Talk:Coeliac disease

Coeliac/Celiac: Please read prior discussions regarding the name of this article at /Archive 1#Requested move.

Do we need nasty images without warnings?

Would it be possible to show a simple drawn diagram, instead of an actual photograph of something that nasty? Or have a warning where people have to click on something before showing it. http://en.wikipedia.org/wiki/Image:Celiac_3.jpg is the image I'm referring to. I personally would like to read the article, without having that image on the side grossing me out. Dream Focus (talk) 10:57, 8 October 2008 (UTC)

I asked my friend, who specializes in cuteness, to draw a more suitable picture of a colonoscopy for you. Image:Happycolon.png How does that rub you?--Perceive (talk) 03:39, 31 December 2010 (UTC)

I'm sorry, but... no and no. Please see Wikipedia:Options to not see an image for some options you can implement over at your end :) Fvasconcellos (t·c) 11:32, 8 October 2008 (UTC)

Sorry, Dream Focus, I don't really see what's nasty about a duodenum. If no caption had been provided, I'm sure you could have easily mistaken it for a tunnel in an underground network on another planet. JFW | T@lk 21:07, 9 October 2008 (UTC)

Well we need a better picture, the image shown is not classic. I will work on it -- Samir 04:51, 14 June 2009 (UTC)

1) This is mild (heck, compared to the really bad stuff we have, I think it doesn't even reach "mild level"). 2) Wikipedia:Perennial proposals#Censor_offensive_images also specifically discuss this. Circeus (talk) 15:29, 14 June 2009 (UTC)

Indo-europeans not are a biologic group

indo-europeans are a linguistic group with very races converted to the aryan culture(for example: indians and iberics) —Preceding unsigned comment added by 189.71.19.89 (talk) 04:34, 27 December 2008 (UTC)

Please make comments on the talk page rather than inserting them in the lead (which I've removed). However, I would be interested to know which source uses the term "indo-european" for the 1% figure, and whether there is a better classification. Also, the term is not repeated in the Epidemiology section, and the lead should be a summary of the body. Colin°^Talk 10:24, 27 December 2008 (UTC)

I know i am going to be two technical with this, but here goes. The gene(s) primarily responsible for celiac disease is DQ2.5, DQA1*0501:DQB1*0201 haplotype. There have been some recent discoveries concerning this type, however I will give the background, first. This haplotype is found in three nodes in Europe. 1. Irish, 2. Sardinians 3. Basque (1 and 3 and 2 and 3 have some haplotype similarities). With more detailed haplotype information is appears that the Basque and Irish ("AH8.1" extended haplotype) have descent from common ancestor in the Pleistocene epoch. The Sardinian node, while in Europe, may have been the result a more recent migration from Africa.

Irish DQ2.5 - A1-Cw7-B8-DR3-DQ2.5 ("AH 8.1" all DQ2.5 is found with DR3 and all DR3 is found with DQ2.5) closest "living ancestral population" Basque - Indoeuropean-No

Sardinian DQ2.5 - A30-Cw5-B18-DR3-DQ2.5 closest "living ancestral population" North Africa - Afroasiatic.

(Several papers have now been written on the natural history/evolution of AH8.1)

AH8.1 spread in Europe during the epipaleolithic period from NW spain or SW France (Iberian refuge) in a quadrant that extended to what is now the Ilses, Scandinavia, Switzerland. It re-spread prior to and during the Migration Age into Eastern Europe (Goths), Russia(Norse), Yugoslavia(Slavs), Northern Italy(Germanics). In the Industrial age it spread into North America(anglo), Latin America(Basque), Australia(Anglo), South Africa(Anglo and Futch). 57% of people in these regions that have A1-Cw7, B8, or DR3-DQ2.5 also have the entire haplotype HLA A1-B8-DR3-DQ2 haplotype. It is said to be in selective linkage disequilibrium and spread from a recent common european ancestor. That ancestor did not likely speak European language (20 to 30 kya). Previously AH8.1 was believed to have been carried by Anglos into India, however, a recent study of Indian AH8.1 shows that only the DR3-DQ2.5 haplotype are linked to Irish AH8.1. The genes in the class III region (between HLA-B and HLA-DR) are all dissimilar, indicating that AH8.1-india is a fortuitous recombination, likely of Dravidian ancestral origin. I personally have spent an alot of time trying to determine precise origin of AH8.1 and basically the trail goes 'dry' in Northern Spain. West Africa has both A1-B8 haplotype and DR3-DQ2.5 but no evidence that AH8.1 formed in West Africa. Morocco has B8-DR3-DQ2.5 but the A1 bearing haplotype is not obviously present. I suspect that the components in Iberia come from West Africa, more than likely we are talking about a Berber origin and language placement is an issue. (Most berbers now speak a hamito-semetic language). A recent paper on these two variants suggest a common ancestor 80,000 years ago.

Finally there is an Asiatic version of DR3-DQ2.5. It is frequently found with a minority of DRB1*0302 (likely of African origin). The haplotype in which it is found more commonly is A33-B58 haplotype. There is no cohesive publication on this material. It is found in West Africa, Sudan, Western Pakistan, Central Asia, China, Thailand. Trace amounts of DQ2.5 are found in Korea, none in Japan. Given the Yayoi migration (2nd Mil BC to 4th century AD) and generally close alignment of Korean and Japanese HLA, I infer that almost all of the DQ2.5 in Korea came from the Asian interior after Yayoi migration, probably with the Mongol invasion of the previous millenium. This appears to be how much of DQ2.5 spread in the east, it is almost always found in cultures with a rich Chinese ancestry. Asian DQ2.5 peaks in Kazakhstan - However the most probable origin in Asia is from the Balochi peoples in SW Pakistan and these people probably arrived at this from W. Africa from a concurrent Sub-saharan/sahul language. This haplotype likely arrived in the holocene and may explain how African cereals spread through Asia.

Contribution of Indoeuropean language to early spread of DQ2.5 -none. Haplotypes common in Anatolia and proximal Europe are at highest frequencies in Europe (Paris basin, Belgium, parts of germany) where Ancestral European haplotypes are at there lowest frequencies. HOWEVER, with Indoeuropean language came advanced wheat cultivation, and this is the major risk factor for celiac disease. Because it is now clear that neolithization was largely non-genetic, it largely failed to displace genes adapted to the mesolithic lifestyle. In Europe, beyond where early neolithization stopped its advance north, or into highlands, the frequency of DQ2.5 is highest. This indicates the role of environment for wheat cultivation, genetics of migration and/or selection. The last peoples to enter the neolithic phase were the Irish, they have they highest level of AH8.1, so that we cannot 'unlink' IE from celiacs either. West Africa has very high DQ2.5 levels and yet CD is low in most areas in which African cereals are exclusively grown. So that the Indoeuropean language spread over a backdrop of preexisting DQ2.5 frequencies in Europe, Sardinia, India, parts of Pakistan and Central Asia but is more associated with the agricultural process of Westeurasian Neolithization.

Statistical concerns.

Risk and associated Risk.

DQ2.5/x risk is 65/100

DQ2.5/DQ2.5 homozygote ~12/100

DQ2.5/DQ2.2 homozygote ~17/100 cases

As frequency increases for DQ2.5 or DQ2.2

• disease frequency will increase more rapidly
• the proportion of DQ2 homozygotes in disease will increase.
• threshold levels of wheat consumption and age of onset will lower.

Here is an example. DQ2.5 spread into northern Mexico with the basque, the combination DQ2.5/DQ8 heterozygotes (highest risk factor for type 1 diabetes) is second highest in Jalisco, Mexico. And yet type 1 diabetes is typically only found in peoples who identify themselves with European culture and virtually absent in people who identify more with mestizo or other native american peoples. In fact, within the indigenous populations of Mexico, where DQ8 (highest single gene risk factor for T1D) can run as high as 95% in gene frequency, inflammatory abnormalities of the immune system are very low. In the Andes of South America, when celiac disease is identified it is more commonly found with DQ8 and almost always found in people transitioning toward a more western lifestyle. Celiac disease is mediated by HLA-DQ variants, however, as these instances show it really is a disease of culture (affluence) that has resulted from peoples in transition from indigenous lifestyles into more Westeurasian cultural patterns in the last 2000 years this frequently was accompanied by a shift to an IE language. Indoeuropean speakers brought about the largest spread of western culture, including wheat, into indigeonous populations. Wheat culture has reached, however, beyond this group into cultures of Asia, and with this disconcerted spread comes the spread of celiac disease (e.g. Japan - DQ8, No DQ2.5). PB666 ^yap 15:07, 31 December 2008 (UTC)

The funny thing is that the Basque and the Irish speak, or spoke originally, bastards of Celtic. I am too lazy to look up whether these technically fall under IE languages but I do assure you that their structure is completely different and weird. Look at Basque or Gaelic, the helloworld sentences suffice, they are about as far away from the Western IE languages as Finnish is. --92.78.3.54 (talk) 17:58, 11 September 2009 (UTC)

Basque isn't usually considered a 'Celtic' language. In fact, it appears to be a 'language isolate', with no obvious relationship to any other language or group of languages, including Celtic. Celtic languages do fall under IE languages. And 'weird' is a rather subjective judgement. Irish certainly has a lot of commonalities with other IE languages. Have a look at the numbers, they're a better indicator than greetings. ANB (talk) 11:03, 12 April 2011 (UTC)

What does this line mean in the opener?

1/3rd of the below sentence doesn't seem to convey meaning very well (the quoted part).

Symptoms include chronic diarrhoea, failure to thrive (in children), and fatigue, but these may be absent "...and symptoms in all other organ systems have been described."

Maybe it's a common phrasing I'm just unfamiliar with?Xetxo (talk) 01:06, 7 February 2009 (UTC)

Maybe the quoted part should be changed to "symptoms in all other organ systems have been reported." —Preceding unsigned comment added by 72.209.5.49 (talk) 23:51, 16 April 2009 (UTC)

The point is that it's possible to have coeliac disease affecting only the skin, nervous system etc. JFW | T@lk 17:58, 17 April 2009 (UTC)

Van Weel is back

http://gut.bmj.com/cgi/content/full/58/4/473 - recent advances in the genetics of coeliac disease. May end up being useful. JFW | T@lk 01:31, 14 April 2009 (UTC)

There is a new Lancet review, doi:10.1016/S0140-6736(09)60254-3. Work to do, I reckon. Perhaps time we get rid of the BSG references and update them with this article, given its advantages. JFW | T@lk 23:46, 25 April 2009 (UTC)

Thanks Jeff I will look at both as soon as I have a chance.PB666 ^yap 23:54, 21 June 2009 (UTC)

With regard to Van Heel, I am not going to comment about his review per say, but the discussion of the major 'other' gene 4q27. Its actually associated with 6 diseases all of which show an increased prevelance in coeliac disease patients, and frequently a clinical prelude to CeD diagnosis. These diseases are

• type 1 diabetes -Linked to DR4-DQ8 and DR3-DQ2.5
• rheumatoid arthritis - Linked to DR4 and DR1
• juvenile idiopathic arthritis
• ulcerative colitis
• graves disease
• SLE
• psoarasis
• psoarasis arthritis

The problem arises in how are the tested individuals drawn into the study, if they are not drawn in randomly (for example random biopsy or random DQ/ATA screening) then all they are doing is picking up common autoimmune disease risk factor, possible increased in CeD, but also possibly drawn in because of the diagnosis process. Or to rephase, what percent of diagnoses celiacs have one or more of the above 6 diseases before showing up in the clinic?

There is a reference to DQ2.5cis, DQ2.5 and the semi-homozygote DQ2.5cis/DQB1*02 (As I said, this oblique terminology was starting to get around) on page 474.

The question we have to ask ourselves here since we have posted information on genetic associations and that information later needed to removed, do we want to add updated information on genetics now, that later will have to be removed when new studies reveal the inadequacies of the past approached. I quote from Van Heel because I think we align on this issue

MISSING HERITABILITY:SOMEWHAT PUZZLING... We estimate that the current coeliac disease risk SNPs account for only 3-4% of disease genetic heritability, with HLA accounting for a further 30%. So where is the rest [>75%] of the heritability of coeliac disease, known from twin and family studies? First we suggest many other associations are still to be found. Odds ratios (ORs) for the newly associated variants, are in the range of 0.7-1.4.

::and most of those are between .85 and 1.15 such that if we accumulated all the risk we still could not explain more than 30% of disease, at best. My opinion which does not account for much here, is that Coeliac disease outside of HLA is quasi-inherited and that there is a fascinating blend of environmental and genetic predispositions, possibly epi-genetic contributions. For example, in NW Europe almost no disease is associated with DQ2.2 and in Italy a surprising proportion is associated with DQ2.2, why should there be such a geographic distinction? There is a basic problem in these studies, early studies showed one locus was associated in place A and in place B not associated. That lead many to believe that the locus associated in place A was just a random association, what if they are not, what if place specific associations are the modus operandus for celiac disease genetics, and by doing genome-wide studies in wide samplings of the population we are simply diluting all the various regional associations and thus picking up diagnosis bias making the these regional susceptibility factors even harder to find. Two of the last two projects of this same kind I have worked on, when one narrowed the clinical subset (parsed according to strict clinical presentation), what appearred to be normal suddenly became significantly different. What Van Heel is saying is that 'we' have to do much better with the genetics.PB666 ^yap 01:29, 22 June 2009 (UTC) BTW I could not download the Lancet article.

Here are two recent papers discussion both issues:

• Tissue Antigens. 2009 Mar;73(3):225-35. Variants within protectin (CD59) and CD44 genes linked to an inherited haplotype in a family with coeliac disease.
• Celiac Disease Revealed in 3% of Swedish 12-year-olds Born During an Epidemic. J Pediatr Gastroenterol Nutr. 2009 May 25.
• BMC Microbiol. 2008 Dec 22;8:232.Imbalances in faecal and duodenal Bifidobacterium species composition in active and non-active coeliac disease.

There is a paper out also on the Genetic Structure of Europeans: A view from the North-East:

Compounding by population stratification [because few regional cohorts of disease exceed 10,000 in number] heterogeneity between studies samples can give false positive results in association studies, as the association with the trait may be the result of the systematic ancestry difference in allele frequencies between groups.

The paper goes onto detail the 3 pole 2 component plots of Europeans. Notably in this image the Irish/Anglo pole in missing.PB666 ^yap 03:28, 22 June 2009 (UTC)

Reliable sources

A user added this source, and it was added back in by another user after reversion: Spersud, Erik and Jennifer (January 3, 2008). Everything You Want To Know About Recipes And Restaurants And Much More. USA: Authorhouse. p. 144. doi:10.1007/b62130. ISBN 9781434360342.. The book is self-published; Authorhouse is a self-publishing company. This book does not meet WP:MEDRS, so it cannot be used as a source for the statement: "Other cereals, such as maize (corn), quinoa, millet, sorghum, chia seed, and rice, are safe for patients to consume". Fences and windows (talk) 15:14, 17 April 2009 (UTC)

There must be better sources for that claim. JFW | T@lk 17:58, 17 April 2009 (UTC)

NICE guideline

The NICE guideline is out. It focuses mainly on diagnosis and not so much on follow-up, http://guidance.nice.org.uk/CG86. JFW | T@lk 20:58, 1 June 2009 (UTC)

Section Order

I notice that a recent edit has moved Screening down to its proper place, as per WP:MEDMOS#Sections, which is great. While even MEDMOS identifies it as a minor concern, I'm wondering if we should change the rest of the sections to match that standard as well (they're close, but a couple are switched around)...at least in my mind, consistency is a good thing. Does anybody else have any opinions?

Also, as part of this, consider whether Screening should be bumped back up (and how far back up), following the guideline in MEDMOS that suggests leaving more-technical sections till lower.

I have no particular opinion on this, so in the absence of any other feedback, I'll switch the ordering to MEDMOS standard in a couple of days. But if there's consensus to use a different order, I'll happily switch it to that. --Rob (talk) 21:26, 13 June 2009 (UTC)

I'm cool either way -- Samir 04:51, 14 June 2009 (UTC)

Endo pic

Need a better one! -- Samir 04:51, 14 June 2009 (UTC)

Antioxidant study

I've reverted the addition of a claim that an in vitro study of macrophages "suggests that the natural antioxidants lycopene, quercetin and tyrosol may help to control the inflammation of coeliac disease." For starters, it doesn't belong in a section on "treatment". Nor does it belong in the "experimental treatments" since it isn't an experimental treatment (in humans). If the article has a section on basic research then this sort of thing might belong, but per WP:MEDRS, we should citing reliable literature reviews to get a balanced picture of the current state of research in this field. All basic-life-science articles (with positive results) conclude that their study on X "suggests" something "may help". This is standard boasting of researchers drumming up funds for future research in the field. It has no significance beyond the intended readership (other researchers). It certainly isn't significant enough to warrant space in a general encyclopaedia. Colin°^Talk 09:11, 19 July 2009 (UTC)

This was the reason I originally removed this study. WP:MEDRS is very clear about including primary studies, especially when they are lightyears removed from being replicated in man. I can already hear the complaint: "But these are natural treatments and therefore no drug company cash will be available to conduct these expensive studies in people..." JFW | T@lk 10:10, 19 July 2009 (UTC)

Agree, and the other problem here is that getting something in a natural dose may have positive or neutral benefits but taking a supplement may have a negative benefit. Two of the compounds are aromatics, and certain aromatic compounds have been identified as sensitizing agents in some people for allergic disorders. WP should not be in a position of making medical recommendations (implied or otherwise).PB666 ^yap 15:38, 31 July 2009 (UTC)

you are putting up straw men, making arguments that have nothing to do with what I wrote, or with why I wrote it. this is a peer-reviewed paper, Scopus shows 11 other peer-reviewed papers that cite it. does it occur to you that the authors may have a deeper understanding of coeliac disease than you do? macrophage activation is at the core of the pathogenesis of coeliac disease, in vitro research has always been essential to learning about this disease and to understanding what is observed in vivo. —Preceding unsigned comment added by 71.182.132.247 (talk) 16:31, 21 July 2009 (UTC)

Please don't make personal attacks. They distract from the subject under discussion. JFW | T@lk 21:58, 21 July 2009 (UTC)

Coeliacs/Celiacs vs Coeliac Disease

Can someone please fix this article by not calling people who suffer from coeliac disease coeliacs (or celiacs for the Americans). It is incorrect to call someone a coeliac. They have coeliac disease, it does not define their person and it is, IMHO, quite offensive and gramatically incorrect to call someone a coeliac. We don't call people with Chron's disease Chronies... Well at least not to their face or in an encyclopedia. —Preceding unsigned comment added by 124.169.176.25 (talk) 15:59, 14 August 2009 (UTC)

I'd be happy to go through the article and make the required changes, provided that we have consensus to do so. I'm just thinking, though, that this may not be an open-and-shut case - after all, we regularly refer to people with several other conditions or attributes by one-word terms: diabetics, paraplegics, disabled (more often "the disabled" or "disabled people, I'll grant), brunettes, lesbians, etc. Oh and contrary to your assertion about Crohnies, around here we do call at least one person a Crohnie: this one. ;) --RobinHood70 (talk) 20:38, 14 August 2009 (UTC)

See WP:MEDMOS and People-first language. Generally, I support people-first terminology. Just because people regularly do something doesn't make it right. However, some medical conditions seem to carry no or little stigma or implications that one is disabled as a person. Both diabetes and coeliac disease could be in that category, and I note that coeliac.org.uk regularly uses the term "coeliacs" and celiac.com uses the term "celiacs". However, NICE is careful to only use "people with coeliac disease" in their guidelines. I find the over-use of the word "patients" in this article to be more problematic: this is not a medical textbook (the word is fine when discussing people actively interacting with healthcare professionals, such as during diagnosis or treatment). Colin°^Talk 22:38, 14 August 2009 (UTC)

Coeliac/Celiac

Not to annoy anyone, but it should be noted that by the numbers, more people will recognize Celiac versus Coeliac (mostly beacuse there are more people who use Wikipedia who speak American English than British English.) Of course there is the redirect, but if Coleiac is seen on another page, it may not be recognized, thus causing signifigant confusion. Now, I don't have a problem with the usage of British English on pages pertaining to the UK and commonwealth nations, but on an international page, the most used spelling would be appropriate. —Preceding unsigned comment added by 71.171.220.67 (talk) 23:32, 26 August 2009 (UTC)

See WP:ENGVAR. JFW | T@lk 21:49, 16 September 2009 (UTC)

Also have a look at the discussion mentioned at the top of this page. Here's a copy of the link to save you time. —RobinHood70 ^{(talk • contribs)} 23:59, 16 September 2009 (UTC)

Should be Celiac - recognized as such around the world, including jolly England. And should be changed. I've never seen this screwed-up spelling before Ever. Confusing for someone new doing research. —Preceding unsigned comment added by 71.169.26.61 (talk) 20:17, 26 July 2010 (UTC)

Please moderate your language. There are plenty of redirects that make the content easy to find, and in England the spelling is coeliac. In fact, if you Google "celiac disease", this article comes up second despite the commonwealth spelling. JFW | T@lk 08:16, 27 July 2010 (UTC)

I'll second that. I've read several European articles that use the spelling "Coeliac". There is no pressing reason to change the spelling to Celiac other than to cater to us North Americans. :) —RobinHood70 ^{(talk • contribs)} 15:53, 30 July 2010 (UTC)

False positive serology

False Positive Serology results? Is it possible to receive a false positive blood test result? Forgive me for bad formatting or for placing this in the wrong section. I am new at this, but would suggest information about false positive blood test results be placed in the main article. Thank youTunalucy (talk) 19:15, 2 September 2009 (UTC)

This is not discussed in the sources, so probably not that much of a problem. Serology is pretty specific. JFW | T@lk 19:56, 2 September 2009 (UTC)

Re: False positive serology

It would seem that the following information would be helpful to get accurate (rather than false positive) results, but when I added it to the article it was removed on the grounds that by posting the portion I linked to the original place I found the information was 'incorrect' formatting. That I should put it 'in my own words' then have a link with the vital information below. I honestly do not feel that something this exact should be 'put in my own words'. I do not break any copyright law as I am quoting directly with a link to it's source at the bottom. Following is the information I attempted to add, exactly as I added it. Please suggest changes more specifically (if that is possible) that can be made to my contribution that would not step on copyright law and still be scientifically as well as clinically correct:

Blood tests

Blood Tests for Celiac Disease

There are a total of 6 tests that can be run for Celiac disease. (1) Anti-Gliadin (AGA) IgA (2) Anti-Gliadin (AGA) IgG (3) Anti-Tissue Transglutamise (tTg) IgA (4) Total Serum IgA

(5) Anti-Tissue Transglutamise (tTg) IgG (6) Endomesial Antiobody (EMA) IgA

Note that AGA is simply the abbreviation for Anti-Gliadin antibody, tTg is for Tissue transglutimase and EMA for Endomeisial antibody. Sometimes you see the letters instead, because writing and saying the words is a pain. The tests with IgA test for the IgA antibody in the system. The IgG tests test for IgG antibodies in the system. The most indicative tests of Celiac are the tTg-IgA (number 3 above) and the EMA (number 6 above).

What is often referred to as the “Celiac Disease Panel” consists of the first 4 tests above. These are the “standard” tests that should always be run to test for Celiac disease. Number 4 - Total Serum IgA is critical to include. This will tell you if the body is able to produce IgA antibodies. Some people (10% of the population) can’t produce the IgA antibodies and are considered IgA deficient. If you cannot produce IgA antibodies, the IgA tests above (number 1, 3, and 6) will never come back positive for Celiac disease, even if you have Celiac disease. Therefore, you have to have the IgG numbers. They usually only run #5 if Total Serum IgA indicates a deficiency and/or if the AGA IgG (number 2 above) is the only one that is abnormally high.

The EMA (number 6) is very sensitive for CD. However, it is a test that is more difficult to read – meaning that you have to have an experienced lab tech reading the results or there could be an error. The tTg-IgA test is more “idiot proof” in the lab and cheaper to do, so it has become more of the standard instead of the EMA. You can have both done, but it isn’t necessary.

Special note for young children: The total IgA is not really considered accurate until the age of 4 or so (at least that is what I have read), so when those results come back, a diagnosis of IgA deficiency would not be made if the child was under the age of 4.

Nobodyz (talk) 12:54, 20 October 2009 (UTC)

Latent coeliac

A mortality study from Sweden that will need to be mentioned: http://jama.ama-assn.org/cgi/content/abstract/302/11/1171 JFW | T@lk 21:48, 16 September 2009 (UTC)

Am I reading this right

The absolute mortality rate was 10.4 (95% CI, 10.0-10.8) per 1000 person-years in celiac disease, 25.9 (95% CI, 25.0-26.8) in inflammation, and 6.7 (95% CI, 5.7-7.6) in latent celiac disease. Excess mortality was 2.9 per 1000 person-years in celiac disease, 10.8 in inflammation, and 1.7 in latent celiac disease. This risk increase was also seen in children. Excluding the first year of follow-up, HRs decreased somewhat.

.

10.4 per 1000 person years is not that bad, 6.7 sounds like a really low mortality risk, what is the risk in person-years for the normal population.PB666 ^yap 21:39, 20 October 2009 (UTC)

CD and DH severity by autoantibody levels

Dahlbom I, Korponay-Szabó IR, Kovács JB, Szalai Z, Mäki M, Hansson T (2009). "Prediction of Clinical and Mucosal Severity of Coeliac Disease and Dermatitis Herpetiformis by Quantification of IgA/IgG Serum Antibodies to Tissue Transglutaminase". J. Pediatr. Gastroenterol. Nutr. ([Epub ahead of print]). doi:10.1097/MPG.0b013e3181a81384. PMID 19841593. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)PB666 ^yap 13:41, 24 October 2009 (UTC)

“ Immunoglobulin (Ig)A antibodies against tissue transglutaminase (IgA-TGA) were detected in all of the patients with CD and in 95% of the DH patients. The IgA-TGA and IgG-TGA levels were higher in group I (P < 0.001). The IgG-TGA levels and positivity rate in group I (100%) were higher than in group II (81%), group III (73%), and the DH group (67%). Elevated IgA-TGA and IgG-TGA levels in combination predicted a more severe small intestinal atrophy (P < 0.0001) with a specificity of 99% for Marsh IIIb-IIIc (flat) lesions. The kinetics of the IgA-TGA decrease during diet differed between groups I and II. ”

CD in MG

Freeman HJ, Gillett HR, Gillett PM, Oger J (2009). "Adult celiac disease with acetylcholine receptor antibody positive myasthenia gravis". World J. Gastroenterol. 15 (38): 4741–4. PMC 2761549. PMID 19824105. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

“ One of 23 (or, about 4.3%) was positive for both IgA-endomysial and IgA tissue transglutaminase antibodies. Endoscopic studies subsequently showed duodenal mucosal scalloping and biopsies confirmed the histopathological changes of celiac disease. Celiac disease and myasthenia gravis may occur together more often than is currently appreciated. The presence of motor weakness in celiac disease may be a clue to occult myasthenia gravis, even in the absence of intestinal symptoms. ”

I did an unpublished study of patients with MG and anti-gliadin antibodies, I looked strictly at patients with DQ2.5 or DQ8 haplotypes and found 2 of 20 with high levels, which indicates that >1 in 25 had elevated levels of anti-gliadin (aplha/beta/gamma). I am going to add this citation to the secondary conditions page, by MEDRES its too premature for this page.PB666 ^yap 13:57, 24 October 2009 (UTC)

Ciclitira's guideline

Colin correctly pointed out that the British Society of Gastroenterology has removed links to its "interim guideline" from its website (link). I totally agree that 7 years is very long for an "interim" guideline, and I must admit that for a medical featured article it has many drawbacks as a WP:MEDRS.

PMID 19394538 in the review by Di Sabatino and Corazza in the Lancet this year. It seems pretty good and certainly separates chaff from corn (no pun at all intended) with regards to some of the data about CD. Does everyone agree that this source should be used as much as possible to replace the "interim guideline" as much as possible. JFW | T@lk 11:50, 29 November 2009 (UTC)

This is the UK paediatric guideline. JFW | T@lk 11:51, 29 November 2009 (UTC)

PMID 18431060 is the first reference of Lancet2009, a historical review of coeliac disease. I will need to find the fulltext, but I reckon it can replace the website that we are currently using for much of the historical context. JFW | T@lk 14:39, 29 November 2009 (UTC)

Great, having removed Ciclitira's guideline I have now found a number of other documents that we definitely need to refer to, such as the NASPGHAN guideline (USA) and the NICE CG86 (UK, diagnosis only). The AGA review is still fairly topical, and of course much of what needs to be cited can still be traced to VanHeelWest and Lancet. The following two claims currently are uncited, and I will need to look for replacements:

• Need for osteoporosis investigations - which patients?
• Bloods to be monitored at follow-up. Not only to monitor for malabsorption, but also are patients having micronutrient deficiencies due to a restrictive diet? JFW | T@lk 12:40, 13 December 2009 (UTC)

Death

In regards to the recent addition, I'm noticing that the wording of the study implies that only those who were gluten-consuming were studied, since they mention those with Marsh stages 1-3 and for Marsh stage 0, they refer to it as "latent Celiac Disease" and mention a positive serology (which I believe becomes negative when you're gluten-free). If someone can confirm my understanding of it, I think we should change the wording to "active coeliac disease" or something to that effect...I'm not sure what the best way of saying that is. —RobinHood70 ^{(talk • contribs)} 07:39, 1 December 2009 (UTC)

I have temporarily removed the addition. It was in the wrong section (should be in "prognosis" beause death is not a symptom) and needs some qualifiers without sounding alarmist. JFW | T@lk 00:20, 8 December 2009 (UTC)

Update tracker

Right then, I've finally managed to bring myself to update this article. There's a fair amount of crud that has accumulated since the FA drive in 2007, much of which is WP:MEDRS-incompatible material. As stated above, there are a number of excellent sources available (and more in the bag if needed), and hence no excuse to source stuff to small papers in borderline impact factor journals.

1. Signs and symptoms  Done
2. Diagnosis  Done
3. Pathophysiology
4. Screening  Done

   Major update with Lancet and NICE now possible

5. Treatment
6. Epidemiology
7. Social and religious issues

   Could do with some tightening and scrubbing

8. History  Done
9. References
10. External links

    Could be reduced in size and ported to DMOZ

Anyone willing to help along is more than welcome. JFW | T@lk 20:41, 13 December 2009 (UTC)

Blood test table

In regards to the Blood test table, I'm noticing that it talks about the HLA DQ2 and DQ8 tests, but these aren't actually mentioned in the Blood test section. Does this table actually make sense to be where it is, or should it be moved down to the Pathophysiology section (or a sub-section thereof)? I don't understand the medicine involved, so I'm completely clueless here. If it does make sense to stay where it is, I'm thinking that perhaps we should move it to the top of the section and let the text wrap around it, to remove the white-space that it causes now. —RobinHood70 ^{(talk • contribs)} 01:22, 15 December 2009 (UTC)

I think "pathophysiology" may need to be moved up for the "diagnosis" section to make sense. The table could be reformatted in the process. JFW | T@lk 20:09, 15 December 2009 (UTC)

"Patients with coeliac"

One issue I'm noticing in some places in this article, which I've noticed in many Coeliac articles from various sources, is the question of whether the phrase "patients with coeliac (disease)" applies in context to patients with coeliac who aren't gluten-free, those who are gluten-free, or both. (And just to complicate matters, those who have recently become gluten-free may still be suffering from the effects of not having been for a long period of time, so may apply to different groups, depending on context.) The specific context may not be available much of the time, but wherever possible, we should try to differentiate. —RobinHood70 ^{(talk • contribs)} 02:04, 15 December 2009 (UTC)

There was some debate as to whether you're allowed to refer to a person as a "coeliac" to begin with. Once that label has been applied, one is always at risk of relapse unless on GFD and therefore the condition is still regarded as chronic even though the changes may have healed. JFW | T@lk 20:11, 15 December 2009 (UTC)

It seems to me that that would be an important distinction to make, regardless of how you label them. While there are many people with coeliac who ignore the GFD completely (or whenever they're tempted, at least), there are a great many who are extremely strict about it, for whom a relapse is, for all intents, an impossibility. I would tend to think that for that group, many of the statements broadly applied to "coeliacs" would not apply to them. On the flip side, I know some statements still do apply to all of us — for example, I remember coming across a report some time ago that suggested that deficiencies in some of the B-complex vitamins were still a concern, even for GF-compliant individuals, where other vitamin/nutrient deficiencies (I don't remember which) were not. But I suppose in many cases, this will be a concern to be dealt with in the original studies, not necessarily with the article. Nevertheless, where identified in the studies, I think it makes sense to identify whether the GFD or lack thereof was taken into consideration in the results. —RobinHood70 ^{(talk • contribs)} 00:42, 16 December 2009 (UTC)

Reviews, reviews

Gastroenterology this month carried this review doi:10.1053/j.gastro.2009.09.008. No need for any primary sources now! JFW | T@lk 22:18, 22 December 2009 (UTC)

It's free as well. Expect me to quote it a lot when I finally rewrite "pathophysiology", thus also eliminating lots of the primary research that crept in. JFW | T@lk 22:51, 26 December 2009 (UTC)

Liver damage and Coeliac disease

I have been reading about the disease and I came across this issue which was not mentioned in our article, so how about we add a section about that, there is this free review that can help allot :-) MaenK.A._Talk 18:09, 27 April 2010 (UTC)

Abnormal liver enzymes are discussed, as are some related autoimmune liver conditions. Also, your review is in Spanish and hence less ideal as a source for an English article. JFW | T@lk 18:59, 27 April 2010 (UTC)

Genetics, Again

Well, folken, its that time again where somehow we decide what to do about the genetics. Van heel has published a new study on Celiac Disease (Nature genetics 42:295-302. It is not a review, but it does cover many of the problems presented in the previous paper. Other than HLA-DQ there appears to be no common genetic ('weak evidnece') association that appears consistent across all populations (12) in their study. In addition it would appear that if you are a DQ2.5cis homozygote (which they expressly mention by name) all other associations appear to be weak, possibly unneccesary. IOW DQ2.5cis homozygosity by its 'genetic' self, may be sufficient with environmental factors to cause Celiac Disease. They describe the faults in the previous studies, which I mentioned here as a reason for removing the non HLA portion of the genetics, and appear to have redressed the problems. The wording they use is not exactly clear, so some aspect of their conclusions may not be worthy of the main article. The following loci are positively associated with very low random probabilities.

[pra = probability of random association mag = magnitude of the probability, less that -9 is considered to be an association with celiac disease as these probabilities are not corrected for the size of the SNP database]

LPP - 3q28 - Lipoma-preferred partner - OR = (1.25-1.34, positive association) pra <-39 Mag. The protein is involved in cell adhesion and extracellular matrix formation. Note a potent target of gliadin-tTG reactive Eosinophiles and Killer Cells is the extracellular matrix, where tTG becomes localized in the villi. LPP and IL1R genetically interact in celiac Disease according to the paper.

IL12A- 3p12-q13.2 - Interleukin 12 alpha chain, OR = 1.36 (1.29-1.44, positive association) pra <-27 mag. This gene encodes a subunit of a cytokine that acts on T and natural killer cells, and has a broad array of biological activities.

IL2, IL21 - Because of haplotype linkage at this locus delineation of the involved locus is not clear - Interleukin 2 and Interleukin 21 - the minor allele is negatively associated. (OR = 0.74) pra < -27.

These three associations can be added to the genetics section as the differential random probabilities are less than 10E-18. Adding these three would not clutter up the genetics section.

SH2B3 - 12q24 - Alias lymphocyte adaptor protein; LNK. LNK Mediates the interaction between the extracellular receptors and intracellular signaling pathways for T-cell activation. - OR ~ 1.2 and pra = -21 corrected = -11.

TNFAIP3 - 6q23 - Several SNP at this locus have been found involved in autoimmune disorders. locus associates strongly with rhuematoid arthritis and type 1 diabetes, it is an inflammatory, disregulation fails to dampen inflammatory immune responses. OR ~1.2 pra = -18, corrected = -9

CCRx loci - 3p21.3 - Chemokine receptor - Different receptors of this class respond to different stimuli, can produce innate response to superantigens, like LPS. Different CCR are found in different T-cells types. The G protein-coupled receptor encoding RNA was isolated from human eosinophils. Eosinophils also expressed a much lower level of a second chemokine receptor, CC CKR1, which appeared to be responsible for the effects of MIP-1-alpha; see CMKBR1 According to Dubois CCRx act synergistically with HLA-DQ genes (figure 1).

These are 6 loci with unquestionable involvement in Celiac Disease susceptibility. However if the patients are not randomly draft other autoimmune diseases may associate with testing. So that the really outstanding loci are those that have no other autoimmune association.

LPP has the highest association is not currently associated with any other autoimmune disease. It has a high odds ratio, a very low corrected probability, and its function appears to be a potential a target of degradation caused by tTG reactive Eosinophiles. IL12A is also a T1D association however, its OR is fairly high, much higher than the percentage of CD who have T1D and therefore part of its risk should be independent of T1D. IL2/IL21 contains a third gene that is not mentioned in this paper, causative function is ambiguous at best. SH2B3 is found in association with a half dozen autoimmune diseases. TNFAIP3 is associated with rheumatoid arthritis, coronary artery disease, psoriasis, celiac disease, type 1 diabetes, inflammatory bowel disease, and systemic lupus erythematosus. CCR loci individually are involved in different diseases.

Conclusions: I do not have a problem adding information concerning Lipoma-preferred partner (LLP) since its highly positively associated with CD, and it appears not to be enriched as a consequence of autoimmune pathways toward celiac disease clinical detection. We can discuss the value of adding IL12A to the main page, if someone believes or has reason to suggest it is of particular mention at this point. PB666 ^yap 22:31, 20 July 2010 (UTC)

Malabsorption-related list is very incomplete

The list is missing many problems related to malabsorption. I frequent the Celiac's forums and find that it is common for us to have Rickets, Scurvy, and severe fatigue. The severe fatigue I believe is really just unrecognized BeriBeri from vitamin B1 deficiency. I had all 3 of these which are now nearly all gone due to my Gluten free diet. My mother has also just gotten diagnosed properly(due to my demanding the doctors to test her for it. Sad hey.) Anyway she has had it a lot longer and the evidence of Rickets is so obvious in her hands it's not even funny. Her fingers are all very crooked especially her thumbs, and her legs too. Yet the docs called it Arthritis before she was diagnosed with celiac's properly. So ya lets get this list corrected to include what everybody on the forums knows to be true already. That is, Rickets, Scurvy, and probably BeriBeri too, are all likely complications due to Celiac's. —Preceding unsigned comment added by 24.231.143.47 (talk) 17:59, 3 September 2010 (UTC)

I wrote much of the content, and in none of the review articles that I used did experienced doctors mention either low thiamine or ascorbate. Rickets are a consequence of low vitamin D (mentioned in the article) but adults who have not suffered rickets in childhood would experience osteomalacia rather than rickets. Neither thiamine nor ascorbate are fat-soluble vitamins, so villous atrophy is less likely to interfere with their absorption.

We have to be very careful and distinguish between self-diagnosis (which may be incorrect) and clinical diagnosis (which is sometimes incorrect but probably less so on the basis of the doctor's training and experience). Self-diagnoses in internet forums can be completely incorrect and based on misperceptions, and sometimes even intended to mislead (especially when then mentioning the name of an expensive supplement product).

Please provide us will a reliable source with regards to thiamine and ascorbate deficiency, and we can review the matter. JFW | T@lk 18:07, 3 September 2010 (UTC)

Fix the spelling

Can someone please fix the spelling of "diarrhea" in the first paragraph? I don't think the spelling given (with an "o") is proper in any variation of English.

In the UK it is spelled "diarrhoea", consistent with the remainder of the article, which is written in British English. See WP:ENGVAR. JFW | T@lk 23:54, 12 January 2011 (UTC)

We also sometimes use "diarrhoea" in Canada, though "diarrhea" is more common, I think, probably due to the US influence. – RobinHood70 ^talk 01:18, 13 January 2011 (UTC)

Only 1 in 10

Only 1 in 10 Celiacs have stomach pain, diarrhea or fail to thrive. That is why it is known as the "ice berg disease." Only 10% of Celiacs have obvious symptoms. The other 90% can have many seemingly unrelated symptoms such as mood swings, crying spells, iratability, inability to lose weight, loss of apetite for weeks at a time, elevated liver enzymes, depression within 2 hours of eating gluten, neurological changes. So the three symptoms listed in the first paragraph are misleading. Those three symptoms listed are the RARE symptoms. Common symptoms include depression and mood swings. I suggest you do some research about the MOST COMMON CELIAC SYMPTOMS. Later in life the most common symptom is osteoporosis and arthritis.

Also, wikipedia should provide a link to the 300 symptoms of Celiac Disease: http://glutenfreeworks.com/gluten-disorders/celiac-disease/symptom-guide/ (Search Google for "300 symptoms of Celiac Disease.")

Please, correct the first paragraph!!! —Preceding unsigned comment added by 24.203.221.236 (talk) 23:07, 14 January 2011 (UTC)

Wikipedia medical articles work primarily on the basis of peer-reviewed medical studies. Due to the preponderance of self-serving medical information out there, it cannot be based on the opinions expressed in a book unless that book has been peer-reviewed (and testimonials don't really count as peer-reviewed). You may wish to read WP:MEDRS for more information. – RobinHood70 ^talk 23:30, 14 January 2011 (UTC)

Footnote #3 doesn't support

Footnote #3 doesn't support an incidence range of 1/1750 to 1/105 as indicated. I'm not sure why this footnote is connected with this text - the nih document shows a very low level of certainty. 67.169.49.52 (talk) 02:05, 5 June 2011 (UTC) (forgot to sign)