What?"The important thing to take away from this study is that people who have IBS symptoms have celiac disease"False!!!IBS patients have a specific "cluster" of symptoms from IBS, minus red flags.Celiac disease patients have bowel symptoms from Celiac.Again they are not the same disorders.and""Symptoms of these diseases--celiac disease, gastroesophageal reflux disease (GERD), food allergies, lactose intolerance, and eosinophilic gastroenteritis--can sometimes coexist or be confused with a functional GI disorder. Depending upon the history and symptom presentation, these diseases may need to be considered when making a diagnosis.
Significantly, they all have distinguishing characteristics that can differentiate them from functional GI disorders. "There is of course no problem asking your doctor about celiac or any other condition that can MIMICK some bowel symptoms of IBS or if you think you have red flag symptoms. Especially if you have other family members with it.Irritable Bowel Syndrome: How far do you go in the Workup?"What about celiac disease? This disorder should always be considered in evaluating IBS, because the diarrhea and abdominal discomfort due to proximal small intestinal villous atrophy and inflammation will specifically respond to a gluten-free diet. Therefore, making a diagnosis early may be cost-effective. The prevalence of celiac disease in the US is reported to range from 1:250 to 1:1500 (17). However, this is influenced by the method of assessment as well as the prior probability of the disorder being present in the population under study. With regard to the method of assessment, in a study set in Olmstead County (18), the reported prevalence was 1:4,600, and the cases were identified by clinical and pathological criteria. In contrast, when serological methods are used, the prevalence is at 1:250 or even higher (19), and in one recent study the prevalence for women was 1:125 compared to males at 1:250 (20). So, when clinically suspected, primary care physicians and specialists may now obtain anti-gliadin and anti-endomysial IgA antibody serologies. These are reasonably effective screening tests, given that the sensitivities and positive predictive values range from 90% - 100% (17). However, in populations where the prevalence of this disorder is low, many positive serological tests will be false positives. Therefore, because the gold standard of diagnosis requires upper endoscopy with duodenal biopsy, endoscopy is almost always needed for confirmation of the diagnosis. But can we be satisfied that these studies are enough to exclude celiac disease? In this issue of Gastroenterology, Wahnschaffe et al.(21) raise concerns about the possibility of missing a diagnosis of latent or potential celiac disease among persons thought to have IBS. Patients with latent or potential celiac disease have a genetic susceptibility for the disease, but do not have the histopathological findings (i.e., no villous atrophy or notable mucosal inflammation) when exposed to a gluten diet, so a small bowel biopsy will not make this diagnosis. In contrast to potential celiac disease, latent disease is characterized by mucosal changes that occurred at some point in time and recovered on a gluten-free diet. The authors propose that both these groups may still respond clinically to a gluten free diet. This creative study attempted to identify patients with latent or potential celiac disease (i.e., who presumably had negative serological screens for celiac disease) in a sample of 102 IBS patients. They evaluated a variety of serological, intestinal and genetic markers, and compared the findings to control groups with treated and untreated celiac disease, latent celiac disease and normal controls. They found two surrogate markers: a) the expression of HLA-DQ2 alleles DQA1*050/DQB1*0201, a genetic marker for celiac disease, and
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an increased intestinal IgA titer against tissue-transglutaminase and/or gliadin were elevated in the small sample of patients with latent celiac disease. Notably, the assessment of intestinal (rather than serological) antibodies is a unique aspect of this study; it is a diagnostic method for celiac sprue that is not commonly done. Then, when evaluating the IBS patients, they found that 35% had expression of the HLA-DQ2 genotype, and this subgroup of IBS patients had significantly increased IgA antibodies against the celiac disease-associated antigens gliadin and/or tissue-transglutaminase in the duodenal aspirate, as well as increased intra-epithielial lymphocytes (also characteristic of celiac disease) when compared to IBS patients without expression of the HLA-DQ2 genotype. Furthermore, 26 IBS patients were put on a gluten-free diet for 6 months. The 13 patients who were positive for the HLA-DQ2 alleles and for the intestinal celiac disease-associated antibodies had a significant reduction in stool frequency and intestinal IgA antibody titers for the celiac disease-associated antigens. This improvement did not occur in the remaining IBS patients on gluten free diet who were negative for HLA-DQ2 gene expression. They conclude that the presence of these two markers in patients with IBS may identify a subgroup with latent or potential celiac disease that may respond to dietary restriction. These findings must be put into a clinical perspective. First, the authors identified the IBS patients as those who had a "…variable combination of abnormal bowel habits in the absence of endoscopic, histopathological, laboratory and microbiological abnormalities." However, these criteria are not sufficient for diagnosing IBS. We do not know how many of these patients actually had abdominal pain, the key symptom criterion for a diagnosis of IBS. Clinically, patients with diarrhea and no pain are considered separate from IBS ("functional diarrhea"), and they define a group where celiac disease is more likely than patients with typical IBS having abdominal pain. In fact, if many of these patients did not have pain, and therefore did not fulfill criteria for IBS, then the findings of the study and its implications for IBS may be quite different. Second, the sample sizes for some of the cells were small. Only 5 patients had latent celiac disease, and the improvement in response to gluten restriction occurred in a sample of 13 patients with IBS who were HLA-DQ2 positive. It will also be valuable to conduct this study in a controlled fashion using a large group of patients with IBS not having celiac disease markers in order to determine the placebo response rate to a gluten free diet. Even the reduction in serologies with a gluten free diet may not provide complete evidence for a clinical response, since dietary restriction of gluten might reduce the antigenic challenge to the immune system, leading to a serological response that is unrelated to the changes in stool frequency. Despite these limitations, this study has raised some important concerns regarding our sense of "security" in accepting normal histopathology to exclude celiac disease in patients having symptoms of IBS, and has opened the door to pursuing these issues in larger clinical trials. "
http://www.romecriteria.org/reading1.html
iagnoses made prior to celiac disease included anemia (40%), stress (31%), and irritable bowel syndrome (29%)
