Liu, Edwin Section of Pediatric Gastroenterology, Hepatology, and Nutrition, The Children's Hospital, University of Colorado Health Sciences Center, Aurora, Colorado.
Last reviewed:March 2018
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- Toxicity of gluten
- Biochemistry of pathogenesis
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An autoimmune disorder caused by gluten sensitivity that damages the small intestine and leads to the malabsorption of nutrients from food. Celiac disease (CD) is an autoimmune condition of the small intestine that is believed to be T-cell (T-lymphocyte)–mediated and triggered by the consumption of gluten proteins found in foods containing wheat, rye, and barley. Symptoms can be overt and related to abdominal pain, diarrhea, weight loss, and other signs of intestinal malabsorption, or they can be subtle and present later in life as osteoporosis or iron-deficiency anemia. Conservative estimates place celiac disease at a prevalence of about 1 in 150 people in the United States, meaning that the majority of individuals remain undiagnosed. Screening is now simple with assays that detect autoantibodies against tissue transglutaminase (tTG) in patient serum. Diagnosis is confirmed by an intestinal biopsy showing villous atrophy (Fig. 1), with implications of a lifelong condition that can be treated only by eliminating dietary gluten. Once gluten is removed from the diet, the autoantibodies, intestinal injury, and symptoms resolve over time. If the patient is rechallenged with gluten, disease and symptoms will recur. Celiac disease is associated with other autoimmune diseases, notably type 1 diabetes and autoimmune thyroid disease, because of shared human leukocyte antigen (HLA) gene predisposition. See also: Antibody; Autoimmunity; Barley; Diabetes; Gastrointestinal tract disorders; Immunology; Intestine; Malnutrition; Rye; Wheat
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