Article ID Journal Published Year Pages File Type
3086585 Pediatric Neurology 2007 5 Pages PDF
Abstract

Celiac disease is an immune-mediated enteropathy triggered by the ingestion of gluten in genetically susceptible individuals. Many reports mention the association between epilepsy and celiac disease and the occasional presence of occipital corticosubcortical calcifications. We investigated 255 children with idiopathic epilepsy. Evaluation included use of routine, easily obtainable studies. Patients were screened for immunoglobulin A (IgA), immunoglobulin G (IgG) antigliadin antibodies and immunoglobulin A antitissue transglutaminase antibodies. Moreover, presence of IgA antiendomysial and antireticulin antibodies was screened. Patients with positive IgA antigliadin antibodies underwent a small intestinal biopsy. Controls consisted of 280 healthy children. Intestinal histopathologic changes, positive IgA antigliadin antibodies or IgG antigliadin antibodies, antireticulin antibodies, and antitissue transglutaminase IgA antibodies were found in five epileptic children but not in control subjects (P = 0.0241). Intracranial calcifications were not found in epileptic children with celiac disease. The findings indicate that prevalence of silent celiac disease is increased among children with idiopathic epilepsy; the type of epilepsy does not appear to play a role. Serum antitissue transglutaminase IgA antibodies could be a good marker for celiac disease screening. Occipital corticosubcortical calcifications are rarer in children with celiac disease and epilepsy.

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