Misplaced Pages

This is an old revision of this page, as edited by BallenaBlanca (talk | contribs) at 20:56, 10 March 2016 (Treatment: moved, completed and updated refs.). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

This is the user sandbox of BallenaBlanca. A user sandbox is a subpage of the user's user page. It serves as a testing spot and page development space for the user and is not an encyclopedia article. Create or edit your own sandbox here. Other sandboxes: Main sandbox | Template sandbox Finished writing a draft article? Are you ready to request review of it by an experienced editor for possible inclusion in Misplaced Pages? Submit your draft for review!

Coeliac disease, also spelled celiac disease, is an autoimmune disorder of the small intestine that occurs in genetically predisposed people of all ages. It is not only a gastrointestinal disease but may involve to several organs and cause a variety of non-gastrointestinal symptoms. Classic symptoms include gastrointestinal problems such as chronic diarrhoea, abdominal distention, malabsorption, lose of appetite, and failure to thrive (in children), is the least common presentation of the disease and affects predominantly children younger than two years of age. Non-classic symptoms are more common especially in older children and adults. It is characterized by milder or absent gastrointestinal symptoms and a wide number of symptoms that can involve any organ of the body, and very frequently may be completely asymptomatic both in children (at least in 43% of the cases) and adults. Coeliac disease is associated other autoimmune diseases, such as diabetes mellitus type 1, thyroiditis, gluten ataxia, psoriasis, vitiligo, autoimmune hepatitis, dermatitis herpetiformis, primary sclerosing cholangitis, and more.

Coeliac disease is caused by a reaction to gluten protein found in wheat, and similar proteins found in the crops of the type Triticeae, which includes other grains such as barley and rye, and all their species and hybrids (such as spelt, kamut, and triticale). Avenin present in oats may be also toxic for coeliac people. Its toxicity depends on the cultivar consumed. Furthermore, oats is frequently cross contaminated with gluten-containing cereals. 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. In some cases, that may lead 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. While the disease is caused by a reaction to wheat proteins, it is usually classified as different from the other forms of wheat allergy.

Globally coeliac disease affects between 1 in 100 and 1 in 170 people. Rates vary between different regions of the world from as few as 1 in 300 to as many as 1 in 40. Increasingly, diagnoses are being made in persons without symptoms as a result of increased screening. Most cases remain unrecognized, undiagnosed and untreated, and exposed to the risk of long-term complications, including cancers such as intestinal lymphoma and greater mortality. People may have severe disease symptoms and be subjected to extensive investigations for many years, before a diagnosis is achieved. Added difficulties for diagnosis are the fact that serological markers (antibodies to tissue transglutaminase) are not always present and many people may have minor mucosal lesions, without atrophy of the intestinal villi. The only known effective treatment is a strict lifelong gluten-free diet, which leads to recovery of the intestinal mucosa, improves symptoms and reduces the risk of developing complications in most people.

This condition has several other names, including celiac sprue, nontropical sprue, endemic sprue, and gluten enteropathy. The term "coeliac" is 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.

1. See American and British English spelling differences.
2. ^ Ciccocioppo R, Kruzliak P, Cangemi GC, Pohanka M, Betti E, Lauret E, Rodrigo L (Oct 22, 2015). "The Spectrum of Differences between Childhood and Adulthood Celiac Disease". Nutrients (Review). 7 (10): 8733–51. doi:10.3390/nu7105426. PMC 4632446. PMID 26506381.{{cite journal}}: CS1 maint: unflagged free DOI (link)
3. ^ Ludvigsson JF, Card T, Ciclitira PJ, Swift GL, Nasr I, Sanders DS, Ciacci C (Apr 2015). "Support for patients with celiac disease: A literature review". United European Gastroenterol J (Review). 3 (2): 146–59. doi:10.1177/2050640614562599. PMC 4406900. PMID 25922674.
4. ^ Rostami Nejad M, Hogg-Kollars S, Ishaq S, Rostami K (2011). "Subclinical celiac disease and gluten sensitivity". Gastroenterol Hepatol Bed Bench (Review). 4 (3): 102–8. PMC 4017418. PMID 24834166.
5. ^ Fasano A (Apr 2005). "Clinical presentation of celiac disease in the pediatric population". Gastroenterology (Review). 128 (4 Suppl 1): S68-73. doi:10.1053/j.gastro.2005.02.015. PMID 15825129.
6. Tonutti E, Bizzaro N (2014). "Diagnosis and classification of celiac disease and gluten sensitivity". Autoimmun Rev (Review). 13 (4–5): 472–6. doi:10.1016/j.autrev.2014.01.043. PMID 24440147.
7. ^ Vriezinga SL, Schweizer JJ, Koning F, Mearin ML (Sep 2015). "Coeliac disease and gluten-related disorders in childhood". Nat Rev Gastroenterol Hepatol (Review). 12 (9): 527–36. doi:10.1038/nrgastro.2015.98. PMID 26100369.
8. ^ Lundin KE, Wijmenga C (Sep 2015). "Coeliac disease and autoimmune disease-genetic overlap and screening". Nat Rev Gastroenterol Hepatol (Review Research Support, Non-U.S. Gov't). 12 (9): 507–15. doi:10.1038/nrgastro.2015.136. PMID 26303674.
9. ^ Tovoli F, Masi C, Guidetti E, Negrini G, Paterini P, Bolondi L (Mar 16, 2015). "Clinical and diagnostic aspects of gluten related disorders". World J Clin Cases (Review). 3 (3): 275–84. doi:10.12998/wjcc.v3.i3.275. PMC 4360499. PMID 25789300.{{cite journal}}: CS1 maint: unflagged free DOI (link)
10. ^ Penagini F, Dilillo D, Meneghin F, Mameli C, Fabiano V, Zuccotti GV (Nov 18, 2013). "Gluten-free diet in children: an approach to a nutritionally adequate and balanced diet". Nutrients (Review). 5 (11): 4553–65. doi:10.3390/nu5114553. PMC 3847748. PMID 24253052.{{cite journal}}: CS1 maint: unflagged free DOI (link)
11. ^ Di Sabatino A, Corazza GR (April 2009). "Coeliac disease". Lancet. 373 (9673): 1480–93. doi:10.1016/S0140-6736(09)60254-3. PMID 19394538.
12. Comino I, Moreno Mde L, Sousa C (Nov 7, 2015). "Role of oats in celiac disease". World J Gastroenterol (Review). 21 (41): 11825–31. doi:10.3748/wjg.v21.i41.11825. PMC 4631980. PMID 26557006.{{cite journal}}: CS1 maint: unflagged free DOI (link)
13. Vivas S, Vaquero L, Rodríguez-Martín L, Caminero A (Nov 6, 2015). "Age-related differences in celiac disease: Specific characteristics of adult presentation". World J Gastrointest Pharmacol Ther (Review). 6 (4): 207–12. doi:10.4292/wjgpt.v6.i4.207. PMC 4635160. PMID 26558154. In addition, the presence of intraepithelial lymphocytosis and/or villous atrophy and crypt hyperplasia of small-bowel mucosa, and clinical remission after withdrawal of gluten from the diet, are also used for diagnosis antitransglutaminase antibody (tTGA) titers and the degree of histological lesions inversely correlate with age. Thus, as the age of diagnosis increases antibody titers decrease and histological damage is less marked. It is common to find adults without villous atrophy showing only an inflammatory pattern in duodenal mucosa biopsies: Lymphocytic enteritis (Marsh I) or added crypt hyperplasia (Marsh II){{cite journal}}: CS1 maint: unflagged free DOI (link)
14. ^ Elli L, Branchi F, Tomba C, Villalta D, Norsa L, Ferretti F, Roncoroni L, Bardella MT (Jun 21, 2015). "Diagnosis of gluten related disorders: Celiac disease, wheat allergy and non-celiac gluten sensitivity". World J Gastroenterol (Review). 21 (23): 7110–9. doi:10.3748/wjg.v21.i23.7110. PMC 4476872. PMID 26109797. The signs of gluten-related enteropathy out of duodenal biopsy range from an increase in the intraepithelial lymphocytes to villous atrophy, as staged by Marsh et al and successively by Oberhuber et al.{{cite journal}}: CS1 maint: unflagged free DOI (link)
15. ^ Molina-Infante J, Santolaria S, Sanders DS, Fernández-Bañares F (May 2015). "Systematic review: noncoeliac gluten sensitivity". Aliment Pharmacol Ther (Review). 41 (9): 807–20. doi:10.1111/apt.13155. PMID 25753138. Furthermore, seronegativity is more common in coeliac disease patients without villous atrophy (Marsh 1-2 lesions), but these 'minor' forms of coeliac disease may have similar clinical manifestations to those with villous atrophy and may show similar clinical–histological remission with reversal of haematological or biochemical disturbances on a gluten-free diet (GFD).
16. ^ Fasano, A; Catassi, C (Dec 20, 2012). "Clinical practice. Celiac disease". The New England Journal of Medicine (Review). 367 (25): 2419–26. doi:10.1056/NEJMcp1113994. PMID 23252527.
17. van Heel DA, West J (2006). "Recent advances in coeliac disease". Gut (Review Research Support, Non-U.S. Gov't). 55 (7): 1037–46. doi:10.1136/gut.2005.075119. PMC 1856316. PMID 16766754.
18. Lebwohl B, Ludvigsson JF, Green PH (Oct 2015). "Celiac disease and non-celiac gluten sensitivity". BMJ (Review). 5: 351:h4347. doi:10.1136/bmj.h4347. PMC 4596973. PMID 26438584. Celiac disease occurs in about 1% of the population worldwide, although most people with the condition are undiagnosed. It can cause a wide variety of symptoms, both intestinal and extra-intestinal because it is a systemic autoimmune disease that is triggered by dietary gluten. Patients with celiac disease are at increased risk of cancer, including a twofold to fourfold increased risk of non-Hodgkin's lymphoma and a more than 30-fold increased risk of small intestinal adenocarcinoma, and they have a 1.4-fold increased risk of death.
19. Levy J, Bernstein L, Silber N (Dec 2014). "Celiac disease: an immune dysregulation syndrome". Curr Probl Pediatr Adolesc Health Care (Review). 44 (11): 324–7. doi:10.1016/j.cppeds.2014.10.002. PMID 25499458.
20. Rodrigo L, Garrote JA, Vivas S (Sep 6, 2008). "[Celiac disease]". Med Clin (Barc) (Review) (in Spanish). 131 (7): 264–70. doi:10.1016/S0025-7753(08)72247-4. PMID 18775218. Estos marcadores presentan en general una elevada sensibilidad y especificidad (cercanas al 90%) en presencia de atrofia marcada de las vellosidades intestinales. Sin embargo, muestran una notable disminución de la sensibilidad (del orden del 40-50%) en casos con atrofia vellositaria leve o cambios mínimos. These markers generally have high sensitivity and specificity (around 90%) in the presence of marked atrophy of the villi. However, they show a marked decrease in sensitivity (of the order of 40-50%) in cases with mild villous atrophy or minimal changes.
21. Lewis NR, Scott BB (Jul 1, 2006). "Systematic review: the use of serology to exclude or diagnose coeliac disease (a comparison of the endomysial and tissue transglutaminase antibody tests)". Aliment Pharmacol Ther (Review). 24 (1): 47–54. doi:10.1111/j.1365-2036.2006.02967.x. PMID 16803602.
22. Bold J, Rostami K (2011). "Gluten tolerance; potential challenges in treatment strategies". Gastroenterol Hepatol Bed Bench (Review). 4 (2): 53–7. PMC 4017406. PMID 24834157.
23. See JA, Kaukinen K, Makharia GK, Gibson PR, Murray JA (Oct 2015). "Practical insights into gluten-free diets". Nat Rev Gastroenterol Hepatol (Review). 12 (10): 580–91. doi:10.1038/nrgastro.2015.156. PMID 26392070.
24. Adams F, translator (1856). "On The Cœliac Affection". The extant works of Aretaeus, The Cappadocian. London: Sydenham Society. pp. 350–1. Retrieved 12 December 2009. {{cite book}}: |last= has generic name (help); External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help)
25. Losowsky MS (2008). "A history of coeliac disease". Dig Dis. 26 (2): 112–20. doi:10.1159/000116768. PMID 18431060.