagues Prof. Lingner and the Swiss Institute. At the instigation of CK were Vgeführt since October 1908, which came in January 1909 for completion. Thereafter, the Swiss Serum and Vaccine Institute has committed itself to support the establishment of the Saxon Serum plant and frees up markets. As head of the serum to be founded Saxon work professor Dr. Otto Heller was used. Heller qualified as a lecturer and was at the Bern University Institute for infectious diseases among active colleagues. His research topics of the trial was one for making a non-infectious vaccine against rabies [193]. Professor Kolle insured against the Swiss Serum works to lead the senior scientific leadership in Dresden for three years. Lingner undertook to pay ten percent per year in net income (minimum: 8,000 dollars) for ten years at the Swiss Serum plant. In addition, Lingner had one lump sum to pay 50,000 marks. Of these, 6,000 marks and two colleagues received from the net income per share 3000 Mark year of activity.<br> <br>After the contract was Lingner Board Member of the Swiss Serum and Vaccine Institute, Berne. He granted the Swiss Institute a loan of 5,000 francs, time and reason are unknown [41]. Lingner said in February 1909 with the Ministry of the Interior, that he intends "to take equipment for the manufacture and distribution of medicinal Sera" on the road Löbtauer 45th For this purpose he rented from the corresponding shares Gambrinus brewery building. Heller's leadership came under the administration rooms, laboratories, stables for 30 horses for serum collection and cooling, storage, bottling and packaging facilities.<br> <br>In the years 1909 to 1910 was the establishment of the Saxon Serum Institute of Bakteriotherapie and work on the Löbtauer Str.45. In addition, Lingner tried to obtain the formal approval for the planned production of serum. In addition to the Interior Ministry, the district chief of Dresden and the team had Medizinalpolizei the trade office act.<br> <br>Lingner in 1910 showed the trade office's intention to open the Dresden Saxon Serumwerk and Institute for Bakteriotherapie. By letter dated July 19, 1910 Office of the tissue Lingner ultimately receives the permission, "... for the production and distribution of Heilseris". On 17 Was registered in October 1911, the Saxon Serum Plant and Institute for Bakteriotherapie as GmbH in the Commercial Register at Amtsgericht Dresden. The Directorate was staffed by Otto Heller and the men appointed as managing directors and Reichelt Bethke, George Seiring also was involved in the management of the company. Lingner did as Chairman of the Board relevant shares. Initial successes achieved, the Saxon Serum Plant with the comprehensive provision of sera and vaccines against cholera and typhoid in the first Balkan war 1912-13. The resulting profits allowed the costly tests to produce a serum for the fermentative cancer detection of cancer. For this purpose, the serum plant invested about 100,000 gold marks. From 1912, a bacteriological-serological investigation resulted in serum plant site including the Aquarius? Chemical reaction for syphilis diagnostics.<br> <br>The First World War, this intensive research, however, for the time being, as was the front cover of a great need for tetanus serum. Sera were also against diphtheria, dysentery, cholera, gas gangrene and needed Streptound pneumococcal and plague and manufactured. Seiring describes the situation as follows: "The war brought back but other tasks. They had generally expected a short war and therefore not made provisions for a long time. The medical service was mostly in the residue. Would lack e.g. Tetanus serum almost completely. I took over the operational management of the Saxon work, and serum was immediately inoculate 200 horses, which we got from the army command made available to if possible to quickly obtain the important serum. In addition to its own production, the Saxon Serum Plant acquired on behalf of the German army administration sera abroad, it could have used his connections to the Lingner Swiss Serum and Vaccine Institute. After World War II, the Saxon Serum Plant worked primarily in the field<br> <br>the fight against syphilis, the protein-body therapy and tuberculosis control. According to Lingner's death was paid according to the testamentary disposition of the employees and workers of the Saxon Serumwerk one-time cash grant in the total height of about 6,700 marks. Lingner's shares could be sold in February 1917 with a profit of 30,000 marks. After the conversion to a stock corporation in 1922 in the sense Lingner, a representative of the state government of Saxony has been delegated to the Supervisory Board, to secure the interests of the community in the fight against endemic diseases. Relations with the Swiss Serum and Vaccine Institute remained with the appointment of its director, Paul Gardinaux exist in the board of the Saxon Serum plant<br> <br><br> <br><br> <br><br><br><br><br><br><br><br><br><br><br><br><br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-65128614309795115032011-07-17T06:41:00.000-07:002011-07-17T06:42:08.141-07:00Coley's Toxins -Clinical Trials Fraud<i>this is quotable!!</i><br><br><b>Why Coleys Toxins has not been widely used despite it's results<br></b><br><font size="1">Submitted by CancerHusband on Wed, 08/18/2010 - 14:26<br></font><br>Back in 2008, we asked our oncologist at Stanford University about immunotherapy. My wife had completed surgery, radiation and chemotherapy. Yet, despite having gone through all that, the odds of recurrence for Synovial Sarcoma are very high, at 50%. And upon recurrence, death almost always follows shortly. Hence, we were actively looking for anything else that could give us an edge.<br> <br>Our former oncologist told us that sarcomas are not immunogenic. By this, she meant that all evidence indicates that sarcomas do not respond to modern immunotherapy. By then, I had already researched Coley's Toxins to a reasonable extent and read numerous case studies of large, bulky sarcomas, melting away completely and staying away for years. Thus, I was perplexed by the apparent discrepancy.<br> <br>A common misconception <br><br>Our former oncologist explained that Coley's Toxins is one of the fringe alternative therapies that have no evidence of working for sarcomas. If I remember correctly, she said that Coleys has been tried only for lung cancer, and not for sarcomas -- and even so, there wasn't any real evidence that it worked (for lung cancer).<br> <br>With all due respect, her view of Coley's was incompatible with what I had researched. William Coley, after all, was head of the bone sarcoma unit at the predecessor of Sloan Memorial Hospital in NYC. He treated mainly sarcoma patients with his toxins. This contradicted our the assertion that it had been tried for lung cancer but not sarcomas.<br> <br>Furthermore, Coley observed that his toxins seemed to work better for sarcomas than carcinomas. Yet another contradiction to the statement that "sarcomas are not immunogenic". To be fair, the "sarcomas aren't immunogenic" statement applies to "modern" immunotherapy used from the 1970s, 80s and 90s. Indeed, these have not been very successful. In recent years, however, immunotherapy has been making a comeback. The news is now filled with companies announcing their cancer immunotherapy products ad trials.<br> <br>It would seem that our former oncologist (along with many other doctors) was not aware of the rich and extensive history behind Coley's Toxins, dating further back to the early 1890s -- a history that may yield hope and promise for some cancer patients.<br> <br><b>Failure by our FDA. The American Cancer Society blacklist.<br></b><br>In fact, Coley's Toxins was used by many physicians in the US since William Coley's time until the 1950s . The critical turning point came <b>in 1963</b> when the <b>FDA ruled Coley's treatment a "new drug"</b> and therefore made it illegal to administer in the US. The <b>FDA refused to grandfather Coley's toxins</b> into existing practice, <b>as it did with aspirin and other long established products</b>. By this time, Coley's Toxins had already been <b>used </b>in the US <b>for </b>a whopping <b>70 years</b>!<br> <br>The net result was a severe blow to cancer patients. Oncologists trained after 1963 eventually never heard about Coleys Toxins. This was further compounded by the American Cancer Society's absurd claim that Coley's Toxins was mere quack therapy. The ACS blacklisted it along with other alternative cancer treatments, thus dooming it into "quack-therapy land" for decades. It was only in the 90s, that the ACS finally withdrew Coley's from their blacklist -- thanks to the efforts of Dr. Lloyd Old and Helen Coley Nauts.<br> <br>For some, it wouldn't be too far fetched a leap to imagine that the pharmaceutical industry lobbyists may have been responsible behind the ACS' push to suppress alternative treatments - treatments that may divert patients away from lucrative chemotherapeutic drugs. But again, this is all supposition that's impossible to prove.<br> <br>This brings me to another important point why Coley's virtually disappeared and may never, ever make it back to mainstream medicine. According to this academic analysis, it takes $802 million to bring a new drug to market .<br> <br>The FDA rules have GOT to change<br><br>As it stands, any drug that cannot earn a minimum of $802 million will probably not make it through FDA trials.<br><br>In order to pass the FDA trial process, the drug needs to be tested in a well controlled setting via clinical trials. While this sounds good and in the interest of the consumer, in practice, it takes LOTS of money. A friend of ours explained her perspective on this issue.<br> <br>This friend works for a company that runs clinical trials for the likes of big pharmaceuticals such as Pfizer, Johnson and Johnson etc. She told us that some doctors love to run clinical trials for the money - lots of it! For example, for each patient recruited to a trial, the doctor may receive $5000 to $10,000. That's what they may receive for recruiting the patient. On top of that, whenever the patient returns to the doctor for periodic evaluation, more money is paid.<br> <br>You can imagine then, if a physician is able to recruit 100s of patients, there's the potential to make serious money for that one trial. And that's only one trial site. Most trials have multiple trial sites. All this money comes from the drug company trying to get their drug approved.<br> <br>Assuming all this is true, and that our friend is not misrepresenting the facts, it discourages me to think that money is the reason why something like Coley's will probably NEVER make it past the FDA clinical trial process - unless a large pharmaceutical company finds it profitable to market.<br> <br>It doesn't matter if Coley's Toxins has shown compelling evidence of achieving significantly better results compared to conventional chemotherapy or radiation. It doesn't matter if it's the only modality that offers any credible evidence of being able to cause large, widespread sarcomas to melt away (and stay away), with no indication of long term toxicity. It doesn't matter if 8 out of 19 advanced stage breast cancer patients resistant to conventional treatment achieved full and complete regression of their cancers.<br> <br>If it cannot be patented or protected (intellectually) to earn back more than $802 million, it ain't going to get through the FDA trial process.<br><br>That's the bottom line. Discouraging isn't it? In it's enthusiasm to protect consumers, the FDA has essentially excluded any drug or treatment that's too cheap to make . Again, a cynic might say that this dynamic has been deliberately put in place by drug companies as a protective moat around their development process.<br> <br>Has modern oncology failed us?<br><br>Even more frustrating is the failure by modern oncology to see beyond these restrictive dynamics. In our personal experience, all the oncologists we have personally encountered have been extremely caring individuals. We believe they have meant only the best for my wife, and always operated in her best interest. Yet, for a disease that holds no definite cure (and one where there is often subjectivity in determining the best treatment plan) -- caring and operating in best interest is not enough. It behooves oncology to go the extra mile and step outside the box.<br> <br>Consider that the "box" is essentially defined by the FDA, which in turn, is defined by financial dynamics that preclude unpatentable drugs. Failing to explore outside the box is a fatal flaw that will divert attention towards managing details (such as minimizing toxicity, balancing side effects with quality of life). This, in turn, leads to missing the big picture -- that is, adopting a whole different approach to that may offer significant benefit - or perhaps even a cure.<br> <br>For many of us cancer patients, the odds are simply too high. We cannot afford to merely follow the official treatment guidelines. Following those guidelines are undoubtedly the right thing to do for a great many cases. However, there are many other cases where they are insufficient. They may be safe and convenient. But they may not be the best thing to do for the patient. When there is enough evidence that an unapproved treatment modality may offer serious benefit to a cancer patient whose prognosis is grim, isn't it then unthinkable NOT to pursue or at least investigate that modality to the utmost?<br> <br>It simply isn't good enough to say "let's wait for the clinical trial process to weed out what works". Again, what if something like Coley's Toxins really does work much better than chemo (for certain cases). And yet, it will never make it through the trial process because of financial reasons?<br> <br>From a moral standpoint, it simply is not right to fall behind official guidelines and wait for someone "else" to prove it. If William Coley hadn't gone scouring the tenements to track down Fred Stein, but rather, remained satisfied to stay within the four walls of his surgical ward to treat patients coming to him, the world would never have benefited from his discoveries.<br> <br>Will any physician or oncologist go that far for their patient today? Will you not take up the challenge, make that mental leap beyond official treatment guidelines, and evaluate the evidence for yourself (rather than relying on potentially flawed meta-analyses)? What if infusing the patient with something so safe that it has no evidence of any long term toxicity can cure - yes CURE - your patient of cancer when nothing else works? Should you not <b>at least take a long, hard look at it</b>?<br> <br><br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-9082710933309633552011-07-16T04:59:00.001-07:002011-07-16T04:59:46.717-07:00mostly German: 2002 hergestellt? WO ist der Nierenkrebs Impfstoff denn nun?<br><font size="6">ELECTROFUSION</font><br>CANCER VACCINE<br><br><a href="http://www.fresenius.de/internet/fag/de/faginpub.nsf/AttachmentsByTitle/geschaeftsbericht_00/$FILE/gb_00.pdf">http://www.fresenius.de/internet/fag/de/faginpub.nsf/AttachmentsByTitle/geschaeftsbericht_00/$FILE/gb_00.pdf</a><br> <br>Seite 71<br><br> BioCore hat auf dem Gelände der Universität Göttin- <br>gen mit dem Bau eines Labors zur Herstellung dieser <br>zellulären Produkte begonnen. Als erstes Produkt wird <br>im Jahr 2002 für klinische Prüfungen ein Impfstoff zur <br> Behandlung des Nierenzellkarzinoms hergestellt, ein <br>Krebs, an dem jährlich allein in Deutschland etwa 12.000 <br>Menschen erkranken. Dieser Impfstoff wirkt nicht wie <br>die in der Krebstherapie bislang bekannten Substanzen, <br> sondern aktiviert das körpereigene Immunsystem des <br>Patienten. Dabei wird die Eigenschaft der Tumore ausge- <br>nutzt, ganz spezielle Merkmale an der Oberfläche auszu- <br>bilden, die vom Körper erkannt werden. Der Impfstoff <br> wird durch eine Elektrofusion von Krebszellen des Pati- <br>enten mit Abwehrzellen eines gesunden Spenders er- <br>zeugt. So entsteht durch Verschmelzung eine Zelle, die <br>zum einen die Tumoreigenschaften des Patienten auf- <br> weist und zum anderen die fremden Merkmale des Spen- <br>ders trägt. Diese fremden Merkmale helfen dann dem <br>Immunsystem des Patienten, die Oberflächeneigenschaf- <br>ten der Tumore als krank zu erkennen und aktiv dagegen <br> vorzugehen. Die bisher veröffentlichten Forschungser- <br>gebnisse haben international bei Experten viel Beach- <br>tung gefunden. <br><br><br>========<br><br><a href="http://cancerguide.org/fusionvaccineabstracts.html">http://cancerguide.org/fusionvaccineabstracts.html</a><br> <br>Hybrid cell vaccination safe and effective therapy for renal cell carcinoma!!!!!!<br><br>Abstract:<br><br>Regression of human metastatic renal cell carcinoma after vaccination with tumor cell - dendritic cell hybrids. Nature Medicine March 2000 Volume 6 Number 3 pp 332-336<br> <br>Alexander Kugler1, 7, Gernot Stuhler2, 7, Peter Walden3, Gerhard Z?ller1, Anke Zobywalski2, Peter Brossart2, Uwe Trefzer3, Silke Ullrich1, Claudia A. M?ller4, Volker Becker5, Andreas J. Gross1, Bernhard Hemmerlein6, Lothar Kanz2, Gerhard A. M?ller5 & Rolf-Hermann Ringert1<br> <br>Reports of spontaneous regressions of metastases and the demonstration of tumor-reactive cytotoxic T lymphocytes indicate the importance of the host's immune system in controlling the devastating course of metastatic renal cell carcinoma1-3. Recent research indicates that immunization with hybrids of tumor and antigen presenting cells results in protective immunity and rejection of established tumors in various rodent models4-8. Here, we present a hybrid cell vaccination study of 17 patients. Using electrofusion techniques5, we generated hybrids of autologous tumor and allogeneic dendritic cells that presented antigens expressed by the tumor in concert with the co-stimulating capabilities of dendritic cells. After vaccination, and with a mean follow-up time of 13 months, four patients completely rejected all metastatic tumor lesions, one presented a 'mixed response', and two had a tumor mass reduction of greater 50%. We also demonstrate induction of HLA-A2-restricted cytotoxic T cells reactive with the Muc1 tumor-associated antigen and recruitment of CD8+ lymphocytes into tumor challenge sites. Our data indicate that hybrid cell vaccination is a safe and effective therapy for renal cell carcinoma and may provide a broadly applicable strategy for other malignancies with unknown antigens. <br> <br><br>OLDER and RELATED:<br><br>B-Cell Vaccine Abstracts<br><br>American Society of of Nephrology 1998 Annual Meeting (Oct 1998) S510: HYBRID-CELL-VACCINATION IS A NEW APPROACH IN THE TREATMENT OF METASTATIC RENAL CELL CARCINOMA (RCC)<br> <br>G.A. Muller,1* V. Becker,1* A. Kugler,2* B. Berner,1* F. Strutz,1 B. Raschke,1* C.A. Muller,3* F. Seseke,2* M. Kallerhoff,2* P. Thelen,2* W. Fenner,4* W.Schott,4* R.H. Ringert.2*<br><br>The median time of survival for patients with renal cell carcinoma (RCC) is 12 to 18 months after metastasis for this cancer usually fails to respond to chemotherapy and other therapeutic regimens such as treatment with interleukines or interferrons. However, spontaneous remissions were reported in 1 to 7 % of cases pointing to some immune mediated mechanisms, although a specific tumor antigen has not been identified so far. For this reason, we have chosen a therapy regimen stimulating the immune system by resembling graft rejection disease after transplantation of foreign HLA-antigens. We treated 32 patients with progressive metastatic RCC in a phase I/II study with a hybrid cell vaccine to stimulate tumor specific immune responses. This vaccine was generated according to GPC criteria by electrofusion of either autologous or allogeneic tumor cells with pooled activated allogeneic B-lymphocytes. The B-lymphocytes were obtained from healthy volunteers who had different HLA-A, -B, -C antigens compared with the recipients. The fusion product was lethally irradiated and applied to the patiens by multiple subcutaneous injections. Boostering was performed up to 6 times in 3 months intervals. The mean follow-up was 7.5 months (1-30 months). 4 out of 32 patients (12,5 %) showed a complete response with full regression of their metastases and another 3 patients showed an initial partial response. In 7 patients progressive disease was stabilized for several months. No side effects except mild fever for one day in 5 patients were observed. Seven patients who responded to this vaccination showed a positive DTH reaction when tumor cells were subcutaneously reinjected on day 10 after treatment. Moreover, immunohistological analysis of biopsies from the injection side showed infiltration of CD8+ and CD4+ T-cells as a further sign of stimulation of immune reactions against malignant cells. Thus active specific immunotherapy seems to be a promising new approach in the treatment of metastatic RCC. A multicenter study will now be conducted.<br> <br>Author Affiliations and Contact Info<br><br>1. Dept. of Nephrology & Rheumatology, University of Gottingen<br>2. Dept. of Urology, University of Gottingen<br>3. Section of Transplantation-Immunology and Immunhematology, University<br> of Tubingen<br>4. Dept. of Urology, NZN Hann. Munchen.<br><br>Autologous and allogenic hybrid cell vaccine in patients with metastatic renal cell carcinoma. Br J Urol 1998 Oct;82(4):487-93<br><br>Kugler A, Seseke F, Thelen P, Kallerhoff M, Muller GA, Stuhler G, Muller C, Ringert RH<br> <br>Department of Urology, University of Gottingen, Germany.<br><br>OBJECTIVE: To evaluate the safety, acute and long-term toxicity and therapeutic activity of an allogenic and an autologous hybrid cell vaccine in patients with progressive metastatic renal cell carcinoma (RCC). PATIENTS AND METHODS: Eleven patients were vaccinated with a lethally irradiated hybrid cell vaccine of allogenic RCC tumour cells fused with major histocompatibility complex class I-matched and class II-unmatched activated allogenic lymphocytes. These patients were then followed for a mean of 11 months. Another 13 patients were vaccinated with a hybrid cell vaccine of autologous tumour cells fused with allogenic activated lymphocytes and followed for a mean of 6 months. RESULTS: Six of the 11 patients receiving the allogenic vaccination showed an initial response, with two complete and two partial responses to date. Only three patients who received autologous vaccination responded to treatment. CONCLUSIONS: Hybrid cell vaccination is a promising new approach in the treatment of patients with advanced RCC.<br> <br><br>==============================<br><br><br><a href="http://www.spiegel.de/wissenschaft/mensch/0,1518,67323,00.html">http://www.spiegel.de/wissenschaft/mensch/0,1518,67323,00.html</a><br><br>Medizin - Impfstoff gegen Nierenkrebs<br> <br>Göttinger Wissenschaftler haben einen Impfstoff entwickelt, der Nierentumore zurückgebildet hat.<br><br>Göttingen - Nach Angaben von Gerhard Anton Müller, Direktor der Universitätsklinik Göttingen und einem der leitenden Forscher der zweijährigen Studie, bildeten sich bei sechs der 30 behandelten Nierenkrebspatienten die Tumore oder Metastasen komplett zurück. Bei einer Frau dauert diese Komplettremission bereits 26 Monate an. Drei weitere Erkrankte zeigten eine deutlichere Besserung mit einer Reduktion der Tumore um mindestens 50 Prozent. Nochmals drei Patienten zeigten kein weiteres Fortschreiten der Krankheit.<br> <br>Nach Aussagen der behandelnden Ärzte litten alle Testpersonen an metastasierendem Nierenkrebs. Dieser bilde Metastasen in Lungen, Knochen, Lymphknoten und Leber. Die Lebenserwartung lag vor der Behandlung zwischen sechs und zwölf Monaten.<br> <br>Ansatzpunkt bei der Entwicklung des Impfstoffes war die Tatsache, dass das Immunsystem Krebszellen oft nicht zerstört, weil es sie nicht als solche identifiziert. Das Problem besteht darin, dass Krebszellen körpereigene Zellen sind, die bestimmte Oberflächenmerkmale herunterregulieren und so die Abwehrkräfte täuschen.<br> <br>Der im "Nature Medicine" beschriebene Impfstoff basiert auf einem Verfahren, das Elektrofusion genannt wird. Bei dieser Methode wird eine gesunde Immunzelle einer fremden Person mit einer Tumorzelle des Patienten verschweißt. Eine Bestrahlung hindert die Krebszelle am Wachstum. Die entstandene Hybridzelle wird anschließend dem Erkrankten injiziert. Die körpereigenen Abwehrzellen werden auf das Gebilde aufmerksam und registrieren gleichzeitig, dass noch weitere Krebszellen im Körper existieren. Daraufhin werden diese vom Immunsystem attackiert.<br> <br>Alle 30 Patienten der Göttinger Studie erhielten eine Impfung, die bei einer erkennbar positven Wirkung alle drei Monate wiederholt wurde.<br><br>Das Deutsche Krebsforschungszentrum in Heidelberg hat indessen mit Zurückhaltung auf die Nachricht vom Nierenkrebsimpfstoff reagiert. "Es ist noch viel zu früh, um von einem Durchbruch zu sprechen", sagte Dirk Schadendorf vom Zentrum. Dazu seien größere kontrollierte Studien notwendig als die Behandlung von 30 Patienten. Ähnliche Forschungsansätze gäbe es zudem "in der ganzen Welt".<br> <br>Auch Gerhard Müller hatte sich entsprechend geäußert. "Wir freuen uns darüber, dass dieses Verfahren bei einem Teil der Patienten so erfolgreich ist. Endgültige Schlüsse können aber erst nach Abschluss unserer derzeitigen Vergleichsstudien gezogen werden", sagte Müller.<br> <br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-3978129502196920562011-07-11T07:33:00.001-07:002011-07-11T07:33:33.789-07:00SURGERY RISK -- RCC and XGP<img alt="http://plasticsurgerymanhattan.net/wp-content/uploads/2009/01/skull.bmp" src="http://plasticsurgerymanhattan.net/wp-content/uploads/2009/01/skull.bmp"><br><br>Abstract ... Objective<br><br> To present the complications from our first 100 cases of laparoscopic nephrectomy, a technically demanding procedure requiring lengthy experience, and to define the risk factors.<br> Patients and methods<br><br> Indications for laparoscopic nephrectomy included patients requiring nephrectomy for benign pathology and those requiring nephroureterectomy for upper tract transitional cell carcinoma confined to the upper ureter and/or renal pelvis. All patients were operated on by one surgeon (D.A.T.) via a transperitoneal route and data on diagnosis, outcome and complications collected prospectively.<br> Results<br><br> The overall complication rate was 18%, of which 3% were major and 15% minor complications. Five cases were converted to open surgery electively. Complications and conversions were associated with a history of pyonephrosis, previous renal surgery, staghorn calculi, polycystic kidney disease, and xanthogranulomatous pyelonephritis. While there was no discernible decline in the decrease in complications with experience, operative duration decreased from a mean of 204 min for the first 20 cases to 108 min for the last 20. Complications and conversions were more closely associated with diagnosis than with the surgeon's experience.<br> Conclusion<br><br> Laparoscopic nephrectomy and nephroureterectomy can be undertaken for a variety of indications with reasonable complication and conversion rates. Although inflammatory conditions increase the difficulty of these procedures, we feel that patients requiring nephrectomy for benign disease should be offered a trial of laparoscopic surgery.<br> Introduction<br><br>Laparoscopic nephrectomy is a demanding procedure requiring extensive experience. Several investigators have noted the advantages to the patient inherent in the laparoscopic approach, including less need for postoperative narcotics and a faster return to normal activities [ 1, 2]. We previously reported that laparoscopic nephrectomy and nephroureterectomy compare well with the open procedures in terms of overall morbidity, length of stay and operative duration [ 3]. Laparoscopic nephrectomy also compares well with open nephrectomy in terms of cost, as measured in the UK National Health Service [ 2].<br> <br> The complications reported for laparoscopic nephrectomy are generally similar to those of open nephrectomy, but a few are unique to the laparoscopic approach, including injuries related to trocar placement, and carbon dioxide retention or embolization. In addition, the technical difficulty of laparoscopic nephrectomy has led to musculoskeletal injuries related to prolonged operation [ 4].<br> <br> Several risk factors have been associated with complications and conversions. In a large multicentre study, laparoscopic tumour nephrectomy had a higher complication rate than laparoscopic simple nephrectomy [ 4]. In addition, complications were most likely to occur in the first 20 cases, suggesting that this reflected sufficient experience and training to minimize the rate. We present the complications from the first 100 cases at our institution, all performed by one surgeon, and attempt to identify risk factors for complications and for conversion to open surgery.<br> <br><br>Patients and methods<br><br>Between September 1992 and March 1997, 100 patients (38 male, 62 female; mean age 50.5 years, range 15–91) underwent laparoscopic nephrectomy (n=79) or nephroureterectomy (n=21) at our institution. The indications for nephrectomy are listed in Table 1. Our policy has been to offer a trial of laparoscopy to all patients with benign pathology, including those with inflammatory conditions and previous surgery. We have also offered laparoscopic nephroureterectomy to patients with TCC in the upper ureter and/or renal pelvis. All the present patients were operated on by one surgeon (D.A.T.).<br> <br><span class="tTitle"></span><a href="http://onlinelibrary.wiley.com/doi/10.1046/j.1464-410x.1998.00847.x/full#"><img style="display: block;" src="http://onlinelibrary.wiley.com/store/10.1046/j.1464-410x.1998.00847.x/asset/image_n/bju847_t1.gif?v=1&t=gpzipp25&s=78cb3b64d3bad3bae551793e638b531f4a68ec0f" alt="Thumbnail image of " title="Thumbnail image of "></a><div class="section" id="ss3"> <br><br>The steps of the technique used for laparoscopic nephrectomy were: the patient is placed in the flank position, the first trocar placed at the edge of the rectus level with the umbilicus, and the second and third trocars placed in an anterior axillary line. The colon is reflected medially, Gerota's fascia entered and when required, a fourth trocar is placed in the mid-axillary line. The hilum is dissected while the kidney is retracted laterally. Endoclips are used for the artery and EndoGIA staples (Autosuture Inc, USA) for the vein. Peri-renal dissection is used to free the kidney and the ureter divided last. The specimen is then removed in an organ-retrieval bag.<br> <br> Initial access to achieve pneumoperitoneum was performed under direct vision, using the Hasson technique, to minimize the risk of injury from the Veress needle. For nephroureterectomy, the initial step was to resect the ureteric orifice transurethrally. After repositioning the patient, the ureter was clipped before laparoscopic dissection of the kidney and ureter, which were removed intact by extension of the inferior port site.<br> <br> Data were collected prospectively; the clinical records of all patients were reviewed, noting either complications or conversion to open surgery, to identify any potential risk factors.<br><br><br><br>Results<br><br> The overall complication rate was 18% ( Table 2), of which 3% were major and 15% minor. Three patients had major complications; the first, aged 59 years, had bilateral TCC and a previous history of percutaneous resection, underwent nephroureterectomy, and sustained an aortic injury, treated by open repair. The second, aged 52 years, had hypertension and no renal function, underwent nephrectomy, sustained a vena caval injury, that was treated by open repair. The third patient, aged 77 years, had a history of obesity, coronary artery disease and transient ischaemic attacks. He underwent nephroureterectomy lasting 180 min for renal pelvic TCC, which had previously been resected percutaneously. Postoperatively, he developed a haematoma in the renal bed, a bleeding diathesis and a fatal myocardial infarction 3 days after surgery.<br> <br><br><br><div class="imageTable" id="t2"><span class="tTitle"><span class="label">Table 2. </span> Minor complications </span><a href="http://onlinelibrary.wiley.com/doi/10.1046/j.1464-410x.1998.00847.x/full#"><img style="display: block;" src="http://onlinelibrary.wiley.com/store/10.1046/j.1464-410x.1998.00847.x/asset/image_n/bju847_t2.gif?v=1&t=gpzipp2c&s=227db1f063dae80e450e83750a124853782fe466" alt="Thumbnail image of " title="Thumbnail image of "></a></div> <span class="tTitle"><span class="label"><br><br><br><br><br>Ten patients required transfusions; the number of units transfused per procedure was 0.38. There was one complication with a delayed presentation, in a patient who presented with a superficial wound infection 12 days after surgery. There were no intra-operative port-related complications and no injuries to bowel. Compared with a contemporary series of open nephrectomies performed for benign indications at our institution, the complication (18% vs 28%) and transfusion rates (0.38 vs 0.89 units per procedure) were lower for laparoscopy [ 3].<br> <br> Patients with minor complications had a similar mean operative duration (141 vs 143 min) but a longer hospital stay (6.2 vs 4.8 days) than patients with no complications. In contrast, patients who required conversion to open surgery or who had a major complication had a longer mean operative duration (315 min) and length of stay (11.8 days).<br> <br> The complication rate was similar for both laparoscopic nephrectomy (17.5%) and nephroureterectomy (18%). However, when patients with inflammatory conditions such as pyonephrosis, staghorn calculi, xanthogranulomatous pyelonephritis (XGP) and those with previous renal surgery were excluded, there was a higher incidence of minor complications and conversions to open surgery ( Table 3). All but one of the local infectious complications occurred in this group of patients. Overall, 29 of 42 patients with inflammatory conditions (69%) underwent laparoscopic nephrectomies without complication or conversion to open surgery, compared with 87% in those patients without these risk factors. The mean operative duration was longer in the inflammation group, but the mean length of stay was only marginally longer ( Table 3).<br> <br><br>Table 3. </span> Conversions and complications in patients with transitional cell carcinoma and inflammatory conditions, compared with those without </span><a href="http://onlinelibrary.wiley.com/doi/10.1046/j.1464-410x.1998.00847.x/full#"><img style="display: block;" src="http://onlinelibrary.wiley.com/store/10.1046/j.1464-410x.1998.00847.x/asset/image_n/bju847_t3.gif?v=1&t=gpzipp2i&s=52fe0d9f6f66f12578bc16278dc721a046353196" alt="Thumbnail image of " title="Thumbnail image of "></a><span class="tTitle"><br> In addition to the two cases of vascular injury noted earlier, five cases were electively converted to open surgery; four for failure to progress (two with staghorn calculi/pyonephrosis, one with locally advanced TCC and one with XGP), and one to remove a large polycystic kidney, where entrapment of the kidney failed. All cases requiring elective conversion were in patients with underlying inflammatory conditions or previous surgery.<br> <br> Even with accumulating experience, there was no discernible trend over time in complications and conversions ( Table 4), with the exception of the last 20 cases, which we attribute to the relative paucity of inflammatory conditions in this group of patients (three of 20). The effect of experience was more evident in the decreasing operative duration (Table 4).<br> <br><br> </span><a href="http://onlinelibrary.wiley.com/doi/10.1046/j.1464-410x.1998.00847.x/full#"><img style="display: block;" src="http://onlinelibrary.wiley.com/store/10.1046/j.1464-410x.1998.00847.x/asset/image_n/bju847_t4.gif?v=1&t=gpzipp2l&s=1172e20d64330ea429d8fd6f80686ec56bad26ec" alt="Thumbnail image of " title="Thumbnail image of "></a></div> <div class="section" id="ss4"><br><br><br>Discussion<br><br>There were 18 complications and five elective conversions in this series of 100 patients undergoing laparoscopic nephrectomy and nephroureterectomy. Our policy has been to offer a trial of laparoscopy to all patients with benign conditions and selected patients with TCC. The series included 42 patients with a variety of inflammatory conditions, e.g. XGP, pyonephrosis and previous surgery, all of which proved to be significant risk factors for complications and conversion to open surgery. Nevertheless, we believe that the overall benefits of a laparoscopic approach usually outweigh the risks, even in this difficult group of patients. We do not presently offer laparoscopic nephrectomy to patients with suspected RCC or XGP.<br> <br> Several technical points should be detailed for the avoidance of complications: strict attention to basic surgical principles; trocars should be placed under direct vision; extra care should be taken to avoid even minor haemorrhage, as blood in the field obscures vision dramatically; the renal hilum should be approached before perirenal or ureteric dissection if at all possible; adequate exposure and retraction are essential; early conversion to open surgery for failure to progress; appropriate selection of patients, including preoperative CT in patients with suspected XGP or known upper tract TCC, to exclude tumour extension; and finally, a regular team of surgeons and nurses, to reduce unnecessary delays and frustration.<br> <br> The present complication and conversion rates are broadly similar to those published previously. Complication rates in the largest reported series were 2.8–37% [ 1, 5] and conversion rates 2.8–10.3% [ 6, 7]. Gill et al. [ 4] reported a 6% rate of conversion to open surgery and a 16% rate of complications in a multi-institutional study. Complications in that series tended to occur in the first 20 cases and were more common in patients undergoing laparoscopic radical nephrectomy. Rassweiler et al. [ 7] recently reported a 5.8% complication rate and a 10.3% rate of conversion to open surgery. However, a more detailed analysis of these series is limited by their multi-institutional nature, given the wide range of operative techniques used.<br> <br> The nature of complications encountered in the present series was similar to that of other series [ 1, 4, 7[8]–9], with a few minor exceptions. We encountered no bowel injuries or intra-operative complications related to trocar access, which we attribute to our use of the open-access (Hasson) technique and strict adherence to basic surgical principles. In addition, there were no postoperative musculoskeletal complications, possibly because of the shorter operative duration. There were several minor infectious complications in patients with a history of staghorn calculi, XGP and pyonephrosis, despite the prophylactic use of broad-spectrum antibiotics. Perhaps this can be attributed to the limited irrigation of the operative field through the laparoscopic approach.<br> <br> The relatively long operative duration reported by most investigators [ 1, 6, 10] for laparoscopic nephrectomy and nephroureterectomy has been used by critics to argue against the widespread adoption of these techniques. The present mean duration was 153 min, which compares well with a contemporary open surgical series [ 3]. The current mean is 111 min in our last 40 cases. By maintaining the operative duration in line with that for open surgery, we support those reports rating laparoscopic nephrectomy as less expensive than open nephrectomy [ 2].<br> <br> As shown in Table 4, increased experience shortens operative duration but does not necessarily reduce complication and conversion rates, which appear to be more closely related to the patient's underlying disease process. Most of these complications were minor and had little or no effect on the patients' recovery. Peters [ 11], in a survey of the laparoscopic experience of paediatric colleagues, reported that complication rates diminished significantly only after 100 cases. Given the greater difficulty involved in performing laparoscopic nephrectomy compared with diagnostic laparoscopy, a longer period of training and experience should perhaps be expected. This requirement for extensive experience of laparoscopic nephrectomy may have contributed to earlier reports which tended to overestimate its cost [ 12] and may mask some of its inherent advantages [ 13].<br> <br> Laparoscopic nephrectomy can be performed safely and efficiently, but thus far has been limited to few referral centres. The way forward is to simplify the techniques and improve training, thereby making it more accessible to the general urologist. To this end, hand-assisted laparoscopy may bridge the gap between the experts and the novice by reducing the necessary experience required [ 14].<br> <br><br>1<br>Kerbl K, Clayman RV, McDougall EM et al. Transperitoneal nephrectomy for benign disease of the kidney: a comparison of laparoscopic and open surgical techniques. Urology 1994; 43: 607 13<br><br> CrossRef,<br> PubMed,<br> Web of Science®<br><br>2<br>Wilson BG, Deans GT, Kelly J, McCrory D Laparoscopic nephrectomy: initial experience and cost implications. Br J Urol 1995; 75: 276 80<br>Direct Link:<br><br> Abstract<br> PDF(423K)<br> References<br><br>3<br>Sharma NK, Stephenson R, Tolley DA Should laparoscopic nephrectomy/nephroureterectomy be the preferred treatment option for most renal pathology? A comparative study. J Urol 1996; 155: 491A, abstract 722<br> 4<br>Gill IS, Kavoussi LR, Clayman RV et al. Complications of laparoscopic nephrectomy in 185 patients: a multi-institutional review. J Urol 1995; 154: 479 85<br><br> CrossRef,<br> PubMed,<br> Web of Science®<br> <br>5<br>Fahlenkamp D, Turk I, Degar S, Loening SA Complications of laparoscopy, observations after 903 cases. J Urol 1997; 157: 140A abstract 547<br>6<br>Ono Y, Katoh N, Kinukawa T, Matsuura O, Ohshima S Laparoscopic radical nephrectomy: Nagoya experience. J Urol 1997; 158: 719 24<br> <br> CrossRef,<br> PubMed,<br> Web of Science®<br><br>7<br>Rassweiler JJ, Fornara P, Fahlenkamp D et al . Laparoscopic nephrectomy — the Austro-German experience. J Urol 1997; 157: 403A abstract 1582<br>8<br>Cadeddu JA, Regan F, Kavoussi LR, Moore RG The role of computerized tomography in the evaluation of complications after laparoscopic urological surgery. J Urol 1997; 158: 1349 52<br> <br> CrossRef,<br> PubMed,<br> Web of Science® Times Cited: 8<br><br>9<br>Eraky I, El-Kappany HA, Ghoneim MA Laparoscopic nephrectomy: Mansoura experience with 106 cases. Br J Urol 1995; 75: 271 5<br>Direct Link:<br> <br> Abstract<br> PDF(421K)<br> References<br><br>10<br>McDougal EM, Clayman RV, Elashry OM Laparoscopic radical nephrectomy for renal tumor: the Washington University experience. J Urol 1996; 155: 1180 5<br><br> CrossRef,<br> PubMed,<br> Web of Science® Times Cited: 153<br><br>11<br>Peters CA Complications in pediatric urological laparoscopy: results of a survey. J Urol 1996; 155: 1070 3<br><br> CrossRef,<br> PubMed,<br> Web of Science®<br><br>12<br>Winfield HN, Rashid TM, Lund GO, Troxel SA, Donovan JI Comparative financial analysis of laparoscopic versus open nephrectomy. J Urol 1994; 151: 342A abstract 460<br><br> PubMed,<br> Web of Science® Times Cited: 34<br> <br>13<br>Gill IS, Clayman RV, McDougall EM Advances in urological laparoscopy. J Urol 1995; 154: 1275 94<br><br> CrossRef,<br> PubMed,<br> Web of Science®<br><br>14<br>Keeley FXJr , Sharma NK, Tolley DA Hand-assisted laparoscopic nephroureterectomy. J Urol 1997; 157: 399A abstract 1565<br> <br> Web of Science® Times Cited: 129<br><br><br></div> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-43889471406622853672011-07-05T03:21:00.001-07:002011-07-05T03:21:45.804-07:00Coley's good against Arthritis (LANCET, Klein)<br><br>The Lancet, Volume 358, Issue 9276, Pages 155 - 156, 14 July 2001<br>doi:10.1016/S0140-6736(01)05369-7Cite or Link Using DOI<br><br>Infection and cancer<br><br>Johan Haux -- jhaux [a} <a href="http://operamail.com">operamail.com</a><br> <br>Sir<br><br>Fran Balkwill and Alberto Mantovani (Feb 17, p 539),1 I think, should have included the name of William B Coley (1862—1936) in their review of Rudolf Virchow's work.<br>I will by no means depreciate Virchow, but stress the clinical relevance of Coley's work for the inflammation-cancer connection. Coley translated the observation of tumour regression concomitant with infection into a treatment—the Coley toxins (Coley's mixed toxins or Coley's vaccine) consisting of heat-killed or sterile filtrated cultures of Streptococcus pyogenes and Serratia marcescens. Thus, the toxins contained some of the most potent immune-regulatory substances, such as lipopolysaccharides, exotoxins (also as superantigens), enzymes such as streptokinase, as well as an unimaginable amount of other bacterial antigens.<br> That the Coley toxins could cure patients with extensive inoperable tumours is documented, but the results were unpredictable, which is not surprising considering where bacteriology and immunology stood at that time.2<br> <br>Tumour necrosis factor (TNF) was the first discovered molecule that directly linked the Coley toxins to an eventual anticancer effect. Today several new members in the TNF superfamily are under fierce investigation as potential anticancer agents, such as TNF related apoptosis inducing ligand, and the picture becomes increasingly complex. TNF kills tumour cells under certain circumstances, but can also promote the malignant state.1 TNF antagonists were first approved for the <b>treatment of rheumatoid arthritis</b> and are now also assessed in clinical cancer studies.1<br> <b>Less known today, the Coley toxins were also very effective in relieving the symptoms of arthritis, and arthritis was the sole indication for some doctors to use them. The very pronounced effects on pain and stiffness occurred after 1-2 weeks of treatment.</b>3 This may show that a decrease or blockade of TNF was a major clinical effect of the Coley toxins instead of an increase of TNF as has been proposed for explaining the anticancer effects.4<br> <br>Another constituent of the Coley toxins, streptokinase, may also have favourable effects in cancer treatment for tumours producing vascular endothelial growth factor (VEGF) leading to extravasation of fibrin and thus possibly shielding the tumour cells from immune attacks.5 It has taken half a century to reveal a few of the molecular mechanisms which may explain the anti-cancer effects of the Coley toxins, but still we are far from the whole scenario.<br> <br>To scrutinise the original Coley toxin concept in a clinical setting with the knowledge and technology of today is probably the only way to get the final answer concerning their mechanisms of action and effectiveness. Such an approach may be a shortcut to find out how to trigger an immune reaction against malignant tumours.<br> <br>References<br><br>1 Balkwill F, Mantovani A. Inflammation and cancer: back to Virchow?. Lancet 2001; 357: 539-545.<br><br><br> THE USE OF COLEY'S MIXED TOXINS IN THE <br> TREATMENT OF CHRONIC ARTHRITIS. <br> BY THOMAS KLEIN, M.D., <br><br> PHILADELPHIA, PA. <br><br> One need not look very far into the endless literature to realize <br>fully the perfectly hopeless task of finding a suitable classification <br> of the various forms of chronic arthritis. It is also not within the <br>bounds of this short paper to enter into any lengthy discussion. <br>Suffice it to say that the term chronic arthritis as here employed <br> embodies those types which are variously classified as: Chronic non- <br>suppurative arthritis; Rheumatoid arthritis; Chronic infectious <br>arthritis; Chronic -osteo arthritis or arthritis deformans. Gout or <br> gouty arthropathies being a purely metabolic disease is not here <br>considered. The same holds true to the arthropathies of nervous <br>origin or those occurring in tabes dorsalis (Charcot joints) and in <br> syringomyelia. The chronic hypertrophic osteo arthropathies occur- <br>ring in the course of pulmonary tuberculosis, bronchiectasis, chronic <br>bronchitis, malignant tumors of the lung, and various chronic cardiac <br> conditions are again distinct and are not included in the above term <br>chronic arthritis as here used. Syphilitic arthritis is again a more or <br>less distant entity and is not here considered. Villous arthritis is <br> probably a stage of chronic osteo arthritis and will be considered as <br>such. Fibrositis and panniculitis will be described as a part of the <br>chronic infectious process so frequently occurring in this type of case. <br> Thevast majority of the remaining caseswill fall into that group <br>in which we are primarily interested. This group is characterized at <br>the beginning by swelling of the smaller joints, both meta-carpo- <br> phalangel and metatarso-phalangel. The process may be unilateral <br>but is more often bilateral. In the early stages the joints gradually <br>swell with little or no pain. This gives them the characteristic fusi- <br> form appearance. Upon examination they have a distinct doughy <br>feeling. At times there is a questionable effusion into the joint. <br>Pathologically this enlargement is due to swelling and hypertrophy <br>of the synovial membrane and capsular ligament. Pain is only <br> present upon pressure and active or passive motion. The disease <br>progresses with definite periods of acute exacerbations, characterized <br>by fever and its accompanying symptoms; increased pain and stiff- <br> ness in joints and surrounding structures -frequently by focal <br>manifestations as increased swelling and redness in the joint struct- <br>ures themselves. These periods are also associated with a slight <br> increase in leucocyte count as compared during the stage of quies- <br>cence. In all respects it follows clinically the course of an infection. <br>During this time the disease progresses upward involving the larger <br> joints, namely the wrist, elbow, shoulders, ankle, knee, hip and the <br>joints of the spine. <br> Soon after the beginning of the process which in itself is essen- <br>tially an hypertrophy of the periarticular structures, we have an <br> atrophic process set up: -The atrophy involves the muscles, sub- <br>cutaneous fat and skin. These atrophic changes are undoubtedly <br>due in many instances to a reflex atrophy. Vulpains idea, namely <br> that impulses carried from irritated articular nerves alter the trophic <br>activity of the cells in the anterior horns without causing a lesion, <br>but sufficient to cause atrophy and weakness, is an extremely good <br> one and is the best explanation offered. It is the glossy atrophic <br>condition of the skin, atrophy of the subcutaneous fat and muscles <br>plus their subsequent contractures which gives the characteristic <br> deformity. The extensor groups of muscles always suffer greater <br>damage than the flexors. Hence flexor contractures always predomi- <br>nate. This is explained by the fact that the nerves which supply the <br> extensors also supply the joints themselves, consequently they bear <br>the blunt of the irritation and the greatest atrophy. <br> Associated with this degenerative process is a fibrositis involving <br>both the aponeurosis and the muscles themselves. In fleshy individ- <br> uals the subcutaneous fat is also caught in the process in the form of <br>a panniculitis. These two conditions account for a good deal of the <br>patient's suffering and as wewill see later form a very important part <br> of the treatment. <br> The feeling that this type of case is always due to a chronic <br>infection is fast gaining ground. Even though the causative organism <br>is not found, the clinical course with its frequent, regular, acute <br> exacerbation associated with fever, increased swelling, pain and red- <br> ness of the joints, increased leucocytes as compared with the quies- <br> cent period, is sufficient to establish this fact. Consequently, when <br> such a case presents itself for treatment we immediately look for a <br> focal infection. Teeth and tonsils correctly occupy the foreground <br> as the most frequent sites of focal infection. Following these are the <br> sinuses, gall-bladder, prostrate, infected ingrown toe-nails, ulceration <br> along the intestinal tract, mediastinal lymph nodes, etc. The femal <br> pelvis has not been found an important factor in our groups of cases. <br> In one case now under treatment the mucous membrane of the mouth <br> afforded repeated rich groups of a hemolytic streptococcus; otherwise <br> no source of infection could be found. The prostate and seminal <br> vesicles are frequently overlooked and when found as a source are <br> too often looked upon as gonorrheal. The streptococcus may long <br> persist without any gonococci being found. Non-surgical biliary <br> drainage, done in an aseptic way offers many opportunities for the <br> study of the gall tract for infection. Too often we overlook the <br> bacteriology of the feces, as here is not an infrequent source of <br> streptococcus infection. <br> Again we must remember that in the vast majority of cases, we <br> are dealing with not one focus of infection but many. The eradica- <br> tion of a dental abscess or a pair of tonsils does not mean that we <br> have removed all the source of infection. When one considers a <br>mediastinal lymph node or an intestinal ulceration as a focus he will <br> readily realize the difficulties in their removal. It is because of this <br> fact and the repeated failure in not getting good results, that lead us <br>to the utilization of a streptococcus vaccine. The vaccine also has <br>further assets. It probably stimulates antibody formation to over- <br> come any focus not eradicated and at the same time seems to aid in <br>a causation of a retrograde process in the periarticular structures <br>themselves. <br> During the past seven years Dr. Robert G. Torrey and myself <br> have been using Coley's Mixed Toxins (amixture of the streptococ- <br>cus of erysipelitus and bacillus prodigiosus) in the treatment of this <br>type of case with surprisingly good results. This vaccine was selected <br> solely because of the potency or virulency of the streptococcus used <br> (.01 cc. of the cultures being sufficient to kill a white mouse in <br>twenty-four hours). It is again easily obtainable in the market <br> Which is a distinct advantage to many men. The action of this <br> vaccine is undoubtedly that of a high powered foreign protein but on <br> the contrary after observing quite a series of cases one cannot help <br> but wonder if it is not in some way a specific. It suggests the <br> thought that the strain of streptococcus causing this disease is in <br> someway related to the streptococcus of erysipelas. Thus far I have <br> treated a series of twenty-one cases. Of these twenty-one cases, <br> twelve have been cured, seven are still under treatment with marked <br> improvement (diminution of pain, swelling of joints, decrease of <br> ankylosis, acute exacerbation being lessened in frequency and <br> severity, and finally abolished, with general improvement in health <br> and gain in weight). Twocases stopped treatment because of severe <br> focal and local reactions. The type of cases treated have been in the <br> vast majority of cases far advanced. The earliest case treated was <br> that of three months duration. The oldest case of fifteen years <br> standing. The average length of duration previous to treatment was <br> 31 years. The length of treatment varied equally as well. The <br> earlier the case was started, the shorter was the duration of treat- <br> ment. In the earliest case the vaccine was given over a period of <br> three months. In the longest case the vaccine was carried over a <br>period of fifteen months. <br><br> MODE OF TREATMENT. <br> When the case presents itself the patient is studied thoroughly <br> from all standpoints, especial attention being paid to focal infection, <br>teeth, tonsils, sinuses, gall-bladder, stools, etc. If the patient presents <br> gastro-intestinal symptoms fractional gastric analysis, feces examina- <br>tion and x-ray studies are made. The colonic stasis which is rather <br>frequent in this type of case is corrected by diet and frequent colonic <br> irrigation, using large quantities of water. The patient is usually <br>undernourished, especially so in young people and I always encour- <br>age forced feeding; diets of special food have not proven satisfactory <br> in any other way. For the past few years I have been making com- <br>plete blood studies including complement fixation tests and the <br>examination of urea, nitrogen, blood sugar, uric acid, creatinin and <br> the chlorides. It has proven very discouraging with the exception <br> of an occasional high uric acid content. This I believe is of extreme <br> importance in helping to differentiate some of these cases. One of <br> my cases has a combination of a rheumatoid and gouty arthritis. <br> She runs a rather persistent high blood uric acid. When the gall- <br> bladder is under question the bacteriology of the bile is studied after <br> asceptic transduodenal lavage. Surgery is only employed after a <br> proved focus has been found. Needless to say that other various <br> x-ray studies are made as indicated, including the joints themsleves. <br> These patients are usually placed in hospitals for a short time during <br> the starting of the vaccine. Rest is a very essential element in these <br> cases and a few weeks in bed usually affords benefit. At the same <br> time it accustoms the patient to the reaction of the vaccine. <br> In starting the vaccine it is very essential to start with a small <br> dose, usually i minim in 1 cc. salt solution or sterile water. This is <br> given subcutaneously. Three types of reaction are experienced, focal, <br> local and general. It has been my practice to tell these people that <br> after the vaccine injection they will have pain in joints heretofore <br> unknown to be involved. The pain in the joints is invariably <br> increased after the first four or five injections. This thereafter will <br> gradually be diminished and the period of freedom from pain will <br> gradually be increased. At the site of injection a marked erythe- <br> matous area develops. The fluid is quite irritating and at times you <br>will think of abscess formation. This I have not experienced but <br> for a week or more the hard indurated nodules persist. These <br> patients are very hypersensitive to the vaccine and the dose must be <br>increased very slowly. This hypersensitivity persists surprisingly <br>throughout the course of treatment and varies with each individual. <br> The largest dose of vaccine given was 10 minims and that after eight <br>months treatment. In the case of fifteen years duration in which <br>we obtained a beautiful result, I could never give over four minims <br> without causing a general reaction. It is to be remembered that in <br> these cases of long standing the patient is usually anemic and <br>markedly undernourished. Thepain has been severe and their nerve <br>has been broken. Consequently it is important to try and avoid a <br> general reaction. While this does not do the patient any harm, it is <br>bad from a psychological standpoint. In addition they have been <br>through so many hands and tried so many forms of treatment that <br> they are always dubious of any new form of treatment and especially <br> so if they are to have more pain in the beginning. <br> The time interval of the injections varies from three to four days <br>at the beginning, gradually being lengthened to five or six days, as <br>the symptoms improve. It has been my rule to gage the time of <br> injection and the size of the dose entirely upon the local reaction. If <br>it be severe the same dose is repeated. At times it is necessary to <br>repeat the same dose as many as four or five times before increasing <br> the vaccine. Especially is this true as the larger doses are used. The <br>vaccine is continued until the patient is clinically well. Unfortu- <br>nately the time of stopping the vaccine is entirely emperical as I <br> know of no way of telling when the infection has been entirely <br>killed out. <br> The benefits derived are a diminution of pain plus a loosening <br>up of the joints. The acute exacerbations which are so characteristic <br> of the disease gradually diminish and are finally obliterated. It is <br>remarkable to see the rapidity of diminution in the size of the joint. <br>The patient through his own efforts will begin to move the joint and <br> loosen it up as soon as the pain subsides. In the febrile cases the <br>temperature gradually returns to the normal course. The patient's <br>general health improves and he soon loses his toxic appearance. The <br> gain in weight is quite remarkable. Onepatient who has been under <br>treatment for the past seven months has gained forty-two pounds. <br> At the beginning of the treatment in addition to clearing up foci <br>of infection, rest and vaccine therapy, the patient is given daily <br> electric bakes to the joints involved; this quite frequently being a <br>general body bake. Care is taken not to massage the joints or the <br>atrophic surrounding structures until after the acute tenderness and <br> swelling have subsided to a great extent. When the massage is <br>started it is of the most gentle character, care being exerted not to <br>traumatize an already diseased tissue. Manipulation, extension, <br> deep massage and other mechanical devices are only resorted to when <br>the patient is well toward recovery. The fibrositis in some cases <br>persists and occasionally it is necessary to stretch the muscles under <br> an anesthetic. Casts are applied but are removed each day for the <br>bake, massage and manipulation. <br> In conclusion it must be said that the treatment of these cases <br>is as complex as their source of infection. The more thoroughly they <br> are studied the more frequently I believe we will find definite <br>evidence of streptococcus infection. Unfortunately the streptococcus <br>does not lend itself to the formation of agglutinins or precipitins; <br> consequently serological tests, so far have failed to give us any <br>definite information. Coley's mixed toxins when used cautiously and <br>over a prolonged period of time have in our hands given us a very <br> satisfactory and pleasing result. <br><br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-71075502770896784052011-07-04T07:11:00.000-07:002011-07-04T07:12:10.579-07:00GERMAN - Vitamin C in der Tumortherapie - ein Review<a href="http://www.naturheilkunde-online.de/naturheilkunde/fachartikel/onkologie/VitaminC.html">http://www.naturheilkunde-online.de/naturheilkunde/fachartikel/onkologie/VitaminC.html</a><br><br>Vitamin C in der Tumortherapie - ein Review<br> <br>Von Heinz Kreher, Mühltal<br><br>Zusammenfassung<br><br>Welche Möglichkeiten gibt es mittels hochdosierter Vitamin- C- Therapie, das Krebsgeschehen positiv zu beeinflussen? Gibt es Erfahrungen, Berichte, Ergebnisse welche die Wirksamkeit der Vitamin-C- Therapie belegen? Sind diese fundiert und sind sie auch in der Praxis reproduzierbar? Dieser Beitrag soll eine Bestandsaufnahme der Literatur zum Thema Vitamin- C- Therapie sein. Es gibt viele Berichte und Bücher und allen wurde versucht Rechnung zu tragen, doch sind wir Heilpraktiker und nicht Statistiker: das Ergebnis zählt, zum Wohle des Patienten.<br> <br> <br><br>Einführung<br><br>Der Krebs, und dazu gehören auch die bösartigen Erkrankungen des lymphatischen und blutbildenden Systems, ist die Ursache von 22 Prozent aller Todesfälle in den Vereinigten Staaten. In jedem Jahr erkranken in den USA etwa 600000 Menschen an dieser Krankheit, in Deutschland sind es jährlich rund 350000 Neuerkrankungen. Ein Großteil von ihnen, rund 420000 in den USA und etwa 220000 in Deutschland, sterben daran. Die durch den Krebs verursachten Leiden sind sehr viel größer als bei den meisten anderen Krankheiten. Aus diesem Grund haben z.B. die USA der Krebsbekämpfung einen besonderen Vorrang eingeräumt und stellen jährlich mehrere hundert Millionen Dollar für die Krebsforschung zur Verfügung. Allein im Jahre 1985 war es eine Milliarde Dollar. Trotz der hohen Beträge und der intensiven Bemühungen, die für die Krebsforschung aufgewendet wurden, ist man in den vergangenen 25 Jahren nur sehr langsam vorangekommen. In den letzten 30 Jahren ist es gelungen, die Überlebenszeit nach der ersten Diagnose wesentlich zu verlängern, vor allem durch Verbesserungen der Operationstechniken und der Anästhesie. Während der vergangenen 25 Jahre sind die Behandlungsmethoden für bestimmte Krebsarten vor allem durch die Anwendung von Strahlen- und Chemotherapie verbessert worden, aber bei den meisten Krebsarten ist es weder gelungen, die Zahl der Erkrankungen zu verringern, noch die Überlebenszeit nach der Diagnose zu verlängern. Es ist unverkennbar, daß wir neue Ideen brauchen, wenn wir diese Geißel der Menschheit erfolgreicher bekämpfen wollen.<br> <br>Eine dieser Ideen war, daß man bei der Krebsvorbeugung und Behandlung hohe Dosen Vitamin C verabreichen könne. Die wichtigsten Arbeiten in dieser Richtung hat Dr. Ewan Cameron, der ehemalige Chef der chirurgischen Abteilung im Vale of Leven Hospital, Loch Lomondside, Schottland, und medizinischer Direktor am Linus Pauling Institute of Science and Medicine geleistet. Irwin Stone behandelte in seinem 1972 erschienenen Buch The Healing Factor: Vitamin C Against Disease die ersten Berichte darüber, daß das Vitamin in Dosen von einem bis vier Gramm täglich, die manchmal zusammen mit höheren Dosen Vitamin A verabreicht wurden, offensichtlich bei einigen Patienten die Krebsbehandlung günstig beeinflussen konnte. Diese Arbeit wurde größtenteils in den Jahren 1940 bis 1956 geleistet. Obwohl es Hinweise darauf gab, daß das Vitamin C in diesen Dosen bei der Krebsbehandlung positiv wirkt, erfolgte in den ersten Studien keine gründliche Untersuchung der möglichen Vorteile, welche die Anwendung von Vitamin C in diesem Zusammenhang erbrachte. Auch über mit Tieren vorgenommene Studien gab es günstige erste Berichte, aber man hatte den ersten Arbeiten auf diesem Gebiet keine weiteren gründlichen Untersuchungen folgen lassen.<br> <br> <br><br>Vitamin C-Resorption und Ausscheidung<br><br>Von Seiten der offiziellen Ernährungsmedizin wird bis heute postuliert, 60-70 mg täglich seien zur Deckung des Tagesbedarfs ausreichend; eine darüber hinausgehende Menge des Vitamins könne im Körper nicht gespeichert werden und wird einfach ausgeschieden. Normalerweise brauche man demnach man keine Vitamin-C-Pillen. Diese Behauptungen sind falsch. Die Beobachtungen, die man über die Konzentration von Ascorbinsäure im Blutplasma im Verhältnis zur Kapazität des Mechanismus für die tubuläre Resorption bei verschiedenen Personen gemacht hat, sagen etwas über die biochemische Individualität hinsichtlich des Vitamins C aus. In einer Studie mit 19 Versuchspersonen schwankte die Kapazität zwischen 10 und 20 mg pro Liter (Friedman, Sherry und Ralli 1940). Andere Forscher haben ähnliche Schwankungen festgestellt. Ascorbinsäure findet sich in den verschiedenen Körperflüssigkeiten und Organen, besonders in den Leukozyten und im Blut. Auch die Konzentration im Gehirn ist hoch. Wenn eine Person, die nicht ausreichend mit Ascorbinsäure versorgt ist, eine größere Menge davon aufnimmt, wird sie sehr schnell aus dem Blutserum in die Leukozyten sowie in andere Zellen und Organe, wie zum Beispiel die Milz, transportiert. Die Menge, die im Blutserum verbleibt, kann geringer sein, als die Kapazität des Mechanismus der tubulären Resorption, sodaß nur sehr wenig mit dem Urin ausgeschieden wird. Harris und Ray haben 1935 ein Testverfahren entwickelt, um zu zeigen, mit welcher Affinität die Gewebe Ascorbinsäure aus dem Blutserum aufnehmen. Bei diesem sogenannten Belastungstest bekommt die Versuchsperson oral oder intravenös eine bestimmte Dosis Vitamin C, und nach sechs Stunden wird der Urin analysiert und sein Ascorbinsäuregehalt festgestellt. Wenn eine Dosis von etwa 1 g oral gegeben wird, dann lassen sich bei den meisten Personen, deren Blutserum nicht völlig frei von Ascorbinsäure war, nach sechs Stunden im Urin noch 20 bis 25 Prozent des ausgeschiedenen Vitamins nachweisen.<br> <br>Eine Person, die einen geringeren Prozentsatz der aufgenommenen Ascorbinsäure ausscheidet, kann das entweder tun, weil sie in ihrer Nahrung eine nicht ausreichende Menge des Vitamins aufgenommen hat, so daß im Gewebe keine Ascorbinsäure mehr enthalten ist, oder weil eine biochemische Abnormität im Körper dafür sorgt, daß die Ascorbinsäure im Blutserum sehr rasch abgebaut wird, möglicherweise deshalb, weil sie sich sehr schnell in andere Substanzen verwandelt. Vanderkamp hat 1966 berichtet, daß Patienten mit einer chronischen Schizophrenie mit einer zehnmal höheren therapeutischenDosis Ascorbinsäure behandelt werden mußten, als sie bei anderen Personen notwendig war, um einen Teil davon im Urin nachweisen zu können. Diese Beobachtung wurde (1967) von Herjanic und MossHerjanic bestätigt. In dieser Studie erhielten 44 kürzlich mit akuter Schizophrenie in eine Klinik eingelieferte Patienten und 44 andere Versuchspersonen jeweils 1,76 g Ascorbinsäure oral verabreicht. Anschließend wurde die innerhalb von sechs Stunden mit dem Urin ausgeschiedene Menge gemessen. Bei der Menge der ausgeschiedenen Ascorbinsäure ließen sich individuelle Unterschiede bis zum Zwanzigfachen feststellen. Sie variierte von zwei bis 40 Prozent, wobei die Schizophreniepatienten nur etwa 60 Prozent dessen ausschieden, was im Urin der anderen festgestellt wurde. Diese Variationen sind wahrscheinlich sowohl durch die unterschiedliche Ernährung als auch durch genetische Faktoren bedingt. Die Verteilungsmuster lassen den Schluß zu, daß es im Hinblick auf die Verarbeitung der Ascorbinsäure drei verschiedene Typen von Menschen gibt, und zwar Personen, die geringe, mittlere und große Mengen ausscheiden. Diese Frage ist bisher jedoch noch nicht ausreichend untersucht worden. Einige Versuchspersonen, die sich für diese Studie zur Verfügung gestellt hatten, bekamen acht Tage lang täglich 1,76 g Ascorbinsäure. Nach der letzten Dosis wurde festgestellt, welche Menge Ascorbinsäure während der darauf folgenden sechs Stunden ausgeschieden worden war. Von 16 Personen, die zunächst nur eine sehr geringe Menge ausgeschieden hatten (weniger als 17 Prozent), gehörten acht jetzt nicht mehr zu dieser Gruppe, während die übrigen acht auch weiterhin nur sehr wenig Ascorbinsäure ausschieden. Danach darf man vermuten, daß diese Personen das von ihnen aufgenommene Vitamin C nicht normal verarbeiten. Vielleicht brauchten sie sehr viel größere Mengen Ascorbinsäure, um gesund zu bleiben.<br> <br> <br><br>Korrelationen zwischen Krebserkrankungen und dem Vitaminstatus<br><br>Die enge Korrelation der Plasma- oder Gewebespiegel unterschiedlicher Vitamine mit dem Auftreten bestimmter Krebserkrankungen wird in epidemiologischen Studien sichtbar. In den letzten Jahren wurden einige in dieser Hinsicht interessante Arbeiten veröffentlicht, ihre Ergebnisse sind im folgenden stichwortartig aufgelistet:<br> <br>Bei regelmäßiger Vitamin C-Aufnahme durch Obst und Gemüse zeigen Frauen ein reduziertes Lungenkrebsrisiko (Steinmetz 1993).<br><br>Das Risiko zur Ausbildung von zervikalen Dysplasien steigt mit der ungenügenden Zufuhr der Vitamine A und C, Riboflavin und Folsäure (Liu 1993).<br> <br>Vitamin C reduziert das Risiko an zervikalen Dysplasien besonders bei Raucherinnen (Potischman 1993).<br><br>Der Folatspiegel in Serum und Nahrung und der Vitamin C-Gehalt in der Nahrung ist umgekehrt proportional zum Auftreten von zervikalen intraepithelialen Neoplasmen (VanEenwyk et al.). 1992).<br> <br>Der Vitamin C-Spiegel steht, durch seine Eigenschaft der Bildung von Nitrosaminen entgegenzuwirken (Yang 1992), in umgekehrter Proportionalität zum Auftreten von Magen- und Oesophaguskrebs.<br><br>In Kombination mit ß-Carotin verringert Vitamin C das Auftreten oraler Leukoplakien (papillomatöse Schleimhautveränderungen).<br> <br>Der Einfluß des Vitamin C-Spiegels auf die Häufigkeit von zervikalen Dysplasien, Zervixkrebs, oralen Leukoplakien, atrophischer Gastritis und Magenkrebs wurde von Singh und Gaby 1991 untersucht.<br><br>Ein niedriger Plasmaspiegel an Vitamin C oder eine unzureichende Vitamin C-Aufnahme erhöhte das Risiko an den aufgeführten Krebsarten bzw. -vorstufen zu erkranken (Singh und Gaby 1991).<br> <br>Bei hormonunabhängigen Krebsarten übte Vitamin C in 33 von 47 durchgeführten Studien eine Schutzwirkung aus. Hierzu gehören Oesophagus-, Larynx-, Mundhöhlen-, Pankreas-, Magen-, Rektum-, Brust- und Zervixkrebs.<br><br> An den beobachteten protektiven Einflüssen werden wahrscheinlich noch weitere chemopräventive Nahrungskomponenten beteiligt sein. Vitamin C beeinflußt jedenfalls in offenbar vielfältiger Weise das Krebsgeschehen.<br><br> Reduktion karzinogener und mutagener Stoffe im Organismus:<br> <br>In Kombination mit Vitamin E reduziert Ascorbinsäure mutagene Substanzen in den menschlichen Fäzes auf 10% der Ausgangsmenge (Hanck 1983).<br>Ascorbinsäure verhindert die Bildung von Nitrosaminen (Weisburger 1991, Tannenbaum 1991).<br> Vitamin C-Defizit äußerte sich bei acht untersuchten Probanden in einem Anstieg von bestimmten Mutagenen in den Fäzes und einer verstärkten oxidativen Modifizierung der Spermien-DNA (Jacob et al.). 1991).<br><br>Schon 1951 wurde berichtet, daß Krebspatienten gewöhnlich eine sehr geringe Vitamin-C-Konzentration im Blutplasma und in den Leukozyten im Blut aufweisen, oft nur etwa die Hälfte des Wertes, der bei anderen Personen festzustellen ist. Diese Beobachtung ist während der vergangenen 30 Jahre immer wieder bestätigt worden. So haben im Jahre 1979 Cameron, Pauling und Leibovitz 13 Studien aufgeführt, die alle zeigten, daß die Vitamin-C-Konzentration bei Krebspatienten sowohl im Plasma als auch in den Leukozyten stark reduziert war. Der Ascorbinsäurespiegel in den Leukozyten von Krebspatienten ist gewöhnlich so niedrig, daß die Leukozyten ihre wichtige Funktion der Phagozytose nicht mehr ausreichend erfüllen können, mit der sie gewöhnlich Bakterien und andere körperfremde Zellen einschließlich bösartiger Zellen einschließen und enzymatisch abbauen. Der niedrige Vitamin-C-Spiegel im Blut von Krebspatienten läßt sich vielleicht damit erklären, daß ihr Körper das Vitamin bei der Bekämpfung der Krankheit verbraucht. Die geringe Vitaminkonzentration im Körper legt nahe, diesen Patienten große Dosen Vitamin C zu verabreichen, um die Körperabwehr so funktionstüchtig wie möglich zu erhalten.<br> <br> <br><br>Langzeitsubstitution mit Vitamin C<br><br>Nur in einem der frühen Berichte über die Zusammenhänge zwischen Vitamin C und Krebs wird die Anwendung hoher Dosen des Vitamins C über einen Zeitraum von bis zu 18 Monaten behandelt. 1954 veröffentlichte Dr. Edward Greer aus Robinson/Illinois, einen Bericht über einen bemerkenswerten Patienten, der seinen Krebs (eine chronisch-myeloische Leukämie) augenscheinlich über einen Zeitraum von zwei Jahren mit der oralen Aufnahme sehr großer Dosen Vitamin C erfolgreich behandelt hat. Dieser Patient, ein älterer leitender Angestellter einer Ölgesellschaft, litt außerdem an einer Reihe anderer, den Krebs begleitender Krankheiten. Im September 1951 entwickelten sich bei ihm eine chronische Herzkrankheit, und im Mai 1952 soll er an einer durch Alkoholmißbrauch entstandenen Leberzirrhose und an Polyzythämie erkrankt sein. Im August 1952 wurde die Diagnose einer chronisch-myeloischen Leukämie gestellt und von einem unabhängigen Hämatologen bestätigt. Nachdem ihm einige Zähne gezogen worden waren, rieten ihm seine Ärzte, Vitamin C zu nehmen, um die Heilung des Zahnfleisches zu beschleunigen. Er begann sofort, sehr große Dosen zu nehmen täglich 24 bis 42g. Er sagte, er habe sich diese hohen Dosen selbst verordnet, weil er sich danach soviel besser fühle. Der Patient sprach immer wieder über sein Wohlbefinden und setzte seine Berufstätigkeit fort. Zweimal verlangte Dr. Greer, er solle das Vitamin C absetzen. Aber beide Male vergrößerten sich nach dem Absetzen des Vitamins seine Milz und seine Leber, wurden schmerzempfindlich, seine Temperatur stieg auf 38,3°C an, und er klagte über allgemeines Unwohlsein und Müdigkeit, die typischen Leukämiesymptome. Sein subjektives Befinden und die Symptome besserten sich sofort, wenn er das Vitamin C wieder einnahm. Er starb im März 1954 im Alter von 73 Jähren an akutem Herzversagen. Seine Milz war zu dieser Zeit unauffällig, und die Leukämie, die Polyzythämie, die Zirrhose und die Myocarditis hatten sich während der achtzehn Monate seit dem Beginn der Einnahme großer Dosen Vitamin C nicht verschlechtert. Greer schloß daraus, daß die Einnahme großer Dosen Ascorbinsäure offenbar wesentlich zum Wohlbefinden des Patienten beigetragen hat.<br> <br> <br><br>Vitamin C als Radikalenfänger<br><br>Radikale sind hochaggressive biochemische Verbindungen. Sie entstehen durch körpereigene Stoffwechselprozesse oder werden durch Umweltgifte oder Strahlen induziert. Radikale schädigen Proteine, Enzyme, Lipoide und die Erbsubstanz. Untersuchungen an menschlichem Blutplasma zeigen, daß Vitamin C von allen getesteten Substanzen (Proteinthiole, Bilirubin, Harnsäure, ß-Carotin, Vitamin E) am effektivsten im Schutz gegen Peroxidradikale ist (Frei et al., 1989). Vitamin C regeneriert oxidiertes Vitamin E und bewirkt hierdurch einen Schutz der Lipidmembranen (Henson et al. 1991).<br> <br>Vitamin C gehört damit in der Behandlung neben Glutathion, und den Vitaminen A und E zu den stärksten Radikalenfängern.<br><br> <br><br>Stärkung des Immunsystems:<br><br>Vitamin C steigert in vielfältiger Weise die Abwehrmechanismen des Organismus (Bayer und Schmidt 1991, Prinz 1977, Werbach 1990, Cheraskin 1985). Sogar inGegenwart der Karzinogene Dibutylamin und Natriumnitrit (beides Nitrosaminbildner), die normalerweise zu einer Verminderung der zellulären und humoralen Immunantwort führen, steigert Vitamin C das Abwehrgeschehen (Medhat 1991).<br> <br>Membranintegrität:<br><br>Dem Vitamin C kommt eine wichtige Funktion in der Aufrechterhaltung derMembranintegrität zu. Vitamin C ist für die Integrität des Endothels unerläßlich (Reinecke 1995 und Matsuda 1993).<br><br> Stabilität des Bindegewebes:<br><br>Vitamin C ist essentiell für ein stabiles Bindegewebe. Es ist für die ausreichende Modifizierung der Aminosäuren Lysin und Prolin verantwortlich. Nur die modifizierten Aminosäuren sind zur Ausbildung einer stabilen Tripelhelix, dem Grundgerüst des Kollagens fähig (Hanauske-Abel zitiert in Peterkofsky 1991). Des weiteren ist Vitamin C für den Auf- und Abbau des Bindegewebes von Bedeutung. Hierbei verschiebt es das Gleichgewicht in Richtung Bindegewebsaufbau und -erhalt (Anderson 1991).<br> <br>1968 haben Cheraskin und seine Mitarbeiter eine synergistische Wirkung zusätzlicher Ascorbinsäuregaben auf die Reaktion von Patienten mit squamösen Karzinomen am Gebärmutterhals auf die Bestrahlung beschrieben. 27 Patientinnen erhielten täglich 750 mg Acorbinsäure beginnend eine Woche vor der Strahlenbehandlung drei Wochen nach ihrer Beendigung. Außerdem bekamen sie ein aus Vitaminen und Mineralien bestehendes Präparat und allgemeine Diätvorschriften (Verringerung der Saccharosemengen in der Nahrung). Die Kontrollpersonen waren 27 ähnliche Patienten, denen keine Vitamine oder Diätvorschriften verordnet wurden. Die Strahlendosis war für beide Gruppen gleich intensiv. Die Ansprechquote auf die Bestrahlung war bei den diätetisch behandelten Patientinnen wesentlich höher (die durchschnittliche Quote lag bei 97,5%) als bei den Kontrollpersonen (63,3%). Das läßt vermuten, daß Krebspatienten, die sich einer Strahlentherapie unterziehen, einen erhöhten Bedarf an Ascorbinsäure haben, und daß die Befriedigung dieses erhöhten Bedarfs vor einigen schädlichen Auswirkungen der Bestrahlung zu schützen vermag und zugleich die therapeutische Wirkung verstärkt.<br> <br> <br><br>Skorbut und Vitamin C<br><br>Der inzwischen verstorbene Dr. William McCormick aus Toronto scheint der erste gewesen zu sein, der erkannt hat, daß die allgemeinen Veränderungen des Bindegewebes, die beim Skorbut auftreten, identisch sind mit den lokalen Bindegewebsveränderungen, die in der unmittelbaren Nachbarschaft eingedrungener Neoplasmazellen beobachtet werden (McCormick 1959). Er nahm an, daß der Nährstoff (Vitamin C), von dem bekannt war, daß er solche Veränderungen beim Skorbut verhindert, bei Krebs eine ähnliche Wirkung haben könnte. Die Tatsache, daß fast alle Krebspatienten an einem Vitamin-C-Mangel leiden, unterstützte diese Auffassung. Es gibt aber auch andere interessante Parallelen zwischen Skorbut und Krebs. In der historischen Literatur wird häufig erwähnt, daß beim Skorbut die Häufigkeit von Krebsen und Tumoren zunimmt. Die Abhandlung über den Skorbut von James Lind (1753) enthält Sätze wie den folgenden: "Alle Teile waren so miteinander vermischt, daß sie nur noch eine Masse oder einen Klumpen bildeten und die einzelnen Organe nicht mehr identifiziert werden konnten". Das ist die sehr anschauliche Schilderung einer Neoplasmainfiltration durch einen Pathologen aus dem 18. Jahrhundert. Andererseits sind die beim fortgeschrittenen menschlichen Krebs auftretenden prämortalen Symptome wie Anämie, Auszehrung, extreme Schlaffheit, Blutungen, Geschwürbildungen, Infektionsanfälligkeit und ein abnorm niedriger Ascorbinsäöurespiegel im Gewebe, im Plasma und in den Leukozyten mit einem Ausfall der Nebennierenfunktionen kurz vor dem Tod praktisch identisch mit den prämortalen Symptomen eines fortgeschrittenen Skorbuts beim Menschen.<br> <br> <br><br>Epidemiologie<br><br>Epidemiologische Erkenntnisse zeigen, daß die Häufigkeit von Krebserkrankungen in großen Populationen in einem umgekehrten Verhältnis zur täglichen Aufnahme von Ascorbinsäure steht. Von den zahlreichen Untersuchungen, die praktisch zu den gleichen Ergebnissen kamen, erwähne ich die Arbeit des norwegischen Forschers Bjelke, der 1973/74 umfangreiche Studien über Patienten mit Magen-Darm-Krebs veröffentlicht hat. Dazu gehörten auch schriftliche Umfragen über die Ernährung der Patienten und die kontrollierte Untersuchung einzelner Fälle. Seine Arbeit, bei der er die Daten von mehr als 30.000 Personen in den Vereinigten Staaten und Norwegen berücksichtigte, schließt die Zusammensetzung der Ernährung dieser Patienten differenziert, bis zum Tabakgenuß und andere Lebens- und Ernährungsgewohnheiten mit ein. Eine negative Wechselbeziehung stellte er zwischen dem Verzehr von Obst, Beeren, Gemüse und Vitamin C auf der einen und dem Auftreten von Magenkrebs auf der anderen Seite fest, während stärkehaltige Nahrungsmittel, wie Kaffee und gesalzener Fisch zu einem häufigeren Auftreten von Magenkrebs führten. Er schloß daraus, daß die beiden wichtigsten Faktoren die Gesamtmenge der Vegetabilien in der Nahrung und der Vitamin-C Gehalt im Essen waren. Je höher der Anteil an Vegetabilien und Vitamin C in der Nahrung war, desto geringer war die Zahl der Krebserkrankungen.<br> <br> <br><br>Tierexperimentelle Studien<br><br>Eine sorgfältige Studie der Beziehungen zwischen Vitamin C und dem spontanen Brustkrebs bei Mäusen wurde, 1981 bis 1984 in einem Institut in Pab Alto durchgeführt. Diese Studie ist die bisher sorgfältigste und zuverlässigste mit Tieren durchgeführte Studie über die Zusammenhänge zwischen dem Vitamin C und Krebs (Pauling u. a. 1985).<br> <br>Die bei diesen Untersuchungen verwendeten Mäuse des Stammes R III erkranken im Alter von etwa 40 Wochen an einem ertastbaren Brustkrebs. An der Tumorbildung ist ein Virus beteiligt, das mit der Muttermilch von der Mutter auf die Tochter übertragen wird. Der Zeitpunkt, zu dem sich der erste Tumor nach der Inkubationsperiode entwickelt, ist konstant. Das heißt, nach diesem Zeitpunkt besteht bei allen Mäusen ohne Tumoren jede Woche die gleiche Wahrscheinlichkeit für das Auftreten des ersten Tumors.<br> <br>Bei den Untersuchungen wurden sieben aus jeweils 50 Mäusen bestehende Gruppen, die ein sorgfältig zubereitetes Futter bekamen, das jeweils 0,076, 1,86, 2,9, 4,2, 8,0, 8,1 oder 8,3 Prozent zusätzliche Ascorbinsäure enthielt. Dieses Futter wurde ihnen im Alter von neun Wochen bis zum Alter von 14 Wochen verabreicht. An Tumoren erkrankte Mäuse wurden getötet, um ihnen ein langes Leiden zu ersparen. Es wurde festgestellt, daß sich die Inkubationszeit mit der Erhöhung der Vitamin-C-Dosis stetig verlängerte, und zwar vom Alter von 38 Wochen für 0,076 Prozent Vitamin C auf ein Alter von 52 Wochen für die Tiere, die 8,3 Prozent Vitamin C bekamen. Auch die Häufigkeit des Auftretens des ersten Tumors in jeder Gruppe von Mäusen nahm prozentual stetig ab, und zwar von 2,7 Prozent in der Woche für 0,075 Prozent Vitamin C auf 0,7 Prozent in der Woche für 8,3 Prozent Vitamin C. Die biostatistische Auswirkung der Ergebnisse zeigt, daß der Zuverlässigkeitswert für die Schlußfolgerung, daß erhöhte Dosen Vitamin C im Futter zu einer Abnahme des Auftretens eines spontanen Brustkrebses bei diesem Mäusestamm führt, extrem hoch ist. Die Wahrscheinlichkeit, daß es sich hier um ein zufälliges Ergebnis handelt, ist eins zu einer Million. Aus dieser Studie geht hervor, daß das Alter, in dem der Tumor sich bildet, mit der Erhöhung der Vitamin-C-Dosis wesentlich zunimmt. Das Durchschnittsalter, in dem die Hälfte der Mäuse einen Tumor entwickelt, nimmt von 66 Wochen für die kleinste Dosis des Vitamins bis zu 120 Wochen für die größte Dosis zu. Die Entwicklung des Krebses wird im Mäusestamm R III vom mittleren Alter bis zum extrem hohen Alter verzögert.<br> <br>Auswirkungen des Vitamin C auf das Tumorgewebe:<br><br>Neue Hinweise auf die antineoplastische Wirkungsweise des Vitamin C auf Basal-Zell und Squamosus-Zell-Karzinom erhielt man bei Ratten und Mäusen. Die Tumorinitiation erfolgte durch Applikation von 3-Methylcholanthren. Durch die anschließende Gabe von Vitamin C p.o. in einer Dosierung von 50 mg/kg KG pro Tag wird die DNA-, RNAund Proteinsynthese in den Krebszellen signifikant reduziert (Lupulescu 1991).<br> <br>Untersuchungen bei Hamstern am Wangenepithellum verdeutlichen die Vitamin C abhängigen Mechanismen in der Pathogenese oral induzierter Karzinogenese. Durch Exposition des Epitheliums (topisch) mit kanzerogenen Chemikalien allein und in Gegenwart von Vitamin C zeigen sich beträchtliche Unterschiede. Makroskopisch reduziert Vitamin C die Häufigkeit des Auftretens epithelialer Tumore. Mikroskopisch bewirkt die Vitamin C-Gabe die Ausbildung papillarer, epideroider Karzinome mit minimaler Invasion, wogegen in der Abwesenheit von Vitamin C gut diflerenzierte Squamosus-Zell-Karzinome entstehen. Diese Beobachtungen legen die Vermutung nahe, daß Vitamin C in der Lage ist, das Wachstum der inituerten Zellen zu beschränken und die Invasion ins Subepithellum zu verhindern (Potdar 1992).<br> <br> <br><br>Die Dosierungsfrage<br><br>Die hochdosierte Vitamin C-Therapie sollte bei Krebspatienten niemals abrupt abgebrochen werden, da der Vitamin C-Spiegel ansonsten weit unter die Ausgangswerte absinken kann (,,rebound eftect"). Aus diesem Grund bevorzugt Cameron kontinuierlich durchgeführte Vitamin C-lnfusionen vor periodisch durchgeführten (mit einigen Tagen Zwischenraum).<br> <br>Am ersten Tag wurden 4 unterschiedliche Dosierungen, beginnend mit 0,5 g bis zu 2,0 g Vitamin C intravenös gegeben. Am zweiten Tag beginnt die Dosierung bei 2,5 g Vitamin C, sie wird bis auf 10 g Vitamin C pro Tag gesteigert und für die folgenden Tage beibehalten. In unserer Praxis hat sich jedoch die Verabreichung von 15g als optimal herausgestellt.<br> <br>Auch weitaus höhere Dosierungen wurden bereits angewendet. Als mögliche Nebenwirkung kann es durch die Konzentration an Natriumionen zur Wasserretention mit Ödembildung in den Gelenken kommen. Bei Patienten mit Herzbeschwerden können sich gefährliche pulmonale Ödeme bilden, die zur Kontrolle einer umgehenden Behandlung bedürfen. Eine seltene Nebenwirkung stellt der septische Schock dar, der durch einen massiven Tumorzerfall ausgelöst wird. Die Behandlung dieser lebensbedrohlichen Komplikation wird auf der lntensivstation durchgeführt.<br> <br>Nach Beendigung der intravenösen Vitamin C-Therapie wird mit der oralen Vitamin C-Gabe fortgefahren. Die Einnahme soll über den Tag verteilt erfolgen (alle 6 Stunden). Die Dosierung liegt zwischen 10 und 30 g. Eine Plasmakonzentration von 3 mg/dl wird empfohlen. Oftmals erreichen die Patienten durch die Vitamin C-Therapie schnell einen Zustand mit stark verbessertem Allgemeinzustand, der oftmals Monate bis Jahre anhalten kann. Dann kommt es jedoch zu einem abrupten Abbruch mit explosiver Metastasierung. Bei den ersten Anzeichen einer Verschlechterung sollte eine erneute Vitamin C-lnfusionstherapie erfolgen. Trotzdem kann eine Reaktion des Patienten auf diese erneute Vitamin C-Therapie niemals exakt vorausgesagt werden.<br> <br>Über einen Zeitraum von 3 Jahren bewirkte die Vitamin C-lnfusionstherapie bei einem Patient mit disseminiertem Leiomyosarkom fünfmal eine deutliche Verbesserung des Zustandes, bei der sechsten Anwendung des Infusionszyklus reagierte er jedoch nicht mehr auf die Therapie. Einige Patienten zeigen schon beim ersten Mal der Therapie keine Reaktion. Es sollte jedoch nach Aussage Camerons auf jeden Fall ein Versuch unternommen werden.<br> <br>Beschriebene Wirkungen der Vitamin-C-Therapie:<br><br>Verbesserung des Wohlbefindens und des Karnofsky-lndexes wird innerhalb von 5-7 Tagen erkennbar. Grund für diese Verbesserung ist die geförderte endogene Carnitinsynthese, für die Vitamin C erforderlich ist. Carnitin ist für den Transport der Fettsäuren in die Mitochondrien notwendig und fördert somit die Energieversorgung des Organismus.<br> <br>Erleichterung der Schmerzen bei skelettalen Metastasen nach 5 - 7 Tagen. Absetzen von Opiaten möglich.Skelettale oder viscerale Metastasen sind oftmals Ursache einer erhöhten Ausscheidung von Hydroxyprolin. Dies spiegelt einen verstärkten Kollagenabbau wieder. Innerhalb von 5 Tagen nach Beginn der Vitamin C-Therapie kommt es zum Abfall der Hydroxyprolinexkretion.<br> <br>Die Tumorreaktion auf die Vitamin C-Therapie wird in einem Absinken der Sedimentationsrate und der Proteintumormarker im Serum (CEA etc.) deutlich.<br><br>In günstigen Fällen wurde die Resorption maligner Pleuraergüsse und Reduktion der pulmonalen Metastasengröße beobachtet (Cameron 1991).<br> <br> <br><br>Adjuvante Vitamin C-Therapie in der Strahlentherapie<br><br>Gerade hier zeigen sich beachtliche Erfolge.<br><br>Bei allen Patienten wurde 3-4x pro Woche, vor der Bestrahlung, 15g Vit.C (2 x 7,5 g Fa. Pascoe) infundiert. Alle Patienten konnten die vorgesehenen Bestrahlungstermine en Block durchführen, alle hatten während der Bestrahlungszeit (ca. 6 Wochen, 2 Gy/Tag) eine hohe Lebensqualität konnten Ihren Hobbys nachgehen und sogar Gartenarbeit verrichten. Die Patienten lernten sich in den 6 Wochen untereinander kennen und es wurde gleich registriert, wenn ein Mitpatient wegen eines sogenanten Strahlenkater, einem Zustand dem eine schwere Grippe nur in etwa nahe kommt, fehlte. Alle Vitamin-C behandelten Patienten konnten jeden Tag erscheinen.<br> <br> <br><br>Vitamin C als Infektionsprophylaxe<br><br>Wie gesagt, weiß man schon seit vielen Jahren, daß Krebspatienten einen niedrigen Vitamin-C- Spiegel im Blut haben und daß diese Patienten, besonders an Krebs erkrankte Kinder, sehr anfällig gegen Infektionen sind. Infektionen sind eine häufige Todesursache bei den an Krebs erkrankten Kindern, zum Teil deshalb, weil die Krebstherapie das Immunsystem schädigt.<br> <br>Der niedrige Vitamin-C-Spiegel im Blut sollte natürlich bei allen Krebspatienten durch die Verabreichung hoher Dosen dieses Vitamins ausgeglichen werden. Diese hohen Vitamindosen sollten zudem einen gewissen Schutz vor Infektionskrankheiten gewähren und eine wertvolle Ergänzung der konventionellen Therapie bei der Behandlung von Infektionskrankheiten und des Krebses selbst sein Die Ascorbinsäure im menschlichen Körper ist entscheidend daran beteiligt, toxische Substanzen zu eliminieren oder zu neutralisieren. Es reagiert hier in der Regel gemeinsam mit den Enzymen der Leber im Sinne einer Hydroxilierung und Ausscheidung toxischer Substanzen über die Nieren. Wir wissen noch nicht, wie weit eine optimale Dosis Vitamin C uns vor karzinogenen Substanzen schützt, die mit der festen und flüssigen Nahrung und durch die Umwelt in unseren Körper gelangen, aber einige Beispiele zeigen, daß diese Schutzwirkung sehr groß sein könnte.<br> <br> <br><br>Vitamin C und Magen- Blasen- und Darmkrebs<br><br>Nitrite und Nitrate in Lebensmitteln wie Speck und anderen geräucherten Fleischsorten reagieren im Magen in Verbindung mit den Aminen im Mageninhalt und bilden Nitrosamine, die als Karzinogene Magenkrebs verursachen. Hohe Dosen Vitamin C verhindern den Umbau von Nitrosaminen zu Nitraten und hemmen damit die Entstehung von Magenkrebs. Gegenwärtig werden große Anstrengungen unternommen, um den Nitrit- und Nitratgehalt in den Lebensmitteln zu reduzieren, um die Krebsgefahr zu verringern. Die Erhöhung des Vitamingehalts in der Nahrung kann solche Bemühungen unterstützen.<br> <br>Es liegen auch Berichte vor, nach denen der bei Rauchern oft beobachtete Blasenkrebs sich zurückbildet, wenn der Patient genügend hohe Dosen Ascorbinsäure -1 g täglich oder mehr- einnimmt. Schlegel, Pipkin, Nishimura und Schultz (1980) haben festgestellt, daß der Ascorbinsäurespiegel im Urin bei Rauchern etwa halb so hoch ist wie bei Nichtrauchern, besonders niedrig aber bei Patienten mit Blasentumoren. Außerdem stellten sie fest, daß Mäuse nach der Implantation eines Kügelchens aus 3-Hydroxyan-thranilinsäure (eines Derivats der Aminosäure Trvptophan) in der Blase Blasentumore entwickelten, wenn die Mäuse normal gefüttert wurden, nicht aber, wenn ihr Trinkwasser mit Ascorbinsäure angereichert wurde. Die Verfasser meinen, daß die Ascorbinsäure die Oxydation der 3-Hydroryanthranilinsäure in ein karzinogenes Oxydationsprodukt verhindert. Sie schrieben: "Augenscheinlich gibt es gute Gründe für die Annahme, daß die günstigen Auswirkungen eines angemessenen Ascorbinsäurespiegels im Urin (der einer täglichen Dosis von 1,5 g entspricht) eine geeignete Präventivmaßnahme gegen die Entstehung und das Wiederauftreten von Blasentumoren ist."<br> <br>Dr. Robert Bruce, der Direktor der Zweigstelle des Ludwig-Krebsforschungsinstituts in Toronto, berichtete 1977, daß es im Darminhalt von Menschen wahrscheinlich mutagene und karzinogene Substanzen gibt. Später berichteten er und seine Mitarbeiter, daß die Verabreichung hoher Dosen Vitamin C die Menge dieser Substanzen wesentlich reduzieren könne (Bruce 1979). Auf diese Weise und außerdem durch die Abkürzung der Zeit, in der sich die Abfallprodukte im Körper befinden, hilft eine angemessene Versorgung mit Vitamin C den unteren Darmtrakt vor Krebs zu schützen.<br> <br>Die Dickdarm-Polyposis ist eine durch die Bildung zahlreicher Polypen im Dickdarm und Mastdarm gekennzeichnete erbliche Krankheit. Diese Polypen sind gutartige Tumoren, aber ihr Vorhandensein ist schon seit langer Zeit als Vorstufe der Malignität erkannt worden. Willis schreibt 1973: ,,Die Opfer der bekannten Polyposis sterben fast immer schon frühzeitig an Dickdarm- oder Mastdarmkrebs. Doch jetzt dürfen sie neue Hoffnung schöpfen. Untersuchungen von De Cosse u.a. (1975), Lai u.a. (1977) und Watne u.a. (1977) an 16 Personen mit Polyposis haben ergeben, daß die regelmäßigeVerabreichung von 3g Vitamin C täglich die Polypen bei fünfzig Prozent der Patienten zum Verschwinden brachten. Es besteht die reale Möglichkeit, daß sich die Krankheit bei anderen Patienten mit einer größeren Dosis von 10 oder 20 g täglich heilen ließe.<br> <br> <br><br>Vitamin C bei disseminierten Krebserkrankungen<br><br>Nach den Enttäuschungen, die Cameron bei seinen Versuchen mit verschiedenen Hormonen erlebt hatte, glaubte er jetzt, daß die Behandlung mit Vitamin C für seine Patienten einen großen Nutzen haben werde, und verordnete mehreren hundert Patienten mit fortgeschrittenem Krebs während der folgenden zehn Jahre große Dosen dieses Vitamins. Es handelte sich bei ihnen fast ausschließlich um Patienten, bei denen alle konventionellen Behandlungsmethoden ausgeschöpft waren. Er und seine Mitarbeiter veröffentlichten eine Reihe wissenschaftlicher Berichte über ihre Beobachtungen. In einem dieser Aufsätze berichteten sie, daß das Vitamin C offensichtlich so wesentlich zur Schmerzlinderung beitrug, daß Patienten, die große Dosen Morphin bekommen hatten, auf eine weitere Behandlung mit diesen Betäubungsmitteln verzichten konnten (Cameron und Baird 1973). Er veröffentlichte auch einen detaillierten Bericht über die ersten 50 Patienten mit fortgeschrittenem Krebs, die mit hohen Dosen Vitamin C behandelt werden sollten (Cameron und Campbell 1974). Hierunter war eine eindrucksvolle Dokumentation über einen Patienten, der unter einer Vitamin C-Behandlung augenscheinlich vollkommen vom Krebs geheilt worden war, bei dem der Krebs jedoch erneut auftrat, als die Behandlung mit Vitamin C eingestellt wurde. Eine erneute Therapieaufnahme führte wiederum zu einer vollständigen Tumorremission.<br> <br>Zunächst beobachtete Cameron, daß sich der Zustand der meisten mit Ascorbinsäure behandelten Patienten eine Zeitlang deutlich besserte und auch eine klinische Besserung festzustellen war. Die Vorteile für die Mehrzahl der Patienten waren neben der Besserung des Allgemeinbefindens eine Linderung der Schmerzen, eine Abnahme der Zahl bösartiger Zellen, sowie eine deutliche Verringerung tumorbedingter Komplikationen (Pleuraergüsse, Hämaturien, Hepatomegalie und Ikterus). In nahezu allen Fällen war auch eine Besserung der Blutsenkungsgeschwindigkeit zu registrieren. Das ließ den Schluß zu, daß sowohl die Besserung des Allgemeinbefindens als auch die offensichtliche Verlängerung der Überlebenszeit Ergebnisse der signifikanten Wirkung der Ascorbinsäure waren, und zwar, entweder direkt oder über den natürlichen Schutzmechanismus des Körpers, oder durch Wirkung auf das Tumorgeschehen selbst.<br> <br> <br><br>Erste kontrollierte Studien<br><br>1973 schien es Cameron an der Zeit zu sein, einen kontrollierten Versuch zu unternehmen, bei dem die Hälfte der Patienten, die durch das Los bestimmt werden sollten, täglich 10 g Vitamin C bekamen, während den anderen ein Placebo verabreicht wurde. Inzwischen war Cameron jedoch so vom Wert des Vitamins C für Patienten mit fortgeschrittenem Krebs überzeugt, daß er aus ethischen Gründen nicht bereit war, diese Behandlung einem Krebspatienten vorzuenthalten, für den er die Verantwortung trug. Obwohl jetzt kein Doppelblindversuch mit willkürlich ausgewählten Versuchspersonen durchführt wurde stand es frei, einen kontrollierten Versuch vorzunehmen. Das Vale of Leven Hospital ist ein großes Krankenhaus mit 440 Betten und nimmt jährlich etwa 500 neue Krebspatienten auf. Obwohl Cameron als Chef der chirurgischen Abteilung mit 100 Betten für deren Verwaltung verantwortlich war, gab es dort nur wenige Krebspatienten, die von ihm selbst ärztlich versorgt wurden. Zunächst gab keiner der anderen Ärzte oder Chirurgen seinen Patienten große Dosen Vitamin C, und auch in späteren Jahren sind viele Krebspatienten im Vale of Leven Hospital nicht mit Ascorbinsäure behandelt worden. Sie konnten bei der Untersuchung die Rolle der Kontrollpersonen übernehmen.<br> <br>1976 wurde die Überlebensdauer von 100 tödlich erkrankten Krebspatienten registriert, die zusätzliche Dosen Ascorbinsäure erhielten, und von 1000 anderen Patienten, die in einem ähnlichen Zustand eingeliefert und von den gleichen Klinikern im selben Krankenhaus behandelt worden waren, und zwar bis auf die Verabreichung der Ascorbinsäure genauso wie die ersteren. Diese 1000 Patienten stellten nun für jeden mit Ascorbinsäure behandelten Patienten zehn Kontrollpersonen, die hinsichtlich des Geschlechts, des Alters, des Typs ihres primären Tumors und ihres klinischen Zustandes der "Nichtbehandelbarkeit" diesem einen Patienten entsprachen, Cameron: "Wir zogen einen nicht zum Stab des Krankenhauses gehörenden Arzt hinzu, der die Überlebenszeiten der mit Ascorbin behandelten Patienten nicht kannte, und baten ihn, die Krankheitsgeschichten aller Kontrollpatienten zu prüfen und für jeden einzelnen die Überlebenszeit zu registrieren - die Anzahl der Tage vom Zeitpunkt des Abbruchs der konventionellen Behandlung bis zum Todestag. Am 10. August 1976 waren alle 1000 Kontrollpersonen gestorben, während 18 der 100 mit Ascorbinsäure behandelten Patienten noch lebten Zu diesem Zeitpunkt war die durchschnittliche Überlebenszeit nach dem Eintritt der ´Nichtbehandelbarkeit´ bei den mit Ascorbin behandelten Patienten 4,2mal so groß wie bei den ihnen entsprechenden Kontrollpersonen. Die 100 mit Ascorbinsäure behandelten Patienten hatten im Durchschnitt mehr als 300 Tage länger gelebt als die entsprechenden Vergleichspatienten, und außerdem hatten wir nach dem klinischen Befund durchaus den Eindruck, daß sie sich in dieser letzten Lebensperiode wohler gefühlt hatten als die anderen. Einige von ihnen leben sogar noch heute und nehmen immer noch ihre tägliche Dosis Natriumascorbat. Und einige von ihnen können sogar als von ihrer bösartigen Krankheit ´geheilt´ angesehen werden, denn sie zeigen keine erkennbaren Manifestationen des Krebses mehr und führen ein ganz normales Leben."<br> <br> <br><br>Wegen der großen Bedeutung des Krebsproblems wurden die Krankengeschichten der Patienten im Vale of Leven Hospital 1978 noch einmal überprüft und der Versuch wiederholt mit 100 Patienten, denen Ascorbin verabreicht wurde, und 1000 entsprechenden Kontrollpersonen (Cameron und Pauling 1978). Zehn der ursprünglichen 100 mit Ascorbin behandelten Patienten, in der Hauptsache solche mit seltenen Krebsarten, für die man nur schwer entsprechende Kontrollpatienten finden konnte, wurden gegen neue ausgetauscht, und die 1000 Kontrollpatienten wurden unabhängig davon ausgewählt, ob sie schon an der vorigen Studie teilgenommen hatten oder nicht (etwa die Hälfte von ihnen hatte zu den ersten 1000 Kontrollpatienten gehört). Die 100 mit Ascorbinsäure behandelten Patienten und die zu ihnen passenden Kontrollpersonen (mit dem gleichen Typ des Primärtumors, dem gleichen Geschlecht und dem gleichen Alter mit einer Toleranz von fünf Jahren) wurden in neun Gruppen aufgeteilt,und zwar je nach dem Typ des Primärtumors. Unter ihnen befanden sich zum Beispiel 17 mit Ascorbin behandelte Patienten und 170 Kontrollpatienten mit Dickdarmkrebs. Die Überlebenszeiten wurden von dem Zeitpunkt an berechnet, zu dem eine Weiterbehandlung des Patienten nicht mehr sinnvoll erschien, das heißt, man glaubte, mit den konventionellen Therapien keine Wirkung mehr erzielen zu können. Zu diesem Zeitpunkt oder wenige Tage später wurde mit der Ascorbinbehandlung begonnen.<br> <br>1978 war die Überlebenszeit bei den neun Gruppen zwischen 114 und 435 Tage länger für die mit Vitamin C behandelten Patienten als bei der Kontrollgruppe. Das war ein Durchschnitt von 255 Tagen für alle Gruppen, der sich ständig erhöhte, weil acht Prozent der Vitamin-C-Patienten noch lebten, nachdem alle Patienten aus den entsprechenden Kontrollgruppen gestorben waren.<br> <br>Aufgrund der Ergebnisse der Studien hat Cameron empfohlen, jedem Krebspatienten neben der angemessenen konventionellen Therapie und sobald wie möglich nach Auftreten der Krankheit hohe Dosen Vitamin C zu verabreichen.<br> <br>Wie vielen Menschen könnte auf diese Weise geholfen werden? Die quantitativen Informationen, gründen sich hauptsächlich auf die Beobachtung von Patienten mit fortgeschrittenem Krebs in Schottland, die täglich 10 g Vitamin C erhielten. Als Ergebnis der Beobachtung von einigen hundert Patienten kam Cameron zu den folgenden Schlüssen über die Wirkung dieser Vitamin-C-Dosen bei Patienten mit fortgeschrittenem Krebs:<br> <br>Kategorie I: Keine Reaktion der Tumoren, aber gewöhnlich eine Besserung des Allgemeinbefindens etwa 20%<br>Kategorie II: Eine recht geringe Reaktion der Tumoren etwa 25%<br>Kategorie III: Verlangsamung des Tumorwachstums etwa 25%<br> Kategorie IV: Keine Veränderung der Tumoren (Stillstand) etwa 20%<br>Kategorie V: teilweise Rückbildung der Tumoren etwa 9%<br>Kategorie VI: Vollständige Rückbildung etwa 1%<br><br> <br><br>Bessere Ergebnisse werden mit größeren Dosen als 10 g täglich erzielt.<br> <br>In dem Buch Cancer and Vitamin C erklärt Cameron :,,Diese einfache und ungefährliche Therapie, die Verabreichung hoher Dosen Vitamin C, hat einen entschiedenen Wert bei der Behandlung von Patienten mit fortgeschrittenem Krebs. Obwohl es noch keinen ganz überzeugenden Nachweis dafür gibt, glauben wir, daß das Vitamin C für die Behandlung von Krebspatienten im Anfangsstadium der Krankheit, ebenso aber auch für die Krebsvorbeugung einen noch größeren Wert hat".<br> <br>Die Verwendung des Vitamins C als Ergänzung der angemessenen konventionellen Therapie bei der Behandlung von Krebspatienten hat viele Vorteile. Vitamin C ist nicht teuer. Es hat keine ernsten Nebenwirkungen, sondern regt den Appetit an, wirkt sich günstig auf Depressionen aus, unter denen Krebspatienten häufig zu leiden haben, verbessert den allgemeinen Gesundheitszustand und steigert die Fähigkeit des Patienten, sich am Leben zu freuen. Für jeden Patienten besteht die Chance, daß die Krankheit durch die Verwendung des Vitamins neben einer angemessenen konventionellen Therapie und einer aus geeigneten Nährstoffen bestehenden Diät viele Jahre unter Kontrolle gehalten werden kann.<br> <br>Weitere Literatur zu diesem Thema mit beigefügtem Literaturverzeichnis kann bei der Firma Pascoe Pharmazeutische Präparate GmbH, Postfach 100755, D-35337 Gießen, kostenlos angefordert werden<br><br>________________________________<br> <br>Friedmann GJ, Sherry S, Ralli EP: Mechanism of Excretion of Vitamin C by Human Kidney at Low and Norrmal Plasma Level of Ascorbine Acid, Journal of Clinical Investigations 19:685-689 (1940)<br><br>Herjanic M, Moss-Herjanic ML: Ascorbine Acid Test in Psychiatric Patients. Journal of Schizophrenia 1:257-260 (1967).<br> <br>Steinmetz KA, Potter JD Folsom AR: Cancer Res. 53 (3), 536-43 (1993)<br><br>Liu T, Soong SJ, Wilson NP, Craig CB, Cole P, Macaluso M, Potischman N J, Nutrition 123 (2 Suppl), 424-9 (1993)<br><br>VanEenwyk J, Davis FG, Colman N: Cancer Epidemiol. Biomarkers. Prev. 1 (2), 119-24 (1992)<br> <br>Singh VN, Gaby SK: American Society for Clinical Nutrition 53, 386-90 (1991)<br><br>Hanck A in: Vitamins in medicine recent therapeutic aspects, 87 - 104, Hans Huber Publishers, Bern (1983)<br><br>Weisburger JH: American Society for Clinical Nutrition 53, 226-37 (1991)<br> <br>Jacob RA, Kelley DS, Pianalto FS, Swendseid ME, Henning SM, Zhang JZ, Ames BN, Fraga CG, Peters JH: Am. J. Clin. Nutr. 54, 13029 (1991)<br><br>Bayer W, Schmidt K: Vitamin C, in: Vitamine in Prävention und Therapie, 2, 264, Hippokrates Verlag, Stuttgart (1991 )<br> <br>Medhat AM, el Din Abdelwahab KS, el Aaser AA, al Nagdy SA: Tumori 31 , 77(5), 372-8 (1991 )<br><br>Anderson R: American Society for Clinical Nutrition 53, 358-61 (1991)<br><br>Lupulescu A: Internat. J. Vit. Nutr. Res. 61, 125-129 (1991)<br> <br>Potdar PD, Kandarkar SV, Sirsat SM: Funkt. Dev. Morphol. 2 (3), 16 (1992)<br><br>Cameron E: Medical Hypotheses 36, 1 90 - 1 94 (1991)<br><br>LAI HY, SHIELDS EK, WATNE AL: Effect of Ascorbic Acid on Rectal Polyps and Rectal Steroids, in: Federadon Proceedings 35, 1061 (1977).<br> <br>WATNE AL, LAI HY, CARRIER J, COPPULA W: The Diagnosis and Surgicai Treatment of Patients with Gardner's Syndrome in: Surgery 82, 327-333 (1977).<br><br>CAMERON E, BAIRD G: Ascorbic Acid and Dependence on Opiates in Patients with Advanced Disseminated Cancer, in: IRCS Letter to the Editor, August 1973.<br> <br>CAMERON E, CAMPBELL A: The Orthomolecular Treatment of Cancer, II. Clinical Trial of High-dose Ascorbic Supplements in Advanced Human Cancer. Chemical-Biological Interactions 9, 285-315 (1974).<br><br>CAMERON E, PAULING L: Experimental Studies Designed to Evaluate the Management of Patients with Incurable Cancer. Proceedings of the National Academy of Sciences USA 75, 6252 (1978).<br> <br>Anschrift d. Autors:<br><br>Hp Heinz Kreher<br><br>Im Ebing 15, D-64367 Mühltal<br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-28142585444373510072011-07-04T03:27:00.000-07:002011-07-04T03:28:19.759-07:00XGP SOLVED with abscess drainage and IV antibioticsCASE REPORT <br><br>Year : 2007 | Volume : 18 | Issue : 4 | Page : 613-616<br><br>Xanthgranulomatous Pyelonephritis Associated with Staphylococcus Aureus<br><br>Abdulla K Al- Hwiesh<br><br>Department of Internal Medicine, King Fahad Hospital, Al-Khobar University, Al-Khobar, Saudi Arabia<br> <br> Abstract <br><br>A 44-year old man with xanthogranulomatous pyelonephritis presented with abdominal distention, left lumber pain, fever, loss of appetite, and loss of weight. He had been known to have diabetes mellitus type II for 20 years, and he was diagnosed to have a left renal stone three months prior to this presentation. The patient's urine and the left psous abscess grew staphylococcus aureus.<br> <br>Keywords: Xanthogranulomatous pyelonephritis, Diabetic mellitus, Renal stone, Staphylococcus aureus<br><br>How to cite this article:<br>Al- Hwiesh AK. Xanthgranulomatous Pyelonephritis Associated with Staphylococcus Aureus. Saudi J Kidney Dis Transpl 2007;18:613-6<br> <br>How to cite this URL:<br>Al- Hwiesh AK. Xanthgranulomatous Pyelonephritis Associated with Staphylococcus Aureus. Saudi J Kidney Dis Transpl [serial online] 2007 [cited 2011 Jul 4];18:613-6. Available from: <a href="http://www.sjkdt.org/text.asp?2007/18/4/613/36522">http://www.sjkdt.org/text.asp?2007/18/4/613/36522</a><br> <br> Introduction<br><br><br>Xanthogranulomatous pyelonephritis (XPN) is an unusual variant of chronic pyelonephritis that is complicated by urinary obstruction in two-thirds of the cases and associated with infected renal stone.[1],[2],[3],[4],[5],[6] Affected patients usually have massive destruction of the kidney that requires nephroctomy. The inflammation rarely extends beyond the renal capsule to retro-peritoneal and adjacent tissue. The space-occupying nature and rapid expansion makes the differentiation between XPN and neoplasm difficult. [2] The coexistence of XPN and Staphylococcus aureus Scientific Name Search has been reported in few cases previously. Here we describe a case of XPN secondary to Staphylopcoccus aureus infection that extended beyond the renal capsule and was associated with diabetes mellitus and renal stone.<br> <br><br> Case Report<br><br><br>A 44-year-old Saudi man was admitted to our hospital in July 2005 with complaint of abdominal distension and left lumber pain for 20 days prior to presentation. The patient had a known case of poorly controlled type II diabetes mellitus complicated by diabetic kidney disease and retinopathy.<br> <br>The patient was apparently well until three months prior to admission when he developed frank hematurea, left lumber pain, dysurea, and frequency and urgency of urination. Intravenous pyelogram revealed a small renal stone in the left kidney. He required 10 days of antibiotics for the associated urinary tract infection. Two months later, the patient started to develop abdominal distension associated with intermittent colicky left lumber pain that increased with movement and lifting his left leg, interfered with his daily activities, and limited his ability to walk. These symptoms were accompanied with high grade fever, nausea, vomiting, profuse sweating, loss of appetite loss of weight, and constipation.<br> <br>There was no history of contact with jaundiced patients or with birds or animal or patients with tuberculosis. The physical examination revealed a middle age man in pain but oriented to time, place, and person with BP 110/70 mmHg, pulse 120/min, respiratory rate 20/min, and temperature 39 o c. The lungs were clear for precaution and auscultation, and the cardiovascular system was unremarkable. The abdomen was distended with palpable 3x4 cm tender mass in the left abdominal region. The bowel sounds were within normal limits and the rectal exam was unremarkable. There was limited flexion of the left leg, decreased sensation on L3-L4 distribution, and a decrease of left knee reflex.<br> <br>The initial clinical assessment was compatible with acute pyelonephritis with possible emphysematous pyelonephritis, xanthgranulomatous pyelonephritis, or malignancy.<br><br>The laboratory investigations revealed WBC 15.7x1000 /µL (neutrophils 90%), hemoglobin 90 g/L, platelets 455 x1000/ µL, BUN 16 mmol/L, creatinine 150 µmol/L, NA 125 mmol/L, K 4.5 mmol/L, Cl 90 mmol/L, CO2 21 mmol/L, Anion Gap 14, total bilirubin 0.3 mg/dl total protein 69 g/L, albumin 20 g/L, alkaline phosphates 233 U/L, SGOT 43 U/L, GTP 20 U/L, LDH 125 U/L,GGTP 184 U/L, and erythrocyte sedimentation rate 133 1 st hour. The urinalysis revealed cloudy urine with protein 1g/L leukocytes 3040 RBC 30-50 and bacteria +3. The urine culture grew staphylococcus aureus however, the blood culture was negative. Prothrombine time, partial thromboplastine time, calcium, phosphorus, magnesium, and uric acid were within normal. The tuberculin skin test (PPD), and urine for acid fast bacilli (AFB) early morning were negative three times. The kidney urinary bladder (KUB) x-ray was within normal limits. Abdominal ultrasound revealed a heterogeneously echoic lesion at the lower left psoas muscle and infiltrating the lower left renal pole. The computerized tomography (CT) of the abdomen confirmed the findings of the ultrasound [Figure - 1].<br> <br>The patient received initially broad spectrum antibiotics that was adjusted later for Staphylococci aureus. Incision and drainage of the abdominal mass produced 400 ml of pure pus. [Figure - 2], discloses the lesion on CT of the abdomen after drainage. The renal biopsy was also performed [Figure - 3]. The microscopic examination of the XPN reveals inflammatory cells that are largely lipid-laden macrophages [Figure - 4].<br> <br><br> Discussion<br><br><br>XPN often occurs in middle age women who frequently have history of recurrent urinary infection. [2] The typical presenting symptoms include flank pain, fever, malaise, anorexia and weight loss. A unilateral renal Mass is usually palpable on physical examination. Blood tests usually reveal nonspecific abnormalities that include anemia, increase in erythrocyte sedimentation rate, and impaired liver function tests. The urinalysis reveals pyuria and bacteruria. The urine culture demonstrates typically gram negative organisms ( Escherichia More Details coli, proteus, mirabilis, klebsiella and providencia); staphylococcus aureus is rarely involved. In our patient both the urine culture and the necrotic tissue culture grew staphylococcus aureus.<br> <br>The diagnosis of XPN is confirmed by renal ultrasound and/or abdominal CT image. The gross examination of the affected kidney discloses an enlarged and destroyed kidney by the inflammatory process with necrotic yellow material surrounded by a layer of orange colored tissue, and staghorn calculi are usually present within the mass. On microscopic examination, the lesion comprises three layers centered by a calyx. [7] The inner zone consists of necrosis, leukocytes, lymphocytes, plasma cell, and macrophages. The middle zone contains vascularized granulation tissue interspersed with hemorrhage. The inflammatory cells are largely lipid-laden macrophages. Furthermore, the outermost part of the lesion is characterized by giant cell and cholesterol clefts. XPN is most frequently confused with renal carcinoma. The evidence of chronic urinary tract infection and the findings on abdominal CT scan usually allow this disorder to be distinguished from neoplasm. However, XPN and renal cell carcinoma can coexist. [2],[3],[4],[5]<br> <br>The usual treatment of XPN is nephrectomy and IV antibiotic. However, in our patient, the XPN related to staphylococcus aureus was treated with abscess drainage and IV antibiotics, and the disease completely resolved.<br> <br> <br> References<br><br>1. Parson,MA, Harris,SC, Longstaff, AJ, Grainger, RG. Xanthogranulomatous pyelonephritis: apthological, clinical and etiological nalysis of 87 case diag hospital 1983; 6:203. Back to cited text no. 1 <br> 2. Chuang CK, Lai MK, Chang PL, et al. Xanthogranulomatous pyelonephritis: Experience in 36 cases. J Urol 1992;147: 333-6. Back to cited text no. 2 [PUBMED] <br>3. Oosterhof GO, Delaere KP. Xanthogranulomatous pyelonephritis. A review with 2 case reports. Ural Int 1986;41:180-6. Back to cited text no. 3 <br> 4. Malek RS, Elde JS. Xanthogranulomatous pyelonephritis. A critical analysis of 26 cases and of the literature. J Urol 1978;119: 589-93. Back to cited text no. 4 <br>5. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises case 2-1995. A 71-year-old man with masses in the pancreas, presacral region, and left kidney. N Engl J Med 1995;332:174-9. Back to cited text no. 5 <br> 6. Watt I, Roylans J. Pyonephrosis. Clin Radial 1975;27:513. Back to cited text no. 6 <br>7. Hill GS. Renal infection. In: Uropathalogy, 1st ed. Hill GS, ed. Churchill Livingstone: New York;1989. p.333-429. Back to cited text no. 7 <br> <br><br>Correspondence Address:<br><br>Abdulla K Al- Hwiesh<br>Department of Internal Medicine, King Fahd Hospital of the University, P.O. Box 40246, Al Khobar 31952<br>Saudi Arabia<br>Login to access the Email id<br><br> PMID: 17951953 <br><br><br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-6596505409423182852011-07-04T02:25:00.001-07:002011-07-04T02:25:33.009-07:00Weak Hydrochloric Acid injections<p align="justify"><b>Is Hydrochloric Acid Better Than an Antibiotic? </b><br> </p><p align="justify"><img alt="http://www.apothecary-bottles.com/uploads/tx_extendedshop/ap051.jpg" src="http://www.apothecary-bottles.com/uploads/tx_extendedshop/ap051.jpg" height="248" width="150"></p><p align="justify"> <br></p><p align="justify"><font size="+1"><font color="#0000ff">These days one regularly hears of deaths in hospital from antibiotic resistant strains of bacteria such as MRSA. And it is well documented that antibiotics are becoming increasingly less effective in the fight against bacteria in general.<br> <br> But is there a better way to combat them?<br> <br> There is a saying that "the old ways are the best". In this article, Wayne Martin suggests an old way that may well be not only an answer to the problem of hospital disease deaths, but an instant and inexpensive answer. And it might even make antibiotics redundant<br> <br> All we have to do now is hope that someone will have the courage to try it.</font></font> </p> <hr class="c9" width="95%"> <p> This is to write about intravenous hydrochloric acid infusions, one part per 1,000 in the treatment of bacterial infections. This treatment had been developed by Burr Ferguson M.D. of Birmingham AL in about 1925. Dr. Ferguson had been a battle surgeon during World War 1 and he had seen the wounded die by the hundreds from infections. He quickly found that when an iv of 10 cc of one in 1,000 hydrochloric acid is given, there is almost at once a big increase in the white cell count.<br> <br> The first patient treated with 10 cc of one in 1,000 hydrochloric acid suffered from a infected gun shot wound. Almost at once the patient's temperature became normal and the infection was abolished.<br> <br> There was then a medical journal, Medical World, and in the years 1932 to 1935 it published many pages of letters from a score of doctors telling of success in the use of ivs of 1 in 1,000 hydrochloric acid in the treatment of bacterial infections. As a student at Purdue University in the years 1932 and 1933 I took the Medical World.<br> <br> I feel now that this treatment of bacterial infections was so effective that there was never the need for the discovery of antibiotics.<br> <br> Two things restricted the general use of ivs of dilute hydrochloric acid in the treatment of bacterial infections. One was that there was no major drug firm to foster its use to doctors. The other thing was that, in the 1930s, orthodox medical thinking held that nothing should be put in the vein, however there were many not so orthodox doctors who used ivs of 10 cc of 1 in 1,000 hydrochloric acid to treat bacterial infections, with dramatic success.<br> <br> I am going to give the case of a dramatic use of this treatment in 1931. I told of this case in my letter in the Townsend Letter for Doctors in the December 2001 issue. I am going to retell of the case here. The report was in Medical World. The doctor was William Howell M.D. of Lexington, Tennessee.<br> <br> He told of the following case: </p> <blockquote> The patient was age 15 and she was delivered of a very large baby that lived only for two hours. She lived in a log cabin in the woods. The delivery was done with the best aseptic condition that could be had in a log cabin. The patient weighed only 90 pounds. There were some small lacerations. On day three after delivery there was a message that the patient had a chill and high fever. She lived in a river bottom and I was in hope that it was malaria and I sent quinine. On the fifth day there was another message telling of the grave condition of the patient. In going into the sick room I saw at once that the message had been urgent. The girl was delirious, temperature was 106, pulse was 140, respiration was 40 and there was a discharge from the vagina with a fetid odor. Every other case I had seen like her had died of the infection.<br> <br>I had some one in 1,500 hydrochloric acid with me but had feared to use it. I injected 10 cc of 1 in 1,500 hydrochloric acid into a vein with much trepidation. The following minutes were anxious ones for me as I hardly knew what to expect. I had never heard of hydrochloric acid being used to treat puerperal sepsis. I was thinking of the warnings of the fatal results of an injection of acid in the vein. I was holding the radial pulse when of a sudden there was sweat on the patient's neck and forehead and a slowing of the pulse. In a few more minutes the patient was bathed in a profuse perspiration and there was a stop to the chatter of her delirium. Thirty minutes after the injection she was conscious and I asked her how she felt. She said that she felt much better she wanted to go to sleep.<br> <br> Within an hour of the injection, her temperature had dropped to 103, her pulse had dropped to 100 and respiration had decreased to 22. On the next four days I repeated the injections. On day six, temperature was 99, pulse was 72 and respiration was 19. Two days later I was called and told that her fever had returned. Her temperature was 101 and there was a free discharge from the vagina. I gave her one more injection of 10 cc of acid. All signs of the infection she had had completely disappeared.<br> </blockquote><br> <p align="justify">A few days ago I was watching CNN on the TV. The subject was antibiotic resistant staph infections in hospitals now. A case was given of a 50 year old woman how went to a hospital in Indianapolis for a minor surgery. She was infected with a resistant staph infection. There followed a sad story. The infection spread from one organ to another and after two months, death. In the CNN report it was said that this was not an isolated case.<br> <br> How much better would it have been if early on in her infection she had been treated with ivs of one in 1,500 hydrochloric acid.<br> <br> This leads to another line of thought. In the M.J. Anderson Bulletin for May-June of 1979, Dr. Birger Jansson had a report on the appendix and colon cancer. In this report he said that patients who had the appendix removed were at twice the risk of having colon cancer. He said that the appendix is an important part of our immune defense, that it produces our cancer killing cells. If this were true, the appendix should be protecting us from cancer in general. Dr. Jansson suggested that we think of ways to keep an infected appendix. He made no suggestion as to how this may be done but the appendix is removed when one has a bacterial infection of the appendix.. It is suggested that when one has an infected appendix, one should consider injections for two days with 10 cc of one in 1,000 hydrochloric acid to see if surgery my be avoided and the appendix saved.<br> <br> The Torrance Company of Portage, MI has 50 cc bottles of one in 500 hydrochloric acid for sale. Their phone is 800 327 0722.<br> <br> Wayne Martin BS ChE <br></p><p align="justify"><br></p> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-30315427972871042142011-07-02T06:38:00.000-07:002011-07-02T06:39:16.457-07:00GERMAN (compressed Book content) Chapter about Coley<br>Ein sehr guter Essay<br><a href="http://www.google.de/search?q=">http://www.google.de/search?q=</a>"merkwürdige+fall+eines+mannes+namens+stein"<br>(amazon 9.95 eur)<br><br>STICHWORTE AUS DEM BUCH "DAS MEDIZINKARTELL"<br> <font size="1"><span style="font-weight: bold;">Langbein, Kurt / Ehgartner, Bert</span>: Das Medizinkartell. Die 7 Todsünden der Gesundheitsindustrie; Piper-Verlag, München 2002; Zusammenfassung von Michael Palomino</font><br><br>1891: Forschung von Coley: der Fall von Fred Stein, der an Infektionen gesund wurde<br>Coley sucht nach Parallelfällen und findet den Fall Fred Stein, dessen Geschwulst 4 mal operiert worden war, 4 mal kam der Tumor zurück, zuletzt mit Angriff auf lebenswichtige Organe, so dass keine Operation mehr möglich war. Dazu kam eine Infektion mit Wundrose. Da wird Stein mit anderen infektiösen Patienten in einem Zimmer isoliert und macht so eine Infektion nach der anderen durch. Nun passierte die Sensation: Der Krebs ging zurück. Langbein/Ehgartner: "Mit jeder neuen Attacke wich jedoch, völlig überraschend für die behandelnden Ärzte, der Krebs ein Stück zurück." Stein wird gesund entlassen (S.265).<br> <br>Coley findet Stein (S.265-266) und Coley meint, man könne Bakterien gezielt gegen Krebs einsetzen. Ebenso forscht in Deutschland Friedrich Fehleisen von der Universität Würzburg, mit Berichten über einige Hundeversuche und Menschenbehandlungen (S.266).<br> <br>Behandlung des krebskranken Zola mit Windrose-Bakterien<br>Coley beginnt 1891, die Wundrose-Auslöser streptokokkus pyogenes auf einer konzentrierten Rinderbouillon zu züchten und behandelt seinen ersten Krebspatienten Zola damit (mehr ist vom Namen nicht in den Akten), der mit Mandeltumor nicht mehr schlucken kann und Geschwüre am Hals und offene Wunden von einer Operation hat (S.266). Die Wundrose wird direkt in die offene Wunde am Nacken eingespritzt und die Bakterien wirken: Die Tumoren schrumpfen ein wenig, aber die Wundrose bekommt Zola nicht (S.267).<br> <br>Coley lässt sich aus Deutschland von Robert Koch Wundrosen-Kulturen schicken und spritzt diese Zola ein. Die Koch-Wundrosen-Kulturen wirken extrem, am 1.Tag bis 40°C Fieber, am 2.Tag schrumpft der grosse Tumor, in 2 Wochen ist er vollständig verschwunden, Zola kann wieder essen. Zolas Spur verliert sich in Italien in seiner Heimat (S.267).<br> <br>Coley heilt mit Windrosen-Gift 100e Krebspatienten<br>Weitere alternative Experimente werden nur von Rockefeller unterstützt (S.268). Die Spitäler wollen nämlich keine Wundrose-Erreger in den Spitälern haben (S.267). Coley kann nun einen eigenen Pavillon einrichten. Die Behandlungen zeigen:<br> <br>-- 2 von 12 Krebspatienten sterben an der Wundrose, die anderen alle nicht<br><br>-- die Immunabwehr ist lernfähig<br><br>-- es müssen neue Infektionen her, um das Immunsystem herauszufordern, macht Coley aber nicht, sondern er isoliert das Gift der Bakterie und spritzt das Gift selbst: Dies ist weniger gefährlich und die Immunabwehr kann nicht reagieren<br> <br>-- ein Patient, John Ficken, wird von bösartigem Tumor geheilt, und mit ihm 100e weitere Patienten (S.268).<br><br>Coleys Mankos:<br>-- er geht nicht standardisiert vor<br>-- er beginnt mit niedrigen Dosen und dann je nach Reaktion des Immunsystems, geht also individuell vor<br> -- [es geht Coley um Heilung, nicht um den Beweis der Wirksamkeit einer Methode]<br>-- die PatientInnen sind völlig heterogen<br>-- Coley beschreibt die Ausgangsstadien kaum, sondern beschreibt den Ausgangszustand der PatientInnen einfach mit dem Wort "inoperabel"<br> -- und die Metastasendiagnostik ist noch kaum entwickelt (S.269).<br><br>Ab 1895:<br>Propaganda gegen Coley und die Immunsystem-Methode durch die Röntgen-Lobby<br>-- Coleys Methode sei gefährlich<br>-- Coleys Methode sei unwissenschaftlich<br> -- die PatientInnen hätten wohl gar nicht an Krebs gelitten (S.269).<br><br>Coleys Förderer Rockefeller glauben der Röntgen-Lobby und schwenken um<br>und lassen Coleys Heilungsansatz leerlaufen, Coley ist nicht mehr "Mode", weil man nichts beweisen kann, weil man nichts sieht, und trotzdem ist Coley der Begründer der Immuntherapie (S.270).<br> <br>Ab Ende 19.Jh.: alternative Forschung zum Krebs mit Immuntherapie<br>Am Cancer Research Institute in Manhatten (S.262-263) wird fieberhaft geforscht (S.263). Insgesamt arbeiten einzelne Ärzte mit der Immuntherapie, v.a. in Deutschland (S.270).<br> <br><br><br><br>1991: Studie von Abel: Fieber stärkt das Immunsystem gegen Krebs<br>gemäss Medizinbiometriker Ulrich Abel, der Krankengeschichten untersucht hat:<br>-- Krebspatienten hatten wenig fieberhafte Infekte<br><br> -- Leute mit "3 oder mehr banal fieberhaften Infekten pro Jahr" haben "ein um das Fünffache geringere Risiko, an Krebs zu erkranken." (S.313)<br><br>Dagegen: Häufiges Antibiotika unterdrückt Fieber und schwächt das Immunsystem (S.313).<br> <br>Die Leute meine, sie leben gesund, wenn sie nie Fieber haben, und dann haben sie den krebs, weil sie nie Fieber hatten. (S.314)<br><br><br>Fiebertherapie gegen Krebs von Arzt Wolfgang Wöppel: alle geheilt!<br>in Bad Mergentheim<br> -- mit Bakterieninjektionen<br>-- mit Ernährungsumstellung<br>-- mit weiteren alternativen Therapien<br>->> dann heilt der Krebs (S.314).<br><br>Dabei ist jedes Schicksal völlig individuell, denn jedes Immunsystem hat nur seine eigene Zusammensetzung (S.314). Dabei sind unter den geheilten Krebskranken alle möglichen Schichten vertreten: Todkranke, Nicht-Todkranke, Gesundheitsapostel, Depressive, die nur noch getrunken und schon ihren "Abschied" gefeiert haben ... sie sind alle geheilt worden vom Krebs! (S.314-315).<br> <br>[Folge: Eine einheitliche Fiebertherapie ist unmöglich, und die Schul-"Medizin" akzeptiert die Individualität der Menschen nicht].<br><br><br>1992: Coleys Arbeiten werden aufgegriffen - Coley ist der Schul-"Medizin" gleichwertig<br> Die Immunsystem-Methode ist den technischen Methoden gleichwertig, stellt Stornes in einer Arbeit fest. Die 5-Jahres-Überlebensrate beträgt bei Coley 47%, mit den technischen Methoden 10-50% (S.269).<br><br>In: Stornes, C.O.: Coley's toxins; In: Nature 1992; 360, S.23<br> <br>Aber Coleys Ansatz wird von der Pharma-Industrie weiterhin nicht beachtet (S.269) [denn man hat ja geldbringende Krebs-"Medikamente" auf dem Markt].<br><br>Arbeiten von Klaus Kölmel über Immuntherapie<br>Die Coley-Toxine werden auch nicht mehr hergestellt (S.270). Einzelne Ärzte arbeiten noch mit der Immuntherapie, zuletzt z.B. Klaus Kölmel, Chef der Universitäts-Hautklinik Göttingen (S.270). In seiner Studie über Coley-Toxine an 15 KrebspatientInnen kommt klar zum Ausdruck:<br> <br>PatientInnen, die nicht auf die Coley-Gifte angesprochen haben<br> <br><br>PatientInnen, die teilweise mit Fieber auf die Coley-Gifte angesprochen haben<br> <br><br>PatientInnen mit hoher Fieberreaktion auf die Coley-Gifte<br> <br>sterben alle<br> <br><br>überleben, haben aber Rückfälle<br> <br><br>sind geheilt, Anzahl: 3<br><br> <br> <br><br>(S.271)<br><br><br>In: Kölmel, K.F. / Abel, U. / Kuhn, B. / Vehmeyer, K. / Wieding, J.U.: Behandlung des metastasierenden malignen Melanoms mit einem Endotoxin enthaltenden Bakterienlysat - Ergebnisse einer Pilotstudie; In: Waclawiczek, H.W. u.a. (Hrsg.): Das maligne Melanom - Derzeitiger Stand in Diagnose und Therapie. Springer, Berlin 1991, S.238-239.<br> <br>Kölmel ist überzeugt vom Faktor Fieber gegen Krebs. Umfragen beweisen ihm:<br><br>Studie von Kölmel über krebsfreies Leben mit vielen Infekten<br><br>krebsfreie Personen<br> <br><br>KrebspatientInnen<br><br>hatten viele Infekte<br> <br><br>hatten wesentlich seltener Infekte<br><br>haben über 2 fieberhafte Infekte in 5 Jahren<br> <br><br>haben unter 2 fieberhafte Infekte in 5 Jahren<br><br>Krebsrisiko: Faktor 1<br> <br><br>Krebsrisiko: Faktor 10 (90% höheres Krebsrisiko)<br> <br> <br><br>(S.271)<br><br><br>In: Kölmel, K.F. / Gefeller, O. / Haferkamp, B.: Febrile Infections and Malignant Melanoma: Results of a Case-control Study; In: Melanoma Res. 1992; 2, S.207-210<br><br>Fieber gemäss Langbein/Ehgartner "verschlechtert [...] die Lebensbedingungen der Bakterien. Jene der Immunstoffe aber verbessern sich." Es ist alles per Elektronenmikroskop nachweisbar (S.312).<br> <br>Die Schul-"Medizin" der Onkologischen Gesellschaft boykottiert Kölmel<br><br>Die plötzlichen Heilungen von Krebs sind bei 1/3 der Fälle durch Fieber-Infektionen ausgelöst. Die Onkologische Gesellschaft reagiert aber kaum. Kölmel hat vor, die Coley-Studie zu wiederholen. Die Onkologische Gesellschaft blockt ab. Die Schul-"Medizin" boykottiert Kölmels Bakterientherapie, weil die Wirkungsweise "nicht geklärt" sei. Gleichzeitig hat die Schul-"Medizin" aber keine Rezepte, geschweige denn bessere, so der Professor und Medizinmathematiker Ulrich Abel aus Heidelberg (S.272).<br> <br><br><br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-29238692826032243972011-07-02T06:28:00.001-07:002011-07-02T06:28:39.612-07:00GERMAN TEXT (mediocre overview COLEY history)<br>Coleys Toxins<br><br>m Herbst 1890 wurde bei Elizabeth Dashiell, einer jungen,<br>zarten, siebzehnjährigen Frau, Knochenkrebs in der rechten<br>Hand diagnostiziert. Da sich die Krankheit noch im Frühsta-<br>dium befand, nahm man ihr den betroffenen Unterarm ab –<br> dennoch starb sie wenige Monate später. Ihr am New Yorker<br>Memorial Hospital, dem späteren Memorial Sloan-Kettering Cancer<br>Center, behandelnder Arzt war der damals achtundzwanzig<br>Jahre alte William Coley, Absolvent der Harvard Medical School.<br> Zutiefst betroffen begann er, alte Patientenakten zu studieren,<br>ohne zu wissen, wonach er eigentlich suchte. Beim Lesen der<br>verstaubten Krankenberichte fiel ihm auf, dass die meisten<br>Krebstherapien scheiterten, die meisten Krebs-Patienten star-<br> ben also. Doch er fand auch die Akte eines Patienten, der unter<br>einem Sarkom (einer Krebsgeschwulst des Bindegewebes) im<br>fortgeschrittenen Stadium gelitten hatte und wieder geheilt<br>worden war.<br><br>Der bereits todkranke Mann war im Herbst 1884 mit einer<br> an zwei Stellen ausgebrochenen schlimmen Wundrose (Erysi-<br>pel) ins Krankenhaus eingeliefert worden. Diese mit hohem<br>Fieber verbundene, durch Streptokokken verursachte Hautin-<br>fektion hatte sein Immunsystem aktiviert. Das pf laumengroße<br> Geschwür unter seinem linken Ohr begann zu schrumpfen, der<br>Patient kam wieder zu Kräften und wurde völlig gesund. Als<br>der hartnäckig weiterforschende Coley ihn etwa sieben Jahre<br>später aufsuchte, ging es dem Mann immer noch gut. Der Krebs<br> war nicht wieder ausgebrochen.<br><br>Da Coley seine Entdeckung vor über hundert Jahren machte,<br>zu einer Zeit also, als das Immunsystem noch ein unerforschtes<br>Gebiet war, verstand er nicht, wieso sich der Krebs durch eine<br> Streptokokken-Infektion zurückbilden konnte. Dennoch glaub-<br>te der Wissenschaftler in ihm, dass er vielleicht über etwas<br>Wichtiges gestolpert war – einen neuartigen Weg der Krebsbe-<br>handlung –, und begann eine Versuchsreihe mit Sarkom-Pati-<br> enten.3 In seinem ausgezeichneten Buch A Commotion in the<br>Blood4 (deutsch: Aufruhr im Blut) beschreibt Stephan Hall mit ei-<br>ner Begeisterung, die ansteckend wirkt, Coleys Anstrengungen,<br>das nachzuahmen, was die Natur auf so vollkommene Weise<br> vorgemacht hatte. Coleys erste Versuche, einen Sarkom-Pati-<br>enten mit lebenden Streptokokken-Kulturen zu impfen, schlu-<br>gen fehl. Doch schließlich gelang es ihm, besonders an-<br>steckende Bakterien zu besorgen, die bei dem Mann, der das<br> Glück hatte, sie injiziert zu bekommen, hohes Fieber und Haut-<br>infektionen auslösten. Nach nur wenigen Wochen bildeten sich<br>die Tumoren im Nacken dieses Patienten zurück. Schließlich<br>verschwanden sie ganz und kamen viele Jahre lang nicht wieder.<br> Der junge Arzt schrieb darüber seine erste Arbeit, die veröf-<br>fentlicht wurde.<br><br>Mit lebendigen, bösartigen und ansteckenden Bakterien zu<br>arbeiten war natürlich gefährlich (und tatsächlich starben zwei<br>von Coleys Patienten an diesen Streptokokken-Infektionen).<br> Also entwickelte der Arzt eine sicherere Methode, indem er ei-<br>nen Impfstoff erfand. Nachdem er Bakterien gezüchtet hatte,<br>tötete Coley die Kolonien oder filterte sie heraus, denn er ging<br>davon aus, dass die von den Bakterien produzierten Giftstoffe<br> wenigstens zum Teil dafür verantwortlich waren, dass die Tu-<br>moren sich zurückbildeten.5 Außerdem fügte Coley die Gift-<br>stoffe eines zweiten Krankheitserregers hinzu, der heute unter<br>Serratia marcescens bekannt ist. Diese Kombination stellte sich als<br> sehr erfolgreich heraus. Bei fortgeschrittenen, inoperablen Sar-<br>komen erzielte er mit seiner Behandlungsmethode eine Hei-<br>lungsquote von fast 20 Prozent. Wurde seine Therapie mit To-<br>xinen nach der ersten Behandlung weitere sechs Monate ange-<br> wandt, so stieg die Rate der Rückbildungen, bei denen der<br>Krebs auch nach fünf Jahren nicht wieder ausgebrochen war,<br>sogar auf 80 Prozent. Das besagt jedenfalls die Statistik, die Co-<br>leys Tochter im Nachhinein erstellte.6 Diese Zahl entspricht<br> den heutigen Statistiken zur Sarkom-Behandlung und über-<br>trifft diese sogar, lässt man die Langzeitwirkungen von Chemo-<br>therapien und Bestrahlungen unberücksichtigt.<br><br>Für kurze Zeit war Coleys Therapie mit Toxinen (auch<br> „Fiebertherapie" genannt, weil sie hohes Fieber auslöste) die<br>einzige bekannte Krebstherapie neben der operativen Entfer-<br>nung, doch wurde diese einfache bakterielle Immuntherapie in<br>wissenschaftlichen Kreisen nie wirklich anerkannt. Ein Grund<br> dafür war die Qualitätskontrolle, denn es gab weder eine ein-<br>heitliche Toxinvorgabe noch eine empfohlene Dosis, und viele<br>Ärzte, die nur geringe Mengen verabreichten, erzielten damit<br>keine guten Ergebnisse.7,8 Hinzu kam, dass eine Therapie mit<br> Impfstoffen für die pharmazeutische Industrie nicht interessant<br>war, denn damit ließ sich – damals wie heute – nicht genug<br>Geld verdienen. Und da die Medizin Ende des 19. Jahrhunderts<br>noch nichts von einem Immunsystem wusste, fehlten den Wis-<br> senschaftlern zudem die Voraussetzungen, um verstehen zu<br>können, weshalb die Toxine wirkten.9 Mit Aufkommen der<br>Bestrahlungstherapie schwand das Interesse an der Therapie mit<br>Toxinen.<br><br>Anfangs wendeten die Ärzte oft noch beide Therapieformen<br> an. Aber bei Stephan Hall können wir nachlesen, dass die Be-<br>strahlung so sehr in Mode kam, dass Coleys übereifriger Chef,<br>Dr. James Ewing, der damalige Leiter des Memorial Hospital,<br>seine Ärzte anwies, nicht nur Knochenkrebs mit hoch dosierter<br> Strahlung zu behandeln, sondern auch alle anderen Fälle von<br>„lang anhaltenden unerklärlichen„ Knochenschmerzen.10 Un-<br>terdessen wurden Coleys Toxine uninteressant, obwohl seine<br>Behandlungsmethode erfolgreicher war als die Bestrahlung.<br> Von 25 Patienten des Memorial Hospital mit inoperablem Sar-<br>kom, die nur bestrahlt wurden, starben 21, und bei 3 Patienten<br>war die Behandlung noch nicht abgeschlossen, sodass die The-<br>rapieform nicht bewertet werden konnte.11 Im Gegensatz dazu<br> waren von 22 Patienten mit inoperablem Sarkom, die mit Co-<br>leys Toxinen behandelt worden waren (davon manche zusätz-<br>lich mit Bestrahlung), 12 Patienten auch nach fünf Jahren noch<br>ohne neuerlichen Krebsbefund, womit sie aus klinischer Sicht<br> als geheilt galten.<br><br>Aber wer interessierte sich schon für die Statistiken – Ra-<br>dium war der letzte Schrei, Coleys Toxine interessierten nie-<br>manden. Bedenkenlos folgten die Menschen dem Radium-<br>Wahn, der sich unkontrolliert ausbreitete. Versehen mit dem<br> Etikett „Sanfte Radiumtherapie", um sie so von der den Krebs-<br>Patienten vorbehaltenen hoch dosierten Radiumbestrahlung zu<br>unterscheiden, wurden die Radiumpräparate über die La-<br>dentheke verkauft und schnell zum Renner. Radium-Fußsal-<br> ben waren um die Wende vom 19. zum 20. Jahrhundert ganz<br>groß in Mode; für Männer gab es sogar ein Suspensorium mit<br>Radium. Manche Hersteller versetzten selbst Süßigkeiten mit<br>Radium und brachten mit Radium angereichertes Wasser auf<br> den Markt, das sie „Radithor" nannten. Das Gebräu wurde als<br>Energie-Elixier für 1 Dollar angepriesen; es sollte bei 150 „en-<br>dokrinologischen" Leiden helfen – von Rheumatismus und er<br>höhtem Bludruck bis zu Erschöpfung und sexuellen Funkti-<br> onsstörungen.<br><br>In der jeder Flasche „Radithor" beiliegenden<br>Broschüre des Arztes hieß es: „Die belebende Wirkung auf das<br>Nervensystem bringt in der Regel eine Leistungssteigerung der<br>Sexualorgane mit sich." Kein Wunder also, dass über 400 000<br> Flaschen verkauft wurden.<br><br>Schon bald nachdem der Stahlindustriemagnat und ehema-<br>lige Meister im Amateurgolf Eben M. Byers auf den Rat seines<br>Arztes hin anfing, täglich Unmengen von „Radithor" zu trin-<br>ken, um eine Armverletzung zu behandeln, verlor das frei ver-<br> käuf liche Radium jedoch seine Attraktivität. Nach der ersten<br>belebenden Wirkung verdreifachte Byers seine tägliche Dosis,<br>fühlte sich dann jedoch immer erschöpfter und verlor enorm an<br>Gewicht. Als er schließlich die Ursache herausfand, war es zu<br> spät. Die ohnmächtige Food and Drug Administration (FDA: zen-<br>trale Behörde für das Nahrungs- und Arzneimittelwesen in den<br>USA) durfte damals nur Warnungen aussprechen. Nicht so die<br>Federal Trade Commission (FTC: Bundesbehörde für Verbrau-<br> cherschutz in den USA), die den Herstellern der Radium-Eli-<br>xiere umständlich vorwarf, dass ihre Getränke nicht die angege-<br>benen Radium-Mengen enthielten.<br><br>In der Zwischenzeit hatte das Radium bei Byers kurz nach-<br> einander einen Großteil seines Ober- und Unterkiefers aufge-<br>löst und Löcher in seinem Schädel hinterlassen. Die Schmerzen<br>und Entstellungen waren grausam. „Das Radium-Wasser zeigte<br>gute Wirkung, bevor er seine Kinnlade verlor", lautete die lako-<br> nische Überschrift eines Artikels, der im Wall Street Journal er-<br>schien und über Eben Byers verhängnisvolle Erfahrung mit<br>„Radithor" berichtete. Der einst flotte, kräftige Industrielle<br>war auf 46 Kilo abgemagert und wurde, zwischen den gestärk-<br> ten weißen Laken des Doctors' Hospital in New York City lie-<br>gend, immer schwächer, bis er schließlich am 31. März 1932 im<br>Alter von 51 Jahren starb und erneut für Schlagzeilen sorgte.<br><br>Einige Monate zuvor war die FTC endlich aktiv geworden und<br> hatte die Herstellung von „Radithor" verboten. Wenig später<br>wurde die FDA mit der Kontrolle über dieses chemische Ele-<br>ment beauftragt.<br><br>Erstaunlicherweise wirkte sich Byers Tod nicht auf die hoch<br>dosierten Bestrahlungsmethoden aus – vielleicht, weil Coleys<br> Toxine passé waren und es außer der operativen Entfernung<br>keine alternative Krebsbehandlung gab. Als Coley 1936 starb,<br>geriet seine als „übertrieben" eingestufte Immuntherapie völlig<br>in Vergessenheit.<br><br>1965 ging die American Cancer Society (amerikanische Krebsgesellschaft)<br> sogar so weit, Coleys Toxine auf die Liste der „unbewiesenen"<br>Krebsmittel zu setzen, womit seine Therapie zusammen mit<br>Kaffeeeinläufen und Laetrilen als Quacksalberei abgestempelt<br>wurde. Dieses Urteil wurde zwar zehn Jahre später wieder<br> aufgehoben, aber in den USA war der schlechte Ruf dieser un-<br>terschätzten Behandlungsmethode besiegelt.<br>In anderen Ländern hingegen wurde die Impftherapie sehr<br>geschätzt.<br><br>Coleys Impfstoff liefert sehr gute Ergebnisse.<br> <br>Hundert Jahre wissenschaftlicher und politischer Unbeweglich-<br>keit und vor allem die Gier unwissender, unbelehrbarer Men-<br>schen haben jedoch dafür gesorgt, dass die Impftherapie noch<br>immer keine anerkannte Krebsbehandlung ist. Sehr wahr-<br> scheinlich wird Coleys Methode dies auch niemals werden,<br>denn man kann ein hundert Jahre altes Medikament nicht pa-<br>tentieren lassen.<br><br>Viele erstklassige Entdeckungen wurden zunächst nicht nur<br>nicht anerkannt, sondern sogar lächerlich gemacht. (Anderer-<br> seits wurden auch viele Entdeckungen, wie zum Beispiel die<br>Bestrahlungstherapie, eine Zeit lang überbewertet.) Trauriger-<br>weise ist William Coleys Schicksal kein Einzelfall. Er starb ver-<br>gessen und verarmt – nachdem er beim Börsenkrach von 1929<br> sein ganzes Geld verloren hatte.<br><br><br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-55243802362849366232011-06-30T15:19:00.000-07:002011-06-30T15:20:12.716-07:00Wayne Martin - Aminoglutethime Digitalis Bromocriptine Coumadin Cimetidine Urea Azelaic acid Chlorella Hydrocortisone<img alt="http://www.second-opinions.co.uk/images/bg_wm.jpg" src="http://www.second-opinions.co.uk/images/bg_wm.jpg" height="286" width="417"><br>Wayne Martin and Barry Groves, Fairhope AL, November 1998<br><br>From the Townsend Letter for Doctors & Patients july 2003<br><br>Editor:<br> Readers of the <span class="BodyItalic">Townsend Letter</span> may have an interest in what got me involved in medicine.<br> When I was age 15 in 1926, my mother at age 40 was suffering from <a href="http://en.wikipedia.org/wiki/Pernicious_anemia">pernicious anemia</a>. She was bedfast and white as a sheet and not expected to live for long. A young Baptist minister was looking after her salvation in light of her expected early death. One day he came running up our front steps saying that everything was going to be "alright."<br> <br>Two doctors at Harvard, Murphy and Minot, had taken 46 patients with late-stage pernicious anemia and fed them one pound of liver a day. All 46 of them had completely recovered in three weeks' time, showing no sign of anemia. They had published the results in the <span class="BodyItalic">Journal of the American Medical Association</span> in 1926 and the Baptist magazine had picked up the story.<br> I was doing most of the cooking and we all began to eat liver three times a day and my mother was fully restored in three weeks' time. Her doctor, when told of eating liver for pernicious anemia, said 'ridiculous, doctors do not learn medicine from the Baptist magazine.' My mother lived to 94.<br> <br> <b>It was of interest to me that doctors took almost no note of the discovery of Murphy and Minot and very few patients with pernicious anemia were told by their doctors to eat liver.<br> </b><br> In 1926 we had 10,000 deaths in the USA from pernicious anemia. In 1934 we still were having 10,000 deaths from pernicious anemia. In 1934 Murphy and Minot won the Nobel Prize for Medicine for their discovery of 1926. Did that get doctors to tell patients to eat liver for pernicious anemia?<br> <br> What happened was that drug firms came out with a liver extract to be injected in the buttock five cc at a time. The cost was $5.00 an injection and was most painful. My mother was told by her doctor that at last something could be done for her anemia. One injection was enough for my mother. She continued to eat liver.<br> <b><br> The injections of liver extract did some good and by 1938 we were having only 4,000 deaths a year from pernicious anemia where there could have been none, had all pernicious anemia patients been eating liver each day.</b><br> <br> Then in 1948, young Karl Folkers, PhD working for Merck discovered vitamin B12. Injections of one cc a week would completely prevent pernicious anemia. Merck sold it to doctors, putting an end to over 10,000 deaths a year from pernicious anemia worldwide.<br> <br> In 1926 doctors were not reading medical journals and that seems to have changed but little today. Doctors today learn medicine from the sales people of the major drug firms and from little else. I will give a few examples:<br><br><img alt="http://www.townsendletter.com/Images/logo.gif" src="http://www.townsendletter.com/Images/logo.gif"><br> <br> See my letter in the <span class="BodyItalic">TLfDP</span> in the April 2000 issue on the anticancer effect of <a href="http://en.wikipedia.org/wiki/Cimetidine">cimetidine</a>. Cimetidine is a wonderful drug for cancer treatment. Smith Klein had done most of the work to find the anticancer effect of cimetidine but when the patent on it ran out, Smith Klein [<a href="http://en.wikipedia.org/wiki/GlaxoSmithKline" title="GlaxoSmithKline">GlaxoSmithKline</a>] shut up like a clam and will do nothing to foster cimetidine for cancer treatment. There is absolutely no use for this wonderful drug in cancer treatment. There are now about 20,000,000 patients, worldwide taking cimetidine for stomach distress and this may be having the effect of reducing cancer among them.<br> <br> I will not review all that I have in my letter in that issue in 2000. I will review a bit of it: The first indication of the anticancer effect of cimetidine was from the University of Nebraska and reported in <span class="BodyItalic">The Lancet</span> in 1979 (i p 822-3). It reported on two patients with lung cancer. Both were given cimetidine for stomach distress. Both had dramatic complete remissions from cancer. In one patient, the lung cancer was a metastasis from a squamous cell carcinoma on the neck. The lung metastasis was most aggressive. The patient was given cimetidine, 1,200mg a day. Almost at once there was a regression of the lung metastasis. The patient was maintained on cimetidine, 600mg a day and one year later, the tumor could no longer be detected.<br> <br> A second patient had a brain metastasis from a non-small cell carcinoma primary of the lung. The patient was given steroids for the brain tumor and cimetidine 600 mg a day. Very soon after she was given cimetidine, the lung tumor decreased in size. The brain tumor was removed by surgery and one year later the lung tumor no longer could be detected. The patient was continued on cimetidine at 600 mg a day.<br> <br> The authors said that there was no indication in the medical literature that cimetidine is an anticancer drug but there was no doubt in their minds that cimetidine was responsible for these two remarkable remissions of lung cancer.<br> <br> By 1982 it was understood that cimetidine inhibits T-suppressor cells and helps to liberate our cancer-killing lymphocytes. A report from Ireland was in <span class="BodyItalic">The Lancet</span>, 1982 (11, p 328), of the treatment of four melanoma patients: All were far advanced with metastases in the internal organs, in the lungs and liver. One young man had severe stomach distress, with many tumors. He was given cimetidine, 1,000 mg a day and almost at once he had regressions of his many tumors. In two weeks' time, he was able to return to work.<br> <br> At this time, their other three patients were given cimetidine, 1,000mg a day. Two of them had dramatic remissions of cancer. One patient was not helped and died. All these patients were tested for T suppressor cell counts. All had their T suppressor cells decreased by cimetidine. All four of these patients were being maintained on coumarin. There had been no benefit from coumarin although the doctors there thought that coumarin may have acted with cimetidine to produce these remissions.<br> <br> Then there was a report in the <span class="BodyItalic">NEJM</span> in 1983, vol. 308, pp 591-2. The report was from Sweden. Here, six melanoma patients were being treated with interferon. There was no benefit. These patients all had cimetidine added to treatment and there were some exceptional results. There were two complete remissions. One patient had a partial remission. With a fourth patient, progression was stopped. With two patients, there was no benefit.<br> <br> It is in the area of colorectal cancer that there is a pressing need for treatment with cimetidine. During a major surgery, there is a vast increase in T suppressor cells which is highly immunosuppressive at a time when cancer surgery may be sending a shower of cancer cells in the blood to all parts of the body.<br> <br> A trial on cimetidine during surgery for colorectal cancer was done in Australia and reported in <span class="BodyItalic">The Lancet</span> in the December 31, 1994 issue pp 1768-9. Cimetidine was given for seven days only at the time of the surgery. The results were utterly astounding. At three years the survival of the patients who got cimetidine was 93%.Of the ones who got no cimetidine, the survival was only 59%. One could surmise that this treatment might be of great benefit in surgery for other kinds of cancer.<br> <br> There was a trial in Japan reported in <span class="BodyItalic">The Lancet</span> in the July 8, 1995 issue, p 115. Here the patients having surgery for colorectal cancer did not get cimetidine during the critical seven days at the time of surgery when there was a surge of T suppressor cells. In this Japanese trial, the patients were not given cimetidine until two weeks after the surgery.<br> <br> Cimetidine has anticancer effects other than the suppression of T suppressor cells. In the Australian study, more of the cancer cell killing lymphocyte entered the tumors, 63% in the ones who got cimetidine and only 24% in the controls. Cimetidine also inhibits histamine which is also immunosuppressive and may be a tumor growth factor.<br> <br> In the Japanese study, all patients at two weeks after surgery were given 5 fluorouracil, 150mg a day. Half of the patients received 800mg a day of cimetidine. This treatment lasted for one year after surgery. The results were even better than in the Australian study. In this study, rectal cancers and colon cancers were reported separately. Among the rectal cancer patients, 100% of those getting cimetidine survived, whereas only 53.3% of those survived who were not given cimetidine. Among the colon cancer patients, survival among the patients given cimetidine was 96.3%. The survival of the colon cancer patients who were not given cimetidine was 68%.<br> <br> We will have in the USA this year over 50,000 deaths from colorectal cancer. The implication of these two trials is that if all patients in the USA having surgery for colorectal cancer were given cimetidine at 800mg a day from one week before surgery until one year following surgery, deaths from colorectal cancer could drop from the present 50,000 plus to less than 20,000 a year.<br> These two studies were reported in 1994 and 1995. It is doubtful in the past seven years if there has been a single patient to have surgery for colorectal cancer who was given cimetidine. This supports my contention that doctors now do not read medical journals.<br> <br> We will now make a case for dipyridamole. <a href="http://www.tldp.com/issue/202/LettersMartin.htm" target="_blank">See my letter in the <span class="BodyItalic">TlfDP</span> in the May 2000 issue on the anticancer effect of dipyridamole.</a><br> <br> The patent on dipyridamole has also run out and the use of it is small indeed. The European Stroke Prevention Study was reported in <span class="BodyItalic">The Lancet</span> in the December 12, 1987 issue, pp 1,371-4. Here it reviewed the many trials on treating stroke patients with aspirin. There had been no trial of aspirin in stroke prevention that had shown benefit. That is still true today. As a result, in the Stroke Prevention Study, aspirin was kept at 1 gram a day and dipyridamole was added to treatment at 225mg per day. All patients had had a TIA or had survived a stroke. The duration of the trial was two years.<br> <br> Adding dipyridamole to aspirin gave results that were so good as to be incredible. Stroke deaths were reduced by 50% but that was not the end of the benefit. Deaths from myocardial infarction were reduced by 38% and cancer deaths were reduced by 30%. It would seem that few if any doctors in the USA have read or have even heard about the amazing results of the European Stroke Prevention Study.<br> <br> The sales people at Boehringer Ingelheim which firm held the patent on dipyridamole, are no longer telling doctors here that dipyridamole tends to prevent cancer cells in the blood from attaching to the walls of arteries and veins, thus preventing the formation of metastases. Close to 90% of cancer deaths are caused by metastases and the message of the sales people at Boehringer Ingelheim was that dipyridamole at 300mg a day will go far to prevent the formation of metastases.<br> <br> Dr. E.H. Rhodes of the St. Hiler and Kingman Hospital in Surrey, England had a report in <span class="BodyItalic">The Lancet</span> in the March 23, 1985 issue, p. 692 on treating melanoma with dipyridamole, 300mg a day. Thirty melanoma patients were maintained on 300mg of dipyridamole over a period of 11 years. Of them, 26 had type IV disease and four had type III disease. The patients with type IV disease had a five-year survival of 74%. None of the patients with type III disease had died, so for the 30 patients with type IV and III disease, the five-year survival had been 77%.<br> <br> This was most remarkable for the five year survival of type IV melanoma patients was only 32% for the whole of England. I established a friendship with Dr. Rhodes. She was a dermatologist and she was treating only melanoma. She felt that what the Boehringer Ingelheim salespeople were saying about dipyridamole preventing the formation of metastases, was true. She felt that if breast, prostate and colon cancer patients were maintained on 300 mg of dipyridamole, the same increase in survival as was had with her melanoma patients, would be seen.<br> <br> Dipyridamole is a most harmless drug. It is regrettable that doctors do not maintain cancer patients in general on 300mg of dipyridamole in the hope of increasing survival by a factor of two or three, by preventing the formation of metastases. Perhaps there would also be a substantial decrease in stroke and heart attack deaths. <br> <br> Now to the anticancer effect of digitoxin. See my letter in the <span class="BodyItalic">TlfDP</span> on the anticancer effect of digitoxin in the June 1999 issue. Also see the letter from Dr. Johan Haux, MD, PhD in the October 2000 issue on cardiac glycosides vs alkylating agents in medical oncology.<br> <br> Here is an old herbal medication that has been used since 1780 to treat congestive heart disease. It has been found over more than 200 years to be most harmless at a proper dose.<br> <br> In the <span class="BodyItalic">NEJM</span> for February 25, 1982, p 484, Bjorn Stenkvist et al. had a report on treating breast cancer with digitalis. There were 149 breast cancer patients in this trial of which 40 were maintained on digitalis. Of them 34 were given digoxin and six were maintained on digitoxin. As of 1982 at five years, only one of the patients taking digitalis had a recurrence of cancer. Of the 109 patients who did not take digitalis, there were 21 recurrences of cancer. There were 9.6 times as many recurrences of breast cancer among the patients not taking digitalis. It was noted that digitalis made breast cancer cells smaller and more uniform in structure.<br> <br> One would have thought that this might have opened up a whole new vista in the treatment of breast cancer. Such was not the case. Dr. Stenkvist was at University Hospital in Uppsala, Sweden. He was not allowed to treat another breast cancer patient with digitalis. What he was told was that no breast cancer patient should be deprived of the great benefit of chemotherapy or tamoxifen. He tried with no success, to interest the major drug firms in digitalis for treating breast cancer. All drug firms that he approached showed no interest in an old drug on which no patent could be had that cost 17¢ a day for treatment.<br> <br> In 1998, I called the digitalis story to the attention of my friend Johan Haux, MD who was then with the Institute of Cancer Research and Molecular Biology at the Norwegian University for Science and Technology in Trondheim, Norway. He at once made contact with Dr. Stenkvist.<br> Over the past five years Dr. Haux has done an incredible amount of work in tissue cultures, testing the anticancer effects of digitalis, both digoxin and digitoxin. He has learned that the main anticancer effect of digitalis is the induction of apoptic death of cancer cells. He has also found that the natural digitoxin has a much greater anticancer effect than has the synthetic digoxin.<br> By now he has tested the anticancer effect of digitoxin against several kinds of cancer and found that it inhibits cancer cell growth in several kinds of cancer, especially in one most hopeless cancer, glioblastoma. This has been the subject for his doctorate thesis. He has reviewed the possibility for the use of digitoxin in the treatment of several cancers in <span class="BodyItalic">Medical Hypotheses</span> in 1999, 53 (6).<br> <br> Meanwhile, Dr. Stenkvist has traced nearly all the patients in his 1982 trial as of 1998. There was only one patient in this trial of 1998 still alive. She was still free from cancer. She was one of the six to get digitoxin. As of 1998, the number of patients not getting digitalis had increased to 143 and of the patients getting digitoxin, only 32 could be traced. Of the 143 patients not getting digitalis, 48 had died of breast cancer or 33.6% of them. Of the six patients getting digitoxin, none had died of breast cancer. Of the 26 who had gotten digoxin, two only had died of breast cancer. Of the 32 patients who had gotten digitalis, only 6.25% of them had died of breast cancer. One can only say that Dr. Stenkvist's trial on treating breast cancer with digitalis had been a great success.<br> <br> In February 23, 1987 I received the following letter from a breast cancer patient, Sandra Harmon in Wisconsin. <p class="TownsendBody" align="center"><img src="http://www.townsendletter.com/Images/greenbar.gif" height="5" width="200"></p> <p>Dear Wayne:<br> Just a note to let you know how I am doing on the regime you recommended to me for breast cancer.<br> <br> I especially want to thank you for your concern, support and encouragement. It is greatly appreciated. I am very sure that God has a special place reserved for you. You are a shining example of brotherly love. The regimen I am following is as follows:<br> Aminoglutethime 125 Bid<br> Digitalis 0.125 a day<br> Bromocriptine 5mg Bid<br> Coumadin 10mg a day<br> Cimetidine 300mg a day<br> Urea 15 grams a day<br> Azelaic acid 10 grams a day<br> Chlorella 15 grams a day<br> Hydrocortisone 10 mg<br> <br> I am doing very well and feel great. As you remember last December I had surgery on my right leg for a metastasis from my breast cancer. I had a large tumor removed and because of this, I am on crutches but I have little pain and I get around well.<br> <br> At that time, I was told by my family doctor that I had pleural effusions from metastases in both lungs. I had bone metastases in my ribs and at several places in my skull. I was told that I should expect survival of from three to six months. In March, I had a bowel obstruction that required a major surgery. They removed my appendix and my ovaries, both of which had metastases.<br> Now for some good news. When I had returned for this surgery, the metastases in my lungs had improved in dramatic fashion. The physicians were amazed. This had taken place between December and March. I had started on this regime the first of December except for the azelaic acid. I was most fortunate that my family doctor went along with my wishes. He said that all that I was taking was utter nonsense and that I must be on chemotherapy at once, however he wrote the prescriptions for me.<br> <br> The first week of May, I went to Denver to Dr. Doell who supplied me with azelaic acid. My family doctor would not even think about my taking azelaic acid and said that I was insane to take it. So in May, I added azelaic acid and chlorella to treatment. I definitely feel that azelaic acid has been a great help. I have felt stronger and more like a normal person from the time that I started taking azelaic acid.<br> <br> I was told by my doctor that it was thought that I had a liver metastasis. I have just had a liver scan and the doctors were amazed at no liver metastases. I told them it was because of taking urea. They think that I am talking Greek. They do not think that I am free from liver metastases so they are going to do another liver scan. They have done another liver scan and again no liver metastases. They assure me that urea is poison.<br> <br> It is now September and I feel so good. I do not think that I can ask more than that. Thank God for people like you who are so willing to help others. Bless you.<br> <br> Sandra H</p> <p align="center"><img src="http://www.townsendletter.com/Images/greenbar.gif" height="5" width="200"></p> <p> I have spent a lifetime working in the aluminum industry until a year ago. I have been writing letters of a medical nature as a pastime. I am sorry that I did not keep in contact with this patient. I recall a phone call I think from her husband, wanting a new place to get azelaic acid. She was alright in 1991.<br> <br> Since I have quoted the letter from Sandra H. some mention should be made of some other treatments which she used at my suggestion.<br> <br> Azelaic acid is not considered a drug. It is just a chemical. The first that I heard of it in cancer treatment was in a report in <span class="BodyItalic">The Lancet</span> in the May 24, 1980 issue pp 1109-11 by A. Breathnach et al. of the St. Mary's Hospital Medical School in London. Azelaic acid was given to patients before and after surgery for melanoma, 10 to 15 grams a day. <br> <br> In this report, azelaic acid did have a definite benefit in treating melanoma. One anticancer effect of azelaic acid it is said, is that it inhibits tyrosinase and tyrosinase is said to foster several kinds of cancer. Also Breathnach said that it inhibits the mitochondrial oxidoreductases of the respiratory chain and of enzymes concerned with DNA synthesis.<br> <br> I made contact with Dr. Breathnach. He said that azelaic acid is most harmless and should be used in the treatment of many kinds of cancers. He had a report in <span class="BodyItalic">Medical Hypotheses</span> in 1999, 52(3) pp 221-26, with the title "Azelaic acid: potential as a general antitumor agent." In it he says that azelaic acid is ideal in the treatment of breast cancer. He was then with St. Thomas Hospital in London.<br> <br> Coumadin is a high-priced version of warfarin. It prevents the formation of fibrin. In 1958, Professor R.A.Q. O'Meara of Trinity College, Dublin reported in the <span class="BodyItalic">Irish Journal of Medical Science</span>, 1958, 394 pp 474. He said that cancer cells give off clotting factors that tend to coat cancer cells with fibrin. The fibrin coat protects cancer cells from being killed by our cancer cell killing immunocytes.<br> <br> O'Meara had a student, L. Michaels, who as a doctor went to Canada. He reasoned that if O'Meara was right, patients who were treated with warfarin for heart disease would be having fewer deaths from cancer. He then followed patients being treated with warfarin amounting to over 1,500 patient years. There had been expected in this group of patients, eight deaths from cancer. There was only one such death. This was reported in <span class="BodyItalic">The Lancet</span> in the October 17, 1964 issue.<br> <br> In the issue of <span class="BodyItalic">JAMA</span>, 1981, (245), pp 831-5, Professor Leo Zacharski of Dartmouth Medical College et al. reported on treating patients with small cell carcinoma of the lung with warfarin. Patients were treated with chemotherapy and radiation alone or with chemotherapy, radiation and warfarin. The patients treated with warfarin survived twice as long. The patient Sandra H, might have done just as well if dipyridamole had replaced the more dangerous coumadin.<br> <br> On the anticancer effect of chlorella, reference is made to a report of Ralph Moss PhD in his <span class="BodyItalic">Cancer Chronicles #23</span> of September 1994. He tells of Dr. R.E. Merchant of the Medical College of Virginia. He had been giving chlorella to 20 patients with far advanced malignant glioma. Normal survival of these patients is less than a year. Of these 20 glioma patients taking chlorella, 7 were alive and doing well at two years. That was in 1990. Merchant reported in 1996, eight years after one glioma patient started taking chlorella and, the patient was alive and well.<br> <br> Bromocriptine inhibits prolactin. It would seem that prolactin fosters breast cancer in some and perhaps all breast cancer patients. Cimetidine tends to induce prolactin and this may be bad in treating breast cancer. If a breast cancer patient takes cimetidine, she should also take something to inhibit prolactin. However it may be a good thing to inhibit prolactin in the treatment of breast cancer. Dr. F. Grisoli of the La Timone University Hospital in Marseille, France thought this to be the case. He and others had a report in <span class="BodyItalic">The Lancet</span> in the October 3, 1981 issue pp 745-6. They reported on a near miracle in the recovery of a woman with breast cancer with a large brain metastasis. She was given 7.5 mg of bromocriptine a day. In six months' time, the large brain metastasis was gone and it still was 18 months after the start of bromocriptine therapy.<br> <br> In <span class="BodyItalic">The Lancet</span> for September 23, 1978 pp 646-9, there was a report on treating 42 patients with well-advanced breast cancer with aminoglutethimide. Of them, 15 were helped in one way or another. Aminoglutethimide causes the adrenals to stop making both estrogen and prolactin. The results of this trial were not spectacular as were for example, the remission of the brain metastasis with the patient treated with bromocriptine.<br> <br> In the January 25, issue of <span class="BodyItalic">The Lancet</span>, p 123, was a report by Professor Evangelos Danopoulos of Athens, Greece on treating liver cancer with oral urea. In this he reported much success. Since 1974, I have written in several publications about treating liver cancer with urea, 15 grams a day and have had many reports of success in so doing.<br> <br> I had sent the patient, Sandra H, a report in <span class="BodyItalic">The Lancet</span> for June 23, 1984 pp 1369-72 from the Royal Marsden Hospital in London. This was a trial on tamoxifen, compared to tamoxifen, aminoglutethimide, hydrocortisone and danazole in treating disseminated breast cancer. I had sent it to her as part of the material on aminoglutethimide in treating breast cancer. I had not suggested to her that she take hydrocortisone.<br> <br> Her recovery from far advanced breast cancer was most spectacular. I have told of the anticancer effects of the various treatments that she used at my suggestion.</p> Wayne Martin, BS, ChE<br><br><br><div class="c5"> <h1>Wayne Martin BS, CEng</h1> </div> <div style="float: right; margin: 0px; margin-top: 20px; padding-left: 5px" class="noprint"><br> </div> <img src="http://www.second-opinions.co.uk/images/waynemartin.jpg" alt="Wayne Martin in November 1998"><br> <p>Wayne Martin was born on 17 July 1911 in Bloomington Illinois. He first became interested in medicine when, as a boy of nine, he helped a homoeopathic doctor by doing such tasks as trundling wheelbarrow loads of hawthorn and yew which the doctor used in his preparations.<br> <br> At the age of seventeen, Wayne suffered a terrible motorcycle accident in which he lost a leg.<br> <br> Wayne secured a place at Purdue University, Indiana, to study biochemistry, getting around a serious lack of funds by tutoring other students in Math. In his second year, however, he had to relinquish this new field of science for economical reasons. In his senior year, during the Great Depression, he realized that there was little prospect for work in such a fledgling profession, so he switched courses and in 1933 obtained a degree in chemical engineering with major emphasis on biochemistry and bacteriology. His livelihood since then has been in chemistry and metalurgy, but that has not stopped him pursuing his consuming lifetime of interest medicine and reading of the world's medical literature, often resulting in remarkable treatments now used by many complementary / alternative medical practitioners.<br> <br> His professional work in Chemical Engineering also resulted in remarkable findings results of which are unknowingly used by people everywhere. Ninety percent of the beryllium copper alloys used worldwide contain 1.80% of beryllium instead of the more expensive form of 2.2 to 2.5% beryllium set by Germans at the Siemans and Haliske Company. Working at the Beryllium Corporation, Wayne Martin in 1935 discovered that the 1.80% beryllium to copper alloy (Berylco 180) was superior in many ways and less expensive. For more than fifty years automobiles and the general public used Wayne Martin's beryllium alloy.<br> <br> Early in World War II, at the Sperry Gyroscope Company as senior metallurgist , and also as a "dollar-a-year" consultant with The War Production Board (WPB), Wayne Martin developed two National Emergency (N.E.) aluminium casting alloys (319, 380). Ninety-five percent of aluminium castings are made of these two alloys. Sixty million pounds monthly of this aluminium alloy is currently used to produce the modern automobile.<br> <br> At end of World War II, the Beryllium Corporation was stuck with a plant owned by the Atomic Energy Commission for which they wanted a peace-time use. Wayne suggested that it be used to make potassium titanium fluoride. The entire aluminium industry uses it to grain-refine aluminium. After its return to the Atomic Energy Commission, Henry Kawecki, Wayne's friend, formed the Kawecki Chemical Company to manufacture potassium fluoride, becoming a multimillion dollar firm, all on Wayne's ideas.<br> <br> In 1950 Wayne Martin helped to place aluminium/magneisum alloy (AL MG 35) for which there was a large market. In 1960 he developed another aluminium alloy (Precedent 71) which, over a period of 20 years, made his employer, U.S. Reduction Company, a great deal of money.<br> <br> Wayne retired in 1979, becoming a salesman with The Southern aluminium Casting Company of Bay Minette, Alabama. Thereafter each retirement led to further consulting jobs, so he never truly retired. Indeed, right up until his death, he was still in demand as a troubleshooter, speaker and panelist among metallurgists in the aluminium industry.<br> <br> So why is a Chemical Engineer who invented important metal alloys featured as a consultant in medicine?<br> <br> Although the great American depression had steered him elsewhere for survival's sake, he never lost touch with medicine. His enquiring mind synthesized many medical articles and research papers to bring to light remarkable treatments in heart, cancer, and other medical problems.<br> <br> In one example from years gone by, in 1963 Wayne organized the Nutrition Research Products Company dedicated to doing something about the 600,000 deaths each year from heart attacks. His idea was carried to The Royal College of Surgeons and The National Heart Hospital in London, England, where Nutrition Research Products Company spent $200,000, and proved that his ideas were effective in preventing heart disease.<br> <br> His thinking frequently about medical treatment has been reported in <em>Townsend Letter for Doctors & Patients</em> and other medical journals. He was the Townsend Letter's most prolific contributor.<br> <br> In 1977, Wayne Martin published a book, 'MEDICAL HEROES AND HERETICS', about the many scientists over the centuries who have been scorned, vilified and had their lives ruined only to be proved right in the end.<br> <br> Wayne Martin, lived with his wife, Betty, in Fairhope, Alabama, until his death on 12 May 2006. He is survived by Betty , two children and two grandchildren.</p><br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-10316062151546231982011-06-15T17:42:00.001-07:002011-06-15T17:42:56.306-07:0018000 fever injections - one doctor (Germany) - no complicationsFYI,<br><br>In this german document <br><a href="http://zaen.medienartig.com/pdf/1990/1990-05.pdf">http://zaen.medienartig.com/pdf/1990/1990-05.pdf</a><br><br>E. Goehring (info _at- archemed dot de??? ) <br>describes the usage of Coley's Toxins<br> in the Aeskulap Klinik in Bad Rappenau<br>(he has administered Vaccineurin 18,000 times)<br><br>page 35 (pdf) = page 366 (scanned document)<br><a href="http://zaen.medienartig.com/pdf/1990/1990-05.pdf">http://zaen.medienartig.com/pdf/1990/1990-05.pdf</a><br> <br>He says ColeysToxins can <br>"dampen autoimmune reactions and interrupt a circulus vitiosus"<br><br>He says that sicknesses that respond to Fever therapie are the following:<br><br>Gonorrhoe, Typhus, Paratyphus, Pertussis, <br> Pneumonie, Fleckfieber, Meningokokkeninfektionen,<br>Osteomyelitis, Virusinfektionen, wie Poliomyelitis,<br>Hepatitis (even with AIDS patients we were able to<br>advantageously influence the clinical status as <br>well as the Immune status); allergic and skin diseases,<br> like Asthma bronchiale, Ekzeme, Neurodermitis, Erythrodermie,<br>allergic Rhinitis, rheumatic diseases, like Bechterev disease<br>rheumatic fever, degenerative-rheumatic sicknesses and<br>soft-tissue rheumatism, Neuralgien und Neuritiden,<br> Ulcus Ventriculi et duodeni (this becomes especially interesting<br>und the aspect of the probable Campylobacter-Etology)<br>chronic-infectious colon diseases like Colitis ulcerosa<br>and Morbus Crohn; lastly multiple sklerosis.<br> The most thankful of all diseases according to our experience<br>is colitis ulcerosa, which responds highly reliably.<br>We have not encountered any relapse after therapy-end, all<br>patients were able to abandon Cortison and/or <br> Salazosulfapyridin.<br><br>method<br><br>*at first we use 2 million units (lysated bacteria)<br> intravenously (Vaccineurin)<br>*then blood circultaion tonikum "strophantin k" 1/4 mg (1A Kombetin) i.v.<br>*bedrest<br> *every 30 min measure temperature and pulse<br><br>most often a 30 minute duration shudder-shivering develops<br>before reaching temparature-peak.<br>This can lead to nausea, vomiting, headaches and muscle pains,<br>especially back-pains. These can be arrested by 1A. Pentazocin.<br> <br>liquid intake only allowed after reaching temperature maximum,<br>to prevent sweating, which leads to temperature reduction.<br><br>in the evening when the fever has subsided a light meal is allowed.<br><br>I have overseen 18,000 fever-injections without complications.<br> our oldest patient was 80<br>I don't know of any technique in oncological therapy that has a<br>comparable therapeutic index.<br><br>His last sentence is:<br>How can modern Medicine afford to relinquish such an efficient method like<br> the fever therapy, which's basic immunologic operation is <br>considered ascertained???<br><br><br>.......<br><br><br><img alt="http://bestsupplementsforwomen.com/wp-content/uploads/2010/03/Mammogram-cartoon1-282x300.jpg" src="http://bestsupplementsforwomen.com/wp-content/uploads/2010/03/Mammogram-cartoon1-282x300.jpg" height="490" width="461"><br> Mammogram - detect caner - cause cancer (we usually push them both)<br><br> <br> Links for my blog readers:<br> <br><a href="http://en.wikipedia.org/wiki/Coley%27s_Toxins">http://en.wikipedia.org/wiki/Coley%27s_Toxins</a><br> <a href="http://www.mbvax.com/pdf/Hoption_Cann_2003.pdf">http://www.mbvax.com/pdf/Hoption_Cann_2003.pdf</a><br> <a href="http://www.mbvax.com/pdf/Pancreas.pdf">http://www.mbvax.com/pdf/Pancreas.pdf</a><br> <a href="http://kidney-renal-cancer.blogspot.com/2010/07/israeli-article-about-coleys-toxins.html">http://kidney-renal-cancer.blogspot.com/2010/07/israeli-article-about-coleys-toxins.html</a><br> <a href="http://kidney-renal-cancer.blogspot.com/2011/01/spontaneous-regression-by-donald-h.html">http://kidney-renal-cancer.blogspot.com/2011/01/spontaneous-regression-by-donald-h.html</a><br> <br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-50834109445172107422011-06-11T02:37:00.001-07:002011-06-11T02:37:41.180-07:00You must SLEEP to stimulate your Immue Systemfunctions of sleep are as follows.<br><br>[edit] Restoration<br><br>Wound healing has been shown to be affected by sleep. A study conducted by Gumustekin et al.[39] in 2004 shows sleep deprivation hindering the healing of burns on rats.<br> <br>It has been shown that sleep deprivation affects the immune system. In a study by Zager et al. in 2007,[40] rats were deprived of sleep for 24 hours. When compared with a control group, the sleep-deprived rats' blood tests indicated a 20% decrease in white blood cell count, a significant change in the immune system. It is now possible to state that "sleep loss impairs immune function and immune challenge alters sleep," and it has been suggested that mammalian species which invest in longer sleep times are investing in the immune system, as species with the longer sleep times have higher white blood cell counts.[41]<br> <br>It has yet to be proven that sleep duration affects somatic growth. One study by Jenni et al.[42] in 2007 recorded growth, height, and weight, as correlated to parent-reported time in bed in 305 children over a period of nine years (age 1–10). It was found that "the variation of sleep duration among children does not seem to have an effect on growth." It has been shown that sleep—more specifically, slow-wave sleep (SWS)—does affect growth hormone levels in adult men. During eight hours' sleep, Van Cauter, Leproult, and Plat[43] found that the men with a high percentage of SWS (average 24%) also had high growth hormone secretion, while subjects with a low percentage of SWS (average 9%) had low growth hormone secretion.<br> <br>There are multiple arguments supporting the restorative function of sleep. The metabolic phase during sleep is anabolic; anabolic hormones such as growth hormones (as mentioned above) are secreted preferentially during sleep. The duration of sleep among species is, in general, inversely related to animal size and directly related to basal metabolic rate. Rats with a very high basal metabolic rate sleep for up to 14 hours a day, whereas elephants and giraffes with lower BMRs sleep only 3–4 hours per day.<br> <br>Energy conservation could as well have been accomplished by resting quiescent without shutting off the organism from the environment, potentially a dangerous situation. A sedentary nonsleeping animal is more likely to survive predators, while still preserving energy. Sleep, therefore, seems to serve another purpose, or other purposes, than simply conserving energy; for example, hibernating animals waking up from hibernation go into rebound sleep because of lack of sleep during the hibernation period. They are definitely well-rested and are conserving energy during hibernation, but need sleep for something else.[5] Rats kept awake indefinitely develop skin lesions, hyperphagia, loss of body mass, hypothermia, and, eventually, fatal sepsis.[44]<br> <br><a href="http://en.wikipedia.org/wiki/Nocturnal_post_absorptive_catabolism#Restoration">http://en.wikipedia.org/wiki/Nocturnal_post_absorptive_catabolism#Restoration</a><br><br><br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-73223307045691577952011-05-30T02:27:00.001-07:002011-05-30T02:27:53.625-07:00Stanislaw Burzynski and "Antineoplastons" - SAUL GREEN<h2> </h2><b>In 1967, after obtaining his medical degree and while completing his PhD in biochemistry, Dr. Burzynski discovered a strain of peptides in human blood and urine that had never before been recorded in biomedical research. As Dr. Julian Whitaker stated in the film, "discovering something in the urine [and blood] at that time, that had never been discovered before - is like finding a whole bunch of new islands ten miles off the coast of Miami, it came as a big surprise." Dr. Burzynski had no idea what this discovery meant at the time. However, he and his colleagues were extremely excited about this new discovery, and he continued to explore it. After testing the human blood of various different sexes, races, and ages of people - he found that these newly discovered peptides were either absent or revealed a very low count within the blood of those individuals with cancer. He eventually found that this peptide count was virtually identical in both human blood and human urine.<br> <br>Dr. Burzynski simply hypothesized - if he could simply extract these peptides from healthy donors, and administer these peptides to people with cancer, perhaps it would be helpful in treating the disease. Upon this initial exploration, he discovered that extracting the amount of peptides from healthy human blood was very laborious as the amount of blood needed to obtain a necessary amount of peptides far exceeded the amount of blood reasonably available.<br> <br>Upon this realization, he began extracting these peptides from human urine, since it was far easier to obtain large amounts of healthy human urine vs. healthy human blood. Dr. Burzynski began setting up collection containers at state parks, religious institutions, and even prisons.<br> <br><br><a href="http://en.wikipedia.org/wiki/Phenylacetylglutamine">Phenylacetlglutamine</a>, <a href="http://www.google.de/search?q=Phenylacetate+urine">Phenylacetate</a><br><a href="http://www.google.de/search?q=Phenylacetylisoglutamine&nfpr=1">Phenylacetylisoglutamine</a><br> </b><br><br>Burzynski, the Movie is the story of a medical doctor and Ph.D biochemist named Dr. Stanislaw Burzynski who won the largest, and possibly the most convoluted and intriguing legal battle against the Food & Drug Administration in American history. His victorious battles with the United States government were centered around Dr. Burzynski's belief in and commitment to his gene-targeted cancer medicines he discovered in the 1970's called Antineoplastons, which have currently completed Phase II FDA-supervised clinical trials in 2009 and could begin the final phase of testing in 2011ΓΓé¼ΓÇ¥barring the ability to raise the required $150 million to fund them.<br> <br>When Antineoplastons are approved, it will mark the first time in history a single scientist, not a pharmaceutical company, will hold the exclusive patent and distribution rights on a paradigm-shifting medical breakthrough. Antineoplastons are responsible for curing some of the most incurable forms of terminal cancer. Various cancer survivors are presented in the film who chose his treatment instead of surgery, chemotherapy or radiation - with full disclosure of medical records to support their diagnosis and recovery - as well as systematic (non-anecdotal) FDA-supervised clinical trial data comparing Antineoplastons to other available treatments. One form of cancer - diffuse, intrinsic, childhood brainstem glioma has never before been cured in any scientifically controlled clinical trial in the history of medicine. Antineoplastons hold the first cures in history - dozens of them. [Chemo/Rad - PubMed 2005] [ANP - PubMed 2003] [ANP - PubMed 2006]<br> <br>This documentary takes the audience through the treacherous, yet victorious, 14-year journey both Dr. Burzynski and his patients have had to endure in order to obtain FDA-approved clinical trials of Antineoplastons. Dr. Burzynski resides and practices medicine in Houston, Texas. He was able to initially produce and administer his discovery without FDA-approval from 1977-1995 because the state of Texas at this time did not require that Texas physicians be required to adhere to Federal law in this situation. This law has since been changed. As with anything that changes current-day paradigms, Burzynski's ability to successfully treat incurable cancer with such consistency has baffled the industry. However this fact has prompted numerous investigations by the Texas Medical Board, who relentlessly took Dr. Burzynski as high as the state supreme court in their failed attempt to halt his practices. Likewise, the Food and Drug Administration engaged in four Federal Grand Juries spanning over a decade attempting to indict Dr. Burzynski, all of which ended in no finding of fault on his behalf. Finally, Dr. Burzynski was indicted in their 5th Grand Jury in 1995, resulting in two federal trials and two sets of jurors finding him not guilty of any wrongdoing. If convicted, Dr. Burzynski would have faced a maximum of 290 years in a federal prison and $18.5 million in fines. <br> <br>However, what was revealed a few years after Dr. Burzynski won his freedom, helps to paint a more coherent picture regarding the true motivation of the United States government's relentless persecution of Stanislaw Burzynski, M.D., Ph.D.<br> <br><a href="http://www.burzynskimovie.com/">http://www.burzynskimovie.com/</a><br><br><img alt="http://image.bayimg.com/haeibaadg.jpg" src="http://image.bayimg.com/haeibaadg.jpg"><br><br><a href="http://www.youtube.com/watch?v=S81PXHwjMAQ&feature=related">http://www.youtube.com/watch?v=S81PXHwjMAQ&feature=related</a><br> <br>Burzynski.The.Movie-Cancer.Is.Serious.Business.DVDRip.DivX <br><a href="http://torrents.thepiratebay.org/6238349/Burzynski.The.Movie-Cancer.Is.Serious.Business.DVDRip.DivX.6238349.TPB.torrent">http://torrents.thepiratebay.org/6238349/Burzynski.The.Movie-Cancer.Is.Serious.Business.DVDRip.DivX.6238349.TPB.torrent</a><br> magnet:?xt=urn:btih:21fcb2c07ada5426d03d2d51285e0510c5f6d0c6&dn=Burzynski.The.Movie-Cancer.Is.Serious.Business.DVDRip.DivX&tr=udp%3A%2F%<a href="http://2Ftracker.openbittorrent.com">2Ftracker.openbittorrent.com</a>%3A80&tr=udp%3A%2F%<a href="http://2Ftracker.publicbt.com">2Ftracker.publicbt.com</a>%3A80&tr=udp%3A%2F%<a href="http://2Ftracker.ccc.de">2Ftracker.ccc.de</a>%3A80<br> <br><br><br>If you watch the movie, you can a picture, backed up by undoubtedly good evidence and logical arguments<br><br>When you read the detractor's article, you hear hate speech and no facts.<br><br><br><font size="4"><b>Antineoplastons? You gotta be kidding me!</b></font><br> <br><div class="article"><i> Monday, August 9, 2010</i><br><br><div style="float: left; clear: left; text-align: center; margin: 10px 10px 10px 0px; width: 323px;"><img src="http://www.labspaces.net/pictures/blog/4c5e4ec3a0c00_blog.jpg" height="416" width="323"><br> Watch where you step, you might be knee-deep in some bullshit son!</div>So I came across a movie about <a href="http://en.wikipedia.org/wiki/Stanis%C5%82aw_Burzy%C5%84ski" target="_blank">Stanislaw Burzynski</a> and his controversial antineoplastons treatment. So I'm pretty sure you are scratching your head wondering what an antineoplaston is? Apparently Burzynski created this convoluted phrase to use instead of simply saying, its a peptide. But take it from top here gang. In 1968, Burzynski graduated from medical school at age 24 in Poland, at age ~25 he also received a doctorate in biochemistry, making him one of the country's youngest M.D., Ph.D. Are you kidding me, when did he start his MSTP training program at age 17? The claim to the Ph.D. is slightly dubious as the medical school at that time was not known to grant Ph.D.'s and faculty at the Medical Academy of Lubin report that Burzyinski only did one year of a lab research project while in medical school to receive this mystery doctorate. Also the guy never received any specialized training in cancer or cancer therapeutics. So flash forward to 1973, Burzynski has spent the past three years at Baylor COM working in a lab isolating peptides from rat brains. He receives his license and is able to practice medicine in the US and also gets a three year grant to study urinary peptides effect on the growth of cancer cells. This grant is not renewed and in 1976 Burzynski announces that he has found the cure to cancer in antineoplastons (peptides) which can "normalize" cancer cells and cause spontaneous regression of cancer.<br><br>So Burzynski goes on to treat folks with a derivative of one of his earlier antineoplastons. One of his peptides A-10, piperdine-2,6-dione (PAPD), which is treated to form phenylacetyl glutamine (PAG) which is a detoxification product produced by the detoxification of phenylacetic acid in the liver which itself is normal byproduct of metabolism, albeit toxic. Anywho Burzynski claims that A-10 can bind to DNA, however it has yet to be shown to bind to either the minor or major groove of DNA and Burzyinski himself claims that A-10 is <a href="http://www.ncbi.nlm.nih.gov/pubmed/3743376" target="_blank">ineffective against cancer</a>.<br><br>So let me get this straight, we have a guy with some shaky credentials treating patients with unproven therapies of dubious providence. And to put a final nail in the coffin, the NCI, the Japanese NCI, and Sigma-Tau Pharmaceuticals have yet to be able to prove that any of Burzyinski's "antineoplastons" have an effect on cancer. And Burzynski claims to have treated over 8,000 patients in 20 years but does not release any hard data to support that his therapy is working.<br><br>Why is all of this getting my knickers in a bind. Because there is a documentary entitle "Burzynski Movie" out that seems to propagate the myth that Big Pharma and the government are out there holding back a man with the cure for cancer. The documentary is what some would call "one-sided" or as I would call it, a fucking piece of shit. The director only interviews supporters of Burzynski, allows the "physician" to slam chemotherapy and radiation therapy, two proven treatments while allowing him to provide no substantive evidence of his miracle treatment. All this does is incense the tin-foil-hat-wearing-conspiracy-theory-nutjobs and of course their slightly more educated cousins, the alternative medicine believers who dabble in pseudoscience. Don't get me wrong I believe in some alternative medicines, but they have to be proven by "scientific results" and held to the same level of scrutiny as conventional medicine (Tideliar, feel free to jump in and back me up). But what pisses me off, is he is playing with patients emotions and lives. I know all experimental medicines are experimental, but most of them have some decent science behind them and have credentialed and competent clinicians running these trials.<br><br>I predict antineoplastons will go the way of the <a href="http://genrepair.blogspot.com/2009/07/regenocytes-medical-breakthrough-or.html" target="_blank">Regenocyte</a>. I've seen some snippets of the film but am trying to get my hand on a copy of the film to give it full critique. So if you have a copy, can I borrow it? I have no intention of paying for that piece of dross.<br><br>h/t: Saul Green</div><h2>h/t Saul Green (did he write this hate speech?)<br></h2><br><br><h2>QUACKWATCH -- Stanislaw Burzynski and "Antineoplastons" </h2> <h3>Saul Green, Ph.D. </h3> Unlike most "alternative medicine" practitioners, Stanislaw R. Burzynski has published profusely. The sheer volume of his publications impresses patients, but unless they understand what they are reading, they cannot judge its validity. To a scientist, Burzynski's literature contains clear evidence that his data do not support his claims. <h4>Burzynski's Background and Credentials</h4> <p>Burzynski attended the Medical Academy in Lubin, Poland, where he received an M.D. degree in 1967 and an D.Msc. degree in 1968. He did not undergo specialty training in cancer or complete any other residency program. His bibliography does not mention clinical cancer research, urine, or antineoplastons during this period.</p> <p>In 1970, Burzynski came to the United States and worked in the department of anesthesiology at Baylor University, Houston, for three years, isolating peptides from rat brains. (Peptides are low-molecular-weight compounds composed of amino acids bonded in a certain way.) He got a license to practice medicine in 1973 and, with others, received a three-year grant to study the effect of urinary peptides on the growth of cancer cells in tissue culture. The grant was not renewed.</p> <p>In 1976, with no preclinical or clinical cancer research experience, Burzynski announced a theory for the cure of cancer based on his assumption that spontaneous regression occurs because natural anticancer peptides, which he named <i>antineoplastons</i>, "normalize" cancer cells. Since urine contains lots of peptides, he concluded that there he would find antineoplastons. Less than one year later and based only on these assumptions, Burzynski used an extract from human urine ("antineoplaston A") to treat 21 cancer patients at a clinic he opened. His shingle read, "Stanislaw R. Burzynski, M.D., Ph.D."</p> <p>Burzynski's claim to a Ph.D. is questionable. When I investigated, I found:</p> <ul><li>An official from the Ministry of Health in Warsaw informed me that when Burzynski was in school, medical schools did not give a Ph.D. [1]. </li><li>Faculty members from at the Medical Academy at Lubin informed me that Burzynski received his D.Msc. in 1968 after completing a one-year laboratory project and passing an exam [2] and that he had done no independent research while in medical school [3]. </li><li>In 1973, when Burzinski applied for a federal grant to study "antineoplaston peptides from urine," he identified himself as "Stanislaw Burzynski, M.D, D.Msc." [4] </li></ul> <h4>Analysis of Antineoplaston Biochemistry</h4> <p>Tracing the biochemistry involved in Burzynski's synthesis of antineoplastons shows that the substances are without value for cancer treatment.</p> <p>By 1985, Burzynski said he was using eight antineoplastons to treat cancer patients. The first five, which were fractions from human urine, he called A-1 through A-5. From A-2 he made A-10, which was <u>insoluble</u> 3-N-phenylacetylamino piperidine 2,6-dione. He said A-10 was the anticancer peptide common to all his urine fractions. He then treated A-10 with alkali, which yielded a soluble product he named AS-2.5. Further treatment of AS-2.5 with alkali yielded a product he called AS-2.1. Burzynski is currently treating patients with what he calls "AS-2.1" and "A-10."</p> <p>In reality, AS-2.1 is phenylacetic acid (PA), a potentially toxic substance produced during normal metabolism. PA is detoxified in the liver to phenylacetyl glutamine (PAG), which is excreted in the urine. When urine is heated after adding acid, the PAG loses water and becomes 3-N-phenylacetylamino piperidine 2,6-dione (PAPD), which is insoluble. Normally there is no PAPD in human urine.</p> <p>What Burzynski calls "A-10" is really PAPD treated with alkali to make it soluble. But doing this does<i> </i><u>not</u> create a soluble form of A-10. It simply reinserts water into the molecule and regenerates the PAG (Burzynski's AS-2.5). Further treatment of this with alkali breaks it down into a mixture of PA and PAG. Thus Burzynski's "AS-2.1" is nothing but a mixture of the naturally occurring substances PA and PAG.</p> <p>Burzyski claims that A-10 acts by fitting into indentations in DNA. But PAG is too big a molecule to do this, and Burzynski himself has reported that PAG is ineffective against cancer [5,6].</p> <p>PA may not be safe. In 1919, it was shown that PA can be toxic when ingested by normal individuals. It can also reach toxic levels in patients with phenylketonuria (PKU); and in a pregnant woman, it can cause the child in utero to suffer brain damage.</p> <p>Burzynski has never demonstrated that A-2.1 (PA) or "soluble A-10" (PA and PAG) are effective against cancer or that tumor cells from patients treated with these antineoplastons have been "normalized." Tests of antineoplastons at the National Cancer Institute have never been positive. The drug company Sigma-Tau Pharmaceuticals could not duplicate Burzynski's claims for AS-2.1 and A-10. The Japanese National Cancer Institute has reported that antineoplastons did not work in their studies. No Burzynski coauthors have endorsed his use of antineoplastons in cancer patients.</p> <p>These facts indicate to me that Burzynski's claims that his "antineoplastons" are effective against cancer are not credible.</p><h4>About the Author</h4> <p>Dr. Green (1925-2007) was a biochemist who did cancer research at Memorial Sloan-Kettering Cancer Center for 23 years. He consulted on scientific methodology and had a special interest in unproven methods. This article was adapted from his presentation at the American Association for Clinical Chemistry Symposium in Atlanta in July 1997.</p> <h4>References</h4> <ol><li>Nizanskowski R. Personal communication to Saul Green, Ph.D., Jan 15, 1992. </li><li>Kleinrock Z. Personal communication to Saul Green, Ph.D., Nov 22 1993. </li><li>Bielinski S. Personal communication to Saul Green, Ph.D., Nov 22, 1987. </li><li>Burzynski S. HEW grant application 1973, item 20 (credentials). </li><li>Burzynski SR. Purified antineoplaston fractions and methods of treating neoplastic diseases. U.S. Patent No. 4,558,057, 1985. </li><li>Burzynski SR. Preclinical studies on antineoplastons AS-2.1 and AS-2.5. <i>Drugs Exptl Clin Res Suppl</i> 1, XII, 11-16, 1986. </li></ol><br><p align="CENTER"><font face="Arial" size="5">Free Market Medicine<br> </font><font face="Arial" size="3">by Robert W. Lee</font></p> <p align="JUSTIFY"> </p> <table align="right" border="0" width="36%"> <tbody><tr> <td width="100%"> <p align="center"><font face="Times New Roman" size="3"><img src="http://www.vitaminb17.org/burzynski.jpg" align="center" border="1" height="318" width="238"></font></p></td> </tr> </tbody></table> <p align="JUSTIFY"><b><font face="Times New Roman" size="5">F</font></b><font face="Times New Roman" size="3">or more than a quarter century, Washington has waged a high-profile "war" on cancer at a cost to taxpayers of some $30 billion. Figures recently reported in <i>The New England Journal of Medicine </i>indicate how the battle is progressing: Between 1970 and 1994 (the latest available figures), the cancer rate <i>increased </i>by six percent. Similarly, in 1995 the National Cancer Institute (NCI) reported that when frequency of the disease during the period 1975-79 was compared with that for 1987-91, the incidence among males was up 18.6 percent, and that for females increased by 12.4 percent.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">This apparent lack of progress in coping with the dread disease is especially disturbing when one considers the amount of time, effort, and resources expended by the orthodox medical community — including the American Medical Association (AMA), the American Cancer Society (ACS), and the Food and Drag Administration (FDA) — on frenetic efforts to delay or derail promising alternatives to the entrenched regimen of surgery, chemotherapy, and radiation.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">Assaults on such non-traditional remedies as laetrile (the science and politics of which were analyzed by G. Edward Griffin in <i>World Without Cancer) </i>and krebiozen come readily to mind. The most notable advocate of krebiozen, which at one time had nearly 20,000 case-history endorsements, was Dr. Andrew C. Ivy, onetime chairman of the University of Illinois clinical sciences department. Dr. Ivy's "establishment" medical credentials were impeccable. He had authored more than 1,000 articles published in scientific and medical journals, had served as a U.S. representative at the post-World War II Nuremberg trials, and had received bronze, silver, and gold medals from the AMA for his achievements. Even the FDA had sought his medical testimony on occasion for judicial proceedings.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">But once Dr. Ivy began advocating an unorthodox cancer therapy, he was promptly derided as a "quack." At the behest of the FDA, he and three associates were indicted in 1964 on 49 criminal counts for violations of the Food, Drug, and Cosmetic Act, mail fraud, mislabeling, making false statements to the gov</font><font face="Times New Roman" size="3">ernment, and conspiracy related to the production and distribution of krebiozen (which the agency had outlawed the year before). FDA chemists claimed that krebiozen was simply a common amino acid found in man and animals.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">The subsequent trial, which lasted from April 19, 1965 to the end of January 1966, cost taxpayers an estimated $3 to $5 million. During the trial a letter was read into the court record by a doctor who claimed that while treating a cancer patient he had obtained krebiozen from Dr. Ivy's laboratories, and had administered it to a patient, but that the substance had done absolutely no good whatsoever. Under cross-examination, however, he eventually admitted that he had never treated such a patient and had never used krebiozen. Asked why he had lied, he replied that an FDA agent had written the letter and asked him to sign it, which he did because he wanted to help the agency put an end to "quackery." Lies and deception, needless to say, are the very essence of authentic "quackery."</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">When the jury rendered its verdicts, Dr. Ivy and the others were acquitted on all counts. Indeed, the jury added that it believed krebiozen had merit. Yet as journalist and author Michael L. Culbert notes in <i>Freedom From Cancer, </i>"the propaganda campaign paid off, and krebiozen was left in the public mind as another unproven cancer remedy and Dr. Ivy was character-assassinated into the limbo reserved for pioneers who dare operate outside of the medical-governmental axis."</font></p> <p><b><font face="Times New Roman" size="5"><br> W</font></b><font face="Times New Roman" size="3">hich leads us to the contemporary case of Dr. Stanislaw R.</font> <font face="Times New Roman" size="3">Burzynski, founder of the Houston-based Burzynski Institute that treats cancer patients with substances called antineoplastons. On May 27th, after less than three hours of deliberation, a federal jury in Houston acquitted Burzynski on the single remaining count of the 75 for which he and his clinic had been indicted by a grand jury in 1995. It was Burzynski's second trial this year. The first, which began in early January, entailed 20 days of testimony by more than 80 witnesses regarding 34 counts of mail fraud, 40 counts of introducing antineoplastons illegally into interstate commerce, and a single contempt-of-court count alleging that Burzynski and his clinic violated a 1983 federal court order precluding such interstate dispersion of the drugs.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">U.S. District Court Judge Simeon T. Lake III, who also presided at the second trial, declared a mistrial after an evenly divided jury deadlocked on all 75 counts. Lake then issued a directed verdict of acquittal on the 34 mail-fraud counts, asserting that the evidence presented by the government did not come close to justifying a conviction. Federal prosecutors announced that they would retry Burzynski and the clinic on the remaining 41 counts, but on May 19th (the day before the second trial began) they tossed in the towel on all 40 of the counts related to interstate commerce. Since the clinic was also dropped from the case, Dr. Burzynski alone was retried on the remaining contempt charge. Following Dr. Burzynski's acquittal, juror Stephenie Shapiro told reporters, "I just don't think that the state proved their case .... It was very unanimous from the beginning. It's not like anybody had to be talked into it."</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">Weeks earlier, on April 18th, L. Darlene Phillips, a juror in the first trial, wrote to Attorney General Janet Reno to express her disgust at "how my time and tax dollars were wasted on this trial." She noted, "On two separate occasions the FDA had confiscated a total of 300,000 documents (i.e., patient records, MRI scans, progress charts, etc.) and for Dr. Burzynski to be able to continue to treat his patients, he had to purchase a Xerox machine, install it at the FDA office, hire someone to make copies, and to make it even more difficult, he was required to call a day in advance to make an appointment for copies to be made. To this day these documents have not been returned." Phillips also reminded Reno that Amy Lecocq, lead prosecutor for the first trial, "violated at least six federal laws governing subpoenas of journalists when she subpoenaed Dr. Ralph Moss, PhD [who had written favorably of Dr. Burzynski]. When he pointed this out to her, she withdrew the subpoena." The blatantly illegal, broad-brush subpoena had sought to compel Dr. Moss to produce every document in his possession — electronic, magnetic, printed, or otherwise — relating to Dr. Burzynski.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">Ms. Phillips further pointed out that "the prosecution failed to introduce even <i>one </i>witness who could say anything defamatory about Dr. Burzynski's character." She added: "One would think after four years of preparing for this trial they would have found at least <i>one </i>disgruntled patient, former employee, business associate, or colleague who had something negative to say about him." Phillips wondered if "our government has real 'criminals' to prosecute," and implored the Attorney General to "put a halt to the nonsense of a retrial by our federal government (namely the FDA) of Dr. Burzynski."</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">Phillips' plea fell on deaf ears: Reno refused to intervene.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">Had Dr. Burzynski been convicted of all 75 counts in the original indictment, he could have received up to 290 years in prison and been fined in excess of $18 million. Today, for the first time since the grand jury issued its indictment, he is a fully free man. No longer is he under the cloud of a $100,000 bail bond, nor does he have to report to the federal courthouse every two weeks, nor seek permission to travel out of state.</font></p> <p align="JUSTIFY"><b><font face="Times New Roman" size="5"><br> B</font></b><font face="Times New Roman" size="3">orn in Poland in 1943, Dr. </font><font face="Times New Roman" size="3">Stanislaw Burzynski received his medical degree in 1967 from the Medical Academy of Lublin, ranking first in a class of 250. He earned a doctorate in biochemistry the following year. It was while working on his dissertation project that he identified certain naturally occurring peptides (protein fragments comprised of two or more amino acids) which he concluded might have something to do with controlling cancer. Persons afflicted with the disease, he noticed, typically had lower blood levels of the peptides — which he later termed "antineoplastons" — than did healthy individuals.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">When he refused to join the Communist Party (virtually a prerequisite for academic advancement at the time), Burzynski was drafted into the Polish army for an indefinite period which precluded the opportunity to conduct meaningful research on his discovery. In 1970, with the help of influential fellow scientists, he emigrated to the United States, where he would eventually encounter more harassment and persecution at the hands of the FDA and the Justice Department than he had under Poland's Red regime.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">From 1970 to 1977 he was a researcher and assistant professor at Baylor College of Medicine in Houston, where his research was sponsored and partially funded by the National Cancer Institute (NCI). It was during this time that he fleshed out his theory that the peptides he had stumbled across in human blood and urine (he now produces them synthetically) could correct and normalize certain types of malignant neoplastic (tumor) cells. Thus the term "antineoplastons." "We are no longer concerned with killing cells," he asserts, "but with changing the program inside the defective cell so that it will begin to function normally."</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">Most experts agree that we all probably develop cancer millions of times during our lifetime. With trillions of maturing cells, millions of errors can and likely do occur, a problem further aggravated by exposure to thousands of chemical carcinogens, and such physical factors as radiation, bacteria, viruses, and unhealthy stress, that have plagued mankind throughout time. Normal cells, Burzynski explains, specialize to serve particular purposes. Once that specialization occurs, they no longer divide to form new cells. They do what they have been programmed to do, then fade and die, to be replaced by new cells.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">Some cells, however, are affected by carcinogens and other disrupting influences that cause them to become, in a sense, both destructive and "immortal." They neither specialize nor die, but continue dividing until they overwhelm normal cells. The result is cancer, which Dr. Burzynski contends is essentially a disease of cell differentiation. "It is obvious," he points out, "that everybody would de</font><font face="Times New Roman" size="3">velop cancer if we didn't have a certain protective system in the body. This is the biochemical protection system .... Antineoplastons correct the program inside the cell and force it toward normal development" by serving as "biochemical micro-switches" that turn off oncogenes (the genes, found in all cells, that are responsible for cell malignancy) and turn on tumor-suppressor genes that stop them.</font></p> <p align="JUSTIFY"><b><font face="Times New Roman" size="5"><br> T</font></b><font face="Times New Roman" size="3">he concept that cells can be repro</font><font face="Times New Roman" size="3">grammed from abnormal to normal, precluding the need to eliminate them, may explain much of the opposition that Dr. Burzynski has encountered from orthodox medicine and its FDA enforcement arm. The theory offers an alternative to the surgery-chemo-therapy-radiation approach which holds that cancer cells must be either destroyed on-site or excised. As Dr. Julian Whittaker, MD, editor of the newsletter <i>Health & Healing, </i>wrote in March of this year, "Though the FDA is the obvious 'point-man' in the persecution of Dr. Burzynski, the real force is coming from the cancer treatment establishment. Just imagine all the physicians, technology, and medical facilities that feed off chemotherapy, radiation therapy, and surgery. They are now threatened by a more effective and less dangerous therapy that can be administered in a doctor's office or by patients at home."</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">T</font><font face="Times New Roman" size="2">HE</font><font face="Times New Roman" size="3"> N</font><font face="Times New Roman" size="2">EW</font><font face="Times New Roman" size="3"> A</font><font face="Times New Roman" size="2">MERICAN</font><font face="Times New Roman" size="3"> is not qualified to reach conclusions regarding the scientific validity of Dr. Burzynski' s antineoplaston theory. However, since opening his private clinic in Houston in 1977, he has treated some 3,000 advanced cancer patients, most of whom turned to him after exhausting conventional treatments. Hundreds are convinced that antineoplastons literally saved, or have significantly extended, their lives, without the debilitating side effects characteristic of such conventional therapies as radiation and chemotherapy.</font></p> <table align="right" border="0" cellpadding="9" width="47%"> <tbody><tr> <td width="100%"> <p align="center"><img src="http://www.vitaminb17.org/burzynski_3.jpg" border="1" height="238" width="334"><br> <font face="Arial" size="2">Dr. Burzynski with patient Dustin Kunnari:<br> After three years, tumors still in remission</font></p></td> </tr> </tbody></table> <p align="JUSTIFY"><font face="Times New Roman" size="3">Consider, as one example, the case of Dustin Kunnari. In February 1994, when he was two and one-half years old, Dustin was diagnosed with an aggressive type of brain tumor called medulloblastoma. It is the second most common brain tumor found in children, and whether treated with conventional therapy or left untreated entails a life expectancy of only one to four years. Three-fourths of Dustin's tumor was removed surgically, after which his parents, Jack and Mariann of Aurora, Minnesota, were encouraged to enroll him in a study at the University of Minnesota that would initially treat his cancer with chemotherapy, then radiation. The possible side effects, they were informed, included hearing loss, stunted growth, hair loss, learning disabilities, sterility, and leukemia. They were, however, assured that the success rate of such therapy reached as high as 40 percent. But when they requested a few names of those parents whose children had been successfully treated, so they could confirm the results firsthand, their request was denied.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">The Kunnaris opted not to enter Dustin in the program, electing instead to give Dr. Burzynski's treatment a try. It is called freedom of choice, but it goes down hard with establishment medicrats. Jack Kunnari told T</font><font face="Times New Roman" size="2">HE</font><font face="Times New Roman" size="3"> N</font><font face="Times New Roman" size="2">EW</font><font face="Times New Roman" size="3"> A</font><font face="Times New Roman" size="2">MERICAN</font><font face="Times New Roman" size="3"> that when they sought to retrieve Dustin's medical records from the University of Minnesota, they were told that in medical cases the opinions of doctors take precedent over those of parents, and that they could be taken to court unless they agreed to enroll Dustin in the study. "Until the day we left for Houston, there were still threats coming," Mr. Kunnari recalled.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">Dustin's antineoplaston treatment began in April 1994. Within six weeks an MRI (Magnetic Resonance Imaging) scan showed complete remission of the tumor. Following another year of treatment, another MRI indicated that the tumor was recurring. The dosage of antineoplastons was increased, and the tumor once again receded. According to Dustin's latest MRI on May 1 st of this year, the tumor remains in remission. Indeed, he was recently taken off intravenous administration of the drug and is presently receiving only a maintenance dosage via capsules. His parents describe him as a robust and basically healthy six-year-old. The side effects of the therapy have been nil.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">The government's prosecution of Dr. Burzynski, which raised the specter of losing their only source for a drug they are convinced has been of enormous benefit to their son, intensified the Kunnaris' anguish — and their anger. "I guess we were always aware," Jack Kunnari told T</font><font face="Times New Roman" size="2">HE</font><font face="Times New Roman" size="3"> N</font><font face="Times New Roman" size="2">EW</font><font face="Times New Roman" size="3"> A</font><font face="Times New Roman" size="2">MERICAN</font><font face="Times New Roman" size="3">, "that if you go with an alternative [therapy] there would be some opposition. But we never dreamed it would be as intense as it has been. From the time the first MRI showed that Dustin's tumor was gone, there was the feeling that we had accomplished something. We stood up for what was best for our son. We stood up to the University of Minnesota despite the legal threats and such. It was a feeling of such joy and appreciation. Then you get hit with these indictments and court rulings against Dr. Burzynski." Mr. Kunnari recalls that "we had just gone through an emotional fight to get our son to the point where the tumor was gone, restore him to a measure of health, and now our government was stepping in and we had to fight it. I don't know how you can explain the range of emotions, but I guess the best way to describe it is a roller-coaster ride. Initially, your son has a brain tumor, so you're down and feeling pretty bad about things. Then you find out about this doctor and you get a feeling of hope, the MRI looks good, and your hope increases. And then the government steps in and says you can't have the treatment."</font></p> <p align="JUSTIFY"><b><font face="Times New Roman" size="5"><br> I</font></b><font face="Times New Roman" size="3">n a February 19, 1997 letter to Judge Lake, Dr. Robert E. Burdick, MD, summarized his review of 17 Burzynski patients (among 40 of his patients with brain tumors who were included in an FDA-approved trial one year earlier) who had responded to treatment with antineoplastons. Dr. Burdick has practiced medical oncology for nearly three decades and is on the faculty of the University of Washington Medical School. After noting the "frustrations that neuro-surgeons, radiotherapists, and we medical oncologists have regarding our ineffective treatment of malignant brain tumors," and presenting a brief overview of the sundry types of malignant tumors, Dr. Burdick noted that it "is very rare, currently, to ever get a complete remission or cure in a patient who has a malignant brain tumor using our standard modalities of surgery, radiation, and chemotherapy. By the time a tumor is large enough to be clinically detected, it has involved such critical structures that to remove it surgically would result in a patient who is left in a vegetative state or is markedly more disabled than he was prior to the surgery."</font></p> <p align="LEFT"><font face="Times New Roman" size="3">Dr. Burdick noted that, "as a rough es</font><font face="Times New Roman" size="3">timate, neurosurgeons do well to cure 1 in every 1,000 brain cancer patients they operate on. Radiation therapy slows the growth of adult tumors, gaining perhaps one month of life and again may result in a cure of only 1 in 500-1,000 patients, those cures being in the pediatric age group. Similarly, chemotherapy research, despite 30 years of clinical trials, has not resulted in the development of a single drug or drug combination that elicits more than an occasional transient response in primary brain tumors .... In fact, chemotherapy in brain tumors is so discouraging that in many parts of the country patients with brain tumors are not even offered the option of chemotherapy."</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">Based on his careful analysis of each of the 17 patients in the study who responded to treatment with antineoplastons, Dr. Burdick found that "there were 7 complete remissions, one patient having had a second complete remission after he discontinued antineoplaston therapy which resulted in his tumor regrowing. There were nine partial remissions, two cases of stable disease, and no disqualifications. The average duration of therapy with antineoplastons necessary to obtain a complete remission was 10 months with a range of 2 to 20 months. The average duration of antineoplaston therapy necessary to obtain a partial response was 8 months with a range of 1 to 14 months. The average duration of complete remissions is 16+ months with all six complete remissions continuing to remain in remission to the best of my knowledge through January 1, 1997. The duration of complete remissions ranged from 3+ months to 40+ months with the duration of partial remissions averaging 18+ months and ranging from 5 to 78+ months."</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">Summing up, Dr. Burdick told Judge Lake that he was "very impressed with the number of complete and partial responses that I have seen here, compared with the number of such responses that I have seen in my own personal experience. The responses here are also far in excess of any prior series of patients published in the medical literature." Even after two patients were subsequently downgraded from "partial remission" to "stable disease," the response rate (partial or complete remissions) was "an astounding 33% with a complete remission rate of 15%. Such remission rates are far in excess of anything that I or anyone else has seen since research work on brain tumors began." Dr. Burdick asserted that it "is very clear that the responses here are due to antineoplaston therapy and are not due to surgery, radiation or standard chemotherapy." He concluded that research "needs to continue on these very promising agents," to determine such things as "the optimal dose of these agents, the optimal route of administration, the optimal duration of treatment and many other details too numerous to mention."</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="5"><br> D</font><font face="Times New Roman" size="3">r. Burzynski opened his clinic in 1977. Prior to 1985, FDA drug-approval procedures were not incorporated into Texas law, so he was advised by his attorney that he could treat patients with innovative medicine as long as he did not engage in interstate commerce. In <i>The Cancer Industry, </i>Dr. Ralph Moss recalls that Burzynski would have preferred to obtain FDA approval, but the roadblocks inherent in the agency's process were virtually insurmountable. The normal process, Moss writes, "is for a new substance to be discovered at a major medical center and then turned over to a drug company for development. If the company decides it is economically feasible, it will then battle its IND [Investigational New Drug] application through the FDA." But even then "it is often unsuccessful."</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">Since none of the drug companies expressed an interest in Burzynski's compounds, he opted to develop them himself. But Moss writes that with virtually no capital with which to finance a run through the FDA maze, Dr. Burzynski "was caught in a classic catch-22 situation. If he tested antineoplastons in humans, the FDA was sure to come down on him eventually. But if he didn't so test them, he could never win FDA approval, since antineoplastons, being species-specific, are not generally effective in animal treatment experiments." The Declaration of Helsinki, adopted in 1964 by the World Medical Assembly and subsequently endorsed by Congress, states: "In the treatment of the sick person, the doctor must be free to use a new therapeutic measure, if in his judgment it offers hope of saving life, reestablishing health, or alleviating suffering." Burzynski decided to treat patients, compile thorough records, finance future development of the drugs with patient fees, and take his chances with the FDA.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">The FDA first visited Burzynski's facilities in 1978. The event was, in sharp contrast to the harassment and legal turmoil that would follow, quite congenial. Burzynski is first to admit that his manufacturing process at the time was rather amateurish, and that the FDA's constructive criticisms enabled him to make needed improvements.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">At the time, most of his problems were emanating from the local medical establishment. Moss writes: "In 1978 Burzynski became the focus of an investigation by the Board of Ethics of the Harris County Medical Society. The charge was using unapproved medications of his own devising. They repeatedly called him in for interviews and instructed him not to give any interviews to the press." Burzynski complied with the press blackout, but in 1979 <i>Penthouse </i>magazine ran an article entitled "The Suppression of Cancer Cures," which described his plight, and in 1981 ABC' s <i>20/20 </i>featured a segment entitled "The War on Cancer: Cure, Profit or Politics?" during which commentator Geraldo Rivera asserted: "The deeper we looked into the story, the more we realized that Stanislaw Burzynski is really not a maverick at all. His work is very much in the scientific mainstream, that burgeoning field of cancer research that's pin-pointing the body's own natural materials, its own proteins, to control irregular cell growth...."</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">In the wake of such national publicity, hundreds of cancer patients began visiting the Houston clinic for treatment, and no more was heard from the local Board of Ethics. Trouble at the national level, however, was beginning to metastasize.</font></p> <table align="left" border="0" cellpadding="9" width="48%"> <tbody><tr> <td width="100%"> <p align="center"><br> <img src="http://www.vitaminb17.org/burzynski_2.jpg" border="1" height="239" width="349"><br> <font face="Arial" size="2">Burzynski and supporters during 1997 trial:<br> Choice in medical treatment is the issue</font></p></td> </tr> </tbody></table> <p align="JUSTIFY"><b><font face="Times New Roman" size="5"><br> I</font></b><font face="Times New Roman" size="3">n 1983, the American Cancer Society placed Dr. Burzynski on its "unproven methods" blacklist of practitioners with which it disagrees. Later in the year, the FDA filed civil suit in federal court to stop him from manufacturing, or treating patients with, antineoplastons. An indication of the FDA's arrogant attitude was reflected in a motion dated May 2, 1983, in which its chief counsel for enforcement warned, "If this court declines to grant the injunctive relief sought by the government, thus permitting continued manufacture and distribution of antineoplastons by defendants ... the government would then be obliged to pursue other less efficient remedies, such as actions for seizure and condemnation of the drugs or criminal prosecution of individuals...." U.S. District Court Judge Gabrielle McDonald barred Burzynski from shipping the drug outside the state, or otherwise introducing it into interstate commerce, but authorized him to treat patients within the state of Texas. "Nothing contained heroin shall be construed as restraining, enjoining or in any way prohibiting the manufacture, processing, packing, holding, promotion, labeling, sale or distribution of antineoplastons ... when it is undertaken strictly and wholly intrastate," her order stated. This partial victory for Dr. Burzynski infuriated the FDA, which promptly moved to circumvent the court order and, it hoped, close down the clinic. When Dr. Burzynski and some of his patients filed suit against the agency in the hope of ending the harassment, Judge McDonald rejected their request to allow a jury to hear their case, but did find that the FDA had disseminated false and misleading information about Burzynski to prospective pa</font><font face="Times New Roman" size="3">tients, insurance companies, and public officials. Her October 24, 1985 ruling demanded that it stop doing so.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">It was earlier that year that FDA agents raided Dr. Burzynski's clinic and seized more that 200,000 pages of documents, including patient records. Without the records, Burzynski was seriously hamstrung in treating his patients. As noted earlier, he was required to install a copier at FDA headquarters, at his expense, and make appointments in advance to photocopy the needed records.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">In 1986, an additional 100,000 documents were subpoenaed for the first grand jury investigation of his activities. After scrutinizing the evidence, the grand jury declined to indict.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">Judge McDonald's 1983 partial injunction stated that "the jurisdiction of this court is retained for the purpose of enforcing or modifying this injunction and for the purpose of granting such additional relief that hereafter may appear necessary or appropriate." Which meant that government prosecutors had a civil-remedy alternative to criminal prosecution regarding the key question (on which the other charges were based) of whether or not Dr. Burzynski had violated Judge McDonald's directive. As interpreted by Burzynski, the order did not bar his clinic from providing antineoplastons to patients from out of state who traveled to Houston to pick them up, then returned home. He was treating such patients within Texas, and neither he nor the clinic were shipping the drugs elsewhere. Nor, he contended, did the court order apply in instances where patients themselves could not, for health or economic reasons, make trips to Houston, so had representatives (friends, rela</font><font face="Times New Roman" size="3">tives, etc.) secure supplies of the drug from the clinic on their behalf.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">Judge McDonald's order did not specifically preclude such activity, but the government argued that it was illegal for Burzynski or his clinic to provide antineoplastons to persons whom they knew would then travel with or ship the drugs beyond state borders.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">Federal law required that Judge McDonald's order be "of reasonable specificity," but on this key point it was imprecise. The government could have asked her to clarify the matter by restating her intent, but it did not. As Gary Anderson, a juror in the second trial, explained, "What we felt was that the order was ambiguous. And it was our feeling that he [Burzynski] made an attempt to do what he thought he should be doing." Indeed, Burzynski had never tried to hide the fact that he was treating persons from other states at his clinic. Their home addresses were listed on the paperwork he had been submitting to the FDA for years.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">In 1990, a second grand jury was convened in yet another attempt by the FDA to garner an indictment, but it, too, cleared Burzynski.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">In 1994, a third grand jury was convened. Again, there was no indictment, but an Assistant U.S. Attorney assigned to the case was dismissed after local reporters discovered that he had subpoenaed the campaign contribution records of a local politician who was a fervent Burzynski supporter, then leaked to the press a false story indicating that misuse of campaign funds was part of the ongoing investigation of Burzynski.</font></p> <p align="LEFT"><font face="Times New Roman" size="3">Up to that point, then, three separate grand juries had scrutinized the Burzynski record and had refused to indict him on so much as a single count. It was a remarkable series of victories for the beleaguered physician, since, as Representative Joe Barton (R-TX), chairman of the Subcommittee on Oversight and Investigations of the House Committee on Commerce, noted in a September 7, 1995, letter to Attorney General Reno, "It is extraordinarily rare for a grand jury to fail to indict at the request of the U.S. Attorney. As far as I know, a grand jury failing to indict some three to four times on essentially the same base of facts is virtually unprecedented. It would appear that the FDA and the Justice Department are abusing the grand jury process to harass and punish Dr. Burzynski for persuading a federal judge that he is not violating the law by practicing medicine within the State of Texas."</font></p> <p align="JUSTIFY"><b><font face="Times New Roman" size="5"><br> I</font></b><font face="Times New Roman" size="3">n 1994, the FDA's oncology division granted Dr. Burzynski permission to conduct four Phase II (efficacy) clinical trials on antineoplastons. FDA inspectors scrutinized and approved his manufacturing facility. It appeared that a truce between the two sides may have been reached. Then, on March 24, 1995, Dr. Burzynski appeared on the CBS program <i>This Morning </i>with three patients whose cancers had been diagnosed as terminal years earlier, but who now claimed to be free of the malignancies following treatment with antineoplastons. That afternoon the FDA again raided the Burzynski clinic, spending some seven hours rummaging through file cabinets, drawers, and computers, and eventually hauling off numerous boxes crammed with documents. It was the first step on the road to a fourth (this time successful) attempt by the FDA to secure a grand jury indictment.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">For eight months, subpoenas were issued to Dr. Burzynski, many of his present and former employees, and other persons with whom he had been associated or who had spoken or written favorably about his work. It was after publishing a letter vigorously condemning the March raid that author Ralph Moss was served with the bogus subpoena covering every document in his possession relating to Dr. Burzynski.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">On November 15, 1995, FDA Commissioner David Kessler testified before the Barton subcommittee. Questioned about the Burzynski case, Kessler vigorously denied that there was a pattern of retaliation against the physician. Five days later, the U.S. Attorney's office in Houston announced the 75-count indictment by the fourth grand jury.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">There is no need to reprise the testimony from the enormously expensive trial. Judge Lake's directed verdict of acquittal on the mail fraud counts, the prosecution's decision to drop the interstate commerce charges, and Burzynski's swift acquittal on the contempt charge speak for themselves. It should be noted, however, that since late 1996 the FDA, perhaps prodded by pressure generated by the Barton hearings, has allowed the Burzynski clinic to register patients, including those from out of state, under dozens of study protocols qualifying them to receive antineoplastons by mail. Which means that at the time he was twice standing trial for contempt of an ambiguous, ancient court order that supposedly barred him from introducing antineoplastons into interstate commerce, he was legally authorized to ship the drugs to patients anywhere in the country. Jurors, at least those in the first trial, were not told about it.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="5"><b><br> C</b></font><font face="Times New Roman" size="3">onstitutional authority Dan Smoot once observed, "A nation which values anything — even good health — more than it values freedom will lose its freedom." Needless to say, the best prescription for good health <i>is </i>freedom — freedom to choose the type of medical care one prefers, from the practitioners one prefers, who provide medications and other services one prefers. A truly free market in health care would enable innovators such as Dr. Burzynski to make a case for their discoveries in competition with others both within and without the "orthodox" medical establishment, unhindered by a dictatorial government bureaucracy that, in the name of protecting our health, often undermines it.</font></p><br><br><blockquote> <p align="JUSTIFY"><font face="Times New Roman" size="3"><br> In 1991, results of an FDA-approved Phase II (efficacy) trial involving 20 patients with varying stages of astrocytoma (the most common brain tumor in children) were published by Dr. Burzynski in <i>Recent Advances in Chemotherapy</i>. Nineteen had received one or more prior standard therapies to which their tumors did not respond. There was complete remission of the tumors in four patients, partial remission in two others, while ten others were diagnosed with "objective stabilization" (less than 50 percent decrease in tumor size). Later, two of the ten patients in that latter category improved to the point that one was reclassified "partial remission" and the other "complete remission." All told, 16 of the 20 patients stabilized or improved, a startling result considering the severity of their conditions when the trial began.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">In September of last year, Dr. Burzynski submitted brain scans of 29 of his clinical trial patients for review by a neuroradiologist at the Barrows Neurological Institute in Phoenix, Arizona. All 29 had been diagnosed as terminal when their treatment with antineoplastons began. A subsequent report noted complete remissions in 13 patients, partial or initial responses in eight others, and no response to the treatment in the remaining eight.</font></p> <p align="JUSTIFY"><font face="Times New Roman" size="3">There are also some indications, though at present based solely on animal studies, that in addition to <i>treating </i>some types of cancer, antineoplastons may also be helpful in <i>preventing </i>them from developing in the first place. Researchers at the Burzynski Clinic and at Japan's University of Kurume Medical School both found indications that low doses of a synthetic form of one type of antineoplaston administered orally prevented lung, breast, and liver cancers in the test animals. </font><font face="Times New Roman" size="3">—</font><font face="Times New Roman" size="3"> R.W.L.</font></p><p align="JUSTIFY"><font face="Times New Roman" size="3"><br></font></p> </blockquote><br><div class="article-rel-wrapper"> <h2 class="contentheading"> Frequently Asked Questions </h2> </div> <div class="article-info-surround"> <div class="article-info-surround2"> <p class="buttonheading"> </p> <p class="articleinfo"> <span class="modifydate"> Last Updated on Wednesday, 09 March 2011 18:45 </span> </p> </div> </div> <p><em>Since the theatrical and DVD release of this documentary, and since some of the mainstream reviews of this film have been published—there are certain questions that have surfaced on a consistent basis. This section will be updated frequently. We are also assembling a full timeline with downloadable sources to some pertinent parts of this story, as well as a fully interactive transcript of the entire film with accompanying linkable and downloadable sources to be posted by Spring 2011.</em></p> <p><strong>1. I asked my doctor about Dr. Burzynski and antineoplastons, and he said there is no proof that it works. </strong></p><p><br><strong></strong></p><p><img alt="http://www.vitaminb17.org/burzynski.jpg" src="http://www.vitaminb17.org/burzynski.jpg"></p> <p>If you are interested in the treatment methods of Dr. Stanislaw Burzynski and you inquire with a physician about these treatments, there are three questions you might want to ask:<br><br>1. Have you ever reviewed the medical records of any present or past patients of Dr. Burzynski?<br>2. Have you visited his clinic and/or made an attempt to understand the science behind his treatment?<br> 3. Have you read any of the peer-reviewed medical literature published concerning the science behind this treatment—and all of the statistical data published regarding the results from Phase 1 and Phase 2 clinical trials?</p> <p>If a doctor, scientist, or medical professional has answered "no" to any of the above questions, their "opinion" on antineoplastons or Dr. Burzynski may be based on the lack of proper education to responsibly arrive that their opinion. <strong><em>Additionally, science isn't a matter of opinion. The scientific findings published in the peer-reviewed medical literature isn't opinion, it's scientific fact, based on the testing and re-testing of these medicines in strictly designed clinical trial conditions under FDA-authorization and supervision—then scrutinized by other peers of the oncology and scientific community for further verification. </em></strong></p> <p><strong>2. Does Dr. Burzynski currently use animal or human urine to treat cancer?</strong></p> <p><span style="text-decoration: underline;"><span style="text-decoration: none;">Absolutely not.</span></span> <a href="http://www.ncbi.nlm.nih.gov/pubmed/3527634" target="_blank">In 1967, after obtaining his medical degree and while completing his PhD in biochemistry, Dr. Burzynski discovered a strain of peptides in human blood and urine that had never before been recorded in biomedical research. </a>As Dr. Julian Whitaker stated in the film, "discovering something in the urine [and blood] at that time, that had never been discovered before—is like finding a whole bunch of new islands ten miles off the coast of Miami, it came as a big surprise." Dr. Burzynski had no idea what this discovery meant at the time. However, he and his colleagues were extremely excited about this new discovery, and he continued to explore it. After testing the human blood of various different sexes, races, and ages of people—he found that these newly discovered peptides were either absent or revealed a very low count within the blood of those individuals with cancer. He eventually found that this peptide count was virtually identical in both human blood and human urine.</p> <p>Dr. Burzynski simply hypothesized—if he could simply extract these peptides from healthy donors, and administer these peptides to people with cancer, perhaps it would be helpful in treating the disease. Upon this initial exploration, he discovered that extracting the amount of peptides from healthy human blood was very laborious as the amount of blood needed to obtain a necessary amount of peptides far exceeded the amount of blood reasonably available.</p> <p>Upon this realization, he began extracting these peptides from human urine, since it was far easier to obtain large amounts of healthy human urine vs. healthy human blood. Dr. Burzynski began setting up collection containers at state parks, religious institutions, and even prisons.</p> <p><strong><a href="http://www.burzynskiresearch.com/" target="_blank"><strong>Today, Dr. Burzynski synthesizes the chemicals to help your body naturally produce these peptides in his massive 46,000 square foot manufacturing facility in Stafford, Texas</strong></a>—he no longer uses urine as the source of these peptides. The use of human urine as the source for these peptides ceased in the early 1980s. Therefore, it has been nearly 30 years since he has used any urine whatsoever as the source of his treatment.</strong></p> <p>As for animal urine, it seems some of the members of the press who reviewed this documentary such as <a href="http://www.villagevoice.com/2010-06-01/film/quack-quack-goes-burzynski/" target="_blank">The Village Voice</a>,<strong> </strong><a href="http://newyork.timeout.com/articles/film/86174/burzynski-film-review" target="_blank">Time Out New York</a>, and the <a href="http://www.nypost.com/p/entertainment/movies/burzynski_3nGJa6Q38Ubybn1pXu6H1J" target="_blank">New York Post</a> either did not pay any attention, didn't bother to watch the film at all, or they maliciously lied about the contents of the film. (The Village Voice and Time Out New York have since edited their reviews online to exclude the "animal urine" inaccuracy, but the New York Post still stands behind this glaring inaccuracy).</p> <p>The chemicals that are used to enable your body to produce these peptides that make up the active ingredients for Dr. Stanislaw Burzynski's patented, Antineoplastons are:<br>Antineoplaston AS2-1: Phenylacetlglutamine, Phenylacetate<br>Antineoplaston A10: Phenylacetylisoglutamine</p> <p><a href="http://www.ncbi.nlm.nih.gov/pubmed/17695534" target="_blank">Antineoplaston A10 is the first naturally occurring antineoplaston substance in the human body to be chemically identified.</a></p> <p>Anyone today who states that Dr. Burzynski currently uses urine of any sort in the treatment of human cancers is either (a) lacking the necessary resources or motivation to investigate this story thoroughly (b) is very confused by the difference between the initial discovery in 1967 vs. how his operation has been running since the 1980's up until today. Or, sadly... (c) is intentionally lying.</p> <p>If you are currently a client of Aetna insurance, or are simply curious, it's important to note that if you visit their website and search for "Dr. Stanislaw Burzynski" or "Antineoplastons" you will find that they state: <a href="http://www.aetna.com/cpb/medical/data/200_299/0240.html" target="_blank">"</a><span style="font-family: arial,helvetica,verdana,sans-serif; font-size: 13px; line-height: 18px;"><a href="http://www.aetna.com/cpb/medical/data/200_299/0240.html" target="_blank">Aetna considers antineoplaston therapy (auto-urine therapy)..."</a>. "Auto-urine therapy" is the practice of urinating into a cup, and drinking it. This is one of the finest examples of either careless research, or malicious slander by the medical establishment. If urinating into a cup and drinking it was a method for treating any disease, why would one need a doctor to perform this treatment? Or better yet, why would someone need an insurance company to cover such a treatment? Or even better, why would someone want to be insured by a company that is incapable of accurately documenting the simplest of scientific data within it's literature?</span></p> <p><strong>3. What was the outcome of the duplicate patents?</strong></p> <p>Given the confusing and convoluted nature of the Department of Health and Human Services filing "copy cat" patents of Dr. Burzynski's AS2-1—which commenced 17 days <a href="http://www.burzynskimovie.com/images/stories/Sources_FAQ_web/NIH_SiteVisit_1991.pdf" target="_blank">after they visited his clinic on October 4, 1991 and verified for themselves that "anti-tumor activity was documented"</a>, all the while <a href="http://www.burzynskimovie.com/images/stories/Sources_FAQ_web/1991_10_21_US6037376.pdf" target="_blank">using one of Burzynski's own scientists to file the patents</a>—below is the official statement regarding this matter after consulting with Dr. Burzynski and his patent attorneys. <br> <br> "It seems the entire criminal indictment was geared toward placing Dr. Burzynski in prison so he could not defend himself against the criminal theft of part of his discovery (AS2-1). While they did manage to patent PA (phenylacetate) which Dr Burzynski never patented, it also included PAG (phenylacetylglutamine) which was patented previously by Burzynski—however, his AS2-1 patents include both chemicals. Since Dr. Burzynski is a free man now, and even though the 'copy cat' NIH patents were approved, Burzynski can't really successfully sue the NIH or Elan until they actually 'act' on those patents by manufacturing and selling the substance. Right now, the only thing Burzynski can do is to ask the <span id="lw_1276985210_1" class="yshortcuts" style="border-bottom: 2px dotted rgb(54, 99, 136); cursor: pointer; background: none repeat scroll 0% 0% transparent;">patent office</span> for re-examination of the NIH patents. Frankly, Dr. Burzynski has spent enough time fighting, he just wants to put this behind him and continue developing his medicine and treating <span id="lw_1276985210_2" class="yshortcuts" style="cursor: pointer; background: none repeat scroll 0% 0% transparent;">cancer patients</span>."</p> <p>Dr. Burzynski can't exactly walk in the front door asking the Department of Health and Human Services for the approval of his discovery for public use, while simultaneously knocking on their back door with a criminal indictment.</p> <p><strong>4. The opposition keeps saying that there has been no "peer-reviewed" data on his therapy, is this true?</strong></p> <p>No, it is not true. Aside from the numerous "peer-reviewed" medical journal articles referenced in the film, Dr. Burzynski and others have published dozens of studies of Antineoplastons in the peer-reviewed medical literature. <a href="http://www.ncbi.nlm.nih.gov/sites/entrez" target="_blank"><strong>Feel free to visit "pubmed.gov" here</strong></a> and search for "Burzynski Antineoplaston". The next question you might want to ask this person is "have you made an attempt to <em>look</em> for any peer-reviewed data on Dr. Burzynski?" More peer-reviewed publications can be found here as well [<a href="http://www.burzynskiclinic.com/publications.html" target="_blank">click</a>]. One of the most stunning admissions of ignoring the peer-reviewed scientific literature occurred in a Dateline NBC 2/20/11 broadcast [<a href="http://www.burzynskimovie.com/index.php?option=com_content&view=article&id=92&Itemid=76" target="_blank">watch the episode and read the analysis here</a>].</p> <p><strong>5. Have other countries other than the United States allowed Antineoplaston research to commence?</strong></p> <div>Yes. The most notable country to participate in Antineoplaston research is Japan. Cancer researchers in Japan have independently<span style="font-weight: bold;"> <span style="font-weight: normal;">successfully conducted Phase I and Phase II clinical trials of Antineoplastons. Phase III trials will commence in 2010 (Phase III trials are the final phase of testing before being approved for use by the general public). It appears that Antineoplastons might be approved for general public use in Japan before it will be made freely available in the United States. Here is a sample list of Japan's peer-reviewed scientific data on their independent trials:</span></span></div> <div><a href="http://www.ncbi.nlm.nih.gov/pubmed/17695534" target="_blank">2007</a>; <a href="http://www.ncbi.nlm.nih.gov/pubmed/16012735" target="_blank">2005</a>; <a href="http://www.ncbi.nlm.nih.gov/pubmed/12768372" target="_blank">2003</a>; <a href="http://www.ncbi.nlm.nih.gov/pubmed/11748457" target="_blank">2002</a>; <a href="http://www.ncbi.nlm.nih.gov/pubmed/9538158" target="_blank">1998a</a>; <a href="http://www.ncbi.nlm.nih.gov/pubmed/9769368" target="_blank">1998b</a>; <a href="http://www.ncbi.nlm.nih.gov/pubmed/8755117" target="_blank">1996</a>; <a href="http://www.ncbi.nlm.nih.gov/pubmed/7474850" target="_blank">1995a</a>; <a href="http://www.ncbi.nlm.nih.gov/pubmed/8667595" target="_blank">1995b</a></div> <p><strong>6. Some of the mainstream reviews have complained that you didn't include members of the FDA or oncologists or doctors to speak either in support or opposition of Dr. Burzynski's treatment. </strong></p> <p>Actually, if you watch the film you will find many doctors who have come out in support of Burzynski. The FDA doesn't conduct personal on-camera interviews with anyone, much less the press or a film maker—this was clearly demonstrated in the film. I had also asked numerous oncologists and general physicians who were previously treating the patients in this film before they began treatment with Burzynski to participate in the film — <span style="text-decoration: underline;">ALL OF THEM</span> turned it down. I even had oncologists exit the theater in Los Angeles and New York City after the film ended commending me on the film - and when I asked them if they would go on camera, none would agree. If you are a board-certified oncologist reading this now, and would like to go on camera, "for" or "against" Dr. Burzynski, <a href="http://www.burzynskimovie.com/index.php?option=com_contact&view=contact&id=1&Itemid=54" target="_blank">please email me here.</a></p> <p><em>On November 18, 2010: Fox News in Austin, TX expressed having the same problem when investigating Dr. Burzynski - <a href="http://www.myfoxaustin.com/dpp/top_stories/Curing-Cancer-without-Chemotherapy-20101118-ktbcw" target="_blank">click here to watch the segment</a><br> </em></p> <p><em> </em></p> <p><em> </em></p> <p><em> </em></p> <p><em> <p><font face="Trebuchet MS, Arial, Helvetica"><font face="Arial Black"> <font size="4">QUACKERY PILS FOR SALE<br></font></font></font></p><p><font face="Trebuchet MS, Arial, Helvetica"><font face="Arial Black"><font size="4">A10 </font><font size="2"> </font> </font><font size="2"> <br> For energy, detoxification, good health and stronger immune system. 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Seek advice from a qualified physician before replacing standard cancer therapy with Coley toxin therapy.</p> <h2>What does Coley toxin therapy involve?</h2> <p>Coley toxins were developed by William B. Coley, MD, in 1890 and fall within the realm of immunotherapy. According to available historical background literature, after reviewing one hundred cases of sarcoma treated in his hospital, Dr. Coley noted that patients who developed infections fared better than those who did not. Dr. Coley mixed toxins of the streptococcus and bacillus prodigious bacteria and administered them to patients. Regressions of cancer were noted by Dr. Coley, but the treatment fell out of disuse with the advent of chemotherapy. Currently Coley toxins are administered intravenously and now include exotoxins, enzymes, proteins and endotoxin from both S. pyogenes and S. marcescens. The combined toxins are only legal in the U.S. if prepared and administered in a physician's office.</p> <h2>How are Coley toxins thought to treat cancer?</h2> <p>Coley toxins are designed to stimulate the immune system to better fight existing malignant cells and enhance survival. </p> <h2>What has been proven about the benefit of Coley toxins?</h2> <p>The University of Texas M.D. Anderson Cancer Center conducted an extensive human studies literature review and found thirty studies applicable to cancer. Used in conjunction with chemotherapy, radiation and surgery, Coley toxins appear to have a greater response than when used alone. Mechanisms of antitumor effects are reported to include the induction of interferon, augmentation of natural killer cell activity, stimulation of lymphoid tissues, activation of macrophages, induction of serum factors that cause necrosis of tumors and increased release of IL-2.</p> <h2>What is the potential risk or harm of Coley toxin therapy?</h2> <p>Side effects to Coley toxins include fever and nausea and, less commonly, headache, back pain, chills, angina and shock-like reactions. Overwhelming the immune system with Coley toxins might cause a serious infection.</p> <h2>How much does Coley toxin therapy cost?</h2> <p>An adaptation of Coley toxins is <b>administered to patients at the Waisbren Clinic in Milwaukee, Wisconsin</b>. Dose schedules and costs vary with individual patients, but recently one injection of mixed bacterial vaccine cost $75. The cost per year is between $3,000 and $8,000.</p> <h2>For additional information:</h2> <p><strong>The University of Texas M. D. Anderson Cancer Center<br> </strong>1515 Holcombe Boulevard<br> Houston, TX 77030<br> Telephone: (800) 392-1611<br> Web site: <a href="http://www.mdanderson.org/departments/CIMER/" target="_blank">www.mdanderson.org/departments/CIMER/</a></p> <p><strong>Waisbren Clinic<br> </strong>Web site: <a href="http://www.waisbrenclinic.com/" target="_blank">www.waisbrenclinic.com/</a></p><p><br></p><br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-46005088815906959572011-05-10T06:13:00.000-07:002011-05-10T06:14:22.650-07:00must read! -- XGP - 15 cases Histology MicroscopyYear : 1989 | Volume : 35 | Issue : 4 | Page : 209-14<br><br>Xanthogranulomatous pyelonephritis--(a clinicopathological study of 15 cases)<br><br>BV Mittal, BP Badhe<br><br><b> :: Abstract </b><br><br>The clinico-pathological features of 15 patients with xanthogranulomatous pyelonephritis (XGP) are described and the probable histogenesis is discussed. Based on our data and the review of literature, we believe that XGP should be regarded as a destructive and at times tumefactive inflammatory process that may complicate chronic pyelonephritis. The initiation of this process remains obscure, but the features commonly associated with XGP are pelvi-calyceal obstruction, ulceration of the pelvic urothelium with collection of necrotic material and bacterial infection.<br> <br><br>How to cite this article:<br>Mittal BV, Badhe BP. Xanthogranulomatous pyelonephritis--(a clinicopathological study of 15 cases). J Postgrad Med 1989;35:209<br>How to cite this URL:<br>Mittal BV, Badhe BP. Xanthogranulomatous pyelonephritis--(a clinicopathological study of 15 cases). J Postgrad Med [serial online] 1989 [cited 2011 May 10];35:209. Available from: <a href="http://www.jpgmonline.com/text.asp?1989/35/4/209/5687">http://www.jpgmonline.com/text.asp?1989/35/4/209/5687</a><br> <br><b><br> :: Introduction <br></b><br>Xanthogranulomatous pyelonephritis (XGP) is an uncommon variant of bacterial infection of the kidney. It is characterised by accumulation of lipid laden macrophages in sufficient numbers to cause yellow nodules in the renal parenchyma, close to the pelvis. There is a destruction of the involved areas of the kidneys. Other characteristics like fibrosis extending into the perinephric fat, hydronephrosis and renal calculi are often observed. The condition is unilateral and results in a non-functioning kidney.<br> <br>To gain a better understanding into the pathogenesis of the process, we undertook this clinico-pathological study.<br><br><br> :: Material and methods <br><br>Fifteen cases diagnosed as XGP in the last 8 years (1980-1987) were included in the study. Clinical details were obtained from the patients' records. Fourteen patients had undergone a total nephrectomy, while partial nephrectomy was carried out in one case. All the specimens were fixed in 10% buffered formalin and processed for paraffin wax sectioning. The sections were stained with haematoxylin-eosin, elastic Van Gieson (EVG) and Pearl's stain for haemosiderin.<br> <br><br> :: Observations <br><br>The study comprised 8 males and 7 females. Fourteen cases were between 20 and 70 years of age (mean age 45 years). The youngest patient was 2 years old. Loin pain was the commonest presenting symptom, seen in 13 out of 15 cases (86.6%). Pyrexia and burning micturition were noted in 4 cases; one of these cases had recurrent attacks.<br> <br>On examination, renal angle tenderness could be elicited in 11 cases (73.3%). In 7 cases (46.6% ), a palpable lump associated with pyonephrosis and hydronephrosis was seen. In one case, perinephric abscess was drained prior to nephrectomy.<br> <br>On intravenous pyelography, non-functioning kidney was found in 14 cases (93.3%). Unascended kidney lying at L4-5 was seen in one case. Bifid ureter with hydronephrosis was seen in the paediatric patient. Obstructive lesions caused by renal calculi in the pelvis were present in 10 cases (66.6% ). One case had a ureteric calculus as well.<br> <br>Urine culture reports were available in 12 cases. Gram negative micro-organisms (E. coli in 5 cases, Proteus vulgaris in 2 cases and Klebsiella in one case) were isolated in 8 cases, while urine was sterile in 4 cases.<br> <br>Gross pathology<br><br>Ten specimens were from the right kidney, while 5 were from the left kidney. Perinephric abscess was seen in 2 specimens. Increased perinephric fat and adherent capsules were seen in 8 cases, while in 7 cases the capsule could be stripped off easily, indicating no spread of infection to the perinephric tissues. Calculi (staghorn or otherwise) were noted within the renal pelvicalyceal system in 10 cases. Ureteral calculus was seen in one case. A polypoid tumour was seen in the renal pelvis alongwith a calculus in one case. There was diffuse dilatation of the pelvi-calyceal system in all cases. The renal parenchyma was variably scarred and atrophic.<br> <br>Grossly visible, yellow, nodular areas varying from 2-10 mm in size were seen in 8 cases. These were close to the ulcerated, dilated pelvi-calyceal system. Areas of haemorrhage were noted in 5 cases.<br><br>Histological features observed are listed in[Table - 1].<br> <br>Focal ulceration of the urothelium with acute inflammation was universal. Them was a polymorphous inflammation with presence of lymphocytes, plasma cells admixed with neutrophils. There was a background of chronic pyelonephritis characterised by focal, variable renal tubular atrophy, fibrosis, chronic inflammation and tubular dilatation. Superimposed on this background, were the changes of XGP. These varied from small focal aggregates of foamy histiocytes below the urothelium to large, destructive, nodular lesions. The foci of XGP were composed of macrophages, some with eosinophilic granular cytoplasm. <b>In some cases, the foamy cells had the nucleus pushed to the periphery and resembled fat cells</b> [Figure - 1].<br> <br><img style="cursor: -moz-zoom-in;" alt="http://www.jpgmonline.com/articles/1989/35/4/images/jpgm_1989_35_4_209_5687_3.jpg" src="http://www.jpgmonline.com/articles/1989/35/4/images/jpgm_1989_35_4_209_5687_3.jpg" height="283" width="582"><br> <br>Focal squamous metaplasia of the urothelium, lining the pelvis was noted in 2 cases. Grade III transitional cell carcinoma with focal areas of squamous metaplasia was noted in yet another case [Figure - 2]. This tumour had spread to the ureter and to the hilar lymph nodes. All the three cases were associated with calculi in the pelvis.<br> <br><img style="cursor: -moz-zoom-out;" alt="http://www.jpgmonline.com/articles/1989/35/4/images/jpgm_1989_35_4_209_5687_4.jpg" src="http://www.jpgmonline.com/articles/1989/35/4/images/jpgm_1989_35_4_209_5687_4.jpg" height="287" width="583"><br> <br>EVG stained slides revealed a variable degree of intimal thickening and medial hypertrophy of the medium-sized vessels. There was no other arterial or venous abnormality seen. There was no evidence of thrombosis or phlebitis. Areas of haemorrhage, adjacent to the ulcerated pelvis and to the xanthomatous areas were seen in 5 cases. Cholesterol granulomas were seen in 3 of these [Figure - 3].<br> <br><img style="cursor: -moz-zoom-in;" alt="http://www.jpgmonline.com/articles/1989/35/4/images/jpgm_1989_35_4_209_5687_5.jpg" src="http://www.jpgmonline.com/articles/1989/35/4/images/jpgm_1989_35_4_209_5687_5.jpg" height="284" width="592"><br> <br><br>Extension of the XGP process to the ureter with presence of foamy cells and calcification were noted in one case. Inflammatory infiltrate extended to the perirenal fat in 8 cases.<br><br> :: Discussion <br><br>Since the first description of XGP by Schlagenhaufer in 1916 (quoted by Parsons et al[15]), more than 400 cases have been reported in the world literature;[20] the largest series being of 87 cases.[15] This is a rare, so called `inflammatory tumour' of the kidney, involving the calyces, renal parenchyma and renal sinus areas. Unlike chronic pyelonephritis, it may spread into the perinephric tissue with formation of abscesses and even fistula.<br> <br>Two other lesions, megalocytic interstitial nephritis (MIN) and malakoplakia have a common denominator with XGP, in the sense that they all represent varied histologic expressions of chronic renal disease. The hallmark of these lesions is the PAS positive, diastase resistant material in their cytoplasm. In addition to the histiocytes, one can identify a mixed cellular infiltrate composed of polymorphonuclear cells, plasma cells, lymphocytes and fibroblasts. Zollinger (quoted by Heptinstall)[21] described MIN as an extremely rare form of interstitial nephritis affecting mainly the renal cortex. XGP involves the cortex and medulla and is frequently associated with severe renal disease and calculi. Malakoplakia of the kidney is primarily a disease of the renal pelvis with involvement of renal parenchyma and Michaelis-Gutmann bodies are the characteristics of the lesion.[14] The lesions seen in all our cases involved the renal pelvis and the adjacent parenchyma but Michaelis-Gutmann bodies were not seen, hence they were labelled as XGP. Grossly visible, nodular, tumefactive lesions were noted in 53% of the cases while in the remaining cases, foamy cell collections were seen only on microscopic examination.<br> <br>The demographic and clinical features in cases of XGP as reported by various workers are presented in [Table - 2]<br><br>XGP is more common in females.[8],[13] It may occur at any age, in the paediatric population[19] as well as in elderly persons[12] In our series, the sex distribution was nearly equal (8 males and 7 females). The youngest patient seen by us was 2 years old.<br> <br>The lesion is generally unilateral and more often involves the right kidney.[13] In 10 of our 15 cases, the right kidney was involved. None of the cases had bilateral lesions. A non-functioning kidney, with stone and infection or a `tumourous' lesion. in the kidney, indistinguishable from a malignant tumour, are the usual presenting features.[13] Fourteen of the 15 cases that we studied, had a non-functioning kidney.<br> <br>Etiology of XGP remains obscure, though a number of factors have been incriminated as causative factors, viz. urinary tract obstruction,[13],[20] specific inflammatory agent, previous ineffective antibiotic treatment,[12] a block in lipid transport,[6] altered immunologic response,[7] lymphatic obstruction,[5] arterial insufficiency,[17] venous occlusion and haemorrhage[13] and necrosis of peri-calyceal fat.[13]<br> <br>We have analysed our data to find out the pathogenic features which are commonly encountered.<br><br>Urinary tract obstruction was observed in 13 of 15 cases. Calculi were noted in 11 cases, while abnormal ureteric openings in the, bladder were noted in 2 cases. Ulceration of the pelvi-calyceal urothelium with inflammatory infiltrate in the subepithelial area, extending into the parenchyma was noted in all cases. Thus, obstruction and infection seemed to be the commonest features.<br> <br>Experimentally, XGP has been successfully produced by permanent ligation of the ureter and a single intravenous injection of a suspension of E. coli 04: H5 strain.[16] Tan and Heptinstall[19] have also shown similar results with injections of P. mirabilis and Staphylococci. Obstruction and infection thus have been shown to be important factors.<br> <br>In majority of the reported cases, Gram negative bacterial infections, especially E. coli and Proteus species have been noted.[8] In some patients more than one organism[2] even Gram positive cocci (e.g. coagulase negative Staphylococcus aureus) have been incriminated. Occasionally, negative urine cultures are found. These may be due to previous antibiotic treatment. In our study, urine culture reports were available in 12 of the 15 cases; 4 cases revealed sterile urine, while Gram negative microorganisms (E. coli in 5 cases, Proteus vulgaris in two and Klebsiella in one) were isolated from the rest. These findings are in confirmity with the reported literature.<br> <br>Lipid laden cells are seen in these lesions. These foam cells may be PAS positive macrophages related in some way to the infective background. They appear to concentrate in the areas of destruction. The necrotic, purulent material is considered to be the main source of the lipid droplets, though a partial endogenous origin cannot be ruled out. Electron microscopic studies have revealed cytosomes containing myelin figures. Bacterial antigens may also be seen. No intrinsic abnormality of monocytes has been described in association with XGP, but Abdou and associates[1] described a patient with malakoplakia who had monocyte lysosomal abnormalities with decrease in cyclic guanyl monophosphate, corresponding to decrease in bactericidal activities. Since XGP and malakoplakia are related lesions, one cannot rule out the possibility of such an abnormality existing in XGP too. XGP has also been reported in native kidneys of patients with renal transplants receiving immunosuppressants.[4] Thus, abnormality in cellular immune response may be one of the causative factors.<br> <br>Foam cells, the hallmark of this disease process, have also been described in the ureter.[9] One of our cases, too, showed presence of foam cells and foci of calcification in the ureter. The origin of lipid in these cells is not from the lining epithelium, as unlike feline urothelium, normal human urothelial lining does not show presence of stainable fat.[18]<br> <b><br>The role of venous obstruction which can lead to haemorrhage has been emphasized by McDonald.[13] He has proposed that the released lipids from cellular elements undergo phagocytosis by histiocytes. We scanned the elastic Van Gieson stained sections for presence of venous, or arterial abnormalities, thrombi or phlebitis. Pearl stain for haemosiderin deposits was carried out, when fresh haemorrhage was not observed. No abnormal neovascularisation, lymphatic or vascular obstruction were noted in any of the cases. Evidence of haemorrhage, fresh or old, was seen in 5 cases. This was adjacent to the ulcerated pelvi-calyceal epithelium and was thought to be a part of acute on chronic inflammatory process rather than due to venous obstruction. Presence of cholesterol granulomas was observed in 3 cases. Though haemorrhage was present in one third of our cases, inflammatory component was predominant and present in all cases. As polymorphonuclear cells and red blood cells are commonly present in `pus' as well as in haemorrhage, the breakdown product of these cells seems to be a probable factor in the development of foam cells</b><br> <br>Three cases showed foci of squamous metaplasia of the pelvic urothelium. As metaplasias are known to occur in association with calculi, their presence alongwith XGP is not surprising. One of our cases with XGP had calculus obstruction, as well as transitional cell carcinoma (TCC) arising in the pelvis, with spread into the ureter and to the hilar lymph nodes. It is uncertain whether stones and chronic non-specific inflammatory conditions are important in the pathogenesis of cancer of the urothelium however, vesical calculi are common among patients with TCC. Similarly, association between TCC and XGP is known.[3]<br> <br>Reversible hepatic dysfunction has been noted in 50% of the cases by Malek et al.[12] No such abnormalities were noted in our cases.<br><br><b>Before XGP was recognised, the foamy cells were mistaken for renal tubular adenocarcinoma</b>; but even today one can encounter this <b>difficulty in differentiating it from carcinoma</b> while interpreting fine needle aspiration material.[8] Thus, taking into account the difficulties in a clinical, and even at times, histological diagnosis, nephrectomy rather than <b>segmental resection</b> seems advisable.<br> <br><br> :: Acknowledgement <br><br>We sincerely thank the Dean and the Head of the Dept. of Pathology, Seth G.S. Medical College, Parel, Bombay-400 012, for allowing us to use the medical records and the pathology material of K.E.M. Hospital.<br> <br><br><br> <br> :: References <br>1.Abdou, N. I., NaPombejara, C., Sagawa, A., Ragland, C., Stechschulte, D. J., Nilsson, U., Gourley, W., Watanabe, I., Lindsey, N. J, and Allen, M. S.: Malakoplakia: Evidence for monocyte lysosomal abnormality correctable by cholinergic agonist in vitro and in vivo New Engl. J. Med., 297: 1413-1419, 1977. <br> 2.Anhalt, M. A., Cawood, C. D. and Scott, R. Jr.: Xanthogranulomatous pyelonephritis: A comprehensive review with report of 4 additional cases. J. Urol., 105: 10-17, 1971. <br>3.Antonakopaulas, G. N., Chapple, C. R., Newman, J., Crocker, J., Tudway, D, C., Obrien, J. M. and Considine, J.: Xanthogranulomatous pyelonephritis. A reappraisal and immunohistochemical study. Arch. Pathol. Lab. Med., 112: 275-281, 1988. <br> 4.Carson, C. C. and Weinerth, J. L.: Xanthogranulomatous pyelonephritis in renal transplant recipient. Urology, 23: 58-61, 1984. <br>5.Dinn, J. J.: Xanthogranulomatous pyelonephritis. Irish J. Med. Sci., 1: 431-440. 1968. <br> 6.Friedenberg, M. .I. and Spjut, H. J.: Xanthogranulomatous pyelonephritis. Amer. J. Roentgenol., 90: 97-108, 1963. <br>7.Gammill, S., Rabinowitz, J., G., Peace, R., Surgen, S., Hurwitz, L. and Himmelfarb, E.: New thoughts concerning xanthogranulomatous pyelonephritis (X-P). Amer. J. Roentgenol., 125: 154-163, 1975. <br> 8.Grainger, R. G., Longstaff, A. J. and Parsons, M. A.: Xanthogranulomatous pyelonephritis: a reappraisal. Lancet, 1: 1398-1401, 1982. <br>9.Katchy, K. C. and Khwaja, S.: Xanthogranulomatous pyelonephritis with bilharzial ureteric obstruction. East Afr. Med. J.. 60: 645-648, 1983. <br> 10.Kierce, F., Caroll, R. and Guiney, E. J.: Xanthogranulomatous pyelonephritis in childhood. Brit. J. Urol., 57: 261-264, 1985. <br>11.Latham, H. S. and Kay, S.: Malignant tumours of the renal pelvis. Surg. Gynaecol. and Obstet., 138: 613-622, 1974. <br> 12.Malek, R. S. and Elder, J. S.: Xanthogranulomatous pyelonephritis: a critical analysis of 26 cases and of the literature. J. Urol., 119: 589-593, 1978. <br>13.McDonald, G. S. A.: Xanthogranulomatous pyelonephritis. J, Pathol. 133: 203-213, 1981. <br> 14.Michaelis, R. and Gutmann, C.: Uber Einschle SSC in Blasentumoren. Z. Clin. Mea., 47: 208, 1902; as quoted by Heptinstall, R. If. in `Pathology of the Kidney", Vol. III, 3rd edition, Little Brown and Co., Boston, Toronto, 1983, p. 1384. <br> 15.Parsons, M. A., Harris, S. C., Longstaff, A. J. and Grainger, R.: Xanthogranulomatous pyelonephritis: a pathological, clinical and aetiological analysis of 87 cases. Diagn. Histopathol., 6: 203-219, 1983. <br>16.Povysil, C. and Konickowa, L.: Experimental xanthogranulomatous pyelonephritis. Invest. Urol., 9: 313-318, 1972. <br> 17.Saeed, S. M. and Fine, G.: Xanthogranulomatous pyelonephritis. Amer. J. Clin. Pathol., 39: 616-625, 1963. <br>18.Scott, G. B. D. and Quigley, P. J.: Xanthogranulomatous pyelonephritis. A comparison of the disease in the cat and man with special reference to the origin of the fat. J. Clin. Pathol., 25: 397-400, 1972. <br> 19.Tan, H. K. and Heptinstall, R. H.: Experimental pyelonephritis. A light and electron microscopic study of the periodic acid-schiff positive interstitial cell. Lab. Invest., 20: 62-69, 1969. <br>20.Tolio., B. M., Iloreta, A., Freed, S. Z., Fruchtman, B., Bennett, B. and Newman, H. R.: Xanthogranulomatous pyelonephritis: Detailed analysis of 29 cases and a brief discussion of atypical presentations. J. Urol., 126: 437-442, 1981. <br> 21.Zollinger, H. U.: Die Interstitie Ile Nephritis Basall Kargen 1945 as quoted by Heptinstall, R. H. in `Pathology of the Kidney', Vol. III, 3rd edition, Little Brown & Co. Boston, Toronto, 1983, p. 1386. <br> <br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-65210893112909613602011-05-07T06:02:00.000-07:002011-05-07T06:53:20.768-07:00Coley GERMAN info. 19yr old girl - 1953 - 1963 - 1990the excellent <a href="http://ESOWATCH.COM">ESOWATCH.COM</a> wiki is down. wikipedia germany has this info: <a href="http://de.wikipedia.org/wiki/Esowatch">http://de.wikipedia.org/wiki/Esowatch</a><br>Esowatch do get attacked by esoteric people through the courts. But Esoteric people could send tele kynetic, mental-power death rays and bad spells, right? <br> BTW <a href="http://esowatch.org/">http://esowatch.org/</a> is a fake, probably operated by the detractors.<br><br>(Maybe not so) Amazingly, their verdict of Coley's Toxins is neutral, apart from one quote that descirbes CT as "without effect". <br> <br>Here the german article:<br><b><br>Coley-Therapie</b><br><br>foto William Coley im Jahre 1892<br><br>Die Coley-Therapie ist eine mittlerweile in Vergessenheit gelangte Methode aus dem Bereich der unkonventionellen Krebstherapien, die auf den amerikanischen Chirurgen William Coley (1862-1936) zurückgeht (nicht zu verwechseln mit seinem Sohn William Bradley Coley der ebenfalls Chirurg war).<br> <br>Die Coley-Methode zielt darauf ab, das Immunsystem des Kranken derart zu beeinflussen, dass es unter Fieber zu einer spontanen Remission der Krebserkrankung kommt. Das heute nicht anerkannte Verfahren kann zu den Immuntherapien bei Krebs und Fiebertherapien gezählt werden und als eine Form der therapeutischen Hyperthermie angesehen werden. Das Verfahren hat sich nicht bewähren können und gilt heute als wirkungslos.[1] Nach dem Tode von Coley im Jahre 1936 engagierte sich seine Tochter Helen Coley Nauts weiter für das Coley-Verfahren.<br> <br>Der auch heute praktizierte Einsatz einer BCG-Impfung bei einigen Krebserkrankungen (Blasenkrebs) hat mit dem Coley-Verfahren nur am Rande zu tun und ist wegen Nachweises einer Wirksamkeit wissenschaftlich anerkannt.[2][3]<br> <br>William Coley<br><br>1888 hatte Coley erfolglos eine neunzehnjährige Patientin mit einem Knochkrebs (Sarkom) behandelt. Die New Yorker Patientin verstarb jedoch trotz Amputation eines Armes. Die Patientin namens Elizabeth Dashiell war eine Kindheitsfreundin von John D. Rockefeller, Jr. Ihr Tod veranlasste Rockefeller später Geldmittel für die Krebsforschung zu spenden. Coley soll der Legende nach sodann alle Krankenakten der letzten 15 Jahre in seinem Krankenhaus (dem späteren renommierten Memorial Sloan-Kettering Cancer Center) nach Therapieerfolgen bei Knochenkrebs durchmustert haben. Er stieß auf einen Patienten deutscher Herkunft mit Namen Stein, der mit Knochenkrebs an einem Erysipel erkrankte und später von Krebs gesundete. Coley machte den inzwischen entlassenen Patienten wieder einige Wochen später ausfindig und fand geraus daß sein Zustand sich nicht wieder verschlechtert hatte. Das Erysipel ist eine Infektion der Haut durch die Bakterie Streptococcus pyogenes. Auch glaubte Coley erkannt zu haben, dass Krebspatienten eine höhere Überlebenswahrscheinlichkeit zu Zeiten hatten, bevor antiseptische und sterilisierende Massnahmen in der Chirurgie Einzug hielten. Coley versuchte dann einen analogen Heilungsverlauf bei anderen Krebspatienten durch eine gezielte Infektion mit dieser Streptokokkenart zu erreichen, dies noch zu Zeiten, als wirksame Antibiotika für den Fall einer lebensbedrohlichen Infektion unbekannt waren. Seine ersten Versuche verliefen erfolglos, und mindestens zwei seiner ersten Versuchspatienten verstarben an der künstlich gesetzten Streptokokkeninfektion.[4] Später setzte er Streptokokkenkulturen ein sowie bakterielle Toxine und berichtete über einen Erfolg.[5] Der Pharmahersteller Parke-Davis begann auch mit der Produktion des Coley Toxin.<br> <br>Coley Toxin / Vaccineurin<br><br>Das von Coley entwickelte Mittel wurde als Coley toxin, Coley fluid und Coly vaccine bekannt. Um gefährliche und potentiell tödliche Streptokokkeninfektionen zu vermeiden, verwendete er schließlich sterilisierte, abgetötete Streptokokkenkulturen, die er mit Bakterien der Gattung Serratia marcescens vermischte. Diese Mischung wurde als eigentliches Coley Toxin bekannt. Allerdings wurden im Laufe der Zeit mindestens 13 verschiedene Präparate entwickelt. Auch die Applikation wurde laufend verändert. Mal wurde das Mittel intravenös angewandt, oder intramuskulär oder direkt in den Tumor gespritzt.<br> <br>Das Coley Toxin wurde auch von der kleinen deutschen Firma Südmedica hergestellt und als Vaccineurin bis zum Jahr 1990 verkauft, als die Zulassung nicht erneuert wurde.<br><br>Kritik an Coley<br><br>Zu Lebzeiten von Coley war seine Methode trotz der damals noch weniger effektiven anerkannten Behandlungsmethoden umstritten und Coley musste sich wegen erfolgloser Behandlungen mit seinem Coley-Toxin durch andere Ärzte dem Vorwurf gefallen lassen, als Scharlatan bezeichnet zu werden. Ihm wurde insbesondere vorgeworfen selektiv Behandlungserfolge zu zitieren und seine behandelten Patienten nicht in einem follow-up längerfristig weiter zu beobachten. Eine Kritik zu Ende des 19. Jahrhunderts war beispielsweise in einem Artikel der JAMA von 1894 zu finden, der auf eine fehlende Replizierung von Coleys Erfolgen hinwies. Im JAMA Leitartikel heißt es dazu wörtlich: "There is no longer much question of the entire failure of the toxin injections, as a cure for sarcomata and malignant growths. During the last six months the alleged remedy has been faithfully tried by many surgeons, but so far not a single well-authenticated case of recovery has been reported." [6] 1934 war ein weiterer Leitartikel der JAMA optimistischer formuliert[7] und verwies auf die Möglichkeit einzelner spontaner Remissionen durch die Coley-Mittel. In den 1920er Jahren wurden Coleys Behandlungserfolge auch vom Bone Sarcoma Registry skeptisch gesehen, das als eines der ersten Krebsregister versuchte, alle bekannten Krebsfälle zu registrieren und zu analysieren.[8] Man zweifelte bei den Behandlungsfällen von Coley auch die jeweils vor Behandlung gestellten Diagnosen an. 1953 wurde in den USA die Produktion der Coley-Toxine untersagt und 1962 verbot die Food and Drug Administration FDA das Coley Toxin endgültig.[9]<br> Literatur<br><br> * Burdick CG. WILLIAM BRADLEY COLEY 1862-1936. Ann Surg. 1937 Jan;105(1):152-5.<br> * Wiemann B, Starnes CO. Coley's toxins, tumor necrosis factor and cancer research: a historical perspective. Pharmacol Ther. 1994;64(3):529-64. <br> <br>Weblinks<br><br> * <a href="http://en.wikipedia.org/wiki/Coley%27s_Toxins">http://en.wikipedia.org/wiki/Coley%27s_Toxins</a><br> * <a href="http://www.cancer.org/docroot/ETO/content/ETO_5_3X_Coley_Toxins.asp?sitearea=ETO">http://www.cancer.org/docroot/ETO/content/ETO_5_3X_Coley_Toxins.asp?sitearea=ETO</a><br> * <a href="http://www.mdanderson.org/departments/CIMER/display.cfm?id=43EF7F2C-0DAF-11D5-810D00508B603A14&method=displayFull&pn=6EB86A59-EBD9-11D4-810100508B603A14">http://www.mdanderson.org/departments/CIMER/display.cfm?id=43EF7F2C-0DAF-11D5-810D00508B603A14&method=displayFull&pn=6EB86A59-EBD9-11D4-810100508B603A14</a><br> * <a href="http://www.reuters.com/article/health-SP/idUSWNAS439120070620">http://www.reuters.com/article/health-SP/idUSWNAS439120070620</a> <br><br>Quellennachweise<br><br> 1. ? Levine DB. The Hospital for the Ruptured and Crippled: William Bradley Coley, Third Surgeon-in-Chief 1925-1933. HSS J. 2008 Feb;4(1):1-9. 15. Dezember 2007<br> 2. ? Gkialas I, Kalantzis A, Lykourinas M. The response of urological tumours to immunotherapy. J BUON. 2005 Jul-Sep;10(3):329-36<br> 3. ? Razack AH. Bacillus Calmette-Guerin and bladder cancer. Asian J Surg. 2007 Oct;30(4):302-9<br> 4. ? Edward F McCarthy. The Toxins of William B. Coley and the Treatment of Bone and Soft-Tissue Sarcomas. Iowa Orthop J. 2006; 26: 154–158. [1]<br> 5. ? Coley WT. The treatment of malignant tumors by repeated inoculations of erysipelas: with a report of ten original cases. Am J Med Sci 1893;105:487-511<br> 6. ? Editorial. The Failure of the Erysipelas Toxins. JAMA. 1894;24:919<br> 7. ? Erysipelas and Prodigiosus Toxins (Coley). JAMA. 1934 Oct 6;103(14):1067–1069. Editorial.<br> 8. ? McCarthy, EF. The registry of bone sarcoma: a history. Iowa Orthop J. 1995;15:74–78<br> 9. ? Hoption-Cann, SA; van Netten, JP, et al. Dr William Coley and tumour regression: a place in history or in the future. Postgrad Med J. 2003;79(938):672–680<br><br><br>Südmedica GmbH Chem. Pharm. Fabrik, Pharm. Handelsges.<br> Ehrwalderstr. 21<br>81377 München<br>Postanschrift:<br>Postfach 701669<br>81316 München<br><br>Tel.: 089-7144061<br>Fax: 089-7192950<br><br>Internet: <a href="http://www.suedmedica.de">www.suedmedica.de</a><br>E-Mail: <a href="mailto:info@suedmedica.de">info@suedmedica.de</a><br> <br><br> Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-325005598080713936.post-69267558625931995692011-04-29T10:57:00.001-07:002011-04-29T10:57:27.809-07:00XGP Antibiotica treatment LIEGE CIPRO full text - french original paper<div id="titles"> <p id="absttl">A case of Xanthogranulomatous Pyelonephritis managed conservatively</p> <li>Parthasarathy <span class="PrName">Shanmugasundaram</span>, Wollongong Hospital, Australia</li> <li>Dr Maureen <span class="PrName">Lonergan</span>, Wollongong Hospital, Australia</li> <div class="abstxt"><p>Xanthogranulomatous Pyelonephritis (XPN) is a rare form of pyelonephritis characterised by massive destruction of the kidneys often requiring nephrectomy. An 80-year non-diabetic lady presented to the Emergency Department with severe obtundation, reduced oral intake and falling urine. In the past she had episodes of dysuria but no urolithiasis or obstructive uropathy. She was dehydrated, hypotensive BP and afebrile. Her initial results:- serum creatinine 690 umol/L, urea 47.6 mmol/L, potassium 5.4 mmol/L, blood sugar 4.3 mmol/L, albumin 20 g/L, bicarbonate 7 mmol/L and haemoglobin 68 g/L. The urine was grossly pyuric and grew Pseudomonas aeruginosa and Proteus mirabilis. A non-contrast CT of the abdomen demonstrated a small and irregular left kidney but the right kidney was replaced by a large, predominantly hypodense mass with extensive calcification and dilated pelvicalyceal system, features consistent with XPN. The ureter was dilated to the vesico-ureteric junction. Retrograde ureteric stenting was attempted but was unsuccessful. Debris was dislodged. The patient was managed with inotropes, fluids and antibiotics, vancomycin and <b> timentin </b>empirically then <b>ciprofloxacin </b>replacing the former. She also received blood transfusion and intravenous bicarbonate. Her general well-being and renal function improved. Her serum creatinine fell to 168 umol/L at 4 weeks without the need for dialysis. Eleven weeks later the right kidney measured 7.1cms and the left 8.0 cms in length on the ultrasound. Hydronephrosis had improved on the right. Presently she continues to maintain a stable although impaired renal function. Our case demonstrates successful conservative management of XPN, which almost inevitably necessitates nephrectomy.</p></div><br><br><h1 id="page_title">Pyélonéphrite xanthogranulomateuse pseudotumorale : diagnostic par la biopsie percutanée et succès du traitement conservateur</h1> </div> <div class="tx-axdocdb-pi1-singleView-authors">REUL O, WALTREGNY D, BOVERIE J, LEVAL J, ANDRIANNE R</div><div class="tx-axdocdb-pi1-singleView-reference">Prog Urol, 2001, 11, 6, 1274-1276</div><div class="tx-axdocdb-pi1-singleView-category"> Cas clinique</div><div class="tx-axdocdb-pi1-singleView-title">Résumé</div><div class="tx-axdocdb-pi1-abstract-fr"> La pyélonéphrite xanthogranulomateuse est une forme inhabituelle d'infection rénale dont le diagnostic est souvent méconnu avant l'intervention chirurgicale. Nous rapportons le cas d'une jeune fille âgée de 19 ans qui présentait une masse rénale pseudotumorale. Le diagnostic de pyélonéphrite xanthogranulomateuse focale a été suspecté par les caractéristiques de la masse aux différents examens d'imagerie médicale et confirmé par l'analyse histologique d'un fragment prélevé par une biopsie percutanée échoguidée. La guérison a été obtenue avec un traitement antibiotique. Une exploration exhaustive comprenant une biopsie rénale devrait être réalisée afin de poser le diagnostic de pyélonéphrite xanthogranulomateuse avant tout geste chirurgical. Nous préconisons le traitement antibiotique comme traitement de première intention de la pyélonéphrite xanthogranulomateuse focale. </div> <div class="tx-axdocdb-pi1-text-fr"> <h2>Observation</h2> Une jeune fille âgée de 19 ans a été adressée à notre hôpital pour des douleurs lombaires droites importantes, permanentes, présentes depuis 3 semaines et en aggravation depuis 3 jours. Lors de son admission, la patiente était apyrétique et ne signalait aucun symptôme urinaire. Elle n'avait pas d'antécédents d'infection urinaire ou de lithiase. L'examen clinique était sans particularité hormis un point douloureux costo-musculaire droit. Il n'y avait pas d'organomégalie ni de contact lombaire au palper bimanuel. Sur le plan biologique, il n'y avait pas d'anomalie à l'exception d'une élévation de la CRP à 49 mg/l. La leucocytose était de 9780/mm3 dont 64% de neutrophiles et l'hémoglobine est de 12.3g/dl. La fonction rénale était conservée avec une urémie de 0.2 g/l et une créatinémie de 8 mg/l. La culture urinaire était stérile. <br><br>L'échographie rénale a objectivé une masse hétérogène de 5 cm de diamètre au pôle inférieur du rein droit tandis que le rein gauche avait un aspect normal. La tomodensitométrie abdominale a confirmé la présence d'une lésion de 5 cm à zone centrale hétérogène et hypodense entourée d'une coque rehaussée par l'injection de produit de contraste (Figure 1). <div class="tx-axdocdb-pi1-imageAndLegend"><table> <tbody><tr><td class="tx-axdocdb-pi1-legend">Figure 1 : Lors du diagnostic, présence à l'examen tomodensitométrique d'une masse hétérogène à centre hypodense et rehaussée en périphérie par le produit de contraste. Lésion similaire de petite taille au pôle inférieur du rein droit.</td></tr> <tr><td class="tx-axdocdb-pi1-image"><img src="http://www.urofrance.org/fileadmin/documents/data/PU/2001/PU-2001-00111274/Images/Image4.jpg"></td></tr> </tbody></table></div> Une seconde lésion de 1 x 1,2 cm de mêmes caractéristiques densitométriques était visible à la partie antérieure du pôle inférieur du rein droit. A l'artériographie rénale sélective, la lésion était hypovascularisée avec étirement des vaisseaux en périphérie sans caractéristique de vascularisation anarchique tumorale (Figure 4). <div class="tx-axdocdb-pi1-imageAndLegend"><table> <tbody><tr><td class="tx-axdocdb-pi1-legend">Figure 4 : Masse hypovascularisée avec étirement des vaisseaux en périphérie à l'artériographie rénale sélective.</td></tr> <tr><td class="tx-axdocdb-pi1-image"><img src="http://www.urofrance.org/fileadmin/documents/data/PU/2001/PU-2001-00111274/Images/Image1.jpg"></td></tr> </tbody></table></div> L'urographie intraveineuse puis la pyélographie rétrograde, l'UIV étant insuffisante, ont révélé un syndrome de masse avec refoulement des tiges calicielles inférieures. <br><br>Nous avons réalisé deux biopsies percutanées de la lésion la plus volumineuse sous guidage échographique. L'analyse anatomo-pathologique a révélé un envahissement du parenchyme rénal par un infiltrat inflammatoire chronique formé de macrophages d'aspect spumeux associés à des monocytes, lymphocytes et de la fibrose. Cet aspect était compatible avec le diagnostic de pyélonéphrite xanthogranulomateuse. La culture de la deuxième biopsie était positive pour des E. Coli, sensibles aux quinolones. La patiente a été traitée pendant cinq semaines par de la ciprofloxacine per os à raison de 250 mg 2 fois par jour. Une réduction considérable du volume de la masse a été observée à l'examen tomodensitométrique réalisé après un mois de traitement (Figure 2). <div class="tx-axdocdb-pi1-imageAndLegend"><table> <tbody><tr><td class="tx-axdocdb-pi1-legend">Figure 2 : Après un mois de traitement, diminution importante de la taille des lésions en tomodensitométrie abdominale</td></tr> <tr><td class="tx-axdocdb-pi1-image"><img src="http://www.urofrance.org/fileadmin/documents/data/PU/2001/PU-2001-00111274/Images/Image2.jpg"></td></tr> </tbody></table></div> Trois mois plus tard, la tomodensitométrie a révélé des zones cicatricielles au niveau des sites des deux lésions initiales (Figure 3). <div class="tx-axdocdb-pi1-imageAndLegend"><table> <tbody><tr><td class="tx-axdocdb-pi1-legend">Figure 3 : Aspect cicatriciel au contrôle tomodensitométrique après 4 mois.</td></tr> <tr><td class="tx-axdocdb-pi1-image"><img src="http://www.urofrance.org/fileadmin/documents/data/PU/2001/PU-2001-00111274/Images/Image3.jpg"></td></tr> </tbody></table></div> Durant les douze mois suivants, aucune récidive n'a été constatée. L'échographie, à un an, était normale <h2>Discussion</h2> La pyélonéphrite xanthogranulomateuse est une forme de suppuration rénale chronique survenant à tout âge, le plus souvent après 40 ans et touchant trois fois plus fréquemment les femmes que les hommes. La forme focale est de diagnostic difficile car elle est souvent confondue avec un processus néoplasique. L'étiopathogénie de la pyélonéphrite xanthogranulomateuse n'est pas connue avec certitude mais plusieurs facteurs étiologiques ont été incriminés dont l'obstruction de la voie excrétrice (lithiase, sténose, tumeur, ...), l'infection urinaire récidivante plus ou moins décapitée par les antibiothérapies et les déficits immunitaires [5] Aucun des ces facteurs n'est présent dans notre observation. <br><br>Les patients souffrant de pyélonéphrite xanthogranulomateuse focale présentent classiquement une douleur intermittente du flanc, de la fièvre, des frissons ou une altération de l'état général avec perte de poids. La symptomatologie dure habituellement depuis plusieurs semaines avant que le diagnostic ne soit posé. <br><br>Sur le plan biologique, on note des signes d'infection avec élévation des tests inflammatoires (C reactive protein, vitesse de sédimentation, fibrinogène) et hyperleucocytose. La culture urinaire est stérile dans 50 % des cas de pyélonéphrite xanthogranulomateuse mais la culture du tissu rénal est presque toujours positive, comme dans notre observation. Les bactéries les plus souvent en causes sont le Proteus Mirabilis et l'E.Coli. <br><br>La pyélonéphrite xanthogranulomateuse focale doit être suspectée à l'examen tomodensitométrique qui révèle classiquement une masse hétérogène centrée sur une tige calicielle et faiblement rehaussée en périphérie par le produit de contraste [7]. L'absence de lymphonoeuds pathologiques, de thrombus veineux ou de métastases sont des signes importants pour orienter le diagnostic. L'échographie rénale, l'urographie intraveineuse et la pyélographie rétrograde révèlent un syndrome de masse aspécifique. Même si la tomodensitométrie abdominale et l'artériographie ont permis de suspecter fortement la nature inflammatoire et non tumorale des lésions rénales dans le cas présenté, ces deux examens ne peuvent pas exclure formellement le diagnostic de lésion néoplasique. Nous avons donc opté pour la biopsie percutanée de la masse rénale, ce qui a permis de confirmer le diagnostic de pyélonéphrite xanthogranulomateuse. <br><br>Le traitement habituel de la pyélonéphrite xanthogranulomateuse focale est malheureusement souvent la néphrectomie totale ou partielle [3]. Cette approche thérapeutique est attribuable à un diagnostic préopératoire rarement correctement posé [4]. Le traitement conservateur de la pyélonéphrite xanthogranulomateuse pseudotumorale par une antibiothérapie seule est donc une exception, avec de rares cas décrits dans la littérature [1, 2, 6] Pour ces cas décrits comme dans le nôtre, le traitement médical s'est avéré efficace avec une résolution complète des lésions rénales. <br><br>Nous pensons donc qu'une exploration exhaustive suivie d'une biopsie percutanée pourrait être réalisée afin de poser le diagnostic de pyélonéphrite xanthogranulomateuse focale avant tout geste chirurgical. De plus, la culture des biopsies rénales permet d'identifier les micro-organismes en cause et d'adapter le traitement en fonction de l'antibiogramme. Nous suggérons l'utilisation du traitement antibiotique comme traitement de première intention de la pyélonéphrite xanthogranulomateuse focale à condition qu il n'y ait pas de pathologie obstructive sous-jacente telle qu'une lithiase ou une lésion des voies excrétrices. <h2> <br><br>REFERENCES</h2> <h2>Références</h2> <div class="tx-axdocdb-pi1-references"> 1. AIZAWA T., KURATA M., OHKUBO Y. A case of xanthogranulomatous pyelonephritis followed by computed tomographic scan. Hinyokika Kiyo, 1998, 44, 729-732. <br><br>2. BROWN P.S. Jr, DODSON M., WEINTRUB P.S. Xanthogranulomatous pyelonephritis: report of nonsurgical management of a case and review of the literature. Clin. Infect. Dis., 1996, 22, 308-314. <br><br>3. CHUANG C.K., LAI M.K., CHANG P.L.,HUANG M.H., CHU S.H., WU C.J., WU H.R. Xanthogranulomatous pyelonephritis: experience in 36 cases. J. Urol., 1992, 147, 333-336. <br><br>4. EASTHAM J., AHLERING T., SKINNER E. Xanthogranulomatous pyelonephritis: clinical findings and surgical considerations. Urology, 1994, 43, 295-299. <br><br>5. MALEK R.S., ELDER J.S. Xanthogranulomatous pyelonephritis: A critical analysis of 26 cases and of the literature. J. Urol., 1977, 119, 589-593. <br><br>6. MOLLIER S., DESCOTES J.L., PASQUIER D., COQUILLAT P., MICHEL A., DALSOGLIO S., RAMBEAUD J.J. Pseudoneoplastic xanthogranulomatous pyelonephritis. A typical clinical presentation but unusual diagnosis and treatment. Eur. Urol., 1995, 27, 170-173. <br><br>7. SHAH M., HAAGA J.R. Focal xanthogranulomatous pyelonephritis simulating a renal tumor: CT characteristics. J. Comput. Assist. Tomogr., 1989, 13, 712-713.<br><br></div> </div> Unknownnoreply@blogger.com0