IgA anti-endomysium antibody. A new immunological marker of dermatitis herpetiformis and coeliac disease

Abstract

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.

Predictors of Family Risk for Celiac Disease: A Population-Based Study

“…EMA was determined by indirect immunofluorescence on monkey esophagus (BINDAZYME™, The Binding Site Ltd, Birmingham, UK) as previously described. 22 Positive = ≥1:5. HLA class II was typed by low-resolution PCR-SSP (one Lambda Inc., Canoga Park, CA), and by high resolution methods for DQA/B alleles.…”

Calcium activation of tissue transglutaminase in radioligand binding and enzyme-linked autoantibody immunoassays in childhood celiac disease

“…All EMA had been analyzed at the Clinical Microbiology and Immunology, Lund University Hospital, Lund, Sweden, by indirect immunofluorescence [5]. …”

“…For the laboratory diagnosis of celiac disease (CD) determination of endomysial antibodies (EMA) has long been utilized [5]. It has further been shown that tTG is the main autoantigen of EMA [6].…”

Inmunología de la enfermedad celíaca

“…Las únicas situaciones en las que podría mantenerse la utilización de estos marcadores son el control de la dieta sin gluten y la falta de sensibilidad de los anticuerpos antiendomisio (AEm)-IgA por debajo de los 2 años de edad, aunque en estos casos, los AAG se ven superados por sus sucesores naturales, los anticuerpos antipéptidos deaminados de gliadina 53 . La descripción del patrón de AEm-IgA en la dermatitis herpetiforme y la EC por inmunofluorescencia indirecta sobre cortes de esófago de mono 54 o de cordón umbilical humano 55 revolucionó el diagnóstico serológico de la EC, y se alcanzaron unas cifras de sensibilidad y especificidad superiores al 95% 51 . Además de la utilización de los tejidos de mono, el principal problema de estos marcadores es técnico, puesto que la inmunofluorescencia indirecta requiere la interpretación del observador, es, por tanto, subjetiva, y necesita de un entrenamiento especial y experiencia.…”