IgA anti-endomysial antibodies in dermatitis herpetiformis: correlation with jejunal morphology, gluten-free diet and anti-gliadin antibodies

Abstract

Circulating IgA-class anti-endomysium antibodies (EmA) can be detected by indirect immunofluorescence on monkey oesophagus sections. We found EmA in 22 (76%) of 29 patients with dermatitis herpetiformis (DH) on a normal, gluten-containing diet. The highest frequency (100%) of EmA was observed in patients with sub-total villous atrophy. IgA-class antigliadin antibodies (AGA) were found using an ELISA method in 59% of 29 DH patients and in 86% of those with sub-total villous atrophy. There was a significant correlation between EmA titres and AGA levels in individual patients. Gluten-free diet (GFD) treatment caused a rapid decrease in EmA titres; only three of the 12 patients still showed raised EmA after 6-12 months on a GFD and two of these three had failed to adhere to a strict diet. In contrast, no decrease in EmA titres occurred in four patients maintained on a normal diet, and two of the three patients with initially negative EmA developed positive titres when continuing on a normal diet. These results show that both IgA-class EmA and AGA are good indicators of jejunal damage in DH. The rapid fall of EmA titres after gluten withdrawal indicates that this test is also useful for monitoring a patient's adherence to a GFD.

A new model for dermatitis herpetiformis that uses HLA-DQ8 transgenic NOD mice

“…These findings reinforce the autoimmune nature of DH, which is supported by the increased association of DH with other autoimmune diseases (32). Similarly, approximately 70% of DH patients have circulating IgA against reticulin and endomysium, both of which are diagnostic markers for celiac disease (2,44). The recurring positivity of approximately 70% for anti-gliadin, anti-tTG, anti-reticulin, and anti-endomysium antibodies likely reflects the state of enteropathy in DH patients.…”

Specific Circulating Anti-Gliadin IgG-Class Antibody Does Not Mediate Intestinal Enteropathy in Gliadin-Fed Mice

“…Taken together, the available data suggest that im mune-mediated intestinal damage involves an autoim mune element, either due to circulating antibodies to tis sue components [21][22][23][24], or due to cell-mediated immunity against self-antigens [25], or possibly both. This would imply that elevated anti-gliadin antibody titres in patients with coeliac disease may be a contributory factor, but alone arc unlikely to mediate the intestinal lesion.…”

“…In man, there is some evidence that circulating IgA class autoantibodies to endomysium and reticulin are im plicated in the intestinal histopathology of coeliac disease and dermatitis herpetiformis [21][22][23][24], even though IgA an tibodies do not fix complement. In our experimental model, it would appear that circulating IgG antibodies to dietary antigens, despite their ability to fix complement and mediate type III hypersensitivity, do not mediate intestinal damage.…”

IgA Antibodies against Reticulin and Endomysium in the Serum and Gastrointestinal Secretions of Patients with Dermatitis herpetiformis

“…In an unselected population of DH patients, IgA antire ticulin antibodies are present in 10-40% of patients and IgA antiendomysium antibodies in 50-80% [1,2]. When patients with DH are selected by the presence of villous atrophy, the incidence of IgA antireticulin antibodies and IgA antiendomysium antibodies is greater than 90%.…”

“…The origin of the IgA which deposits in the skin of patients with DH is not known; however, the strong associ ation of DH with a gluten-sensitive enteropathy has led to the hypothesis that this IgA is of gut origin. Although IgA antibodies which can bind to human skin have not been detected in the serum of patients with DH, IgA antibodies which bind to connective tissue of the human and rodent liver, kidney and esophagus have been detected in the serum of patients with both DH and isolated gluten-sensi tive enteropathy [1,2],…”