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Found 15 results

  1. Celiac.com 08/31/2017 - A possible mechanism behind the cause of refractory celiac disease and why fecal transplantation (fecal microbiota transfer) may provide a cure was presented in "Synthetic Stool May Advance Fecal Transplant Therapy for Celiac Disease" 02/13/2013.[1] In September 2016, the article "Serendipity in Refractory Celiac Disease: Full Recovery of Duodenal Villi and Clinical Symptoms after Fecal Microbiota Transfer" was published in the Journal of Gastrointestinal and Liver Disease[2] describing the first known case of refractory celiac disease cured by a fecal transplant. The patient in that case was being treated for a recurrent Clostridium difficile infection. This very important milestone article somehow missed the light of the news media at that time. The 68-year old woman patient was a 10-year diagnosed victim of refractory celiac disease on a gluten-free diet. On admission for treatment of severe diarrhea, the patient exhibited Marsh IIIA villous atrophy. The patient was already receiving on-going treatment for refractory celiac disease with drugs. Additional drugs and antibiotics were given to treat the diarrhea. Eventually, the patient tested positive for C. difficile. Antibiotics were ineffective to treat the recurrent C. difficile infection. A fecal microbiota transfer was then performed. The C. difficile infection and diarrhea resolved, and, 6 months after the fecal transplant, villous atrophy resolved and went to Marsh 0. All symptoms of refractory celiac disease were eliminated. The patient remains symptom free on a continuing gluten-free diet. The case clearly demonstrates the need to fully investigate the use of fecal microbiota transfers to treat celiac disease. As suggested in my earlier reference[1], a standardized synthetic stool should be developed to enable full scale clinical trials. Also a full scale research effort into completely healing and restoring the intestinal mucosa with the novel protein R-spondin1 needs to be funded and restarted. Sources: 1. Synthetic Stool May Advance Fecal Transplant Therapy for Celiac Disease. Roy S. Jamron. Celiac.com 2013 Feb 13. 2. Serendipity in Refractory Celiac Disease: Full Recovery of Duodenal Villi and Clinical Symptoms after Fecal Microbiota Transfer. van Beurden YH, van Gils T, van Gils NA, Kassam Z, Mulder CJ, Aparicio-Pages N J Gastrointestin Liver Dis. 2016 Sep;25(3):385-8.
  2. Celiac.com 07/11/2016 - Collagenous sprue is a rare form of small bowel enteropathy characterized by a thickened basement membrane and is considered to be directly related to celiac disease. Doctors have numerous treatment strategies for celiac sprue, but there is currently no effective standardized therapy. One medical team recently described four cases of celiac sprue and proposes thioguanine (6-TG) treatment, based on their results. The research team included Tom van Gils, Tine van de Donk, Gerd Bouma, Foke van Delft, E Andra Neefjes-Borst, and Chris JJ Mulder. They are variously affiliated with the Department of Gastroenterology and Hepatology, VU University Medical Center, Amsterdam, The Netherlands, Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands. The team reviewed 4 cases of celiac sprue. They got their data from the prospective database of patients referred to their celiac centre. The team had an expert pathologist evaluate the small bowel biopsies. None of the patients had ever shown celiac-specific antibodies, and all were negative for HLA-DQ2 and HLA-DQ8 phenotype. Three patients were treated with a combination of 6-TG and budesonide, and 1 patient received 6-TG only. All patients improved remarkably. They found normalized thickening of the basement membrane in 2 patients, and complete histological improvement, including full recovery of villi, in 1 patient. In the third patient, the thickened basement membrane was only very focally recognized. The thickened membrane remained in the last patient, likely due to the short follow-up time. Celiac sprue should be separated from celiac disease. Based on the lack of typical HLA phenotyping and the absence of celiac-specific antibodies, there seems to be no relation with celiac disease in these four patients. A promising treatment option might be 6-TG with or without budesonide. Larger study groups are needed to develop an effective standardized treatment for celiac sprue. This is exciting for folks with celiac sprue, as they previously had no good treatment options at all. Source: BMJ Open Gastro 2016; 3:e000099. doi:10.1136/bmjgast-2016-000099
  3. This article originally appeared in the Spring 2003 edition of Celiac.com's Scott-Free Newsletter. Refractory sprue. The specter of this condition is enough to cause fear in the hearts of many people living with celiac disease, yet this fear is based more on myth and misunderstanding than on medical science. For those who are concerned about their risk for developing refractory sprue, there is much that can be done. For those who have developed the condition, there are treatment options and new hope on the horizon. To begin, however, we must substitute fear with knowledge. What is refractory sprue? This question has been the subject of great scientific inquiry, and there are differing opinions on the relationship between celiac disease and refractory sprue. However, there are several general characteristics of refractory sprue that researchers seem to agree on: Presence of persistently damaged villi in the small intestine that are not repaired after the gluten free diet has been successfully initiated and/or maintained An increased presence of intraepithelial lymphocytes (IEL) in the small bowel Severe malabsorption Researchers think of celiac disease as the beginning of a spectrum of conditions that could, for a small percentage of patients, end up at the other end to be enteropathy associated T-Cell Lymphoma. Most people with celiac disease will respond to the gluten free diet and never move to the next stage in this spectrum. But for those that do, they will experience changes in their immune system and in the cells lining their intestine that could lead to cancer. The spectrum would start with celiac disease, and the next step would be the non-responsiveness of the immune system to the gluten-free diet, in other words, refractory sprue. Then in some cases, a condition called ulcerative jejunitis develops, and finally, the damaged lining of the intestine produces cancer cells that mimic the mutations of the abnormal immune system cells. How many people with celiac disease are affected by refractory sprue? First, there are no reported cases in the medical literature of celiac sprue in people under 20 years of age. Second, the number of celiacs affected by refractory sprue, while not known, appears to be very small. We know this because the current estimates for small bowel cancers in people affected by celiac disease, as reported at the 10th International Conference on Celiac Disease is less than 2.5%. Refractory sprue can result in small bowel cancers, but not in all cases. It is interesting to note that in a recent study of patients with "unresponsive" celiac disease, Dr. Joseph Murray and his colleagues found that of 49 patients evaluated, only nine actually had refractory sprue—25 were found to have gluten contamination in their diets. The most common symptoms presented by the patients who truly had refractory sprue were weight loss, steatorrhea and diarrhea, in that order. What makes refractory sprue different than celiac sprue? Again, there are several medical points of view on this, but all researchers would agree that one marker indicates the presence of refractory sprue, and it is not found in celiac disease. Abnormal Intraepithelial Lymphocytes (Immune Cells) The intraepithelial lymphocytes found in celiac disease have a normal-looking appearance under the microscope and they behave like normal celiac immune cells (they respond to gluten when they shouldnt). These lymphocytes have the ability to communicate with other cells using different types of messages on their cell surfaces. When diagnosing celiac disease, pathologists look for an increased number of IELs as an indication of celiac disease. In refractory sprue, however, there is a different kind of IEL that is found in great numbers. This immune cell does not look normal, and it ignores the presence or absence of gluten. This type of cell does not have the ability to communicate normally with other cells as it would be expected to do. However, it does have the ability to communicate with cancer cells, contributing to their development. It is not clear what causes this type of IEL to develop or mutate, contributing to refractory sprue. It is possible to have refractory sprue without having these abnormal lymphocytes; in this case, treatment with steroids often results in response to the gluten free diet and a reversal of the condition. French researchers have developed a test to determine whether a biopsy specimen reflects a normal course of celiac disease with a slow response to the diet, or the need for further testing because refractory sprue may be present. In paraffin wax, a specimen can be stained to determine whether or not the immune cells express CD8, a protein often found on intraepithelial lymphocytes in celiac disease. If CD8 is positive, the individual has celiac and is responding very slowly to the diet. If the sample is CD8 negative, refractory sprue could be the reason. How is refractory sprue diagnosed and treated? It must be established through a thorough diet history and antibody testing that the individual is adhering to a strict gluten-free diet. Then, all other gastrointestinal diseases have to be ruled out before a diagnosis of refractory sprue is made. Conditions to be ruled out include pancreatic insufficiency, lactose malabsorption, parasite infestation, intolerance to other food proteins, coexisting inflammatory bowel disease, and autoimmune enteropathy, among others. Diagnosis should include a test called an enteroscopy, which is a procedure that explores more of the small intestine, and often finds ulcerative jejunitis, a marker of damage in refractory sprue. In addition, because the abnormal IELs can proliferate throughout the gut, a colonoscopy is recommended to determine if lymphocytic colitis is present. Treatment options include the elemental diet (also used in Crohns Disease), total parenteral nutrition (tube feedings), steroids, immunosuppressive therapies such as Cyclosporine, Infliximab, and in some cases, chemotherapy. Treatment options depend on the extent of refractory sprue found on biopsy and the nature of the clinical symptoms involved. How can I reduce the chances of developing refractory sprue? Researchers agree that most cases of refractory sprue develop in people who were diagnosed very late in life or who didnt follow the diet completely. Note that it doesn't matter how much gluten was consumed in these patients, they still developed refractory sprue. So the best protection against developing refractory sprue is to follow the diet. Be honest with yourself, especially if you cheat a little. What are you eating? Are you sure there isnt a great gluten-free alternative out there? Hey, there's even beer nowadays, so don't dismiss the suggestion of great gluten-free brownies, cakes, pies, pasta, crackers, cookies, or whatever else you are craving. Deal with your feelings too. Its easy to get angry about how life is much harder for people with celiac disease—how everything related to food requires too much planning, preparation, and explanation. These feelings are perfectly justified, but they do not justify cheating on your diet. There are great "quick fix" cookbooks out there, even convenience meals that are gluten free. Do whatever it takes to stay healthy, and gluten-free for life. Don't forget regular visits to your gastroenterologist or internist. Follow-up care for people with celiac disease is incredibly important, even if the medical community hasn't recognized it yet. Regular antibody testing to monitor compliance with the diet is an extra level of protection that every celiac needs. A simple anti-gliadin antibody test (IGG and IGA), six months post diagnosis, a year post-diagnosis and then every year after that for the first three years is key. In fact, the most serious celiac disease complications tend to occur in the first three years after diagnosis. Veteran celiacs should have their antibody levels checked every couple of years. While refractory sprue remains a potential complication for any adult with celiac disease, a majority of adult celiacs in this country will not have to face this difficult condition. For those diagnosed, treatment options continue to improve and the disease is becoming easier to manage. Researchers continue to study refractory sprue in order to better understand how the condition behaves and to develop new treatments. For now, the best defense against refractory sprue is a good offense—living a completely gluten-free life.
  4. Tropical sprue is a disease which causes a food absorption problem, especially with fat. The high risk places for catching tropical sprue are Southeast Asia and South America, and it is not normally found in Africa. The cause is not fully understood, but may be due to a viral infection, and/or from dietary factors. The symptoms are diarrhea (pale large stools), a sore tongue, loss of appetite, and weight loss. In the latter stages of the disease, a patient may develop ostemalacia (softening of the bones), peripheral neutitis, edematous swelling of the extremities, and megaloblasitic anemia. The standard treatment for tropical sprue is folic acid and cyanocobalamin. If diarrhea continues a cycle of tetracycline can be given. Anemia can be corrected by intracenous transfusions if necessary, and iron can be administered if there are any signs of iron-deficiency anemia in addition to megaloblastic anemia. Tropical sprue must be distinguished from gluten sensitivity. It is said that the damage form tropical sprue does not get as severe as that of celiac disease, but it may be very hard to distinguish the two. Arasitic infestations also need to be considered in people who have problems upon returning from underdeveloped areas.
  5. Collagenous Sprue is a distinctive lesion of the intestinal mucosa associated with progressive malabsorption. The intestinal pathology is initially identified with the characteristic flat lesion of untreated Celiac Sprue. Thereafter, bands of eosinophilic hyaline material within the lamina propria become increasingly apparent. As the disease progresses, the mucosa becomes progressively thinner. Therapy, including the gluten-free diet, does not help. Some cases currently designated refractory or unclassified Sprue many prove to be Collagenous Sprue.
  6. The National Celiac Association remains dedicated to the mission of supporting, educating and advocating for individuals with celiac disease and non-celiac gluten sensitivity, their families and communities across the nation. Our grassroots approach hasn’t changed in the 24 years we have been serving the community. Wherever you may reside, you matter to us and we are here to help you! We welcome support groups who would like to team up with us to provide education and support on a local level. Over 70 support groups and former CSA chapters are in the process of joining our team and more would be wonderful. Together our outreach will be both nurturing and empowering. Executive Director Lee Graham Web site: https://www.nationalceliac.org
  7. Celiac.com 12/07/2009 - Collagenous sprue is associated with high morbidity, but the etiology of this condition is poorly understood. There is little data concerning the pathological and clinical manifestations of patients with collagenous sprue. The research team set out shed some light on the etiology, disease manifestations and outcomes of collagenous sprue. A team of researchers recently undertook a clinico-pathological study of 19 patients with collagenous sprue and found that the condition does not always end badly for the patient. The research team was made up of Efsevia Vakiani, Carolina Arguelles-Grande, Mahesh M Mansukhani, Suzanne K Lewis, Heidrun Rotterdam, Peter H Green and Govind Bhagat. They are associated with either the Department of Pathology at New York's Memorial Sloan-Kettering Cancer Center, or with Columbia University's Department of Medicine or of Pathology. The team searched their departmental database covering the periods from 1999–2008 to identify cases of collagenous sprue and to gather clinical and lab data. The team evaluated small bowel histology, including thickness of sub-epithelial collagen, intra-epithelial lymphocyte phenotype and results of T-cell clonality assays. The found nineteen patients (15 women, 4 men, age 22–80 years, mean 57 years). Seventeen (89%) suffered from celiac disease and two from unclassified sprue. 9 of 17 (53%) celiac disease patients had refractory disease; 5 of 15 (33%) presented atypically without diarrhea, including 2 of 6 (33%) with active (untreated) celiac disease, and 3 of 9 (33%) with refractory celiac disease. They found autoimmune disorders in 12 of 19 (63%) patients and microscopic colitis (n¼7), lymphocytic gastritis (n¼2) or collagenous gastritis (n¼2) in nine patients. Thickness of subepithelial collagen increase varied from mild (n¼6), moderate (n¼10), or marked (n¼3), and villous atrophy from total (n¼13) to subtotal (n¼6). In no case did they find phenotypically aberrant intraepithelial lymphocytes. The only patient with refractory celiac disease type II showed a dominant T-cell clone with polymerase chain reaction analysis. 7 of 11 (64%) patients showed histological improvement. Overall, 8 of 19 (42%) responded favorably to a gluten-free diet, including 2 of 9 (22%) with refractory celiac disease. 10 of the 19 patients responded to immuno-modulatory therapy, including 6 of 9 (67%) with refractory celiac disease. Only one patient died from the effects of refractory celiac disease. No patient developed lymphoma. The vast majority of patients with collagenous sprue did have celiac disease. Even though numerous patients required immuno-modulatory therapy to control symptoms, many responded to gluten-free diet alone. The researchers conclude that most collagenous sprue patients have relatively good clinical outcomes. Source: Modern Pathology 23 October 2009; doi:10.1038/modpathol.2009.151
  8. The following report comes to us from The Sprue-Nik Press, which is published by the Tri-County Celiac Sprue Support Group, a chapter of CSA/USA, Inc. serving southeastern Michigan (Volume 7, Number 6, September 1998). The degree of mucosal damage varies from one celiac patient to another. Also, the amount of the small intestine that is affected also varies, with the damage usually progressing from the beginning of the small intestine and then moving downward toward the end of the small intestine. This may explain the variable symptoms in different patients. For example, when a significant portion of the small intestine is involved, diarrhea, malabsorption, and weight loss result. When damage is isolated to only the top portion of the small intestine, the only affect may be iron deficiency. (Incidentally, when iron deficiency is not corrected by iron supplements, it is highly likely that celiac disease is the cause of the deficiency.) Gluten in a celiacs diet causes the immune system to produce gliadin antibodies in the intestine. Some of these leak into the bloodstream where they can be detected in blood tests. These blood tests are useful for screening for celiac disease, though a small intestinal biopsy remains the gold standard for diagnosing celiac disease (celiac disease). There are few diseases for which diet and nutritional issues are more important than for celiac disease. At this time, the only known treatment of celiac disease is the removal of wheat, barley, rye, and oats from the celiacs diet. On the surface this sounds simple, but complete removal of dietary gluten can be very difficult. Gluten-containing grains are ubiquitous in the Western diet. Also, grain-derived food additives such as partially hydrolyzed vegetable protein [and modified food starch] are widely used in processed foods and oral medications. Content labels are often vague or incomplete regarding these additives. What further complicates matters is a lack of significant experience on the part of physicians and dietitians in the dietary treatment of celiac disease. This is mainly because there are so few celiac patients for anyone practitioner. Therefore the best sources of dietary information for a new patient are other knowledgeable, more experienced celiacs. It is very important that the diet be followed with full and strict compliance. Celiacs, especially if theyve had active celiac disease for a longtime, are at higher than normal risk for GI malignancies.(Fortunately, compliance to a good gluten-free diet returns the risk of malignancy and life expectancy to that of the general population.)Another complication of long-term untreated celiac disease is bone loss, which maybe irreversible in older patients. When a large portion of the small intestine is affected by active celiac disease, the result can be a generalized malabsorption problem, resulting in deficiencies of water- and fat-soluble vitamins and minerals. Folic acid deficiency is particularly common in celiac disease because, like iron, it is absorbed in the upper small intestine [where the highest concentration of celiac-related damage generally occurs]. Folic acid is necessary for DNA replication, which occurs in cell turnover. So a deficiency of folic acid can impair the regenerative ability of the small intestine. Vitamin B12, also essential to DNA synthesis, is not malabsorbed as commonly as folic acid. Magnesium and calcium deficiency are also common in active celiac disease, because of decreased intestinal absorption AND because these minerals tend to bind with malabsorbed fat which passes through the system. It is particularly important for doctors to assess the magnesium status of celiacs, because without correction of a magnesium deficiency, low levels of calcium and potassium in the blood cannot usually be corrected with supplements. In severe cases, magnesium supplementation should be done intravenously because of the tendency of oral magnesium to cause diarrhea. Supplemental calcium generally should be provided to celiacs, possibly with vitamin D, to help restore tissue and bone calcium levels to normal. The exact dose of calcium is not known. Dr. Fine usually recommends 1500-2000 mg of elemental calcium per day, divided into two doses, for several years and sometimes indefinitely. [4], [5], [6] Zinc is another mineral that often becomes depleted in patients with chronic malabsorption. Zinc supplementation (usually the RDA via multi-vitamin and mineral supplements) helps avoid skin rashes and restores normal taste. Up to 20% of celiacs will continue to experience loose or watery stools even after going on a gluten-free diet. Sometimes this is due to inadvertent gluten in the diet, but a recent study at Dr. Fines medical center showed that in these cases other diseases epidemiologically associated with celiac disease are present.[7] These include microscopic colitis, exocrine pancreatic insufficiency, lactose intolerance, selective IgA deficiency, hypo- or hyperthyroidism, and Type I diabetes mellitus. When diarrhea continues after beginning a gluten-free diet, a search for these associated diseases or others should be undertaken and treated if found. The use of cortico steroids has been advocated in celiacs when the response to the gluten-free diet is sluggish or absent. This is necessary more often in older than in younger patients. However, pancreatic enzyme supplements (prescribed by a doctor) may be needed to help digestion and resolve ongoing malabsorption in some patients. The endomysial antibody blood test is highly accurate and specific for detecting celiac disease. However, the current method of detecting these antibodies involves an operator looking through a microscope and observing the antibody binding on monkey esophagus or human umbilical cord tissue substrates. The correct interpretation of results is highly dependent on the skill and experience of the technician interpreting the fluorescence pattern through the microscope. Moreover, determination of the amount of antibody present relies upon repeat examinations following dilutions of the blood serum, with the last positive test being reported as a titer. A new discovery was reported by a research group in Germany.[8] The antigen substrate of the endomysial antibodies has been identified. This allows the development of a new test that can detect and measure serum endomysial antibodies in one, chemically-based test run [thus greatly reducing the potential for human error and significantly reducing the time needed for each test--ed.] These new tests should be available for clinical use shortly. In a recent study, Dr. Fine found that the frequency of positive stool blood tests was greater in patients with total villous atrophy relative to partial villous atrophy, and all tests were negative in treated patients without villous atrophy.[9] This suggests that fecal occult blood may be a non-invasive and inexpensive method of following the response of the damaged intestine to treatment. Also, it should be noted that the high frequency of positive tests due to villous atrophy will decrease the accuracy of the tests when used for cancer screening in this same patient population (which is how these tests are normally used by health care providers). There have been two recent reports touting the lack of deleterious effects when 50 grams of oats per day are added to the diet of celiac patients. Although this finding is exciting for celiacs, both studies possess certain limitations. In the first study, published by a Finnish group, the exclusion criteria for symptoms and histopathology were somewhat strict, so that patients with more mild forms of celiac disease seemingly were selected for study. And though no damage to duodenal histology occurred after one year of oats consumption, no physiologic or immunologic parameters of disease activity were measured. Furthermore, several patients in the treatment group dropped out of the study for reasons not mentioned in the article.[10] The second and more recent study involved only 10 patients, studied for twelve weeks. The favorable results of this study must be interpreted with caution because of the small sample size and short study period.[11] Even the one-year treatment period in the Finnish study may be too short to observe a harmful effect, as it is known that small intestinal damage sometimes will not occur for several years following there introduction of gluten to a treated celiac. At the worst, an increase in the incidence of malignancy may result from chronic ingestion of oats, an effect that could take decades to manifest. Therefore, this issue will require further study before oats can be recommended for the celiac diet. 3. From the September 1998 newsletter of the Houston Celiac-Sprue Support Group, a chapter of CSA/USA, Inc. 4. Ciacci C, Maurelli L, et el, Effects of dietary treatment on bone mineral density in adults with celiac disease; factors predicting response, Am J Gastroenterol, 1997; 92 (6): 992-996. 5. Mautalen C, Gonzalez D, et al, Effect of treatment on bone mass, mineral metabolism, and body composition in untreated celiac patients, Am J Gastroenterol, 1997; 2 (2):313-318. 6. Corazza gluten-free, Di Sario A, et al, Influence of pattern of clinical presentation and of gluten-free diet on bone mass and metabolism in adult coeliac disease, Bone, 1996; 18 (6):525-530. 7. Fine, KD, Meyer RL, Lee EL, The prevalence and causes of chronic diarrhea in patients with celiac sprue treated with a gluten-free diet, Gastroenterol, 1997; 112 (6):1830-1838. 8. Dieterich W, Ehnis T, et al, Identification of tissue transglutaminase as the autoantigen of celiac disease, Nat Med, 1997; 3 (7):797-801. 9. Fine KD, The prevalence of occult gastrointestinal bleeding in celiac sprue, N Engl J Med, 1996; 334 (18):1163-1167. 10. Janatuinen EK, Pikkarainen PH, et al, A comparison of diets with and without oats in adults with celiac disease, N Engl J Med, 1995; 333 (16):1033-1037. 11. Srinivasan U, Leonard N, et al, Absence of oats toxicity in adult coeliac disease, BMJ, 1996; 313 (7068):1300-1301.
  9. Celiac.com 05/04/2010 - A team of clinicians recently set out to assess the effectiveness of treating collagenous sprue with a combination of gluten-free diet and steroids. The team was made up of Alberto Rubio-Tapia, Nicholas J. Talley, Suryakanth R. Gurudu, Tsung-Teh Wu, and Joseph A. Murray. They are affiliated variously with the Division of Gastroenterology and Hepatology of the Mayo Clinics in Scottsdale, Arizona, Jacksonville, Florida, and Rochester, Minnesota, and the Division of Anatomic Pathology in Rochester Mayo Clinic. Deposits of subepithelial collagen that form a distinctive band in the small bowel are one of the clinical hallmarks of collagenous sprue. For the study, the team evaluated clinical characteristics, treatments, and outcomes of patients with collagenous sprue. The team looked at medical records for thirty patients with collagenous sprue from the Mayo Clinics from Scottsdale, Jacksonville, and Rochester, for the periods covering 1993 and 2009. 21 of the patients were female (70%), ranging in age from 53–91 years. The majority of patients suffered from severe diarrhea and weight loss. However, collagenous spore is commonly associated with collagen deposits or chronic inflammation in other parts of the gastrointestinal tract, as well as other immune-mediated disorders. 16 patients (53%) were hospitalized to treat dehydration, while 21 patients (70%) suffered from associated immune-mediated diseases, the most common of which was celiac disease. Other common associated diseases included microscopic colitis, hypothyroidism, and autoimmune enteropathy. Subjects showed subepithelial layers of collagen deposits in the small bowel ranging from 20 –56.5μm, and averaging 29 μm thickness. Eight patients showed subepithelial collagen deposits in the colon or stomach. 24 patients (80%) showed a positive clinical response to treatment with a combination of a gluten-free diet and immunosuppressive drugs. Nine patients showed confirmed histologic improvement, while five patients experienced complete remission. Of two patients who died, one succumbed to complications from collagenous sprue, while one died of another illness. Most patients with collagenous sprue show a positive clinical response to a combination of gluten-free diet and steroids. Source: Clinical Gastroenterology and Hepatology 2010;8:344–349. doi:10.1016/j.cgh.2009.12.023
  10. Celiac.com 02/05/2010 - Collagenous sprue is classically understood as a disorder of the small intestinal mucosa marked by persistent diarrhea, severe malabsorption with multiple nutrient deficiencies, and progressive weight loss. H. J. Freeman of the Department of Medicine, University of British Columbia Hospital, Vancouver, BC, Canada offers an update on collagenous sprue. Patients with collagenous sprue typically show a severe to variably severe "flattened" mucosal biopsy lesion with distinctive sub-epithelial deposits in the lamina propria region. These deposits contain collagens, as demonstrated by both histochemical stains and ultrastructural studies. Moreover, permanent disappearance of these deposits after resection of a localized colon cancer suggests that this disorder might actually involve a para-neoplastic morphologic marker of an occult malignancy. In collagenous sprue cases, physicians often first consider a diagnosis of simple celiac disease, until the patient fails to respond to a gluten-free diet. Recent studies portray a close association between collagenous sprue and celiac disease, sometimes with concomitant T-cell enteropathy. A number of studies demonstrate gastric and/or colonic associations with the unusual inflammatory mucosal process in collagenous sprue, which suggests that the condition may be more complex and have more varied contributing causes than presently understood. Source: World Journal of Gastroenterology. 2010 Jan 21; 16(3):296-8
  11. Celiac.com 11/25/2003 - Investigators from the Celiac Sprue Research Foundation, a non-profit public charity, and the Palo Alto Medical Foundation are seeking 20 volunteers who have Celiac Sprue to participate in a study called the "Gluten Detoxification Trial". The Gluten Detoxification Trial will test the effects of consumption of an Orange Juice Mixture that has been modified by the addition of gluten pre-treated with an enzyme (PEP) that is intended to "detoxify" the gluten. If the PEP is successful in detoxifying the gluten, then the stage will be set for development of a PEP therapeutic drug, or pill, that may allow Celiac Sprue patients to consume a regular gluten containing diet. The study involves 2 two-week stages, separated by one month off. The first stage will occur during the first two weeks in December. The second stage will occur during late January 2004. Participants in this study will be randomized to consume an Orange Juice Mixture containing gluten daily for 14 days during one stage, and an Orange Juice Mixture containing gluten pre-treated with the PEP daily for 14 days during the other stage. Participants will record symptoms daily during each stage, and will have laboratory tests measured before and after each stage. Participants will undergo a screening physical exam at the beginning, and brief follow-up exams after each stage at the Palo Alto Medical Foundation. Participants in the Gluten Detoxification Trial must meet all of the following criteria: Diagnosed with Celiac Sprue by small intestinal biopsy (participants must be able to provide a copy of the biopsy report). Have had at least one abnormal Celiac antibody test (e.g. transglutaminase (ttg), endomysial (EMA), anti-gliadin) in the past. Be in remission on a gluten-free diet. Be at least 18 years of age. Pre-registration is required to participate in the study. If you can participate, please contact the Celiac Sprue Research Foundation at the above address or e-mail address and request a registration packet/consent. Please call either Dr. Gail Pyle at (408) 655-0384 or Dr. Gary Gray at (650) 327-1144 if you have any questions.
  12. Celiac.com 08/10/2001 - The Celiac Sprue Association, under the new leadership of Mary Schluckebier, has recently taken an important step towards eliminating the lingering confusion surrounding its position on gluten-free foods. According to Janet Rinehart, the CSAs "Basics for a Celiac Diet" guidelines have recently been revised to include the following key changes: Canola oil is not mentioned (except where you might assume the connection for "general recommendations for those with a depressed immune system)." Rather than stating that quinoa, amaranth and teff are not safe for the celiac diet, the document now says: "Some celiacs have demonstrated toxicity or sensitivities to the following cereals: quinoa, amaranth and teff." Distilled vinegar, however, is still on the CSAs "Low Gluten Items to Avoid List." The CSA still maintains that distilled vinegar and alcohol are "questionable," even if there is no detectable gluten/gliadin in them, and even though the Gluten Intolerance Group (GIG), Celiac Disease Foundation (CDF) and the new guidelines from the American Dietetic Association (ADA) all include them on their safe lists . The CSA urges celiacs to ascertain the source of any questionable ingredients from their manufacturers. The CSAs new version of their "Celiac Disease Self-Management Chart for the Clinical Diet" advocates: A "self-management" approach to the diet, where the first stage is to eliminate anything questionable -conservative approach. Zero gluten is the goal. The second stage is to develop good methods for questioning products and controversial items/information. Then introduce new items, one at a time, at least two weeks apart. The third stage is to maintain a stable diet, using as many tools as possible. There is also a sample Food Diary Chart to use when beginning the zero gluten diet to track your meal planning (be sure to include brand names for reference). According to Janet Rinehart the CSAs new guidelines "are not incompatible with the new ADA recommendations in the later stages." Further: "We can use the CSA diet to start with, and then use the ADA recommendations and those published by GIG/CDF, depending on individual food sensitivities." She urges celiacs and support groups to quite blaming the CSA and instead work together to contribute positively to the success of all celiacs in all groups.
  13. Celiac.com 03/19/2002 - For the past several years, Gary M. Gray, M.D. and Chaitan Khosla, Ph.D., both at Stanford University, have been studying the underlying causes of Celiac Disease, with an eye toward finding a therapeutic solution that would not require the strict adherence to a gluten-free diet. For the past two years, I have helped organize the Celiac conference at Stanford University; and we have collected blood from Celiac volunteers for their research. Based on a series of studies involving animal tissue, Drs. Gray, Khosla, and coworkers have developed a hypothesis for the cause of the disease. Their findings in animal studies need to be confirmed on human tissue, and any differences in normal and Celiac intestine must be defined. The Stanford researchers are now in need of volunteers who are scheduled for a follow-up biopsy as part of their optimal care to provide intestinal tissue samples. Volunteers must be biopsy-diagnosed Celiacs who, as part of their care, will be undergoing an upper gastrointestinal endoscopy for recovery of small biopsies from the duodenum. For this research, two small (a few milligrams) of additional tissue will be taken during the biopsy, frozen immediately, and transported to Stanford. Please note that volunteers undergoing procedures at locations other than Stanford Hospital could participate. The small amount of additional tissue does not constitute a significant additional risk over and above that you will undergo due to the endoscopy and routine biopsies for the pathologist to examine. The research has been approved by the Human Subjects Committee at Stanford University Medical Center. If you would like to participate in this study, please contact Kelly Rohlfs at 650-725-4771 or kellyr@bonair.stanford.edu.If you have questions concerning the risks and benefits of this study, please contact Dr. Gray at 650-725-3366 or gray@stanford.edu. Dr. Gray will coordinate the study with your gastroenterologist at the time of your endoscopy.
  14. New England Journal of Medicine, May 2, 1996 -- Volume 334, Number 18 Kenneth D. Fine The New England Journal of Medicine published a study in the May 2, 1996 (Volume 334, Number 18) issue regarding the prevalence of occult gastrointestinal bleeding in patients with celiac sprue. Its goals were to explain the iron deficiency found in many celiacs. The fecal samples of 8 Patients with partial villous atrophy and 28 with total villous atrophy were studied. Their results found 25% of patients with partial villous atrophy and 54% of Patients with total villous atrophy tested positive for blood. They concluded that gastrointestinal bleeding can be found in about 50% of patients with celiac sprue, and should therefore be added to the list of factors that can contribute to iron deficiency in celiacs. The following are comments on this article by Karoly Horvath, M.D., Ph.D., of Baltimore, Maryland, USA. If you have any questions you can e-mail him at: khorvath@umabnet.ab.umd.edu Date: 05/02/96 - 08:20:20 AM. Subject: Re: Fecal Occult Blood, Plus Elevated Liver Enzymes FECAL OCCULT BLOOD: The cited NEJM paper found occult intestinal bleeding in patients who had some degree (partial and total) of intestinal villous atrophy. However, this paper have certain methodological problems. The first, and most important -as you can read in the editorial comment- that they did not place the patient on a specific diet before collecting the stool. It is a rule that the patients should be on a diet which eliminate all the peroxidase containing food. So this may increase the number of false positive cases. The second problem that the hemoccult test is only a screening method, which does not give information about the degree of blood loss. The test can be positive in the presence of small amount of blood in the stool. While this paper has limitations, I should accept that patients with mucosal atrophy and inflammation have small amount of blood loss. So I do not have any doubt regarding the final conclusion of paper, that patients with active celiac disease have blood loss in the stool. This is not surprising and not a novel finding. To avoid any panic in the celiac community I do not recommend to post this finding without appropriate comment to the Celiac List. We should emphasize one sentence from this paper: ALL THE PATIENTS WITH PREVIOUSLY DIAGNOSED AND TREATED CELIAC SPRUE HAD NEGATIVE TESTS FOR FECAL OCCULT BLOOD. LIVER ENZYMES: It is well known that patient with intestinal inflammation may have elevated liver enzymes. The well known examples are patients with inflammatory bowel disease. Because patients with active celiac disease have significant accumulation of inflammatory cells in the mucosa it is not surprising that a percentage of patients with active celiac disease have elevated liver enzymes. However, this is a temporary elevation, which disappears on gluten-free diet. The explanation is not clear for this finding. The simplified explanation is that there is an increased permeability in the inflamed intestinal segments and different toxins, which normally are detoxified by the enterocyte Cytochrom P450 enzyme system, enter the portal circulation and there is an increased toxin load into the liver.
  15. Celiac that do not remain on a gluten-free diet can develop Refractory Sprue. Refractory Sprue and Collagenous Sprue patients who initially respond to a gluten-free diet many subsequently relapse despite maintaining their diet. Such patients are then refractory to further dietary therapy. In contrast, others are refractory to dietary therapy from its inception and, assuming they are truly on a gluten-free diet, may not have celiac disease; these patients are said to have unclassified Sprue. Some refractory patients with celiac disease, typical or atypical, respond to treatment with corticosteroids or other immunosuppressive drugs. In others, there is no response and malabsorption may be progressive. Collagenous Sprue is characterized by the development of a thick band of collagen-like material directly under the intestinal epithelial cells and has been regarded by some as a separate entity from celiac disease. However, subepithelial collagen deposition has been noted in up to 36% of patients with classic Celiac Disease and in Tropical Sprue. Although individuals with large amounts of subepithelial collagen may be refractory to therapy, the presence of collagen does not , a riori, preclude a successful response to a gluten-free diet. Collagenous colitis accompanying celiac disease also has been observed and would be considered in the diagnosis of diarrhea occurring in celiac disease patients on a gluten-free diet.
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