The recently described IgA anti-endomysial antibodies (IgA-EmA) are directed against the intermyofibril substance of the smooth muscle, which may correspond either to a reticulin-like structure or a surface component of smooth muscle fibrils. These antibodies occurred in about 80% of sera of thirty-eight patients with dermatitis herpetiformis (DH), in about 70% of twenty-eight patients with coeliac disease and in about 20% of nine patients with other enteropathies. IgG class anti-gliadin antibodies (AGA) also occur in each of these diseases. Both antibodies were detected on monkey oesophagus by immunofluorescence. The IgA-EmA could not be detected in 122 control sera from patients with other gut or skin diseases, including fifteen cases with ulcerative colitis and fifteen cases with linear IgA bullous dermatosis (LABD). The presence and the titre of IgA-EmA and AGA paralleled the severity of the jejunal changes in patients with coeliac disease.

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Immunoglobulin A (IgA) deficiency is 10 to 15 times more common in patients with celiac disease (CD) than in healthy subjects. Serological tests have become the preferred methods of diagnosing CD in both symptomatic and asymptomatic patients. However, commercially available serological methods are limited in that they detect only the IgA isotype of antibodies (with the exception of IgG gliadin assays); hence, IgA-deficient patients with CD may yield false-negative serology. Fifteen pediatric patients with CD and 10 IgA-deficient pediatric patients without CD were examined for IgA and IgG antibodies to endomysium, gliadin, and tissue transglutaminase. Twenty-five specimens from patients with IgA deficiency were examined. Fifteen were from patients with CD, and 10 were patients without CD. All 15 IgA-deficient patients with CD were positive for endomysium antibodies of the IgG isotype and for IgG gliadin antibodies. All but one of the IgA-deficient patients with CD were also positive for IgG tissue transglutaminase antibodies. None of the IgA-deficient patients without CD were positive for any of the antibody markers. All the specimens examined were also negative for IgA-specific antibodies to endomysium, gliadin, and tissue transglutaminase. IgG-specific antibody tests for endomysium, gliadin, and tissue transglutaminase are useful for the identification of IgA-deficient patients with CD. IgG antibody tests along with tests routinely being used in clinical laboratories can reliably detect all active patients with CD. In addition, the levels of these CD-specific IgG antibodies could be used to monitor patient dietary compliance