Adult celiac disease (gluten-sensitive enteropathy, celiac sprue) is an immune-mediated mucosal disorder of the small intestine that occurs in genetically-susceptible individuals, often leading to diarrhea and weight loss. Usually, antibodies to tissue transglutaminase (as well as others) develop during the disease course. As a result, serological tests have been used as effective screening tools in many populations, particularly in directing biopsy testing to define prevalence of celiac disease. Diagnosis of untreated celiac disease in adults has traditionally been dependent upon a small intestinal biopsy showing the characteristic mucosal pathological changes that have been well-described elsewhere (1–4). Some of these features in untreated patients may include villous blunting, increased crypt length and mitotic activity, increased numbers of lamina propria lymphocytes and plasma cells, and finally, increased numbers of intraepithelial lymphocytes. These have also been classified in different ways, some emphasized to be more cumbersome than others (2, 3) to express the severity of the changes, such as mild, moderate, and severe (1, 4), primarily in the proximal small intestine (5). None of these pathological features are pathognomonic or specific for the diagnosis of untreated celiac disease, even the most severe changes. Indeed, celiac disease (celiac sprue, gluten-sensitive enteropathy) has been recognized for more than a half century by Dicke and his collegues (6) and others as a gluten-dependent disorder, and as emphasized elsewhere (7), a diagnosis of adult celiac disease depends on a critical further conformational step: demonstration of a response to a strict gluten-free diet.
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