| Revision as of 01:55, 9 March 2016 editBallenaBlanca (talk | contribs)Extended confirmed users6,901 edits Coeliac disease - introduction. Added refs. Some corrections.← Previous edit | Latest revision as of 09:44, 22 August 2016 edit undoBallenaBlanca (talk | contribs)Extended confirmed users6,901 edits blanking | ||
| (9 intermediate revisions by 2 users not shown) | |||
| Line 1: | Line 1: | ||
| {{User sandbox}} | {{User sandbox}} | ||
| <!-- EDIT BELOW THIS LINE --> | <!-- EDIT BELOW THIS LINE --> | ||
| '''Coeliac disease''', also spelled '''celiac disease''',<ref>See ].</ref> is an ] disorder of the ] that occurs in ] people of all ages. It is not only a gastrointestinal disease but a systemic disease, because it may involve to several ] and cause an extensive variety of non-gastrointestinal symptoms.<ref name=CiccocioppoKruzliak2015>{{cite journal|vauthors=Ciccocioppo R, Kruzliak P, Cangemi GC, Pohanka M, Betti E, Lauret E, Rodrigo L|title=The Spectrum of Differences between Childhood and Adulthood Celiac Disease|journal=Nutrients|volume=7|issue=10|pages=8733–51|date=Oct 22, 2015|pmid=26506381|pmc=4632446|doi=10.3390/nu7105426|type=Review}}</ref> | |||
| <!-- Signs and symptoms --> | |||
| Coeliac disease with “classic symptoms”, which include gastrointestinal manifestations such as chronic ] and abdominal distention, malabsorption, lose of appetite, and ] (in children), is currently the least common presentation form of the disease and affects predominantly to small children generally younger than two years of age.<ref name=LudvigssonCard2015 /><ref name=RostamiNejadHoggKollars2011>{{cite journal|vauthors=Rostami Nejad M, Hogg-Kollars S, Ishaq S, Rostami K|title= Subclinical celiac disease and gluten sensitivity|journal=Gastroenterol Hepatol Bed Bench |volume=4|issue=3|pages=102–8|date=2011|pmid=24834166|pmc=4017418|doi=|type=Review}}</ref><ref name=Fasano2005Pediatric>{{cite journal|author=Fasano A|title=Clinical presentation of celiac disease in the pediatric population|journal=Gastroenterology|volume=128|issue=4 Suppl 1|pages=S68-73|date=Apr 2005|pmid=15825129|doi=10.1053/j.gastro.2005.02.015|type=Review}}</ref> | |||
| Coeliac disease with “non-classic symptoms” is the most common clinical found type<ref name=RostamiNejadHoggKollars2011 /><ref name=LudvigssonCard2015 /><ref name=TonuttiBizzaro2014>{{cite journal|vauthors=Tonutti E, Bizzaro N|title=Diagnosis and classification of celiac disease and gluten sensitivity|journal=Autoimmun Rev|volume=13|issue=4-5|pages=472-6|date=2014|pmid=24440147|doi=10.1016/j.autrev.2014.01.043|type=Review}}</ref> and occurs in older children (over 2 years old), adolescents and adults.<ref name=LudvigssonCard2015 /> It is characterized by milder or even absent gastrointestinal symptoms and a wide spectrum of non-intestinal manifestations that can involve any organ of the body, and very frequently may be completely asymptomatic<ref name=CiccocioppoKruzliak2015 /><ref name=Fasano2005Pediatric /> both in children (at least in 43% of the cases<ref name=VriezingaSchweizer2015>{{cite journal|vauthors=Vriezinga SL, Schweizer JJ, Koning F, Mearin ML|title=Coeliac disease and gluten-related disorders in childhood|journal=Nat Rev Gastroenterol Hepatol|volume=12|issue=9|pages=527–36|date=Sep 2015|pmid=26100369|doi=10.1038/nrgastro.2015.98|type=Review}}</ref>) and adults.<ref name=Fasano2005Pediatric /> Coeliac disease is associated with some autoimmune diseases, such as ], ],<ref name=CiccocioppoKruzliak2015 /><ref name=LundinWijmenga2015>{{cite journal|vauthors=Lundin KE, Wijmenga C|title=Coeliac disease and autoimmune disease-genetic overlap and screening|journal=Nat Rev Gastroenterol Hepatol|volume=12|issue=9|pages=507–15|date=Sep 2015|pmid=26303674|doi=10.1038/nrgastro.2015.136|type=Review Research Support, Non-U.S. Gov't}}</ref> ], ], ], ], ], ], and more.<ref name=LundinWijmenga2015 /> | |||
| <!-- Cause and pathophysiology --> | |||
| Coeliac disease is caused by a reaction to ], a ] (] protein) found in wheat, and similar proteins found in the crops of the ] ], which includes other common grains such as ] and ],<ref name=TovoliMasi2015>{{cite journal|vauthors=Tovoli F, Masi C, Guidetti E, Negrini G, Paterini P, Bolondi L|title=Clinical and diagnostic aspects of gluten related disorders|journal=World J Clin Cases|volume=3|issue=3|pages=275–84|date=Mar 16, 2015|pmid=25789300|pmc=4360499|doi=10.12998/wjcc.v3.i3.275|type=Review}}</ref><ref name=PenaginiDilillo2013>{{cite journal|vauthors=Penagini F, Dilillo D, Meneghin F, Mameli C, Fabiano V, Zuccotti GV|title=Gluten-free diet in children: an approach to a nutritionally adequate and balanced diet|journal=Nutrients|volume=5|issue=11|pages=4553–65|date=Nov 18, 2013|pmid=24253052|pmc=3847748|doi=10.3390/nu5114553|type=Review}}</ref><ref name="Lancet">{{cite journal | author = Di Sabatino A, Corazza GR | title = Coeliac disease | journal = Lancet | volume = 373 | issue = 9673 | pages = 1480–93 | date = April 2009 | pmid = 19394538 | doi = 10.1016/S0140-6736(09)60254-3 }}</ref> and all their species and hybrids (such as ],<ref name=TovoliMasi2015 /> ], and ]<ref name=TovoliMasi2015 /><ref name=PenaginiDilillo2013 />). ] present in oats may be also toxic for coeliac people.<ref name=PenaginiDilillo2013 /> Its toxicity depends on the ] consumed.<ref name=CominoMoreno2015>{{cite journal|vauthors=Comino I, Moreno Mde L, Sousa C|title=Role of oats in celiac disease|journal=World J Gastroenterol|volume=21|issue=41|pages=11825–31|date=Nov 7, 2015|pmid=26557006|pmc=4631980|doi=10.3748/wjg.v21.i41.11825|type=Review}}</ref> Furthermore, oats is frequently cross contaminated with gluten-containing cereals.<ref name=PenaginiDilillo2013 /> Upon exposure to gliadin, and specifically to three ]s found in ]s, the enzyme ] modifies the protein, and the ] cross-reacts with the small-bowel tissue, causing an ]. In some cases, that may lead to a truncating of the villi lining the small intestine (called villous atrophy).<ref name=VivasVaquero2015>{{cite journal|vauthors=Vivas S, Vaquero L, Rodríguez-Martín L, Caminero A|title=Age-related differences in celiac disease: Specific characteristics of adult presentation|journal=World J Gastrointest Pharmacol Ther|volume=6|issue=4|pages=207–12|date=Nov 6, 2015|pmid=26558154|pmc=4635160|doi=10.4292/wjgpt.v6.i4.207|type=Review|quote=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)}}</ref><ref name=ElliBranchi2015>{{cite journal|vauthors=Elli L, Branchi F, Tomba C, Villalta D, Norsa L, Ferretti F, Roncoroni L, Bardella MT|title=Diagnosis of gluten related disorders: Celiac disease, wheat allergy and non-celiac gluten sensitivity|journal=World J Gastroenterol|volume=21|issue=23|pages=7110–9|date=Jun 21, 2015|pmid=26109797|pmc=4476872|doi=10.3748/wjg.v21.i23.7110|type=Review|quote=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.}}</ref><ref name=MolinaInfanteSantolaria2015>{{cite journal|vauthors=Molina-Infante J, Santolaria S, Sanders DS, Fernández-Bañares F|title=Systematic review: noncoeliac gluten sensitivity|journal=Aliment Pharmacol Ther|volume=41|issue=9|pages=807-20|date=May 2015|pmid=25753138|doi=10.1111/apt.13155|type=Review|quote=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).}}</ref> This ] of nutrients because the ] are responsible for absorption. The only known effective treatment is a lifelong ].<ref name="Lancet"/> While the disease is caused by a reaction to wheat proteins, it is usually classified as different from the other forms of ]. | |||
| <!-- Epidemiology --> | |||
| Increasingly, diagnoses are being made in ] as a result of increased ].<ref name="VanHeelWest">{{cite journal | author = van Heel DA, West J | title = Recent advances in coeliac disease | journal = Gut | volume = 55 | issue = 7 | pages = 1037–46 | year = 2006 | pmid = 16766754 | pmc = 1856316 | doi = 10.1136/gut.2005.075119 | type=Review Research Support, Non-U.S. Gov't}} <!-- PMC 1856316 from 9 Jan --></ref> Globally coeliac disease affects between 1 in 100 and 1 in 170 people;<ref name=NEJM2012>{{cite journal|last1=Fasano|first1=A|last2=Catassi|first2=C|title=Clinical practice. Celiac disease|journal=The New England Journal of Medicine|date=Dec 20, 2012|volume=367|issue=25|pages=2419–26|pmid=23252527|doi=10.1056/NEJMcp1113994|type=Review}}</ref> rates do, however, vary between different regions of the world from as few as 1 in 300 to as many as 1 in 40.<ref name=NEJM2012/> Nevertheless, most cases remain unrecognized, undiagnosed and untreated, and exposed to the risk of long-term complications, including malignancies such as intestinal ] and greater mortality.<ref name=CiccocioppoKruzliak2015 /><ref name=ElliBranchi2015 /><ref name=LebwoholLudvigsson2015>{{cite journal | vauthors =Lebwohl B, Ludvigsson JF, Green PH | title = Celiac disease and non-celiac gluten sensitivity | journal = BMJ | volume = 5 | pages = 351:h4347| date = Oct 2015 | pmid = 26438584|pmc= 4596973 | doi = 10.1136/bmj.h4347|type= Review|quote=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.}}</ref><ref name=LevyBernstein2014>{{cite journal|vauthors=Levy J, Bernstein L, Silber N|title=Celiac disease: an immune dysregulation syndrome|journal=Curr Probl Pediatr Adolesc Health Care|volume=44|issue=11|pages = 324–7|date=Dec 2014|pmid=25499458|doi=10.1016/j.cppeds.2014.10.002|type=Review}}</ref> Patients may suffer severe disease symptoms and be subjected to extensive investigations for many years, before a proper diagnosis is achieved.<ref name=LudvigssonCard2015>{{cite journal|vauthors=Ludvigsson JF, Card T, Ciclitira PJ, Swift GL, Nasr I, Sanders DS, Ciacci C|title=Support for patients with celiac disease: A literature review|journal=United European Gastroenterol J|volume=3|issue=2|pages=146–59|date=Apr 2015|pmid=25922674|pmc=4406900|doi=10.1177/2050640614562599|type=Review}}</ref> Added difficulties for diagnosis are the fact that serological markers (] ) are not always present<ref name=MolinaInfanteSantolaria2015 /><ref name=NEJM2012 /> and many patients may have minor mucosal lesions, without atrophy of the ].<ref name=RostamiNejadHoggKollars2011 /><ref name=BoldRostami2011>{{cite journal|vauthors=Bold J, Rostami K|title=Gluten tolerance; potential challenges in treatment strategies|journal=Gastroenterol Hepatol Bed Bench|volume=4|issue=2|pages=53–7|date=2011|pmid=24834157|pmc=4017406|type=Review}}</ref> | |||
| <!-- History, society and culture --> | |||
| This condition has several other names, including c(o)eliac 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 ].<ref name="Aretaeus">{{Cite book|last=Adams F, translator |title=The extant works of Aretaeus, The Cappadocian |url=https://books.google.com/?id=v4gIAAAAIAAJ&pg=PT1&q= |chapter= On The Cœliac Affection |pages=350–1|chapterurl=https://books.google.com/books?id=v4gIAAAAIAAJ&pg=PA350#v=onepage&q=&f=false |accessdate=12 December 2009 |year=1856 |publisher=Sydenham Society |location=London}}</ref><ref name="Losowsky">{{cite journal | author = Losowsky MS | title = A history of coeliac disease | journal = Dig Dis | volume = 26 | issue = 2 | pages = 112–20 | year = 2008 | pmid = 18431060 | doi = 10.1159/000116768 }}</ref> | |||
| {{listaref|2}} | |||
Latest revision as of 09:44, 22 August 2016
 | 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! |