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== Types ==
The following classification of gluten-related disorders was announced in 2011 by a panel of experts in London, and published in February 2012:<ref>{{cite journal|last1=Sapone|first1=Anna|display-authors=etal|title=Spectrum of gluten-relate disorders: consensus on new nomenclature and classification|journal=BMC Medicine|date=7 February 2012|volume=2012|issue=10:13|pages=13|doi=10.1186/1741-7015-10-13|pmid=22313950|pmc=3292448}}</ref><ref name="Czaja-Bulsa-2014-section9-figure2">{{cite journal |author=Czaja-Bulsa G |title=Non coeliac gluten sensitivity - A new disease with gluten intolerance |journal=Clinical Nutrition (Edinburgh, Scotland) |volume= 34|issue= 2|pages= 189–194| date=August 2014 |pmid=25245857 |doi=10.1016/j.clnu.2014.08.012 |type=Review|doi-access=free }} See section 9 and Figure 2: Classification of gluten-dependent disorders.</ref>
* [[Autoimmunity|Autoimmune]] disorders: [[celiac disease]], [[dermatitis herpetiformis]], [[gluten ataxia]]
* Non-autoimmune, non-allergic: disorder with unknown cause, likely immune-modulated: [[non-celiac gluten sensitivity]] (NCGS)
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=== Autoimmune disorders ===
{{Main|Celiac disease|Gluten-sensitive enteropathy-associated conditions}}
[[Autoimmunity|Autoimmune]] conditions related to gluten include [[celiac disease]], [[dermatitis herpetiformis]], and [[gluten ataxia]]. There is research showing that in people with [[gluten ataxia]] early diagnosis and treatment with a gluten-free diet can improve ataxia and prevent its progression.<ref>{{cite journal |vauthors=Hadjivassiliou M, Sanders DS, Woodroofe N, Williamson C, Grünewald RA |s2cid=13427708 |title=Gluten ataxia |journal=Cerebellum |volume=7 |issue=3 |pages=494–8 |year=2008 |pmid=18787912 |doi=10.1007/s12311-008-0052-x |type=Review}}</ref> The population of people with gluten ataxia and other neurological conditions appears to have a different HLA distribution, in particular more [[HLA-DQ1]], compared to most persons with celiac disease, who have [[HLA-DQ2]] and [[HLA-DQ8]].<ref>{{cite journal |vauthors=Troncone R, Jabri B |title=Coeliac disease and gluten sensitivity |journal=Journal of Internal Medicine |volume=269 |issue=6 |pages=582–90 | date=June 2011 |pmid=21481018 |doi=10.1111/j.1365-2796.2011.02385.x |type=Review|doi-access=free }}</ref>
==== Coeliac disease ====
{{Main|Coeliac disease}}
[[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 [[oats]] and derivatives.<ref name=Biesiekierski2017>{{cite journal| author=Biesiekierski JR| s2cid=6493455 | title=What is gluten? | journal=J Gastroenterol Hepatol | year= 2017 | volume= 32 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 />
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Among extra-intestinal manifestations, NCGS seems to be involved in some [[neuropsychiatric disorder]]s,<ref>{{Cite journal|last1=Bressan|first1=Paola|last2=Kramer|first2=Peter|date=2016|title=Bread and Other Edible Agents of Mental Disease|journal=Frontiers in Human Neuroscience|language=en|volume=10|doi=10.5281/zenodo.1004705|pmid=27065833|doi-access=free}}</ref> principally [[schizophrenia]],<ref name=LebwoholLudvigsson>{{cite journal | vauthors =Lebwohl B, Ludvigsson JF, Green PH | title = Celiac disease and non-celiac gluten sensitivity | journal = BMJ | volume = 351 | pages = h4347| date = October 2015 | pmid = 26438584|pmc= 4596973 | doi = 10.1136/bmj.h4347|type= Review }}</ref><ref name="CatassiBai2013" /> [[autism]]<ref name=LebwoholLudvigsson /><ref name="CatassiBai2013" /><ref name=VoltaCaio2015 /> and [[peripheral neuropathy]],<ref name=LebwoholLudvigsson /><ref name="CatassiBai2013" /> and also [[ataxia]]<ref name=LebwoholLudvigsson /> and [[attention deficit hyperactivity disorder]] (ADHD).<ref name=FasanoSapone2015 />
Gluten is likely responsible for the appearance of symptoms, but it has been suggested than in a subgroup of people with NCGS and symptoms like IBS, other components of wheat and related grains (oligosaccharides like fructans), or other plant proteins contained in gluten-containing cereals (agglutinins, lectins, and [[amylase trypsin inhibitor]]s (ATIs)) may play a role in the development of gastrointestinal symptoms.<ref name=ElliBranchi>{{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 = June 2015 | pmid = 26109797 |pmc= 4476872 | doi = 10.3748/wjg.v21.i23.7110}}</ref> ATIs are about 2–4% of the total protein in modern wheat and 80–90% in gluten.<ref name="FasanoSapone2015" /> In a review of May 2015 published in [[Gastroenterology]], [[Alessio Fasano|Fasano]] ''et al.'' conclude that ATIs may be the inducers of innate immunity in people with coeliac disease or NCGS.<ref name=FasanoSapone2015 /> As of 2019, reviews conclude that although [[FODMAP]]s present in wheat and related grains may play a role in non-celiac gluten sensitivity, they only explain certain gastrointestinal symptoms, such as [[bloating]], but not the [[non-celiac gluten sensitivity#Extraintestinal|extra-digestive symptoms]] that people with non-celiac gluten sensitivity may develop, such as [[neurological disorder]]s, [[fibromyalgia]], psychological disturbances, and [[dermatitis]].<ref name=Verbeke2018>{{cite journal |last1=Verbeke |first1=K |title=Nonceliac Gluten Sensitivity: What Is the Culprit? |journal=Gastroenterology |date=February 2018 |volume=154 |issue=3 |pages=471–473 |doi=10.1053/j.gastro.2018.01.013 |pmid=29337156| quote=Although intolerance to fructans and other FODMAPs may contribute to NCGS, they may only explain gastrointestinal symptoms and not the extraintestinal symptoms observed in NCGS patients, such as neurologic dysfunction, psychological disturbances, fibromyalgia, and skin rash.15 Therefore, it is unlikely that they are the sole cause of NCGS.|doi-access=free }}</ref><ref name=VoltaDeGiorgio2019>{{cite journal| vauthors=Volta U, De Giorgio R, Caio G, Uhde M, Manfredini R, Alaedini A| title=Nonceliac Wheat Sensitivity: An Immune-Mediated Condition with Systemic Manifestations | journal=Gastroenterol Clin North Am | date= March 2019 | volume= 48 | issue= 1 | pages= 165–182 | pmid=30711208 | doi=10.1016/j.gtc.2018.09.012 | pmc=6364564 | type=Review |quote=Furthermore, a role for the FODMAP (eg, fructans) component of wheat as the sole trigger for symptoms is somewhat doubtful, because many patients with NCWS report resolution of symptoms after the withdrawal of wheat and related cereals, while continuing to ingest vegetables and fruits with high FODMAP content in their diets.59 On the whole, it is conceivable that more than one culprit may be involved in symptoms of NCWS (as they are currently defined), including gluten, other wheat proteins, and FODMAPs.60–62 }} </ref><ref name="FasanoSapone2015" /> As occurs in people with coeliac disease, the treatment is a [[gluten-free diet]] (GFD) strict and maintained, without making any dietary transgression.<ref name=VoltaCaio2015 /> Whereas coeliac disease requires adherence to a strict lifelong gluten-free diet, it is not yet known whether NCGS is a permanent, or a transient condition.<ref name=VriezingaSchweizer /><ref name=VoltaCaio2015 /> The results of a 2017 study suggest that NCGS may be a chronic disorder, as is the case with celiac disease.<ref name=VoltaDeGiorgio2019 /> Theoretically, a trial of gluten reintroduction to observe reaction after 1–2 years of strict gluten-free diet might be advisable.<ref name=VoltaCaio2015 />
Approximately one third of personas with NCGS continue having symptoms despite gluten withdrawal. This may be due to diagnostic error, poor dietary compliance, or other reasons. Those afflicted with NCGS may be under the impression that they don't need to follow a strictly [[gluten free diet]]. However, the ingestion of even a small amount of gluten may cause more immediate symptoms in people suffering from NCGS as compared with those afflicted with coeliac disease. People with NCGS should carefully read ingredient labels on food and be aware of potential [[cross contamination]] as a source of gluten in otherwise gluten-free foods. To find out if there are unintended ingestions of gluten, an exhaustive evaluation with the advice of a coeliac disease specialized dietitian could be necessary.<ref name=VoltaCaio2015 />
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People can also experience adverse effects of wheat as result of a [[wheat allergy]].<ref name=ElliBranchi /> Gastrointestinal symptoms of wheat allergy are similar to those of coeliac disease and non-celiac gluten sensitivity, but there is a different interval between exposure to wheat and onset of symptoms. Wheat allergy has a fast onset (from minutes to hours) after the consumption of food containing wheat and could be [[anaphylaxis]].<ref name=NEJM2012 /><ref name=ScherfBrockowQuotation>{{cite journal|vauthors=Scherf KA, Brockow K, Biedermann T, Koehler P, Wieser H|title=Wheat-Dependent Exercise-Induced Anaphylaxis|journal=Clin Exp Allergy [Epub ahead of print]|volume=46|issue=1|pages=10–20|date=September 18, 2015|pmid=26381478|doi =10.1111/cea.12640}}</ref>
The treatment of wheat allergy consists of complete withdrawal of any food containing wheat and other gluten-containing cereals.<ref name=ScherfBrockowQuotation /><ref name=HischenhuberCrevelQuotation>{{cite journal |vauthors=Hischenhuber C, Crevel R, Jarry B, Mäki M, Moneret-Vautrin DA, Romano A, Troncone R, Ward R|title=Review article: safe amounts of gluten for patients with wheat allergy or coeliac disease |journal=Aliment Pharmacol Ther |volume=23|issue=5|pages=559–75|date=March 1, 2006|pmid =16480395|doi=10.1111/j.1365-2036.2006.02768.x|doi-access=free}}</ref> Nevertheless, some people can tolerate barley, rye or oats.<ref name=Pietzak>{{cite journal|author=Pietzak M|title=Celiac disease, wheat allergy, and gluten sensitivity: when gluten free is not a fad|journal=JPEN J Parenter Enteral Nutr|volume=36|issue=1 Suppl|pages=68S–75S|date=Jan 2012|pmid=22237879|doi=10.1177/0148607111426276}}</ref>
=== Other conditions or risk factors ===
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Compared to the [[Coeliac disease#Pathophysiology|pathophysiology of celiac disease]], the pathophysiology of NCGS is far less understood.
A literature review of 2014 found that people suffering from NCGS "are a heterogeneous group, composed of several subgroups, each characterized by different pathogenesis and clinical history, and, probably, clinical course".<ref name="mansueto-etal-2014">{{cite journal|author1=Mansueto P |author2=Seidita A |author3=D’Alcamo A |author4=Carroccio A |title=Non-Celiac Gluten Sensitivity: Literature Review|journal=Journal of the American College of Nutrition|volume=33|issue=1|year=2014|pages=39–54|issn=0731-5724|doi=10.1080/07315724.2014.869996|pmid=24533607|type=Review|hdl=10447/90208 |hdl-access=free}}</ref>
=== Genetics ===
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== Treatment ==
{{Main|Gluten-free diet}}
For people with celiac disease, a lifelong strict gluten-free diet is the only effective treatment to date;<ref name="LamacchiaCamarca2014" /><ref name="Czaja-Bulsa-2014-table2">{{cite journal |author=Czaja-Bulsa G |title=Non coeliac gluten sensitivity - A new disease with gluten intolerance |journal=Clinical Nutrition (Edinburgh, Scotland) |volume= 34|issue= 2|pages= 189–194| date=August 2014 |pmid=25245857 |doi=10.1016/j.clnu.2014.08.012 |type=Review|doi-access=free }} See [http://www.clinicalnutritionjournal.com/article/S0261-5614%2814%2900218-0/fulltext#tbl2 Table 2: Characteristics of gluten-dependent disorders].</ref>
For people diagnosed with non-celiac gluten sensitivity, there are still open questions concerning for example the duration of such a diet. The results of a 2017 study suggest that non-celiac gluten sensitivity may be a chronic disorder, as is the case with celiac disease.<ref name=VoltaDeGiorgio2019 />
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For people with [[wheat allergy]], the individual average is six years of gluten-free diet, excepting persons with anaphylaxis, for whom the diet is to be wheat-free for life.<ref name="Czaja-Bulsa-2014-table2"/>
Preferably, newly diagnosed celiacs seek the help of a dietician to receive support for identifying hidden sources of gluten, planning balanced meals, reading labels, food shopping, dining out, and dining during travel.<ref name="pmid24444577">{{cite journal |vauthors=Pelkowski TD, Viera AJ |title=Celiac disease: diagnosis and management |journal=American Family Physician |volume=89 |issue=2 |pages=99–105 | date=January 2014 |pmid=24444577 }}</ref> Knowledge of hidden sources of gluten is important for people with celiac disease as they need to be very strict regarding eating only gluten-free food.<ref>{{cite journal|vauthors=Cristofori F, Arezzo F, Gentile A, Francavilla R |s2cid=71854723|title=Gluten Sensitivity in Pediatrics: A Clinical Conundrum|journal=Current Pediatrics Reports|date=September 2014|volume=2|issue=3|pages=204–210|doi=10.1007/s40124-014-0053-9|doi-access=free}}</ref> The degree of gluten [[cross contamination]] tolerated by people with non-celica gluten sensitivity is not clear but there is some evidence that they can present with symptoms even after consumption of small amounts.<ref name=VoltaCaio2015 /> Sporadic accidental contaminations with gluten can reactivate [[movement disorder]]s associated with non-celica gluten sensitivity.<ref name=VinagreAragonZis>{{cite journal| vauthors=Vinagre-Aragón A, Zis P, Grunewald RA, Hadjivassiliou M| title=Movement Disorders Related to Gluten Sensitivity: A Systematic Review | journal=Nutrients | year= 2018 | volume= 10 | issue= 8 | page=1034 | pmid=30096784 | doi=10.3390/nu10081034 | pmc=6115931 | type=Systematic Review }} </ref> A part of people with gluten-related neuropathy or [[ataxia#Gluten ataxia|gluten ataxia]] appears not to be able to tolerate even the traces of gluten allowed in most foods labeled as "gluten-free".<ref name=HadjivassiliouGrunewald2002>{{cite journal| vauthors=Hadjivassiliou M, Grünewald RA, Davies-Jones GA| title=Gluten sensitivity as a neurological illness. | journal=J Neurol Neurosurg Psychiatry | year= 2002 | volume= 72 | issue= 5 | pages= 560–3 | pmid=11971034 | doi= 10.1136/jnnp.72.5.560| pmc=1737870 | type=Review }} </ref>
The inclusion of [[oats]] in gluten-free diets remains controversial. [[Oat#Protein|Avenin]] present in oats may also be toxic for coeliac sufferers.<ref name=PenaginiDilillo>{{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 = November 18, 2013| pmid = 24253052|pmc= 3847748| doi = 10.3390/nu5114553}}</ref> Its toxicity depends on the [[cultivar]] consumed.<ref name=CominoMoreno>{{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 = November 7, 2015 | pmid = 26557006 |pmc= 4631980 | doi = 10.3748/wjg.v21.i41.11825}}</ref> Furthermore, oats are frequently cross-contaminated with gluten-containing cereals.<ref name=PenaginiDilillo />
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== Epidemiology ==
In the United States, fewer cases of CD have been found compared to other countries.<ref>Boettcher, Erica and Ramesh K. Gandhi. "Celiac Disease." ''Primary Care Reports'', vol. 18, no. 12, Dec. 2012, pp. 153-167. EBSCO''host'', http://search.ebscohost.com/login.aspx?direct=true&db=a9h&AN=83835158&site=ehost-live&scope=site.</ref> The incidence of celiac disease and of wheat allergy is estimated each to lie at around 1% of the population. There has been a 6.4 increase in the case reports of celiac disease between 1990 and 2009.<ref name="coeliac disease in children"/> The incidence of NCGS is unknown; some estimates range from 0.6% to 6%,<ref name="Czaja-Bulsa-2014-table2"/> and a systematic review of 2015 reported on studies with NCGS prevalence rates between 0.5% and 13%.<ref name="pmid25753138">{{cite journal |vauthors=Molina-Infante J, Santolaria S, Sanders DS, Fernández-Bañares F |title=Systematic review: noncoeliac gluten sensitivity |journal=Alimentary Pharmacology & Therapeutics |volume=41 |issue=9 |pages=807–20 |year=2015 |pmid=25753138 |doi=10.1111/apt.13155 |type=Review|doi-access=free }}</ref>
In Europe, the average consumption of gluten is 10g to 20g per day, with parts of the population reaching 50g or more per day.<ref name="sapone-etal-2010-b"/>
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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.|s2cid=6012463|date=2016-01-01|title=Sensitivity to wheat, gluten and FODMAPs in IBS: facts or fiction?|url=https://gut.bmj.com/content/65/1/169|journal=Gut|language=en|volume=65|issue=1|pages=169–178|doi=10.1136/gutjnl-2015-309757|issn=0017-5749|pmid=26078292|doi-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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