Coeliac Disease

Coeliac disease ( /ˈsiːli.æk/; spelled celiac disease in North America 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 chronic diarrhoea, failure to thrive (in children), and fatigue, but these may be absent, and symptoms in other organ systems have been described.

Increasingly, diagnoses are being made in asymptomatic persons as a result of increased screening; the condition is thought to affect between 1 in 1,750 and 1 in 105 people in the United States. 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).

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. 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, non-tropical 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 in a translation of what is generally regarded as an ancient Greek description of the disease by Aretaeus of Cappadocia.

Read more about Coeliac DiseaseSigns and Symptoms, Pathophysiology, Diagnosis, Screening, Epidemiology, Research Directions, History

Other articles related to "coeliac disease, disease, coeliac":

Gluten Immunochemistry - Innate Immunity - Alpha Gliadin 31-43 - Intraepithileal Lymphocytes and IL15
... The release of IL15 is a major factor in coeliac disease as IL15 has been found to attract intraepithelial lymphocytes (IEL) that characterize Marsh grade 1 and 2 coeliac disease ... innate peptide activation of T-cells in celiac disease is strange ... immunity to IRP peptide is involved in coeliac disease, dermatitis herpetiformis and possibly juvenile diabetes ...
HLA A1-B8-DR3-DQ2 - Importance To Medicine - In Coeliac Disease & Dermatitis Herpetiformis
... typing for HLA-DQ and DR, the association with HLA-A1 and B8 was identified for coeliac disease in 1973 and dermatitis herpetiformis in 1976 ... to identify the genetic risk even though disease causing genes, a DQ2 haplotype, was 1.3 million nucleotides away ... Further information HLA-DQ2 in coeliac disease and HLA-DQ2.5 in gluten immunochemistry Aside from the highly studied link between DQ2.5 and coeliac disease, there are ...
Coeliac Disease - History
... about 9500 BCE) in the Fertile Crescent in Western Asia, and it is likely that coeliac disease did not occur before this time ... His "Cœliac Affection" (coeliac from Greek κοιλιακός koiliakos, "abdominal") gained the attention of Western medicine when Francis Adams presented a translation of Aretaeus's work at the Sydenham ... The diarrhoea manifested as loose stools that were white, malodorous and flatulent, and the disease was intractable and liable to periodic return ...
Anti-ganglioside Antibodies - Triggering Agents - Coeliac Disease
... Antibodies to ganglioside are found to be elevated in coeliac disease ... Recent studies show that gliadin can cross-link to gangliosides in a transglutaminase independent manner, indicating that gliadin specific T-cell could present these antigens to the immune system ...
Samuel Gee - Coeliac Disease
... Samuel Gee gave the first modern-day description of coeliac disease in a lecture at the Hospital for Sick Children, Great Ormond Street in 1887 ... Signs of the disease are yielded by the fæces being loose, not formed, but not watery more bulky than the food taken would seem to account for pale in colour, as if devoid of bile yeasty, frothy, an ... Gee acknowledges earlier findings and terms for the disease and adopts the same term as Aretaeus ...

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