title: Celiac disease-like abnormalities in a subgroup of patients with irritable bowel syndrome.
abstract: OBJECTIVE
  Abdominal symptoms in the absence of mucosal abnormalities are features of both the irritable bowel syndrome (IBS) and latent/potential celiac disease (cd). To identify a possible subgroup of IBS patients with latent/potential cd, surrogate markers of cd were investigated in IBS patients.
  
  
  METHODS
  IBS patients suffering from diarrhea (n = 102), and patients with active cd (n = 10), treated cd (n = 26), and latent cd (n = 5) were included in the study. We measured serum immunoglobulin (Ig) A against gliadin and tissue-transglutaminase, and IgA and IgM against gliadin, tissue-transglutaminase (intestinal cd-associated antibodies), and the dietary proteins beta-lactoglobulin and ovalbumin in duodenal aspirate by enzyme-linked immunosorbent assay. Intraepithelial lymphocytes (IELs) were counted in histology sections, and the expression of HLA-DQ2 (A1*0501/B1*0201) was investigated by polymerase chain reaction. In 26 IBS patients, the effect of 6 months of gluten withdrawal was examined.
  
  
  RESULTS
  Most cd patients expressed HLA-DQ2 and had increased intestinal cd-associated antibodies, whereas cd-associated serum IgA and IEL counts were increased in active cd in contrast to treated or latent cd. In IBS patients, 35% were HLA-DQ2-positive, 23% had increased IEL counts, and 0% and 30% had increased cd-associated antibodies in serum and duodenal aspirate, respectively. Furthermore, stool frequency and intestinal IgA decreased significantly under a gluten-free diet in the subgroups of HLA-DQ2-positive and intestinal antibody-positive IBS patients when compared with IBS patients without these markers.
  
  
  CONCLUSIONS
  HLA-DQ2 expression and increased intestinal cd-associated antibodies are markers that can identify latent/potential cd in a subgroup of IBS patients who consequently appear to profit from a gluten-free diet.
authors.affiliation: Department of Gastroenterology and Infectious Diseases, Universitätsklinikum Benjamin Franklin, Freie Universität Berlin, D-12200 Berlin, Germany. ulliwahn@zedat.fu-berlin.de
authors.forename: U
authors.initials: U
authors.lastname: Wahnschaffe
authors.forename: R
authors.initials: R
authors.lastname: Ullrich
authors.forename: E O
authors.initials: EO
authors.lastname: Riecken
authors.forename: J D
authors.initials: JD
authors.lastname: Schulzke
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000906:Antibodies / Q000032:analysis; D000941:Antigens / Q000276:immunology; D002446:Celiac Disease / Q000150:complications* / Q000276:immunology; D003109:Colonic Diseases, Functional / Q000150:complications* / Q000276:immunology; D004032:Diet; D004386:Duodenum / Q000276:immunology; D005260:Female; D005903:Gliadin / Q000276:immunology; D006801:Humans; D007070:Immunoglobulin A / Q000032:analysis; D007075:Immunoglobulin M / Q000032:analysis; D007782:Lactoglobulins / Q000276:immunology; D008297:Male; D008875:Middle Aged; D010047:Ovalbumin / Q000276:immunology; D012155:Reticulin / Q000276:immunology; D011503:Transglutaminases / Q000276:immunology
chemical_list: D000906:Antibodies; D000941:Antigens; D007070:Immunoglobulin A; D007075:Immunoglobulin M; D007782:Lactoglobulins; D012155:Reticulin; D010047:Ovalbumin; D005903:Gliadin; D011503:Transglutaminases