pean Georges Pompidou Hospital, René

Celiac disease is a unique autoimmune disorder, unique because the environmental precipitant is known. The disorder was previously called celiac sprue, based on the Dutch word sprue, which was used to describe a dis-ease similar to tropical sprue that is characterized by diarrhea, emaciation, aphthous stomatitis, and malabsorption.1,2 Celiac disease is precipitated, in genetically pre-disposed persons, by the ingestion of gluten, the major storage protein of wheat and similar grains.3 Originally considered a rare malabsorption syndrome of child-hood, celiac disease is now recognized as a common condition that may be diag-nosed at any age and that affects many organ systems. The therapy for the disease is a gluten-free diet; however, the response to therapy is poor in up to 30 % of patients, and dietary nonadherence is the chief cause of persistent or recurrent symptoms. Small intestinal adenocarcinoma, refractory sprue, and enteropathy-associated T-cell lymphoma are complications of celiac disease that must be ruled out when alarm-ing symptoms such as abdominal pain, diarrhea, and weight loss develop despite a strict gluten-free diet. Patho genesis Celiac disease results from the interaction between gluten and immune, genetic, an