Identification of a new coeliac disease subgroup: antiendomysial and anti-transglutaminase antibodies of IgG class in the absence of selective IgA deficiency

Objective. The aim of the present study was to increase the sensitivity of the antiendomysial antibody (EMA) test by evaluating also EMAs of IgG1 isot ype. Design and subjects. Over the last 2 years, serum EMAs IgA and IgG1 were de termined in 1399 patients, referred to our gastrointestinal unit due to cli nical suspicion of malabsorption. Serum antitissue transglutaminase (tTG) a ntibodies IgA and IgG, as well as total IgA levels, were also investigated, Furthermore, EMAs IgA and IgG1 were evaluated in biopsy culture supernatan ts. Biopsy specimens were also admitted to histological and immunohistochem ical evaluation. Twenty-six patients with gastroenterological disease other than coeliac disease (CD) were used as a disease control group. Ninety-nin e blood donors were used as a healthy control group. Results. Diagnosis of CD Mras based on histological findings in the 110/139 9 patients showing EMA IgA positivity, and in a further 56/1399 patients pr esenting both EMA IgA and IgG1 positivity in sera as well as in culture sup ernatants. Of the remaining 1233 EMA IgA-negative patients, 60 showed only EMA IgG1 positivity both in sera and in culture supernatants. It is notewor thy that anti-tissue transglutaminase antibodies IgG (anti-tTG) were positi ve in all 60 EMA IgG1-positive patients as well. By contrast. a selective I gA deficiency was found in only 11 out of the 60 EMA IgG1-positive patients , Villous height/crypt depth ratio was < 3:1 in 38 of the 60 EMA IgG1-posit ive patients (63.3%). whilst overexpression of ICAM-1 and CD25 was observed in all these patients. Conclusions. In this study, we observed a group of CD patients who were EMA IgG1-positive even in the absence of EMA IgA positivity and IgA deficiency , The diagnosis was based on the finding of the gluten-dependent clinical a nd histological features typical of CD. Data emerging from the present inve stigation thus suggest that the prevalence of CD should be reassessed and t hat the determination of EMA IgG1 could offer a new tool in the diagnostic armamentarium of CD.