Open AccessGluten‐dependent Small Bowel Mucosal Transglutaminase 2–specific IgA Deposits in Overt and Mild Enteropathy Coeliac Disease
Author(s) -
Koskinen Outi,
Collin Pekka,
KorponaySzabo Ilma,
Salmi Teea,
Iltanen Sari,
Haimila Katri,
Partanen Jukka,
Mäki Markku,
Kaukinen Katri
Publication year - 2008
Publication title -
journal of pediatric gastroenterology and nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 131
eISSN - 1536-4801
pISSN - 0277-2116
DOI - 10.1097/mpg.0b013e31817b6dec
Subject(s) - coeliac disease , tissue transglutaminase , villous atrophy , enteropathy , medicine , immunoglobulin a , gluten , gluten free , gastroenterology , autoantibody , intraepithelial lymphocyte , intestinal mucosa , malabsorption , immunopathology , pathology , immunology , antibody , disease , immunoglobulin g , biology , immune system , enzyme , biochemistry
Objectives: In coeliac disease, immunoglobulin (Ig)A–class autoantibodies against transglutaminase‐2 are produced in the small intestinal mucosa, where they are deposited extracellularly. It remains unclear whether positive intestinal transglutaminase‐2‐targeted IgA deposits in subjects having normal small bowel mucosal morphology are signs of early‐stage coeliac disease. We evaluated the gluten dependency of these deposits in overt and mild enteropathy coeliac disease. Patients and Methods: All together 48 subjects suspected of coeliac disease but having normal small bowel mucosal villi were enrolled; 28 of them had latent coeliac disease. The remaining 20 having positive intestinal IgA deposits adopted a gluten‐free diet before villous atrophy had developed. For comparison, 13 patients with overt coeliac disease and 42 noncoeliac controls were studied. Small bowel mucosal transglutaminase‐2–specific autoantibodies were compared with villous morphology, intraepithelial lymphocyte densities, and serum coeliac autoantibodies. Results: Intestinal IgA deposits were seen in all but 1 of the patients with latent coeliac disease, when the morphology was still intact; the intensity of these deposits increased as villous atrophy developed and decreased again on a gluten‐free diet. In 20 patients with intestinal IgA deposits in normal villi, the intensity of the deposits decreased with the diet similarly to that seen in patients with overt coeliac disease. Mucosal IgA deposits were seen initially only in 5% of noncoeliac controls and in 8% after extended gluten consumption. Conclusions: The response of small bowel mucosal transglutaminase‐2–specific IgA deposits for dietary intervention was similar in overt and mild enteropathy coeliac disease. Detection of such IgA deposits thus offers a good diagnostic tool to uncover early‐stage coeliac disease.