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Diagnostic value of anti-Saccharomyces cerevisiae and antineutrophil cytoplasmic antibodies for inflammatory bowel disease: high prevalence in patients with celiac disease
Authors:Damoiseaux Jan G M C  Bouten Bas  Linders Annick M L W  Austen Jos  Roozendaal Caroline  Russel Maurice G V M  Forget Pierre-Philippe  Tervaert Jan Willem Cohen
Affiliation:(1) Department of Clinical and Experimental Immunology, University Hospital Maastricht, The Netherlands;(2) Department of Immunology, University Hospital Groningen, Groningen, The Netherlands;(3) Department of Gastroenterology, University Hospital Maastricht, Maastricht, The Netherlands;(4) Department of Pediatrics, University Hospital Maastricht, Maastricht, The Netherlands
Abstract:
Both celiac disease and inflammatory bowel disease (IBD) are characterized by chronic diarrhea and the presence of distinct (auto)antibodies. In the present study we wanted to determine the prevalence of serological markers for inflammatory bowel disease, i.e., perinuclear antineutrophil cytoplasmic antibodies (pANCA) and/or anti-Saccharomyces cerevisiae antibodies (ASCA), in 37 patients with biopsy-confirmed celiac disease (Marsh IIIb/c). The majority of the patients was positive for IgA (auto)antibodies typically associated with celiac disease, i.e., antiendomysium antibodies (EMA) (86.5%), antigliadin antibodies (AGA) (73%), and antirecombinant human tissue transglutaminase antibodies (rh-tTGA) (86.5%). Four patients with selective IgA deficiency could be identified by analyzing EMA, AGA, and rh-tTGA for the IgG isotype. The prevalence of pANCA and ASCA, markers that are used for IBD, was unexpectedly high in our cohort of patients with celiac disease: 8 patients were positive for pANCA (IgG) and 16 patients were positive for ASCA (IgG and/or IgA). These results indicate that the presence of pANCA or ASCA in the serum of patients with chronic diarrhea does not exclude celiac disease. A prospective study is required to determine whether pANCA and/or ASCA identify patients at risk for developing secondary autoimmune disease.
Keywords:Inflammatory bowel disease  autoimmune disease  IgA deficiency
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