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[[Coeliac disease]] ([[American and British English spelling differences|American English]]: celiac) (CD) is one of the most common chronic, immune-mediated disorders, triggered by the eating of [[gluten]], a mixture of proteins found in [[wheat]], [[barley]], [[rye]], and derivatives.<ref name=Biesiekierski2017>{{cite journal| author=Biesiekierski JR| s2cid=6493455 | title=What is gluten? | journal=J Gastroenterol Hepatol | year= 2017 | volume= 32 | issue=Suppl 1 | pages= 78–81 | pmid=28244676 | doi=10.1111/jgh.13703 | type=Review | quote= Similar proteins to the gliadin found in wheat exist as secalin in rye, hordein in barley, and avenins in oats and are collectively referred to as “gluten.” The gluten found in all of these grains has been identified as the component capable of triggering the immune-mediated disorder, coeliac disease.| doi-access=free }}{{open access}}</ref><ref name=LebwoholLudvigsson /> Evidence has shown that this condition not only has an environmental component but a genetic one as well, due to strong associations of CD with the presence of HLA ([[Human leukocyte antigen]]) type II, specifically DQ2 and DQ8 alleles.<ref name=Denham>{{cite journal|last1=Denham|first1=JM|last2=Hill|first2=ID|title=Celiac disease and autoimmunity: review and controversies.|journal=Current Allergy and Asthma Reports|date=August 2013|volume=13|issue=4|pages=347–53|pmid=23681421|doi=10.1007/s11882-013-0352-1|pmc=3725235}}</ref> These alleles can stimulate a [[T cell]], mediated immune response against tissue [[transglutaminase]] (TTG), an enzyme in the extracellular matrix, leading to inflammation of the intestinal mucosa and eventually villous atrophy of the small intestine.<ref name=Pasha>{{cite journal|last1=Pasha|first1=I|last2=Saeed|first2=F|last3=Sultan|first3=MT|last4=Batool|first4=R|last5=Aziz|first5=M|last6=Ahmed|first6=W|s2cid=25585961|title=Wheat Allergy and Intolerence; Recent Updates and Perspectives.|journal=Critical Reviews in Food Science and Nutrition|date=2 January 2016|volume=56|issue=1|pages=13–24|pmid=24915366|doi=10.1080/10408398.2012.659818}}</ref> This is where the innate and adaptive immune response systems collide.
[[File:Inflammed mucous layer of the intestinal villi depicting Celiac disease.jpg|thumb|249x249px|Villous atrophy of the small intestine]]
CD is not only a gastrointestinal disease. It may involve several organs and cause an extensive variety of non-gastrointestinal symptoms. Most importantly, it may often be completely asymptomatic. Added difficulties for diagnosis are the fact that [[serological]] markers ([[Anti-transglutaminase antibodies#Anti-tissue transglutaminase|anti-tissue transglutaminase]] [TG2]) are not always present<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=December 20, 2012|volume=367|issue=25|pages=2419–26|pmid=23252527|doi=10.1056/NEJMcp1113994}}</ref> and many people may have minor mucosal lesions, without atrophy of the [[intestinal villi]].<ref name=BoldRostami>{{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}}</ref> Diagnosis of CD should be based on a combination of person's familial history, genetics (i.e. presence of HLA DQ2/DQ8) serology and intestinal histology.<ref name=ElliBranchi />
CD affects approximately 1–2% of general population all over the world,<ref name=LundinWijmenga2015>{{cite journal|vauthors=Lundin KE, Wijmenga C|s2cid=24533103|title=Coeliac disease and autoimmune disease-genetic overlap and screening|journal=Nat Rev Gastroenterol Hepatol|volume=12|issue=9|pages=507–15|date =September 2015|pmid=26303674|doi=10.1038/nrgastro.2015.136}}</ref> but most cases remain unrecognized, undiagnosed and untreated, and exposed to the risk of long-term complications.<ref name="ElliBranchi" /><ref name="Fasano2005Pediatric">{{cite journal |author=Schuppan & Gisbert-Schuppan |date=2019 |title=Wheat Syndromes: How Wheat, Gluten and ATI Cause Inflammation, IBS and Autoimmune Diseases |journal=Book |volume= |issue= |pages= |doi= |pmid= |via=Springer Nature Switzerland AG, Switzerland.}}</ref> People may experience severe disease symptoms and be subjected to extensive investigations for many years, before a proper diagnosis is achieved.<ref name=LudvigssonCard>{{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 = April 2015 | pmid = 25922674 | pmc = 4406900 |doi = 10.1177/2050640614562599}}</ref> Untreated CD may result in the lack of absorption of nutrients, reduced quality of life, [[iron deficiency]], [[osteoporosis]], an increased risk of intestinal [[lymphoma]]s and greater mortality.<ref name=LebwoholLudvigsson /> CD is associated with some autoimmune diseases, such as [[diabetes mellitus type 1]],<ref name="Denham" /> [[thyroiditis]],<ref name=LundinWijmenga>{{cite journal | vauthors = Lundin KE, Wijmenga C| s2cid = 24533103| title = Coeliac disease and autoimmune disease-genetic overlap and screening| journal = Nat Rev Gastroenterol Hepatol| volume = 12| issue = 9| pages = 507–15| date = September 2015 | pmid = 26303674 | doi = 10.1038/nrgastro.2015.136}}</ref> [[ataxia|gluten ataxia]], [[psoriasis]], [[vitiligo]], [[autoimmune hepatitis]], [[dermatitis herpetiformis]], [[primary sclerosing cholangitis]], and more.<ref name=LundinWijmenga />
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== Research ==
Research has attempted to discern, by [[double-blind placebo-controlled trial]]s, between a "fad component" to the recent popularity of the [[gluten-free diet]] and an actual sensitivity to gluten or other components of wheat.<ref name=FasanoSapone2015 /><ref name="CatassiBai2013" /><ref>{{cite journal |vauthors=Di Sabatino A, Volta U, Salvatore C, Biancheri P, Caio G, De Giorgio R, Di Stefano M, Corazza GR |title=Small Amounts of Gluten in Subjects with Suspected Nonceliac Gluten Sensitivity: A Randomized, Double-Blind, Placebo-Controlled, Cross-Over Trial |journal=Clinical Gastroenterology and Hepatology |volume=13 |issue=9 |pages=1604–12 |year=2015 |doi=10.1016/j.cgh.2015.01.029 |pmid=25701700|hdl=11392/2375087 |url=https://www.cghjournal.org/article/S1542-3565(15)00153-6/fulltext |doi-access=free |hdl-access=free }}</ref>
In a 2013 [[blind experiment#Double-blind trials|double-blind]], [[placebo-controlled study|placebo-controlled]] challenge (DBPC) by Biesiekierski ''et al.'' in a few people with [[irritable bowel syndrome]], the authors found no difference between gluten or placebo groups and the concept of NCGS as a syndrome was questioned. Nevertheless, this study had design errors and an incorrect selection of participants, and probably the reintroduction of both gluten and [[whey]] protein had a [[nocebo]] effect similar in all people, and this could have masked the true effect of gluten/wheat reintroduction.<ref name=ElliBranchi /><ref name="AzizHadjivassiliou2015" />
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In a 2015 double-blind placebo cross-over trial, small amounts of purified wheat gluten triggered gastrointestinal symptoms (such as abdominal bloating and pain) and extra-intestinal manifestations (such as foggy mind, depression and aphthous stomatitis) in self-reported NCGS. Nevertheless, it remains elusive whether these findings specifically implicate gluten or proteins present in gluten-containing cereals.<ref name="AzizHadjivassiliou2015" />
A 2016 review of the recent research advancements in understanding diet's role in attenuating IBS patient's symptoms concluded that gluten was a common trigger. However, because on the different compounds responsible for symptoms, many patients that could be inaccurately labelled non-coeliac gluten sensitive; and it may be more appropriate to use nomenclature such as "non-coeliac wheat sensitive" (NCWS), "non-coeliac wheat protein sensitive" (NCWPS), or even FODMAP sensitive when referring to these patients.<ref>{{cite journal |last1=Giorgio |first1=Roberto De |last2=Volta |first2=Umberto |last3=Gibson |first3=Peter R. |title=Sensitivity to wheat, gluten and FODMAPs in IBS: facts or fiction? |journal=Gut |date=1 January 2016 |volume=65 |issue=1 |pages=169–178 |doi=10.1136/gutjnl-2015-309757 |s2cid=6012463 |pmid=26078292 |doi-access=free |hdl=11392/2375077 |hdl-access=free }}</ref>
In a 2018 double-blind, crossover research study on 59 persons on a gluten-free diet with challenges of [[gluten]], [[fructans]] or [[placebo]], intestinal symptoms (specifically [[bloating]]) were borderline significantly higher after challenge with fructans, in comparison with gluten proteins (P=0.049).<ref name="Verbeke2018" /><ref name="VoltaDeGiorgio2019" /> Although the differences between the three interventions was very small, the authors concluded that fructans (the specific type of FODMAP found in wheat) are more likely to be the cause of NCGS gastrointestinal symptoms, rather than gluten.<ref name="Verbeke2018" /> In addition, fructans used in the study were extracted from chicory root, so it remains to be seen whether the wheat fructans produce the same effect.<ref name="VoltaDeGiorgio2019" />
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