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Aims: Tissue transglutaminase (tTG) was recently identified as the major autoantigen in coeliac disease. The aim of this multicentre study was to evaluate the impact of a new immunoenzymatic assay for the detection of IgA anti-tGT antibodies. Methods: Seventy four Italian and French clinical laboratories participated in this study; anti-tTG IgA with an enzyme linked immunosorbent assay (ELISA) method using guinea pig liver extract as the coating antigen, anti-endomysium IgA autoantibodies (EMA), and total serum IgA were determined in 7948 patients, 1162 of whom had coeliac disease (737 untreated cases and 425 on a gluten free diet). A proportion of the sera were then sent to a reference laboratory for anti-tTG retesting with an ELISA method using recombinant human tTG antigen. Results: Seven thousand four hundred and fifty eight (93.8%) sera were EMA/antiguinea pig fig concordant (positive or negative); 490 (6.2%) were non-concordant. The sensitivity of EMA and antiguinea pig fig in the 737 untreated patients with coeliac disease was 92.1% and 94.8%, respectively, and the specificity was 99.8% and 99.2%, respectively. Retesting of the discordant sera showed that of the 162 sera classified as EMA negative/antiguinea pig tTG positive, only 49 were positive for human recombinant anti-tTG, and that 39 of these were also EMA positive. Furthermore, of the 36 sera classified as EMA positive/antiguinea pig tTG negative, only two were confirmed as EMA positive. Conclusions: The antiguinea pig fig assay is more sensitive but less specific than EMA, whereas the antihuman recombinant tTG assay is far more specific and just as sensitive as antiguinea pig tTG. Testing for EMA presents considerable interpretative problems and is difficult to standardise. [ABSTRACT FROM AUTHOR]

Celiac disease (CD) is frequently associated with an autoimmune disorder (AD). The aim of the study was to establish if an AD is more frequent than expected in relatives of CD patients and, in particular, if it is related to the presence of silent unrecognised CD. We also evaluated the prevalence of ADs in CD patients and compared it with that in a control series. A structured questionnaire was used to evaluate the prevalence of ADs in 125 (51 males and 74 females with a mean age of 8.9 years) children with CD (group A), 125 (67 males and 58 females with a mean age of 8.1 years) matched "healthy" children (group B), all 1352 first- and second-degree relatives of the 125 children with CD (group C), all 1238 first- and second-degree relatives of the control group B of "healthy" children (group D), and all 205 first- and second-degree relatives of 20 children with AD (group E). We also used the antiendomysium antibody assay to screen 354 of the 373 first-degree relatives of group C. An AD was present in 9 of the 125 (7.2%) children with CD (group A), in 1 of the 125 (0.8%) healthy children (group B), in 67 of the 1352 (4.9%) relatives of CD patients (group C), in 14 of the 1238 (1.1%) relatives of healthy children (group D), and in 7 of the 205 (3.4%) of relatives of patients with AD (group E). Clinically silent CD was found in 20 of the 354 first-degree relatives of CD patients (5.6%), and the risk of silent CD was significantly higher, reaching 25% (4/16) in the subgroup of relatives also affected by another AD. Relatives of CD patients had an increased prevalence of AD compared to control groups, and relatives of CD patients with ADs, have a risk as high as 25% of being silent celiacs: they should thus be screened for CD. [ABSTRACT FROM AUTHOR]