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Showing results for tags 'excerpts'.
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Celiac.com 11/07/2013 - Several of the world's most prominent scientists, researchers, healthcare practitioners, nutritionists, patients, caregivers and others interested in improving the lives of those living with gluten-related disorders will gather online, November 11-17, 2013, for the first-ever Gluten Summit: A Grain of Truth. An excerpt from two of the iconic speakers is below. Have you ever wondered what "the Godfather of celiac disease diagnosis" thinks about the fact that celiac disease is generally only recognized and treated if a patient has total villous atrophy (all the shags are worn away)? I went to the source! I had the tremendous honor of traveling to Wolfson College, Oxford University in the United Kingdom to interview Dr. Michael Marsh, "the Godfather of celiac disease diagnosis", after whom the Marsh classification of intestinal damage in celiac disease was named. Dr. Marsh has a powerful message for the world about the critical importance of identifying and treating the early stages of celiac disease in patients before it reaches the end-stage of total villous atrophy (Marsh III). In 2006 Dr. Marsh stood up at the International Celiac Disease Symposium in New York and asked the panel the hard question "If a patient has positive blood tests and a negative biopsy, and you do not recommend a gluten-free diet, and the patient dies of lymphoma in two years, which one of you will be able to say that you practiced a good standard of care medicine?" This was a wake-up call to the world, and five years later non-celiac gluten sensitivity was recognized as a separate condition in a consensus by 16 global experts. In the first interview he has ever given, in the 21st birthday year of the Marsh classification system, Dr. Marsh speaks out on: Why normal villi can also be associated with a state of gluten sensitivity Why physicians must not wait for total villous atrophy to occur before treating gluten sensitive patients with a gluten-free diet Why a variety of disciplines beyond immunologists must now join together to study the early stages of celiac disease Dr. Marsh calls them out! Dr. Hadjivassiliou - How GLUTEN can affect your NERVOUS SYSTEM! Dr. O'Bryan: A suggestion that you have made in a number of your papers over the years is that "It is time to move on from gut to brain." Can you tell our listeners what you mean by this? Prof. Hadjivassiliou: Sure. I think it was a comment in relation to try and escape from the existing belief that sensitivity to gluten is primarily or even exclusively a disease of the gut. You can see why it's always been thought of as a gastrointestinal disease, simply because that's where gluten gets ingested and absorbed. However, we are talking about an autoimmune disease, and therefore the manifestations of an autoimmune disease can be very diverse...It's about time we thought of this as a systemic disease that can affect different parts of the body rather than concentrating solely on the bowel. My main interest was whether patients can manifest exclusively with neurological (nervous system) problems. Prof. Hadjivassiliou goes on to explain: The ratio of patients with nervous system issues vs. intestinal issues Why an early diagnosis is CRITICALLY IMPORTANT Why neurological patients may take longer to see results when they start a gluten-free diet The true impact of an accidental gluten exposure on a person whose nervous system is affected by gluten Visit theglutensummit.com for a link to the world's first ever online Gluten Summit, which will take place from Nov.11-17, 2013, to listen to the entire interview with Prof.Hadjivassiliou and many, many more interviews with the experts on gluten-related disorders and diet, and their impact you and your children's health. The Gluten Summit is a unique and FREE event which aims to move the question, "Is gluten the cause?" into today's conversation between patients and healthcare professionals potentially improving the lives of millions now.
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Celiac.com 09/30/2002 - The Canadian Medical Association Journal (Hoey, 2002;166:479-80) published the following, Irritable Bowel Syndrome: Could it be Celiac Disease?, as excerpted below. This was an analysis of a Lancet article (Sander et al, 2001;358:1504-8) called, Association of Adult Coeliac Disease with Irritable Bowel Syndrome: A Case-Control Study in Patients Fulfilling Rome II Criteria Referred to Secondary Care. Here are the CMAJ excerpts: Irritable Bowel Syndrome is found in 10% to 20% of people with the use of standard diagnostic tools such as the Rome II criteria. Rome II criteria is specified below: At least 12 weeks, which need not be consecutive, in the preceding 12 months of abdominal discomfort or pain that has 2 out of 3 features: Relieved with defecation Onset associated with a change in frequency of stool Onset associated with a change in form (appearance) of stool Symptoms that cumulatively support the diagnosis of irritable bowel syndrome: Abnormal stool frequency (more than 3 bowel movements per day or fewer than 3 bowel movements per week) Abnormal stool form (lumpy/hard or loose/watery stool) Abnormal stool passage (straining, urgency or feeling of incomplete evacuation) Passage of mucus Bloating or feeling of abdominal distention Question: What proportion of patients who meet the Rome II criteria for irritable bowel syndrome have celiac disease? Case subjects: The article cites that 300 people (214 women, 86 men ranging in age from 18 to 87, (mean 56 years)) met the Rome II criteria out of 686 new patients who were referred by a family physician to a university hospital gastroenterology clinic. Control subjects were healthy people without irritable bowel syndrome. Also, most control subjects were companions of the patients who were matched to case subjects by age (within 1 year) and sex, as well as questioned in the same manner as case subjects. All case and control subjects underwent a wide range of baseline investigations, including full blood count, measurement of erythrocyte sedimentations rate, blood urea nitrogen and serum electrolyte levels, and thyroid function tests. In addition, they were investigated for celiac disease by analysis of serum levels of IgG antigliadin, IgA antigliadin and endomysial antibodies. Most of the case subjects, particularly those older than 45, underwent colonoscopy or sigmoidoscopy and barium enema. Case and control subjects with positive antibody test results were offered duodenal biopsy to confirm the possibility of celiac disease. Of the 66 case subjects who had positive antibody test results, 49 had elevated levels of only IgG antigliadin 4 of only IgA antigliadin and 6 of only endomysial antibodies Fourteen of the 66 were subsequently found to have histologic evidence of celiac disease; 11 of the 14 were positive for endomysial antibodies. Nine of the of 66 case subjects were lost to follow-up or refused duodenal biopsy; 1 of them was positive for endomysial antibodies. Of the 44 control subjects who had positive antibody test results, 41 had elevated levels of only IgG antigliadin 1 of only IgA antigliadin and 2 of IgG antigliadin and endomysial antibodies Only the last 2 subjects elected to undergo duodenal biopsy, and both were found to have histologic evidence of celiac disease. Commentary: The authors found that a high proportion of patients (about 5%) who were referred to a university hospital gastroenterology clinic and who met the Rome II criteria did have celiac disease. In addition, the clinic specialists uncovered other organic abnormalities in almost 20% of the referred patients. The study had several weaknesses. For instance, although most of the case subjects underwent extensive investigations of the lower gastrointestinal tract, the control subjects did not. Thus, some of the case subjects who were lost to follow-up or refused investigation and many of the age-matched control subjects might have been found to have irritable bowel disease, celiac disease or other gastrointestinal abnormalities. The authors conclude from their findings that patients who meet the Rome II criteria for irritable bowel syndrome and who are referred to a secondary care centre should be investigated routinely for celiac disease. In an editorial accompanying the Lancet article, a gastroenterologist cautioned that more studies are needed. He noted an earlier study in which 121 consecutive patients were referred for investigation of irritable bowel syndrome. Using Rome I criteria and similarly extensive investigation, the researchers detected no cases of celiac disease. Because of the findings from the Lancet study, the editorialist has decided to further lower his threshold for screening for celiac disease among patients referred for investigation of irritable bowel syndrome. Perhaps other gastroenterologists would be wise to do the same. I verified the five percent as cited in the CMAJ as 14 out of the 300 patients who met the Rome II criteria also had celiac disease. The CMAJ also cites the following, Studies in Europe have shown that up to 1% of the adult population may have celiac disease. We can make our own conclusions from this study in Lancet and we might agree that 1% may be understated but further studies have to be performed to corroborate a higher percentage of undiagnosed celiacs; I hope this definitely encourages closer scrutiny of IBS patients like myself who was diagnosed with IBS in 1997 with only a symptom of left side tenderness below my rib cage and a sigmoidoscopy which revealed no abnormalities except a hemorrhoid. Then, in the summer of 2001, I was diagnosed with lactose intolerance and IBS once more before discovering from medical research and my food dairy taken since May 2001, along with corroboration by an allergist in October 2001, that it may be celiac disease, as my malabsorption symptoms grew worse.
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Celiac.com 09/01/2002 - Patients with celiac disease are 20 times more likely than the general population to have epilepsy and often have associated cerebral and cerebellar calcifications imaged by CT and MRI. Depression, dementia, and schizophrenia are all also common in persons with untreated celiac disease. Cerebellar degeneration with resulting ataxia (gluten-associated ataxia) is a known entity in Europe, and the National Institutes of Health (NIH) is currently recruiting subjects with ataxia to examine them for gluten sensitivity and celiac disease. Focal white matter lesions in the brain recently have been reported to occur in children with celiac disease and are thought to be either ischemic in origin as a result of vasculitis or caused by inflammatory demyelination. Parents of children with celiac disease have reported behavioral changes such as irritability, separation anxiety, emotional withdrawal, and autistic-like behaviors that all seemed to improve on a GFD. Although not scientifically validated, the GFD is now also being advocated for children with autism by several groups. Whether or not children with autism are at a higher risk for celiac disease or celiac children have a higher incidence of autism remains to be proven. However, children with Down syndrome, who often have autistic-like behaviors, are at higher risk for celiac disease. It has been hypothesized that gluten may be broken down into small peptides that may cross the blood-brain barrier and interact with morphine receptors, leading to alterations in conduct and perceptions of reality. The serologic tests can be divided into 4 different types of antibodies: antigliadin (AGA), antireticulin, antiendomysium (AEA), and antitissue transglutaminase (tTG). Each antibody varies widely in its sensitivity, specificity, and positive and negative predictive values (Table 2). Table 2 (from Pietzak et al, 2001, compiled data from multiple studies) Test Sensitivity Specificity PPV NPD AGA IgG 57-100 42-98 20-95 41-88 AGA IgA 53-100 65-100 28-100 65-100 AEA IgA* 75-98 96-100 98-100 80-95 Guinea pig tTG† 90.2 95 Human tTG† 98.5 98 * Patients older than 2 years of age. † IgG +IgA antibodies. The AEA IgA immunofluorecent antibody is an excellent screening test for celiac disease, with both a high sensitivity and specificity. This antibody was discovered in the early 1980s and rapidly gained use as part of a screening celiac panel by commercial laboratories in combination with AGA IgG and AGA IgA. Its major drawbacks are that it may be falsely negative in children under the age of 2 years, in patients with IgA deficiency, and in the hands of an inexperienced laboratory. Also, the substrate for this antibody was initially monkey esophagus, making it expensive and unsuitable for screening large numbers of people. Recently, the human umbilical cord has been used as an alternative to monkey esophagus. However, the subjective nature of the AEA assay may lead to false-negative values and unacceptable variability between laboratories. Because tTG had been first described as the autoantigen of celiac disease in 1997, it has been used to develop innovative diagnostic tools. The tTG IgA ELISA test is highly sensitive and specific, using either the commercially available guinea pig tTG or human recombinant tTG. The tTG assay correlates well with AEA-IgA and biopsy. However, it represents an improvement over the AEA assay because it is inexpensive and rapid (30 minutes), is not a subjective test, and can be performed on a single drop of blood using a dot-blot technique. Therefore, this test is ideally suited for mass screenings and in the future could be performed in the general practitioners office, much like the now routine finger-stick hematocrit. For the reasons outlined above, the IgA class human anti-tTg antibody, coupled with the determination of total serum IgA, currently seems to be the most cost-effective way to screen for celiac disease. AEA should be used as a confirmatory, pre-biopsy test, whereas AGA determinations should be restricted to the diagnostic work-up of younger children and patients with IgA deficiency, using the guidelines in Table 3. Table 3 Probability of celiac disease based on three antibodies in combination AEA IgA AGA IgA AGA IgG Interpretation + + + Celiac disease 99% probable + - + probable + + - Celiac disease probable + - - Celiac disease probable - + + Celiac disease less likely* - - + Celiac disease less likely* - + - Celiac disease less likely - - - Celiac disease very unlikely+ * If patient is IgA sufficient: AGA IgG > 100 warrants work-up of enteropathy. + If patient is on a gluten-containing diet. Celiac disease: AEA, antiendomysium antibodies: AGA, antigliadin antibodies.
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