Coeliac disease (/ˈsiːli.æk/; spelled celiac disease in North America[1] and often celiac sprue) is an autoimmune disorder of the small intestine that occurs in genetically predisposed people of all ages from middle infancy onward. Symptoms include pain and discomfort in the digestive tract, chronic constipation and diarrhoea, failure to thrive (in children), anaemia[2] and fatigue, but these may be absent, and symptoms in other organ systems have been described. Vitamin deficiencies are often noted in people with coeliac disease owing to the reduced ability of the small intestine to properly absorb nutrients from food.
Increasingly, diagnoses are being made in asymptomatic persons as a result of increased screening;[3] the condition is thought to affect between 1 in 1,750 and 1 in 105 people in the United States.[4] Coeliac disease is caused by a reaction to gliadin, a prolamin (gluten protein) found in wheat, and similar proteins found in the crops of the tribe Triticeae (which includes other common grains such as barley and rye).[5]
Upon exposure to gliadin, and specifically to three peptides found in prolamins, the enzyme tissue transglutaminase modifies the protein, and the immune system cross-reacts with the small-bowel tissue, causing an inflammatory reaction. That leads to a truncating of the villi lining the small intestine (called villous atrophy). This interferes with the absorption of nutrients because the intestinal villi are responsible for absorption. The only known effective treatment is a lifelong gluten-free diet.[5] While the disease is caused by a reaction to wheat proteins, it is not the same as wheat allergy.
This condition has several other names, including cœliac disease (with œ ligature), c(o)eliac sprue, nontropical sprue, endemic sprue, gluten enteropathy or gluten-sensitive enteropathy, and gluten intolerance. The term coeliac derived from the Greek κοιλιακός (koiliakós, "abdominal") and was introduced in the 19th century...