1999;28:26C30. (TG-IgG). Very low proportions (0 to 8%) of IgA-deficient sera and control sera were positive for TG-IgA, gliadin IgA, EMG, and TG-IgG. Eight of 26 (31%) IgA-deficient serum samples were positive for gliadin IgG, whereas 3 of AZD1080 26 (12%) control serum samples were positive for gliadin IgG, but this difference was not statistically significant. Physicians supplied medical data for 18 of 26 individuals with IgA deficiency; only 4 individuals experienced undergone small-bowel biopsy, AZD1080 and 0 of 4 individuals showed villous atrophy. These findings display that IgA deficiency is found more frequently among sera submitted for screening for EMA inside a research laboratory establishing, but there was no clear-cut serologic or medical evidence of CD in EMA-negative, IgA-deficient individuals. Celiac disease (CD) displays intolerance to gliadin (a component of gluten) from wheat and related proteins from rye and barley. Children typically present with failure to thrive, diarrhea, and malabsorption; adults, in contrast, may exhibit a vast array of symptoms, including dermatitis herpetiformis, recurrent abdominal pain, and anemia (6, 17, 18). CD is histologically recognized by detection of villous atrophy in small-bowel biopsy specimens (6, 17). Individuals with CD are successfully treated by removing gluten using their diet programs (12, 17). Most CD patients create immunoglobulin G (IgG) and IgA antibodies that identify gliadin (7, 23, 24). Via processes only beginning to become recognized (12, 19, 25, 28), gliadin exposure in CD individuals also prospects to the production of autoantibodies that identify endomysium, an intermyofibril compound found in primate smooth-muscle connective cells (8). Recent studies have recognized transglutaminase as CD97 the major autoantigenic component of endomysium (9). Although biopsy remains the gold standard for the analysis of CD, serologic testing is definitely valuable like a display for CD. The single best serologic test for CD is definitely endomysial IgA (EMA) detection, on the basis of its high ( 95%) level of sensitivity and specificity (6, 29). Initial studies that have measured transglutaminase IgA (TG-IgA) demonstrate level of sensitivity and specificity ideals nearing those of checks for EMA, but kits cleared from the U.S. Food and Drug Administration have only recently become available (1, 10, 26). For reasons that remain unclear, checks for neither endomysial IgG (EMG) nor transglutaminase IgG (TG-IgG) are as sensitive or specific as checks for EMA for the detection of CD (1, 2, 11, 26). Checks for gliadin IgG and gliadin IgA present good level of sensitivity and specificity, respectively, but neither assay is as efficient as an assay for EMA (6, 7, 17, 24). Although EMA measurement is considered the best serologic test for CD, the assay does have limitations. In children less than AZD1080 2 years old, EMA detection is less than 90% sensitive (27, 29). Another limitation to the use of EMA detection for serologic detection of CD is the improved rate of recurrence of IgA deficiency in individuals with CD. Approximately 3% of CD patients show IgA deficiency, AZD1080 whereas only 0.3% of the general population offers IgA deficiency (5, 13). Therefore, sera from CD patients who will also be IgA deficient may give a false-negative result for EMA (1, 2, 5, 22, 27). This limitation offers led some investigators to.