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Found 17 results

  1. Celiac.com 12/01/2016 - Alcohol-related cerebellar degeneration is one of the most common forms of acquired cerebellar ataxia. Researchers still do not understand the exactly how alcohol damages the cerebellum. Very little study has been done on auto-reactive immune mediated mechanisms as a possible contributor. Recently, a team of researchers set out to investigate the potential role of alcohol-induced immune mediated cerebellar degeneration. The research team included Priya D. Shanmugarajah, Nigel Hoggard, Stuart Currie, Daniel P. Aeschlimann, Pascale C. Aeschlimann, Dermot C. Gleeson, Mohammed Karajeh, Nicola Woodroofe, Richard A. Grünewald and Marios Hadjivassiliou. They are variously associated with the National Blood Service Sheffield, UK; Department of Immunology, Northern General Hospital, Sheffield, UK and Academic Unit of Radiology, University of Sheffield, UK. For their study, the team recruited patients with ataxia and a history of heavy alcohol use from the Ataxia and Hepatology tertiary clinics at Sheffield Teaching Hospitals NHS Trust. The team determined the pattern of cerebellar involvement both on clinical (SARA score) and imaging (MRI volumetry and MR spectroscopy) parameters. They also evaluated HLA genotyping, serological markers for gluten-related disorders and serological reactivity on rat cerebellar tissue using indirect immunohistochemistry. In all, the team studied thirty-eight patients with ataxia, which negatively impacted the gait in 97% of patients, and stance and heel-shin slide in 89% of patients. The team used MRI volumetric and spectroscopy techniques to show significant structural, volumetric and functional deficiencies of the cerebellum with particular involvement of the cerebellar vermis. They found circulating anti-gliadin antibodies in 34% of patients, compared with 12% of healthy controls. They found antibodies to transglutaminase 6 (TG6) in 39% of patients, but only in 4% of healthy control subjects. Using immunohistochemistry, they found Purkinje cell and/or granular layer reactivity in 71% of patient sera. Alcohol induced tissue injury to the CNS leading to cerebellar degeneration may also involve immune mediated mechanisms, including sensitization to gluten. The team is calling for role of gluten in ataxia to be studied further, to determine the exact mechanism, and the extent of gluten's impact on ataxia patients. Source: Cerebellum & Ataxias 2016, 3:17. DOI: 10.1186/s40673-016-0055-1
  2. The average gluten-containing diet contains roughly 10-40 grams of gluten per day. This figure is based on the amounts of gluten in your average slice of whole wheat bread, which contains around 4.8 grams of gluten (10% gluten by weight), and the amount of gluten in a serving of pasta, which is roughly 6.4 grams of gluten (11% gluten by weight). The smallest amount of gluten which has been shown by a biopsy to cause damage to a celiac is 0.1 gram per day (Catassi et al.). This is approximately the amount of gluten contained in 1/48th of a slice of bread! The biopsies in this study showed an increase in intraepithelial lymphocyte count, one of the earliest signs of damage. The challenge was on 10 patients (children) for 28 days each. Four of the patients showed an increase in IgA antigliadin antibodies. The intestinal permeability test remained normal.
  3. Celiac.com 12/28/2006 – Antonio Tursi and colleagues at the Digestive Endoscopy Unit, Lorenzo Bonomo Hospital, Andria, (BA), Italy have published a study which concludes that any neurological damage caused by celiac disease may be irreversible—even after treatment with a gluten-free diet. Although the study is relatively small, its conclusions are important—especially to those who suffer from the neurological effects of celiac disease. More research needs to be done to determine why antineuronal antibodies persist in treated celiacs. It would be interesting to see if the removal of other common offending proteins (such as casein, soy, corn, eggs, etc.) from the diets of the patients in this study would have any effect on their antineuronal antibody levels. The following article that was recently published on Celiac.com may provide further insight: Gluten Causes Brain Disease! By Prof. Rodney Ford M.B., B.S., M.D., F.R.A.C.P. Below is the abstract of the study: Dig Dis Sci. 2006 Sep 12 Peripheral Neurological Disturbances, Autonomic Dysfunction, and Antineuronal Antibodies in Adult Celiac Disease Before and After a Gluten-Free Diet. Tursi A, Giorgetti GM, Iani C, Arciprete F, Brandimarte G, Capria A, Fontana L. Digestive Endoscopy Unit, Lorenzo Bonomo Hospital, Andria, (BA), Italy. Thirty-two consecutive adult celiac disease patients (pts), complaining of peripheral neuropathy (12 pts), autonomic dysfunction (17 pts), or both (3 pts), were evaluated to assess the presence of neurological damage (by clinical neurological evaluation and electrophysiological study) and antineuronal antibodies and to assess the effect of a gluten-free diet on the course of the neurological symptoms and on antineuronal antibodies. At entry, 12 of 32 (38%) pts showed signs and symptoms of neurological damage: 7 of 12 (58%), peripheral neurological damage; 3 of 12 (25%), autonomic dysfunction; and 2 (17%), both peripheral neurological damage and autonomic dysfunction. The overall TNS score was 105 at entry. Anti-GM1 antibodies were present in 5 of 12 (42%) pts: 3 showed peripheral neurological damage and 2 showed both peripheral neurological damage and autonomic dysfunction. One year after the gluten-free diet was started, histological lesions were still present in only 10 of 12 (83%) pts. TNS score was 99, 98, 98, and 101 at the 3rd, 6th, 9th, and 12th month after the gluten-free diet was started, so it did not improve throughout the follow-up. None of the pts showed disappearance of antineuronal antibodies throughout the follow-up. We conclude that adult celiac disease patients may show neurological damage and presence of antineuronal antibodies. Unfortunately, these findings do not disappear with a gluten-free diet.
  4. Celiac.com 06/02/2014 - Despite following a gluten-free diet, many people with celiac disease continue to have symptoms, and to suffer from ongoing small intestinal inflammation. Can a drug be created to alleviate such symptoms and inflammation, and protect celiacs on a gluten-free diet against small amounts of gluten contamination? San Carlos California-based Alvine Pharmaceuticals is conducting a phase 2 trial to determine whether their drug, ALV003, an orally administered mixture of 2 recombinant gluten-specific proteases can protect celiac disease patients from gluten-induced mucosal damage. For this trial, Alvine is working with researchers Marja-Leena Lähdeaho, Katri Kaukinen, Kaija Laurila, Pekka Vuotikka, Olli-Pekka Koivurova, Tiina Kärjä-Lahdensuu, Annette Marcantonio, Daniel C. Adelman, and Markku Mäki. They are affiliated with the School of Medicine and Tampere University Hospital at the University of Tampere; the Department of Gastroenterology and Alimentary Tract Surgery at Tampere University Hospital and School of Medicine at the University of Tampere, and FinnMedi Oy in Tampere, Finland; the Department of Medicine at Seinäjoki Central Hospital in Seinäjoki, Finland; Liikuntaklinikka, Oulu Diakonissalaitos; and Terveys, Oulu Diakonissalaitos, Oulu, Finland. For their Phase 2 trial, the research team first established two grams of gluten per day as the optimal challenge dose for their 6-week gluten study. They then randomly assigned 20 adults with biopsy-proven celiac disease to receive ALV003, and twenty-one to receive a placebo. Both groups also received 2 grams of gluten each day. The team conducted duodenal biopsies at baseline, and after gluten challenge, focusing on the ratio of villus height to crypt depth and densities of intraepithelial lymphocytes. A total of seven patients dropped out due to adverse reactions. Four were receiving ALV003, and three were receiving the placebo. Sixteen patients given ALV003 and 18 given placebo were eligible for efficacy evaluation. Biopsies from subjects in the placebo group showed evidence of mucosal injury after gluten challenge, with average villus height to crypt depth ratio changed from 2.8 before challenge to 2.0 afterward. (P = .0007; density of CD3þ intraepithelial lymphocytes changed from 61 to 91 cells/mm after challenge; P = .0003). However, the team saw no significant mucosal deterioration in biopsies from the ALV003 group. The two groups showed no significant differences in symptoms, though they did show substantial differences in morphologic changes, and CD3þ intraepithelial lymphocyte counts differed significantly from baseline to week 6 (P = .0133 and P = .0123, respectively). This small, but important, step means that ALV003 did provide significant protection against gluten-induced gut damage for people with celiac disease on an otherwise gluten-free diet, which means that Alvine can continue to the next phases in the development process. If successful, glutenase ALV003 will be the first drug to protect people with celiac disease against gut damage from small amounts of gluten. Source: Clinicaltrial.gov, Numbers: NCT00959114 and NCT0125569
  5. Journal of Clinical Gastroenterology 2003; 36(3):219-221 Celiac.com 03/28/2003 - A study by Antonio Tursi, M.D, et al, was recently conducted to evaluate the correlation between the degree of histologic intestinal damage in celiac patients and their level of positivity (serum value) to anti-tissue transglutaminase antibodies (anti-tTG). The study looked at 119 adult celiac patients who were diagnosed consecutively (47 men and 72 women; mean age, 28 years; range, 22-51 years), and were stratified for histologic damage according to Marsh classification. The final step was to compare their Marsh histologic intestinal damage classification with their anti-tTG serum values. Here are their results: Marsh I lesions were present in 13 patients (10.92%), Marsh II in 24 anti-tTG (20.16%), Marsh IIIa in 27 anti-tTG (22.68%), Marsh IIIb in 31 anti-tTG (26.05%) and Marsh IIIc in 24 anti-tTG (20.16%). Anti-tTG positivity was ranging from 1 of 13 anti-tTG (7.69%) in Marsh I lesions to 23 of 24 anti-tTG (95.83%) in Marsh IIIc lesions respectively (P The researchers conclude that the mean serum value in celiacs with severe enteropathy (Marsh IIIb-c lesions) was higher than in those with only slight enteropathy (Marsh I-IIIa). Further, serologic test results in the absence of histologic evaluation (biopsy) may "underestimate the real prevalence of celiac disease," thus delaying a proper diagnosis and putting patients at risk for a large variety of serious health problems.
  6. Celiac.com 03/22/2013 - Enterocyte damage is one of the common features of celiac disease, and often results in malabsorption. Presently, doctors don't know very much about the recovery of enterocyte damage and its clinical consequences. Serum intestinal fatty acid binding protein (I-FABP) is a marker that allows researchers to study enterocyte damage. A research team set out to determine the severity of enterocyte damage in adult-onset celiac disease, how it responds to a gluten-free diet, and the correlation among enterocyte damage, celiac disease autoantibodies and histological abnormalities during the course of disease. The research team included M. P. M. Adriaanse, G. J. Tack, V. Lima Passos, J. G. M. C. Damoiseaux, M. W. J. Schreurs, K. van Wijck, R. G. Riedl, A. A. M. Masclee, W. A. Buurman, C. J. J. Mulder, and A. C. E. Vreugdenhil. They are affiliated with the Department of Paediatrics & Nutrition and Toxicology Research Institute Maastricht (NUTRIM) at Maastricht University Medical Centre in Maastricht, the Netherlands. For their study, the team first determined I-FABP blood levels in 96 biopsy-proven adults with celiac disease, and in 69 patients following a gluten-free diet. They used 141 individuals with normal antitissue transglutaminase antibody (IgA-tTG) levels as a control group. They found that levels of I-FABP were related to the degree of villous atrophy (Marsh grade) and IgA-tTG. Patients with untreated celiac disease showed higher I-FABP levels (median 691 pg/mL) compared with control subjects (median 178 pg/mL, P < 0.001) and correlated with Marsh grade (r = 0.265, P < 0.05) and IgA-tTG (r = 0.403, P < 0.01). I-FABP blood levels in patients following a gluten-free diet dropped substantially, but not within the range found in control subjects, even though they showed normalization of IgA-tTG levels and Marsh grade. Celiac patients with elevated I-FABP levels who did not respond to gluten-free diet showed persistent histological abnormalities. The team's main finding was that enterocyte damage, as assessed by serum I-FABP, correlates with the severity of villous atrophy in celiac disease at the time of diagnosis. Even though enterocyte damage improves upon treatment with a gluten-free diet, the majority of patients still show substantial enterocyte damage despite the absence of villous atrophy and low IgA-tTG levels. Thus, they conclude that elevated I-FABP levels that do not respond to a gluten-free diet likely point to histological abnormalities and warrant further evaluation. Source: Aliment Pharmacol Ther. 2013 Feb;37(4):482-90. doi: 10.1111/apt.12194.
  7. Celiac.com 07/23/2012 - At 2012 Digestive Diseases Week in San Diego, California, Alvine Pharmaceuticals, Inc. announced the publication of data from Phase 2A trial of its main celiac disease compound, ALV003. The results show that ALV003, orally administered to celiac disease patients on a gluten free diet, significantly reduces gluten-triggered intestinal mucosal damage. For the trial, 41 adults with clinically proven celiac disease who had followed a gluten-free diet for at least one year were randomly given ALV003 or a placebo each day for six weeks. During that time, they also received 2g of gluten in the form of bread crumbs. Participants received a small bowel biopsy prior to randomization and again, at the end of the six week challenge. The results showed that the study met its primary endpoint of a clinically and statistically meaningful reduction in intestinal mucosal damage in celiac patients on a gluten-free diet. Damage was measured by the ratio of the villus height to crypt depth, or Vh:celiac disease between the ALV003 and placebo treated groups over the six week study period. Secondary endpoints included change in intraepithelial lymphocyte (IEL) density, gastrointestinal symptoms as measured by Gastrointestinal Symptom Rating Scale (GSRS) scores, celiac serologies, safety and tolerability. Each subject received small bowel biopsy at the start of the trial, and again after six weeks of daily gluten challenge. When researchers compared biopsy results from 34 patients, they found significantly less small intestinal mucosal damage in patients treated with ALV003 than in placebo-treated patients (p=0.013). Placebo-treated patients suffered worse damage and symptoms. Most often, these included abdominal distention, flatulence, eructation, abdominal pain and diarrhea. The published data shows that: Biopsy results for patients who received ALV003 had significantly reduced small intestinal mucosal damage compared with placebo-treated patients (p=0.0133). For placebo-treated patients, IELs, including CD3+ and CD3+ aB and subsets, which measure cellular inflammation responses, were significantly higher, but were mostly normal in the ALV003-treated patients. ALV003-treated patients had better overall GSRS scores and scores for indigestion and abdominal pain symptoms, compared with placebo-treated patients, though the results were not statistically significant. Patients reported no serious adverse events, however, placebo-treated patients reported more regular and consistent non-serious adverse. Such events that occurred in 10 percent or more patients included abdominal distention, flatulence, eructation, diarrhea, nausea, headache and fatigue. Celiac-disease blood tests revealed no significant changes between the ALV003 and placebo-treated patients, though results did show positive trends for tissue transglutaminase and deamidated gliadin peptide antibody titers in the ALV003-treated group, which indicates improved immune response. Daniel Adelman, M.D., Alvine's Senior Vice President and Chief Medical Officer, says that the trial results represent the first time that any such treatment for celiac disease has met its pre-specified primary endpoint of providing protection against damage from gluten-exposure in celiac disease patients, with data that is both clinically and statistically significant. Such a drug could help to protect gluten-free celiac disease patients against accidental gluten contamination. The company plans to initiate a Phase 2B trial later this year. Read the abstract of the presentation (Sa1342) on the DDW website. Review information on Alvine's current clinical trial titled "Evaluation of Patient Reported Outcome Instruments in Celiac Disease Patients" at the NIH website.
  8. Celiac.com 04/04/2011 - Having been diagnosed with celiac disease, I know from having to follow a strict gluten-free diet that monitoring one's diet and health can be inconvenient, time-consuming, and challenging. Similarly, keeping one's blood sugar level under control for diabetics can be tough, but studies are showing how important this is, as it has been shown to prevent diabetic neuropathy, that is, nerve damage peculiar to diabetics, and its devastating effects. According to Tedd Mitchell, M.D., President of the Texas Tech University Health Sciences Center, there are two types of diabetic neuropathy, peripheral and autonomic. Peripheral neuropathy is "a degeneration of the nerves in the feet and hands," according to Dr. Mitchell, which, as it occurs "slowly but progressively," reduces sensitivity to touch while heightening sensations of pain and itching. The second type is autonomic neuropathy, which is, Dr. Mitchell says, "damage to nerves that control bodily functions, such as digestion, urination, heart rate, blood pressure, sexual function and even sweating." Some of the symptoms of this type are digestive problems, urinary problems, and reductions in blood pressure. The longer one has been diabetic, the higher one's risk for neuropathy. Thankfully, evidence supports that long-term blood sugar control can reduce this risk. It may seem like a challenge for some diabetics to control their blood sugar, but with some determination and effort, it can successfully be achieved. MedicalMoment.org, a website developed by Columbia St. Mary's, an organization of hospitals and clinics, offers various ways to get started controlling your blood sugar. First, in liaison with your health care provider, test your blood sugar and keep a record of your results and pertinent information, on a daily basis. Follow your doctor's prescribed diabetes medicine plan while eating foods low in fat, sugar, and sodium and high in fiber on a regular basis, aiming for the same caloric intake every day. It's important to get regular exercise, starting slowly if need be, such as swimming and walking. Your diet and exercise routine should be geared toward maintaining your ideal weight, which should be determined by your health care provider. You'll want to stay aware of signs of possible nerve damage such as sores that won't heal, blisters, swelling, and ulcers. MedicalMoment.org also offers several tips for keeping blood sugar under control. Low blood sugar should be treated quickly with the use of special glucose gel or tablets. Smoking, which harms the heart and the circulatory system, should be avoided. Next, learn as much as possible about your diabetic condition and treatment; knowledge is power in this case, as I know from being a celiac disease patient. Lastly, avoid stress and get support by staying connected with friends and relatives or a support group who can help you keep your blood sugar under control. It isn't unusual for me to focus some of my work as an author, researcher, and gluten-free and health advocate, on the area of diabetes; after all, according to Celiac.com, evidence is growing which supports that people with Type 1 diabetes are at high risk for celiac disease. In this research, the necessity of maintaining blood sugar is clear. With the help of your medical practitioner and other resources, you can achieve proper self-care in controlling blood sugar level and lower this risk of nerve damage. Resource: Mitchell, Dr. Tedd. "Nerve damage: One more reason to keep blood sugar under control." USA Weekend: July 9-11, 2010.
  9. American Journal of Clinical Pathology, April 2000 - A New Method of Quantitative Fecal Fat Microscopy and its Correlation with Chemically Measured Fecal Fat Output, by Kenneth Fine, M.D. and Frederick Ogunji Ph.D (Celiac.com 07/09/2000) Patients with gluten sensitivity should be evaluated for nutrient malabsorption because if present, this means there is small intestinal damage and institution of a gluten-free diet is imperative to prevent osteoporosis and other nutrient deficiency syndromes. Furthermore, a test at the time of diagnosis serves as a baseline to be compared to later if needed. For more than 50 years, the primary method used to assess for the presence of small intestinal damage and nutrient malabsorption in patients with celiac disease has been a 72-hour quantitative stool collection. However, because this method requires that patients accurately collect all the stools they pass for 3 days (missed stools lead to falsely low results), the test is logistically difficult for medical centers unaccustomed to the procedure, and the voluminous specimens usually are abhorred by patients and laboratory technicians. It poses obvious problems for children who cannot or will not collect all their stools, as well as for patients with chronic diarrhea, who may have bowel movement frequencies reaching 15 or more per day and/or fecal volumes as high as 2 or 3 liters per day. For these reasons, physicians evaluating patients with suspected or proven gluten sensitivity often avoid tests for intestinal malabsorption altogether. Recently, researchers at the Intestinal Health Institute in Dallas, Texas have developed a new method for quantitating fecal fat excretion that requires collection of only a single stool specimen. Development of this method was based on the fact that as more fat is malabsorbed, the fat globules in stool become more numerous and larger. In a study published in the April 2000 issue of the American Journal of Clinical Pathology entitled A New Method of Quantitative Fecal Fat Microscopy and its Correlation with Chemically Measured Fecal Fat Output, Kenneth Fine, M.D. and Frederick Ogunji Ph.D. tested 180 patients and found a highly statistically significant linear correlation between quantitative fecal fat microscopy (the new method) and chemically measured fecal fat output (the old method). They also showed that their microscopic analysis of just one stool gives comparable results to analysis of an entire 3-day collection. These researchers have, thus, shown that a dedicated quantitative analysis of one stool under a microscope can detect the rise in fecal fat due to intestinal malabsorption (or pancreatic maldigestion) as accurately as 3-day stool collections, making this latter test a thing of the past for most patients. This new stool test for intestinal malabsorption and other celiac-testing is available for order online from a laboratory set up by Drs. Fine and Ogunji to serve the needs of celiac patients. It is called EnteroLab and can be accessed at http://www.enterolab.com/.
  10. Celiac.com 09/20/2010 - People with celiac disease face increased risk of cancer and a large amount of circumstantial evidence suggests that oxidatively damaged DNA may be used to help predict future cancer development in celiac patients. To evaluate that hypothesis, a research team set out to assess and describe oxidative stress and oxidative DNA damage in celiac disease patients. Anna Szaflarska-PopÅ‚awska, Agnieszka Siomek, MieczysÅ‚awa Czerwionka-Szaflarska, Daniel Gackowski, RafaÅ‚ Różalski, Jolanta Guz, Anna Szpila, Ewelina Zarakowska and Ryszard OliÅ„ski comprised the research team. They are associated with the college of medicine at Nicolaus Copernicus University, in Bydgoszcz, Poland. They found that children with celiac disease have higher than normal levels of the oxidative DNA damage biomarkers urinary 8-oxodG and 8-oxoGua, regardless of following a gluten-free diet. To measure urinary excretion of 8-oxodG and 8-oxoGua, and levels of oxidative DNA damage in the leukocytes, as well as the level of antioxidant vitamins, the team used high-performance liquid chromatography (HPLC) and HPLC/gas chromatography with isotope dilution mass detection. They observed parameters for DNA damage in a group of children with untreated celiac disease, in a group of children with celiac disease following a strict gluten-free diet, and in a control group of healthy children. They found that the two groups of celiacs showed significantly higher overall levels of 8-oxodG in DNA isolated from the leukocytes and from the urine samples than did the control subjects, without regard to diet. There was no significant difference between treated and untreated celiacs. That means being on a gluten-free diet offered no protection from oxidative DNA damage for all children with celiac disease. One key difference was that the untreated celiac children showed significantly lower levels of retinol and α-tocopherol, vitamin A and E, compared to the treated celiac children. Between group difference of 0.31 and 3.76 µmol/l, respectively, suggests that a gluten-free diet offers some protection against oxidative damage in treated celiacs. From the results indicate that oxidative stress and/or oxidatively damaged DNA in celiac patients cannot be explained by diet alone, and that factors independent of diet play an important role. Supplemental vitamin A and E in celiac disease patients may help minimize the risk of cancer development. Source: Cancer Epidemiol Biomarkers Prev 2010; 19: 1960–1965
  11. Celiac.com 04/27/2006 - Liver abnormalities have been found in a high percentage of celiacs when first diagnosed, around 42% according to some studies. Gluten toxicity and increased intestinal permeability have both been suspected as a cause of liver abnormalities. Serious liver disorders, including cirrhosis, have been found in association with a number of celiac disease cases which appear to resolve upon treatment and maintaining a gluten-free diet. It is not clear whether some damage to the liver may remain long term even after maintaining a gluten-free diet. Below is an interesting study (Hepatology. 2006 Mar 23;43(4):837-846) of the effects of induced liver cirrhosis on the intestinal mucosa which results in oxidative stress and an alteration of intestinal permeability, intestinal bacteria makeup, and bacterial overgrowth. Hence not only does damage to the intestine in response to gluten often result in bacterial overgrowth, but damage to the liver by gluten may also contribute to bacterial overgrowth and mucosal alterations. Damage to the liver caused by celiac disease may also have other consequences, as the liver plays many important roles including storage and production of important compounds and proteins and the removal of fat soluble toxic substances. As we are increasingly exposed to endocrine disrupting xenobiotic environmental chemicals and toxic substances, a dysfunctional livers inability to remove fat soluble toxic substances may leave celiacs more susceptible to adverse effects from these chemicals which can accumulate in adipose (fatty) tissue. In the Winter 2006 issue of Scott Adams' Celiac.com Newsletter, I discuss in detail, in Unraveling Fibromyalgia, how a dysfunctional liver and fat soluble toxic substances accumulating in innervated and vascularlized adipose tissue in the vicinity of joints may be the cause of fibromyalgia. Bacterial overgrowth has also been found in association with fibromyalgia. But clearly, lesser degrees of fatigue, muscle and joint pain, thyroid disorders, and other symptoms could also result from liver dysfunction caused by celiac disease. The inability of the liver to remove xenobiotic chemicals may also increase the risk of breast and other cancers. Recently a new review on liver disorders and celiac disease has appeared (See below - World J Gastroenterol 2006 March 14;12(10): 1493-1502 and 1503-1508): Liver Damage and the Intestinal Mucosa. One cannot ignore the secondary effects and symptoms that liver damage may add to those symptoms caused by glutens effect on the intestinal mucosa. Those unexplained aches and pains and other symptoms and disorders which have frequently been reported by some celiacs may be a result of liver dysfunction. Some notes: Elevated liver enzymes are the result of liver enzymes released by damaged liver cells. The article cites one study stating A gluten-free diet for 1 to 10 years resulted in complete normalization of liver chemistry tests in 95% patients. Normal liver chemistry tests DO NOT necessarily mean that the liver is functioning normally and that no damage remains. See: Special Considerations in Interpreting Liver Function Tests - http://www.aafp.org/afp/990415ap/2223.html Referenced Abstracts: Hepatology. 2006 Mar 23;43(4):837-846 Intestinal mucosal alterations in rats with carbon tetrachloride-induced cirrhosis: Changes in glycosylation and luminal bacteria. Natarajan SK, Ramamoorthy P, Thomas S, Basivireddy J, Kang G, Ramachandran A, Pulimood AB, Balasubramanian KA. The Wellcome Trust Research Laboratory, Department of Gastrointestinal Sciences, Christian Medical College, Vellore, India. Spontaneous bacterial peritonitis is a major cause of mortality after liver cirrhosis. Altered permeability of the mucosa and deficiencies in host immune defenses through bacterial translocation from the intestine due to intestinal bacterial overgrowth have been implicated in the development of this complication. Molecular mechanisms underlying the process are not well known. In order to understand mechanisms involved in translocation of bacteria, this study explored the role of oxidative stress in mediating changes in intestinal mucosal glycosylation and luminal bacterial content during cirrhosis. CCl(4)-induced cirrhosis in rats led to prolonged oxidative stress in the intestine, accompanied by increased sugar content of both intestinal brush border and surfactant layers. This was accompanied by changes in bacterial flora in the gut, which showed increased hydrophobicity and adherence to the mucosa. Inhibition of xanthine oxidase using sodium tungstate or antioxidant supplementation using vitamin E reversed the oxidative stress, changes in brush border membrane sugar content, and bacterial adherence. In conclusion, oxidative stress in the intestine during cirrhosis alters mucosal glycosylation, accompanied by an increased hydrophobicity of luminal bacteria, enabling increased bacterial adherence onto epithelial cells. This might facilitate translocation across the mucosa, resulting in complications such as spontaneous bacterial peritonitis. World J Gastroenterol 2006 March 14;12(10):1503-1508 Hepatobiliary and pancreatic disorders in celiac disease Hugh James Freeman Free full text: http://www.wjgnet.com/1007-9327/12/1503.asp A variety of hepatic and biliary tract disorders may complicate the clinical course of celiac disease. Some of these have been hypothesized to share common genetic factors or have a common immunopathogenesis, such as primary biliary cirrhosis, primary sclerosing cholangitis and autoimmune forms of hepatitis or cholangitis. Other hepatic changes in celiac disease may be associated with malnutrition resulting from impaired nutrient absorption, including hepatic steatosis. In addition, celiac disease may be associated with rare hepatic complications, such as hepatic T-cell lymphoma. Finally, pancreatic exocrine function may be impaired in celiac disease and represent a cause of treatment failure. World J Gastroenterol 2006 March 14;12(10):1493-1502 Gut flora and bacterial translocation in chronic liver disease John Almeida, Sumedha Galhenage, Jennifer Yu, Jelica Kurtovic, Stephen M Riordan Free full text: http://www.wjgnet.com/1007-9327/12/1493.asp Increasing evidence suggests that derangement of gut flora is of substantial clinical relevance to patients with cirrhosis. Intestinal bacterial overgrowth and increased bacterial translocation of gut flora from the intestinal lumen, in particular, predispose to an increased potential for bacterial infection in this group. Recent studies suggest that, in addition to their role in the pathogenesis of overt infective episodes and the clinical consequences of sepsis, gut flora contributes to the pro-inflammatory state of cirrhosis even in the absence of overt infection. Furthermore, manipulation of gut flora to augment the intestinal content of lactic acid-type bacteria at the expense of other gut flora species with more pathogenic potential may favorably influence liver function in cirrhotic patients. Here we review current concepts of the various inter-relationships between gut flora, bacterial translocation, bacterial infection, pro-inflammatory cytokine production and liver function in this group.
  12. Celiac.com 06/09/2009 - Results of a recent small population study done in Spain suggest that a gluten-free diet may change gut bacteria balance by decreasing beneficial bacteria and increasing detrimental bacteria. Certainly, gut health is an issue to most people with celiac disease. Recent studies suggest that people with celiac disease benefit from bifidium and lactobaccilus supplements, so it's possible that such benefit is in part an offsetting of damage due to gluten-free diet; at least, a connection seems possible. The Spanish study follows just ten individuals for just one month on gluten-free diets. A large-scale, long-term study might make very different observations, and reach very different conclusions. The study found no significant differences in dietary intake before and after the gluten-free diet except for reductions (P=0.001) in polysaccharides. Bifidobacterium, Clostridium lituseburense and Faecalibacterium prausnitzii proportions decreased (P=0.007, P=0.031 and P=0.009, respectively) as a result of the GFD analysed by fluorescence in situ hybridisation (FISH). Bifidobacterium, Lactobacillus and Bifidobacterium longum counts decreased (P=0.020, P=0.001 and P=0.017, respectively), while Enterobacteriaceae and Escherichia coli counts increased (P=0.005 and P=0.003) after the GFD assessed by quantitative PCR (qPCR). TNF-alpha, interferon-gamma, IL-10 and IL-8 production by PBMC stimulated with faecal samples was also reduced (P=0.021, P=0.037, P=0.002 and P=0.007, respectively) after the diet. The study doesn't provide any real evidence to support a conclusion one way or the other, especially their conclusion that a gluten-free diet "may constitute an environmental variable to be considered in treated Coeliac disease patients for its possible effects on gut health." The fact is that beneficial, probiotic bacteria in the human gut are influenced by diet. The more fruits, vegetables, and high fiber foods we consume, the healthier our bacteria will be. The Spanish study makes no mention of the subjects' diets. Were they fed high fiber, low fat diets rich in fruits and vegetables, or did they eat a standard western diet with no gluten? It would be interesting to compare the gut bacteria levels of people before celiac disease diagnosis and after celiac disease diagnosis to see if a gluten-free diet improves gut bacteria overall, or if the Spanish results would be seen again. Br J Nutr. 2009 May 18:1-7.
  13. Celiac.com 06/12/2009 - In a medical first, researchers at UCLA have made a connection between intestinal inflammation and systemic chromosome damage in mice, a discovery that may pave the way for early identification and treatment of human inflammatory disorders, some of which raise the risk for various kinds of cancer, according a study published in Cancer Research. Scientists discovered that local intestinal inflammation caused DNA damage to lymphocytes of the peripheral blood circulating throughout the body. So, contrary to conventional medical wisdom, chromosome damage is not limited to the immediate intestine, but involves body tissues far away from the actual inflammation. Their results showed single- and double-strand DNA breaks in the blood, and chromosome damage in peripheral blood indicating systemic genetic damage. Inflammatory diseases have been linked to some lymphomas and abdominal, liver and colorectal cancers, said Robert Schiestl, lead author, and professor of pathology, radiation oncology and environmental health sciences and a Jonsson Cancer Center scientist. Finding inflammation early – before any symptoms surface - and treating the associated causes quickly may prevent the damage that eventually triggers these cancers, he said. Before the study, researchers had no knowledge that "intestinal inflammation causes damage that can be found throughout the body,” said Schiestl, adding that this "may help explain how inflammation leads to these cancers.” Intestinal inflammation can be caused by such maladies as Crohn’s disease, inflammatory bowel disease, ulcerative colitis and Celiac disease. Nearly 1.5 million Americans, and 2.2 million Europeans currently suffer from inflammatory bowel diseases and global incidence is on the rise, Schiestl said. The discovery opens up the possibility of using chromosome damage in the peripheral circulating blood as a biomarker to spot intestinal inflammation before any symptoms surface. Researchers were able to detect chromosome damage in the blood of specially bred mice before the onset of colitis, said Aya Westbrook, a graduate student of the UCLA Molecular Toxicology Interdepartmental Program and the paper's first author. Westbrook added that disease severity correlated directly with higher levels of chromosome damage in the blood. Chromosome damage, according to study author Dr. Jonathan Braun, professor and chairman of the Department of Pathology and Laboratory Medicine at UCLA, may be the “earliest detectable indicator” of intestinal inflammatory disease. Currently, the only way to diagnose patients with inflammatory bowel disease is through full endoscopic exam, which is both invasive and costly. In theory, Braun said, a biomarker blood test might replace the invasive endoscopic exam and allow physicians to identify early inflammatory disease before it develops fully. Spotting disease and being able to ward it off early is one of the Holy Grails of all medicine. This breakthrough could “change the natural history of these diseases,” Braun said. For the first time, doctors might have a tool that can actually help spot inflammation, the earliest precursor to multiple kinds of cancer, at its earliest stages, long before any actual disease develops. This could lead to the prevention of tens of thousands of cancers. UCLA researchers have launched a clinical trial to confirm their findings in humans, Schiestl said. They’re focusing on patients with Crohn’s disease and ulcerative colitis. They're hoping the discovery will permit them to test new strategies for treating smoldering disease, which we’ve never been able to identify before,” Schiestl said, adding that they might be able to assess new drugs for treating early inflammatory disease. The research may also show why some patients with inflammatory disease develop cancers, while others endure chronic inflammation for decades, yet remain cancer-free. Researchers suspect that some unknown molecular mechanisms might work to protect some patients and not others. Finding such mechanisms might lead to tests for predicting which patients with intestinal inflammatory diseases are predisposed to cancer. Cancer Research: June 1 2009, Volume 69, Issue 11
  14. Celiac.com 05/31/2006 - I previously discussed how liver abnormalities are highly prevalent in celiac disease. Why damage to the liver occurs is unknown, and gluten toxicity and increased intestinal permeability have been proposed as factors. The following free full text article appearing in the current issue of Gastroenterology may shed light on why liver damage occurs in celiacs. Toll-like receptors (TLRs) reside on the surface of many cells which participate in the immune system. TLRs sense molecules present in pathogens but not the host, and when the immune system senses these molecules, chemicals are released which set off inflammatory and anti-pathogen responses. One class of molecules recognized by TLRs and common to most pathogenic bacteria is lipopolysaccharides (LPS). Gluten increases intestinal permeability in celiacs. The disruption of the intestinal barrier permits endotoxins, such as LPS, from gut bacteria to reach the portal vein of the liver triggering a TLR response from immune cells in the liver. Proinflammatory mediators are released cascading into the release of more chemicals leading to inflammation and liver damage. This may be the cause of liver damage in celiacs. Gluten itself could also trigger a liver immune response. Kupffer cells in the liver are capable of antigen presentation to T cells, along with liver dendritic cells, and could initiate a T cell response to gluten within the liver. The following article is somewhat technical, but discusses the role of various liver cells involved in the immune process and how intestinal permeability and TLRs contribute to liver injury. The article is a good read and provides valuable information about the liver I have not seen elsewhere. Gastroenterology Volume 130, Issue 6, Pages 1886-1900 (May 2006) Toll-Like Receptor Signaling in the Liver Robert F. Schwabe, Ekihiro Seki, David A. Brenner Free Full Text: http://www.gastrojournal.org/article/PIIS0016508506000655/fulltext
  15. Scand J Gastroenterol. 2003 Jul;38(7):727-31. Effectiveness of the sorbitol H2 breath test in detecting histological damage among relatives of coeliacs. Tursi A, Brandimarte G, Giorgetti GM, Inchingolo celiac disease. Dept. of Emergency, L. Bonomo Hospital, Andria (BA), Italy. Celiac.com 08/07/2003 - An Italian study conducted by Dr. L. Bonomo and colleagues and published in the July 2003 edition of Scandinavian Journal of Gastroenterology concludes that A significant proportion of coeliacs may be missed if relatives are screened by serology only, while the efficacy of sorbitol H2-BT in screening relatives is confirmed. This study confirms that neither a breath test nor serology can replace intestinal biopsy, which remains the gold standard for the diagnosis of celiac disease, thus confirming the continued importance of performing biopsies for diagnosing celiac disease. The studys goal was to determine the diagnostic capabilities of serological tests (antigliadin (AGA), antiendomysium (EMA) and anti-tissue transglutaminase (anti-tTG)) and sorbitol H2 breath test (H2-BT) in the detection of celiac disease in first-degree relatives. The study screened 111 first-degree relatives of 37 celiac families using both test methods to determine candidates for small bowel biopsy. First-degree relatives with abnormal test results underwent a small bowel biopsy, as did those with negative serological and H2 breath test results who had clinical complaints or suspected that they may have celiac disease. The biopsy results were expressed using the Marsh classification system, and celiac disease was diagnosed in 49 of the 111 screened relatives of celiacs, or in 44.14%. A breakdown of the results is as follows: 5 showed Marsh IIIc, 8 Marsh IIIb, 16 Marsh IIIa, 13 Marsh II and 7 Marsh I lesions. 19 relatives showed the classical form of celiac disease, 20 showed the sub-clinical form, and 10 showed the silent form. The serological test results indicated an overall positivity of only 36.73%, with strong positive results only in those with severe intestinal damage and Marsh IIIb-c lesions. The sorbitol H2-BT breath test results showed an overall positivity of 83.67%, and showed strong positivity in patients with slight histological damage (Marsh I-IIIa).
  16. Diabetologia. 2005 Apr 14 Celiac.com 04/29/2005 – According to Italian researchers an improper immune response to wheat may play an important role in the pathogenesis of Type 1 diabetes. The researchers fed one group of female non-obese diabetic (NOD) mice a standard gluten-free diet, while another group of NOD mice was fed a standard gluten-free diet that also included wheat proteins. The researchers then evaluated the small intestinal architecture of the mice and found that the wheat-protein group "showed reduced villous height, increased intraepithelial infiltration by CD3(+) cells and enhanced expression of H2-IA and IFN-gamma mRNA when compared with mice on the gluten-free diet." After 43 weeks the cumulative incidence of diabetes was 65% in the gluten-free group, and 97% in the wheat-protein group. The researchers conclude that the mice that ate wheat proteins had a much higher incidence of diabetes and small intestinal enteropathy that included higher mucosal levels of pro-inflammatory cytokines.
  17. Digestion 2002;66(3):178-85 PMID: 12481164 Ciacci C, Cirillo M, Cavallaro R, Mazzacca G. Department of Internal Medicine, Gastrointestinal Unit, Federico II University of Naples, Naples, Italy. Celiac.com 01/12/2003 - Background and Aims: Celiac disease is the most common severe food intolerance in the Western world and is due to gluten ingestion in genetically susceptible children and adults. Intestinal biopsy is the golden standard for evaluation of mucosal damage associated with celiac disease. Gluten-free diet is the key treatment for celiac disease. Data on the long-term control of celiac disease are few and limited to small series of patients. The study reports data on the control of celiac disease and on its correlates in a large cohort of celiac adults during long-term treatment with gluten-free diet. Methods: The study cohort comprises 91 men and 299 women having undergone treatment with a gluten-free diet for at least 2 years and with complete records for visits at the time of diagnosis of celiac disease (baseline). Data collection included gender, age, education, weight, bowel habit, blood hemoglobin, plasma albumin and cholesterol, serum antiendomysium antibodies (EMA), dietary compliance to gluten-free diet (coded as good, low, or very low), and intestinal damage at biopsy (coded as absent, mild, or severe). Results: The duration of follow-up was 6.9 +/- 7.5 years (mean +/- SD, range 2-22 years). At follow-up visit, intestinal damage was absent in 170 patients (43.6%), mild in 127 (32.6%), and severe in 93 (23.8%). At follow-up, intestinal damage was significantly associated with dietary compliance, EMA, and plasma albumin (follow-up value and change value from baseline to follow-up). Baseline education significantly predicted dietary compliance and intestinal damage at follow-up. Conclusions: Celiac disease is often poorly controlled in the majority of patients on long-term treatment with a gluten-free diet as demonstrated by intestinal biopsy. Lack of adherence to strict gluten-free diet is the main reason of poorly controlled disease in adults. Laboratory and clinical information have a high positive predictive value and low negative predictive value for intestinal damage on long-term treatment. Dietary compliance as assessed by interview is the best marker of celiac disease control due to low cost, noninvasivity, and strong correlation with intestinal damage. Copyright 2002 S. Karger AG, Basel
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