AGA Institute Medical Position Statement on the Diagnosis and Management of Celiac Disease

he Medical Position Statements developed under the aegis of the AGA Institute and its Clinical Practice and Economics Committee were approved by the AGA Institute Governing Board. The data used to formulate these recommendations are derived from the data available at the time of their creation and may be supplemented and updated as new information is assimilated. These recommendations are intended for adult patients, with the intent of suggesting preferred approaches to specific medical issues or problems. They are based upon the interpretation and assimilation of scientifically valid research, derived from a comprehensive review of published literature. Ideally, the intent is to provide evidence based upon prospective, randomized placebo-controlled trials; however, when this is not possible the use of experts' consensus may occur. The recommendations are intended to apply to healthcare providers of all specialties. It is important to stress that these recommendations should not be construed as a standard of care. The AGA Institute stresses that the final decision regarding the care of the patient should be made by the physician with a focus on all aspects of the patient's current medical situation. Celiac disease is a permanent intolerance to gluten, a term that is broadly used to describe the storage proteins in wheat, rye, and barley. Celiac disease is characterized by a chronic inflammatory state of the proximal small intestinal mucosa, which can impair digestion and absorption of macronutrients and micronutrients and results in increased net secretion of water and solute. Celiac disease can present with intestinal symptoms, can present with extraintestinal symptoms (including the intensely pruritic skin rash dermatitis herpetiformis), or may be detected in individuals who are asymptomatic as part of the screening of populations at increased risk for celiac disease. There is a spectrum of small intestinal mucosal injury that ranges from minimal with an increase in intraepithelial lymphocytes to total villous atrophy. However, most symptomatic patients with celiac disease have some degree of villous atrophy. The HLA class II DQ molecules DQ2 or DQ8 are necessary, although not sufficient, for the phenotypic expression of celiac disease.