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RESEARCH PRODUCT

Anti-actin antibodies in celiac disease: correlation with intestinal mucosa damage and comparison of ELISA with the immunofluorescence assay.

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The presence in the sera of celiac disease (CD) patients of anti-actin autoantibodies (AAAs) has been suggested as a marker of severe intestinal villus atrophy (1). AAAs have been detected with an immunofluorescence (IF) technique and seem to contribute to villus cytoskeleton damage and to the pathogenesis of intestinal damage in CD (2). The aims of the present study were to evaluate the relationship between the presence of serum IgA AAAs and severity of intestinal mucosa damage in CD patients and to compare the IF assay with a new ELISA for IgA AAA determination. We enrolled 150 individuals in the study. IgA AAAs were assayed in 58 consecutive CD patients diagnosed between January and December 2003: 30 adults (10 male; median age, 32 years; range, 18–56 years) and 28 children (14 male; median age, 18 months; range, 1–12 years). The sera were collected at CD diagnosis, after overnight fasting, and were frozen at −80 °C for a mean of 9 months before AAA determination. In 20 patients, AAAs were reassayed after 6–12 months of gluten-free diet. CD diagnosis was based on the revised criteria of the European Society of Pediatric Gastroenterology and Nutrition (3). We enrolled 64 patients as “healthy” controls [34 adults evaluated for suspected hypercholesterolemia (15 male; median age, 35 years; range, 18–56) and 30 children with recurrent pharyngotonsilitis (14 male; median age, 3 years; range, 1–12 years)]. None of these controls had symptoms or laboratory signs suggesting CD, and all were negative for anti-endomysium (EmA) and anti-transglutaminase (anti-tTG). We enrolled an additional 28 adults with autoimmune or gastrointestinal diseases other than CD as “disease” controls: type 1 autoimmune hepatitis (AH; 6 cases), type 2 AH (4 cases), systemic lupus erythematosus (4 cases), Sjogren disease (3), primary biliary cirrhosis (2), Crohn disease (4), multiple food intolerance (3), …