Talk:Coeliac disease/Archive 2

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JCI article

This month's JCI contains a large number of gastro-related reviews. Kaganoff has reviewed the immunopathology of coeliac. I will read the article over the weekend and incorporate any interesting material into the article. JFW | T@lk 23:33, 11 January 2007 (UTC)

Wegman's Disease?

Hello. I recently found out that a person who I was aware of (though had never actually gained an acquaintance with or spoke to) was diagnosed with what they called "Wegman's Disease", and briefly described it as an "autoimmune disease". I have since attempted to find out something regarding this disease, but to no avail. I did, however, see a few mentions of "Celiac disease" while googling it, and found it uncanny that Celiac (or Coeliac) disease is also an autoimmune disease. The symptoms described on this article could be applied to the individual I am thinking of (mainly FFT), but like I said I really didn't know the person. Can anyone shed some light on this? (And yes, I know there's a chain of supermarkets called Wegman's) Mattygabe 22:07, 20 February 2007 (UTC)

It gets 101 Google hits, few of which serious. It is not listed on Whonamedit[1]. Whatever it may have been, that doctor should use more useful terminology. JFW | T@lk 23:19, 6 March 2007 (UTC)

1728

Coeliac passion - Ephraim Chambers in 1728. How striking. JFW | T@lk 02:17, 7 March 2007 (UTC)

Constipation

In the following sentence, the "and even constipation is seen" clause appears (to me, on my initial reading) to be a parenthetical remark but the sentence makes no sense without it. Instead, the final clause appears to give some indication of the frequency of constipation. So, could the sentence be rephrased or split?

However, the variety of gastrointestinal symptoms that may be present in patients with coeliac disease is great, and even constipation is seen, in some series comprising up to a third of patients.

The use of the medical jargon "series ... of patients" will be unfamiliar to the lay reader. Additionally, the reader may not appreciate the difference between the frequency in a patient group (esp. if being studied in a tertiary hospital that only gets the difficult cases) and the frequency in the whole coeliac population. If the latter really is as high as one third, then surely the "and even ..." is inappropriate since one third is pretty common. Finally, can you clarify if the patients with constipation also have diarrhoea (at different times, presumably), or is this instead of.

Colin°^Talk 14:25, 7 March 2007 (UTC)

I have no idea. I think the point is that one can have constipation but still be coeliac. I'll look into this. JFW | T@lk 01:07, 8 March 2007 (UTC)

Epidemiology

There's some unusual linking going on here, which is too subtle for the reader to guess take advantage of. Most readers will think those words just link to the appropriate continents/countries.

• Europe → HLA DR3-DQ2#DR2.5 is Nodal in Sardinia and Western Ireland
• African → HLA DR3-DQ2#DQ2.5 Spread Late in Human Evolution
• Japanese & Chinese → HLA DR3-DQ2#DQ3-DR2 East of the Urals

Saharawi is linked to Sahara rather than Saharawi – is there a reason for this?

The phrase "DQ a5ß2 isoform" (a "major susceptibility factor") will confuse the lay reader. The only clue that this is a genetic concept is probably that they will remember getting lost among all the DQs earlier in the Genetics section. This "a5ß2" terminology wasn't used then. The jargon "isoform" could be linked to protein isoform and probably also briefly explained here, or in the Genetics section.

Colin°^Talk 21:31, 7 March 2007 (UTC)

The whole section needs dumbing down. JFW | T@lk 01:07, 8 March 2007 (UTC)

Why UK-centric coeliac and not celiac?

1,100,000 Google hits for coeliac 3,000,000 Google hits for celiac

Yet, we've standardized on the rarer spelling. Why? (No, I'm not American.)

Remember, vital medical information is useful only if people read it, and Google searches don't do the translation automatically (yet.)

Ndaniels 20:57, 10 March 2007 (UTC)

Before I reply, please do not use news articles as sources. If there are academic cites, please use these preferentially. When citing academic work, please use the citation style employed in the remainder of the article.

Once a Wikipedia article has been composed in a particular spelling, it is well-precedented policy not to change that spelling. This policy (see WP:NC for pointers) is not really open for discussion here. JFW | T@lk 21:12, 10 March 2007 (UTC)

Oh, and Google will pick up the American spelling in the intro offered as the second alternative. JFW | T@lk 21:16, 10 March 2007 (UTC)

Ndaniels, If you look further up the talk page, you'll find two previous discussions on the name. One of these was a formal requested move, which was rejected. BTW: celiac will redirect here so folk searching by that name will still find it. Colin°^Talk 21:20, 10 March 2007 (UTC)

You've quite missed my point re the spelling - a host of people will look in Google for specific information and won't be redirected within the Wikipedia article that has the information. Not to be melodramatic, but again, over millions of queries this will result in at least some unnecessary deaths. I did look for the discussion, but no title seemed to match. Sorry to have missed that, but the problem remains, surely. Sometimes one has to mention issues with very significant consequences, even if one suspects others aren't going to agree quickly to remedy anything. Ethically, there's sometimes no other choice.

A Google search for "celiac disease" currently gives this article as the seventh hit; every hit before it is to reliable, non-commercial sources, such as the NIH and Celiac.org. Searches for "celiac treatment" or "celiac diagnosis" and other likely terms do not direct here, but neither do searches for the same terms with UK spelling. I think we can safely assume people searching on Google will either come here or go to an equally excellent resource. Fvasconcellos 21:44, 10 March 2007 (UTC)

If people are using google as their first port of call and not their doctor, deaths resulting could be attributed to natural selection... survival of the fittest, death of the stupid... (that's how i say it anyway :-D). Unfortunately it'd be their babies dying, not them.--KX36 21:37, 3 June 2007 (UTC)

You're right, at the moment Google prefers www.answering-christianity.com/breast_feeding.htm to Wikipedia for one complex query about coeliac disease that I tried. But this may not always be so.

I don't wish to be contentious, if the stakes weren't high I wouldn't be taking the pain of typing on about this, much less taking up anybody else's time. If everyone will always be safe, and always get the information they want without Wikipedia, none of us should be wasting a moment working here. We all believe we are helping to put information in front of people, and I suspect that's often true, and that Wikipedia is worthwhile, in practical terms, as more than a "cheat sheet". I'm not sure all policies and attitudes here reflect that, however, and where the stakes are high, feel obliged to mention it, although I badly want to slap up mlb.tv instead right now.

Pardon the scruples of someone who was BBSing before there was a web, but no more smileys to express disagreement, please (much less direct contradiction of another.) This is simply not proper etiquette, and hasn't been for maybe twenty years. Ndaniels 22:21, 10 March 2007 (UTC)

Smiley removed, and it was not meant as contradiction, simply as irony, and not towards your comment—towards my own, as many may not consider Wikipedia "equally excellent" when compared to more "official" resources. Fvasconcellos 22:26, 10 March 2007 (UTC)

If you disagree with the policy, please raise your points on Wikipedia talk:Naming conventions. Otherwise I think we can rely on the precendent of the previous move request :-). JFW | T@lk 22:27, 10 March 2007 (UTC)

Thanks, I'll do that. Note, however that the previous discussion did not mention the practical consequences, and seems to me to be a wholly separate argument on different, abstract and linguistic points, without significant overlap. :-) Ndaniels 22:46, 10 March 2007 (UTC)

That would apply, mutatis mutandis, to any other health- or safety-related article. JFW | T@lk 22:56, 10 March 2007 (UTC)

Well, here's hoping it would - why not do the greatest good, after all - and I've assumed everyone who reads the point will understand that adversus solem ne loquitor. Even so, there may be no sharper case than the most common genetic disorder which is also one of, if not the, most missed diagnosis, and very capable of causing death.Ndaniels 02:11, 11 March 2007 (UTC)

This whole argument is very silly. You're assuming that people are more likely to search for one because there are more Google hits but there is absolutely no evidence for that. For example, assuming coeliac is more popular in commonwealth countries (which is often the case), then your case is very weak IMHO. Indeed you could argue celiac is more dangerous since Americans tend to have access to a resonably decent health service. However people in poorer developing commonwealth countries like India for example or even Malaysia and of course numerous African countries tend to have fewer and power quality health care options. It is surely then these people who we need to worry about more? Nil Einne 12:11, 10 April 2007 (UTC)

Of course looking at the article it appears that the disease is prevalent amongst people from "Sardinia,[31] Basque Country, Ireland,[32]and Scandinavia." Surely then it is these people we should be most worried about, not Americans (not people from poorer developing countrier either perhaps). Of course, claiming it is the most common genetic disorder seems highly circumspect to me. Genetic disorders affecting those in Western countries tend to get a lot more research then those affecting people in developing countries. There are probably a number of genetic disorders affecting people in said countries which are far more common then this. Nil Einne 12:16, 10 April 2007 (UTC)

Celiac is more common in terms of numbers, I think just because there are more internet users in America. Most countries use coeliac. It is not a UK-Centric term in any way. It is rather that 'celiac' is the American term and most of the rest of the world uses 'coeliac'. —Preceding unsigned comment added by 81.178.194.75 (talk) 02:06, 6 December 2007 (UTC)

Dramatic increase in diagnosis, and possibly incidence, now omitted, as indicated

I've now omitted, after it was edited out:

Celiac is diagnosed 100 times more often than it was 50 years ago.

Since the only source I have is Paul G. Donahue, M.D. - he wasn't impugned, but he published in the wrong media for an editor here.

Note that here, too, underdiagnosis of this illness - the most common genetic disorder - is disabling and even killing very large numbers of people. Underlining the new knowledge of how threatening this illness is, to how many, would save lives. Keeping citations pristine by omitting facts with apparently lesser citations, has, I'm sorry to say, the opposite effect. It is always more comfortable to believe our actions have no, or few, consequences (the topic of "moral self-indulgence" within Philosophy). But we owe others a degree of reflection on the possible consequences to them, as well.

I'm sure no-one means harm, and that improving the quality of citations is a very worthy goal - but there are always trade-offs in life, and for medical articles in particular, consideration of this has to be part of the balance struck. Ndaniels 21:56, 10 March 2007 (UTC)

Without an academic cite, there's little we can do to support the point. A random reply by a physician is not, in my mind, a reliable source. It may be his personal experience. Your philosophical objections miss the point that this is meant to be a reliable article; without a solid source the reliability of the article suffers. JFW | T@lk 22:23, 10 March 2007 (UTC)

You've stated your reasons well - I'd be amazed if a M.D.'s syndicated column didn't have a fact checker, but you may be better informed. Not to cavil, but I do take issue with putative loss of life being called "a philosophical point"; surely that's the exact opposite of a philosophical point. An interesting reversal to make, though, if you'll pardon my saying so. Ndaniels 22:41, 10 March 2007 (UTC)

Is mentioning a statistic of diagnosis on the scale of "putative loss of life"? This is entirely rhetorical. As I stated, the M.D. in question may have been speaking from experience, and in a syndicated column would be forgiven for doing so. Unless a more reliable (read: academic) source is made available we should not be introducing this point into the article. JFW | T@lk 22:45, 10 March 2007 (UTC)

The whole point I'm trying to make is that, in this instance, knowing that your doctor is very unlikely to diagnose this common illness, or that you as a doctor are likely to overlook it; will surely cause second looks and result in more diagnoses and longer lives. This is logic, together with real consequences - in both ways the opposite, in common parlance, of "rhetoric." I used putative to mean something I have suggested, I did not mean to imply any general assumption; and withdraw that word if it has been taken amiss. But even with a mistake in my meaning, this isn't "rhetoric." I will grant that your invoking the dismissive term "rhetoric" is natural enough because it's threatening to all humans (myself included) to imagine that our decisions have dramatic consequences. But as every decent parent knows, it is nonetheless, and often sadly, so. I and everyone else finds at least one opportunity a day to deny just how much difference my choices may make to others, but this is a bad issue upon which to succumb to that tendency, I have suggested. If you follow Trivers on the unconscious, this kind of denial may be the very reason we all have unconscious minds; so it's unsurprising to encounter it more than once here today, given what I've suggested. However since the reasonable statistical guess is that multiple other people's lives probably do hang in the balance over the next decades, let's fight this natural human tendency.

On a smaller point: I personally doubt something as specific as "%15 after age 65" is a guess in the dark from personal experience, but why bring this up at all since I've already ceded to your judgment? It's harder for people to be a good losers if others won't be good winners and take the win. You guys are working me awfully hard today - harder than I personally prefer to work volunteers (even when I'm one myself, just at a higher level.) Typing is costly to me, I will soon install Dragon Naturally Speaking to reduce pain, but haven't yet. Less cavilling today and that might be onboard, now. Ndaniels 02:44, 11 March 2007 (UTC)

I think you are mistaken about the fact that doctors are "likely" to overlook it. Of course I'm not aware of your personal experiences, but as with any other illness there needs to be sufficient information for a doctor to take the step of suspecting the disease to be there. If the symptoms are too subtle, it is equally likely that there are other explanations. Most tiredness is caused by stress and poor sleeping and not by coeliac disease. I wouldn't screen for coeliac in someone complaining of tiredness without at least one more triggering piece of information (e.g. weight loss, anaemia). I think practicing doctors could be forgiven for using the same decision making process.

Screening is now much more common. In the U.K. practically every patient who develops iron deficiency anaemia is now tested for coeliac disease, as per the BSG guidelines. This is likely to yield quite a few cases, keeping in mind that anaemia is a very common finding (present in 60-80% of cases). JFW | T@lk 07:30, 11 March 2007 (UTC)

If most doctors are seeing dozens or hundreds of cases and diagnosing precisely zero, as the cited survey says, then "likely to overlook" is quite an understatement, statistically speaking. (I can't comment re tiredness, not sure how that came in.) HOWEVER I'm very much with you in not blaming doctors here for many reasons, not least that most patients with new symptoms of any kind don't obtain a specific diagnosis on one visit and never have, because life is extremely complex; and because coeliac may (may) be ballooning in incidence, etc. Not to mention that there may still be doctors out there whose practice began before it's discovery. Fifty years is not that long a time. (I rather wish it were possible to shoehorn that sentiment into the article.) But by the same token patients should be clearly warned when it might actually be dangerous to assume infallibility on the part of their physicians - or even adequate competence (re this one disease.) See my soon to be actual if unsatisfactory bio, but I can't claim personal experience with celiac, and don't know anyone with the illness (to my knowledge) for that matter. I'm just going by the studies I've encountered. No agenda.Ndaniels 21:58, 13 March 2007 (UTC)

Breastfeeding under "triggers"

Would it be reasonable to put at least a "see triggers" in the diet section? I can understand that a repetition of the breastfeeding meta-analysis is unwanted, but it seems a little odd to put breastfeeding under triggers since it has the reverse effect; and does not have that effect, so far as we know, because it reduces or is an antagonist for some trigger.

Given that this study suggests we could cut the (phenotype) numbers of the most common genetic illness roughly in half at a stroke with breastfeeding, it's probably important to put this in a place where it would be seen. However, I'm quite unsure where that would be, given that we now have sections that clearly overlap (at least, diet and triggers). I don't feel I have enough experience here to be rearranging sections, however, and may have created enough fuss for one day, anyway. :) Ndaniels 03:09, 11 March 2007 (UTC)

"Triggers" is probably the wrong name for that section. Who says the timing of gluten introduction is a trigger and not a risk modifier?

PLEASE start using full academic references rather than just an URL to the Pubmed page. You can see many examples in the page's other references. To automatically generate a good reference, here is a tool that will help you (just type the PMID into the applet). JFW | T@lk 07:30, 11 March 2007 (UTC)

Maybe a "Causes" section (Etiology being pretentious and unnecessarily obscure here) that could be subdivided into Environment which could be cleaved into "triggers" or "risk factors", etc? (Then further cleaved into Diet !? ... hmm, that doesn't sound altogether felicitous either.) I think "risk factor" would probably be understood by a tenth grade reader, but I'm not the one to ask.

As for refs, I definitely should have used brackets, not the ref tag, with the PMIDs, so the URLs would click through. My bad. Silly of me to assume they would click through, I suppose. However, I can't help thinking that maybe putting in an extra, indirect link to the true link rather defeats the whole purpose of the WWW: you know, direct hyperlinks and all that. PMIDs are permanent, so link loss isn't an issue. Looking properly (or just pretentiously) academic shouldn't get in the way of getting more information (including the abstract) to the interested reader, ASAP, surely? I don't know many people, even myself usually, who skip articles and just want to read the bibliography, but if they do, then I'm wrong. In any case, however sadly, volunteers do what they can do. I have the URLS I have, strict limits on the time I can spend and I know PMIDs are common in Wikipedia. So this may not change quickly, I'm sorry to say.Ndaniels 21:44, 13 March 2007 (UTC)

Large forehead sign

I don't think this "phenomenon" is established sufficiently to be included into this article: PMID 15919249. JFW | T@lk 07:36, 11 March 2007 (UTC)

I may disagree here. There are some quite recent truly bizarre (yet apparently solid) correlations between bone overgrowth (possibly due to mild comorbid collagen formation disorders?) or malformation and various chronic illnesses. The ghost of phrenology makes it psychologically uncomfortable to believe the evidence, but there it is. However, if you really want to be freaked out, try this BBC story Time changes modern human's face: "The scientists said the differences between past and present skull shapes were "striking"." [[2]]

I think it may be worth noting, but not emphasizing.

Included only for amusement, (feel free to delete) a quote from Darwin:

"That my mind became developed through my pursuits during the voyage is rendered probable by a remark made by my father, who was the most acute observer whom I ever saw, of a sceptical disposition, and far from being a believer in phrenology; for on first seeing me after the voyage, he turned round to my sisters, and exclaimed, "Why, the shape of his head is quite altered." "

PS, lemme know if it's bad form to tack this to someone else's comment.Ndaniels 22:15, 13 March 2007 (UTC)

Of course I found it insteresting ;-) Someone may guess why. It's not a matter of phrenology. Simply human skull develops in a non uniform way: the forehead as well as the neurocranium develops earlier, when gluten is not yet introduced in the diet, while the rest of the face develops later, when gluten already made its damages.

The observation it's not about an overgrowth of the forehead but about a relative undergrowth of the rest of the face. It's not easy to make such observation in a multi-racial enviroment (because of the well-known different proportions between popolations), so the study was limited on people that were born and have ancestors in Naples area. Some other researchers confirmed the validity of the observations, but the main difficulty was to compare omogeneous groups.

The paper was also the subject of an article by PH Green et al. (PMID 15978879) from Columbia University College of Physicians and Surgeons who called the "phenomenon" coeliac face. Hope that all the paper cited in the voice are more sufficiently established. But who decides it? Sorry for my very poor English, feel free to correct my contribution to this talk.--Massimo Finizio 16:27, 1 May 2007 (UTC)

What do Green et al have to say about it? Do they dismiss it? A single paper and its commentary may not be sufficient to establish such a sign. And what is its diagnostic use? JFW | T@lk 22:18, 6 May 2007 (UTC)

It seems it's a personal matter for you, so feel free to remove what you want from what you consider your personal property. But just in case you're really interested in the paper (and hoping this is not a copyright violation) PHR Green, P Brar and TT Malahias say the paper is "(...) a translation of a clinical observation into a well conducted clinical research finding. The other message is that physician do not see a particular sign until it is demonstrated as a sign". The paper was cited in the sign section, not in the diagnostic section, I'm sure you know the difference. A sign has its importance even if it is not related to diagnosis, because it helps us to better understand how a particular condition works an a subject. In this case it seems important to me the finding that the sign doen not appear in people with early diagnosis and a regular GF diet.

On the other side can you show me where this was discussed on the talkpage and not found to be ready for prime time as you wrote in the edit history? Since I'm interested in the head growth and believe wikipedia is very important to reach other's opinions, I kindly ask you (or others) to find the time to explain your reasons against inclusion and the sources that confirms your convinctions. --Massimo Finizio 6:31, 7 May 2007 (UTC)

I also agree that it's not ready for prime time (based on one paper and its commentary), but it is interesting. Mind you, I'm basing this on the abstract alone -- I had pulled up the paper in March when this section started, but haven't read it yet. Will do so tomorrow. As an aside, Chris Mulder's double balloon stuff on refractory celiac is very neat. -- Samir 06:40, 7 May 2007 (UTC)

Update for pathologists

PMID 17021129 looks like it's very recent and rather up-to-date on both the serology and the pathology. JFW | T@lk 07:45, 11 March 2007 (UTC)

Persistent villous atrophy

Persistent villous atrophy, even when asymptomatic, predisposes for refractory sprue and malignancy. JFW | T@lk 22:30, 19 March 2007 (UTC)

History

PMID 4595183. JFW | T@lk 00:54, 20 March 2007 (UTC)

Thanks. I'll take that and develop the history further. Colin°^Talk 14:33, 20 March 2007 (UTC)

I've added some more but didn't feel the need need to cite this article due to having both original papers available. Another article that may be useful is History of coeliac disease by S. Auricchio and R. Troncone but I don't have access. Colin°^Talk 13:59, 21 March 2007 (UTC)

Care to add to Samuel Gee as well? Fvasconcellos 14:34, 21 March 2007 (UTC)

Sure. JFW's paper will be useful there. Colin°^Talk 14:53, 21 March 2007 (UTC)

Done. Colin°^Talk 14:54, 23 March 2007 (UTC)

History of the Coeliac Condition Another source of pointers for research (lacks author/citations sadly). Colin°^Talk 16:23, 21 March 2007 (UTC)

Note PMID 4601230 is a Letter in response to PMID 4595183 above. It states that Matthew Baillie gave an earlier modern description in 1814. Baillie observes "some patients have appeared to derive considerable advantage from living almost entirely on rice". (Baillie M (1815), Observations on a Particular Species of Purging, Medical Transactions of the Royal College of Physicians, 5, 166.). Being just a letter, albeit in a respected journal, I'm not sure this counts as a reliable source for the citation. However, Google believes PMID 15124851 (online via Acta Paediatric) also contains a citation. I don't have access to that paper. Thoughts? Colin°^Talk 14:54, 23 March 2007 (UTC)

DM1

PubMed is down (!!!) so I'm linking some references here to look at later:

• PMID 11318836
• PMID 14618956
• PMID 9518950 (screening)

JFW | T@lk 15:53, 21 March 2007 (UTC)

Things not being mentioned at the moment

The link between cerebral calcifications and coeliac is quite well established. Perhaps it should be mentioned explicitly, rather than lumped with the other less specific neurological syndromes.

We should perhaps mention slightly abnormal LFTs and septal fibrosis/portal lymphocytic infiltration.

Older diagnostic modalities, such as the 3 day faecal fat estimation and the D-xylose–absorption test.

We don't quote a fairly recent NEJM review by Farrell & Kelly (2000) PMID 11796853. JFW | T@lk 23:24, 25 March 2007 (UTC)

Mortality

doi:10.1111/j.1572-0241.2007.01111.x suggests that coeliac disease diagnosed in childhood has a 3x elevated mortality. Still low in absolute terms, but very high in relative ones. This somewhat undermines the hypothesis that "undiagnosed" coeliac disease can do life-threatening damage. I need to read the fulltext paper before working it into the "prognosis" section. JFW | T@lk 14:48, 1 April 2007 (UTC)

I just looked at the full text of this paper. If true, it is extremely important. They have good outcome data for a sizeable cohort of former children with early dx. Unfortunately, the validity hinges on the comparability of the matched population and the validity of the mortality stats for that population, and that is only sketchily described in the methods. Finally, even if true, the mechanism proposed ("risk taking" because of the psychological burden of the diagnosis) may not be the right link. For example, what is the parental separation rate after a child is diagnosed with celiac?-- it rises dramatically after the diagnosis of juvenile diabetes. What happens to the socioeconomic status of a family after diagnosis of celiac? Did lower social risk (i.e., better off, better educated) patients disproportionately move away from Lothian during the decades studied? I am just tossing out other possible explanations. This paper is either crucially important to the drive for early diagnosis of asymptomatic children (i.e., DON'T) or it is misleading crap. Not sure yet which. Different interpretation anyone? alteripse 22:32, 6 April 2007 (UTC)

Newer Testing procedures

I'd love to see some of our more qualified readers add a section on some of the newer popular testing procedures. The big name I hear on all the forums is entero labs and their fecal testing https://www.enterolab.com/Home.htm with some of their educational material located here https://www.enterolab.com/StaticPages/Frame_Resources.htm There's a lot of happy users but as far as I can tell Dr. Fine has yet to publish his methodology for peer review.

I'm by nature a skeptic and very much love peer reviewed quality research. Certainly no disrespect meant to the online celiac communities, they have helped me, but there seems to be alot of desperate people looking for answers and help. When a person who sees a naturopath says this test is accurate, my skeptic alarm is running full tilt and I'd really like to see what others more educated in medicine than myself think of his work. At the core I certainly agree that testing to arrive at a diagnosis before one reaches villous atrophy is very necessary. --johncm Unsigned by 75.129.206.98 (talk · contribs)

This webpage is very unhelpful. It does not readily explain how the test works, but it indicates that it is meant to replace small bowel biopsies! One needs very carefully designed studies to prove that claim. It worries me that this doctor is already starting an Intestinal Health Institute. Coeliac can be diagnosed before villous atrophy sets in - read the article. Serology is very sensitive, and picks up latent cases.

I worked a lot on this Wikipedia page to provide unbiased and readily available information for coeliac patients. When Dr Fine's test has been thoroughly evaluated and is ready for prime time we can debate whether it should be included in our article. JFW | T@lk 21:32, 7 April 2007 (UTC)

DCM

Dilated cardiomyopathy seems to occur at an increased rate in coeliacs - exact numbers vague. PMID 10421311 first indicated a link. PMID 11926572 corrobates it, but rather indirectly. The initial group (Curione) has looked at improvement on gluten withdrawal (PMID 12643296) and PMID 16054552 attributes the whole thing to carnitine. Perhaps not quite ready for prime time, but fascinating. JFW | T@lk 10:31, 23 April 2007 (UTC)

Capsule endoscopy

Capsule enteroscopy is good at picking up macroscopic evidence of villous atrophy: doi:10.1111/j.1572-0241.2007.01238.x. JFW | T@lk 15:21, 26 April 2007 (UTC)

In refractory disease, double balloon enteroscopy seems to be useful: doi:10.1111/j.1572-0241.2007.01122.x. JFW | T@lk 15:25, 26 April 2007 (UTC)

Koilia(kos) meaning?

"The term coeliac derives from the Greek κοιλιά (koilia, abdomen)"

A google search brings up several sources with koiliakos instead.[3][4]

Could someone explain this? Xilla 07:20, 7 June 2007 (UTC)

I've had a look for sources and agree that κοιλιακος (koiliakos) is a more direct source but the root is ultimately κοιλιά (koilia). The Oxford dictionary definition for coeliac gives

ORIGIN Greek koiliakos, from koilia 'belly'

Most sources use the first word but I've been unable to track down the original Greek text to check (probably here somewhere). I'm no Greek scholar, but it appears that the difference is that it is the adjectival form of the noun (abdominal vs. abdomen).

One issue that a Ancient Greek editor might help with is whether there are accents:

• κοιλια or κοιλία or κοιλιά.
• κοιλιακος or κοιλιακός.

are all mentioned on various sites, but some might be Modern Greek.

I used a web-based concordance for Biblical (=New Testament) Greek, so that may explain the discrepancy. If a better version is available please let us know. JFW | T@lk 20:09, 13 June 2007 (UTC)

Pesach

69.249.244.99 (talk · contribs) replaced the previous section on Jewish Passover with a very long new section that goes into the relevance of grain in Jewish religion per se[5]. While certainly relevant, the new section was rather elaborate (e.g. the role of grain in Jewish practice per se) and used a lot of unexplained jargon (kitniot, etc). I suspect this may be a bit excessive for this article, given that coeliac disease is not common in Jews to begin with. JFW | T@lk 20:09, 13 June 2007 (UTC)

Case-finding

Dr Fasano has clearly made an impact with his research and has now looked into case finding strategies into the diagnosis of coeliac in the USA. doi:10.1111/j.1572-0241.2007.01173.x JFW | T@lk 12:15, 24 June 2007 (UTC)

Permeability reduction

doi:10.1111/j.1365-2036.2007.03413.x studies a gut permeability modification substance. Hmm. Will it reduce EATL? JFW | T@lk 06:25, 26 June 2007 (UTC)

If diet fails to improve symptoms

... there's always budesonide doi:10.1111/j.1572-0241.2007.01380.x JFW | T@lk 22:08, 2 July 2007 (UTC)

Celiac Disease = Giardia ?

Celiac Disease = Giardia ?

The symptoms of Celiac (also IBS, Crohns, and more....) seem to parellel those of Giardia.

The same cause may have different symptoms in different people !

Problem with Giardia, is that Giardia is difficult to detect, and one test, even though it is negative does not guarantee that you don't have 'giardia', or other 'bacterial parasites'. This creates a logical problem, in that most people don't repeat tests.

In one case a patient spent some 15 years with intestinal problems, the specialist said he had a 'disease' - no cause, no cure. Then an old country doctor stated quite simply, you have an intestinal infection, possibly giardia.

Problem is that it seems we have created 'diseases' that ignore the simple, obvious cause to many diseaes and that is 'bacteria'.

Why ?

-Celiac is a auto-immuno disease, often appears in europe, industriel countries -Giardia is a tropical infectious disease. Name of the bacteria is giardia lamblia

The logic suggests that doctors in 'indusstrialized countries' are failing to test for tropical diseases; with travel, individuals in industrial centers can pick them up quite easily.

I suggest this as a lead to someone to check into a possibility sub-heading.

--Caesar J. B. Squitti  : Son of Maryann Rosso and Arthur Natale Squitti 14:57, 7 July 2007 (UTC)

What you are suggesting is adding a subsection under diagnosis usually called differential diagnosis in medical textbooks and review articles. A differential diagnosis is a list of conditions that resemble the disease being discussed, along with the methods of distinguishing them. One reason we don't have a Differential diagnosis subsection in this celiac disease article is that it would be either a long list of scores of conditions (of little value to most readers), or would be as long as the current article to give a sentence or two about how each condition might resemble celiac and how to distinguish the two. For example the differential diagnosis for chronic diarrhea includes not just celiac disease and giardia but many types of exocrine pancreatic deficiency like cystic fibrosis, many types of digestive enzyme deficiency like lactose intolerance, dietary excesses like too much fruit juice, tumors producing secretory diarrhea, many types of small bowel disease like eosinophilic gastroenteritis, various GI food sensitivities, inflammatory bowel diseases, and finally dozens of types of infection besides giardia. Now, repeat the discussion for all the other ways that celiac disease can present, such as growth failure, anemia, tetany, etc. Bottom line is that most of us don't think an extensive differential diagnosis discussion belongs in most encyclopedia articles, but we are fairly unanimous that an unbalanced mention of a single disease that might resemble celiac in one respect is not a useful addition. If it is of any reassurance to you, both giardiasis and celiac are two of the first things a North American pediatrician will consider as causes of chronic diarrhea in a preschooler. alteripse 15:16, 7 July 2007 (UTC)

Todays 'scientists' are taking a "miscroscopic" approach to disease, that appears to create som many 'uncurable diseases'. Case in point is that some 'specialists' are labelling 'giardiasis' as IBS, or IBD, or perhaps Crohns, or Schizophrenia, as the toxins create a fugue state of mind.

To an individuals seeking 'solutions' a listing of most probable,and curable casues would be my suggestion.

Again, most probable, and curable causes with cures would be a suggestion.

--Caesar J. B. Squitti  : Son of Maryann Rosso and Arthur Natale Squitti 14:13, 19 July 2007 (UTC)

Ulcers

There seems to be some debate as to whether ulcers are indicative of Celiac Disease or not. See the wiki article here: http://en.wikipedia.org/wiki/Aphthous_ulcer#Causes and search for the UK spelling, "Coeliac".

This should be marked as debatable or contested or what-have-you in the main page on Celiac. (My wiki editing skills are not up to this task.)

Wikipedia pages may contradict each other. I agree that the link between coeliac disease and aphtous ulcers is not watertight, and that most cases of aphtous ulceration, even if severe, are idiopathic and not due to coeliac, Crohn's, Behcet's or some other small bowel enteropathy. I disagree that the link is so debatable that it should be marked as such on this page. JFW | T@lk 15:45, 15 July 2007 (UTC)

Okay, that's fine too. I was just following what I thought was the standard. I'm not campaigning for either side. :) --Rob 21:03, 23 July 2007 (UTC)

One cause with many 'different symptoms' welcome to the world of half-truths again corrupting science; Undected bacterial causes seems to be in the lead for a cause. --Caesar J. B. Squitti  : Son of Maryann Rosso and Arthur Natale Squitti 14:15, 19 July 2007 (UTC)

Hmm, if they are undetected then why do you think there are bacteria involved? JFW | T@lk 06:54, 7 August 2007 (UTC)

Predicting risk

This Italian study used genetic markers, mainly HLA, to predict risk in offspring: doi:10.1136/gut.2006.108530 JFW | T@lk 15:45, 15 July 2007 (UTC)

Repaired erroneous genetics section,

7-13-2007. On the genetics section, I have added information on the new IL2/IL21 association genome wide survey done in Britian. On the issue of myoIXB I have added information on a study suggesting it has a general autoimmune association that is not specific to celiac disease. Pdeitiker 03:21, 14 July 2007 (UTC)

7-14-2007. For some reason the corrections of 7-13 did not show up. I corrected the completely incorrect explanation of cis and trans-haplotypes, trying as hard as possible to make it readable in spite of its complexity. I also integrated the new MyoIXB data into the 'other associations' paragraph and added information about IL2 and IL21.

While doing this I found 2 'linking' errors which I did not correct.

1. [[Chromosome 5 (human)|2]] q33

• Should be
• [[Chromosome 2 (human)|2]]q33"?

2. [[Chromosome19 (human)|15]]q11-q13

• Should be
• [[Chromosome15 (human)|15]]q11-q13"?

I am waiting to get an original paper on the Celiac 1 to 5 before making the change to insure that the loci are labeled correctly, (where one error probably more).Pdeitiker 22:38, 15 July 2007 (UTC)

Another Error, Under tissue transglutaminase

Antibodies to gluten do not appear to cross-react to transglutaminase. Antibodies were found that reacted to the tTG-gliadin complexes, but the reference is not provided.Pdeitiker 22:39, 15 July 2007 (UTC)

Capsule endoscopy

Another capsule study, showing that macroscopic appearance is about as good as biopsy in selected patients. doi:10.1111/j.1572-0241.2007.01238.x JFW | T@lk 06:54, 7 August 2007 (UTC)

Enzymes

Hmmm, this is not for inclusion in this article but the enzyme therapy has been trialled on rats doi:10.1053/j.gastro.2007.05.028 JFW | T@lk 09:09, 12 August 2007 (UTC)

Genetics

A new review on genetic risk. doi:10.1111/j.1572-0241.2007.01471.x. I cannot help but notice that it focuses on HLA-D2/D8. Perhaps we should simplify this article's genetics content; clearly we are trying to be too clever. JFW | T@lk 09:38, 12 August 2007 (UTC)

I have created a new page on anti-tranglutaminase antibodies, in which some of the tranglutaminase discussion can be moved to. I agree about the genetics, should we include the discussion there of transhaplotypes, whereas it can be discussed on the DR3-DQ2 page. Better choice is to link to a section on that page. I am going to work on correcting some errors in this section and fixing the Celiac 1 to 5 section.

Regarding the literature and DQ2 and DQ8. The terminologies are clinical but not scientific in my opinion and are missleading. To give an example, two recent papers on refractory celiac disease and severe disease, two papers show that RCD2 and EATL are dominated by DQ2 homozygotes (can be DQ2.5/DQ2.5, DQ2.5/DQ2.2 or DQ2.2/DQ2.2), BUT a third paper shows that almost all high Marsh grade patients are limited to DQ2.5 and particularly DQ2.5 homozygotes. I consider DQ serotyping with coeliac disease to be _lazy_ science. It is by chance adequate with DQ8 since 99.5% of DQ8 is DQA1*03:DQB1*0302. Not everything that is published deserves to be published.

The issue is your target audiance, in consideration here is the patient who has just been typed, more frequently by gene typing. The basic assumption (based on my experience) is that the clinical sources of information are improperly explained to the patients and risk is also not explained. Those patients are then a mixture of serotyped or genotyped, so that they need to understand how the two relate. Also I should point out that people with DQ2.5 and especially those with either DQ2.5/DQ2 or **DQ2.5/DQ2.5** phenotypes are at much greater risk for life threatening complications, RCD2 and EATL, an age-related risk that comes from non-adherance to a gluten-free diet. [I have created a section on RCD and EATL on the GSEA associate conditions page, but I really think it belongs here!)

The issue is whether that level of information needs to be on this page. You might be unaware of the fact that there are 'marginal' independent testing labs in the US that are typing patients and along with that passing out what I consider to be 'very weak' associations with CD. As the paper you referenced stated almost 100% of carefully tested patients are DQ2 and DQ8+. These laboratories are providing associations to DQ1 and other DQ3. DQ3, of course, also has DQ7 and is associated to CD via DQ2.2/DQ7 heterozygote.

I will ask some people who are CD+ to reveiw that information, privately, and see what they think.Pdeitiker 13:53, 17 August 2007 (UTC).

Perhaps we need to make abundantly clear that there are various systems of terminology.

HLA page does that, also HLA-DQ

Just because the genetics terminology is more accurate doesn't mean that the system used by clinicians is obsolete, useless, and not worth referring to.

Serotyping is fine for DQ8. It is not completely obsolete, but for DQ2 its lack of unambiguous functional characterization is problematic.

Is your critique of the ongoing genetics research of coeliac disease shared by other investigators in the field? JFW | T@lk 14:45, 17 August 2007 (UTC)

Yes some papers now state clearly that HLA DQ2.5 or HLA DQB1*0201 (Sensu stricto) is involved in the most severe disease. The assumption 'building' situations occur as a result of older genotyping and serotyping issues. I cannot speak for every institute but the quality of HLA typing varies widely between institutes, our regional capability was good, but we chose better typing capability in-house because of its ability to cross check errors (erroneous typing for CD has been pointed out) and because A1:B1 typing is virtually unambiguous given high linkage disequilibration in most CD susceptible populations.

Use of DQ2 serotyping

Frankly I could waste alot of time discussing the nuances of DQ2 versus genotyping, The best way that I can address the question is this. When HLA DQ was first serotyped three identities came forth, DQw1, w2 and w3. DQw1 recognized DQA1 gene products(DQA1*0101, 0102, 0103 and 0104) that are associated with DQ5 and DQ6 (beta recognized). DQw2 and w3 recognized beta chain. This recognition is simply an artifact of which of 3 major subclasses were first recognized. Since DQ2 (DQw2) recognizes beta chain association studies based on DQ2 are biased toward beta chain associations, alpha chain associations are invisible without some other form of biasing information such as DR or DQA1* typing.

Let us take an important example from 2007. It is now known that DQ2 homozygotes are strongly associated with the severe form of refractory disease RCD2, 2 papers now have been published, ~60% of patients with RCD2 are DQ2 homozygotes. Rather impressive association but does that end there. Actually, we don't know because DQ2 testing is invisible to DQalpha.

So let us look at this example. (all alleles preceded by "HLA DQ" A1*0501 : B1*0201 / A1*0501 : B1*0201 (DQ2.5/DQ2.5) 100% identical DQ isoforms.

What is it? DQ2.5 double homozygote.

A1*0501 : B1*0201 / A1*0201 : B1*0202 (DQ2.5/DQ2.2) 50% identical DQ isoforms.

What is it? DQB1*02 homozygote

These two haplotypes should represent that ~60%. But is that all the homozygotes. Nope.

A1*0501 : B1*0201 / A1*0505 : B1*0301 (DQ2.5/DQ7.5) 50% identical DQ isoforms.

What is it? DQA1*05 homozygote

This homozygote is of the alpha chain. It is possible that a remaining 39% of RCD2/EATL are alpha homozygotes and thus the overwhelming majority of RCD2 disease explained by homozygosity of alpha or beta chain genes. If that is true then this is highly pertinent toward the genetics of CD.

Rather than producing a clear answer as alpha:beta typing would do we are left with a number between 60 and 100% homozygotes (i.e. 96% CI between 40 and 100%) All of that 60% could be DQ2.5/DQ2.5 and the DQ2.5/7.5 not significantly increased in the remaining 40%.

In this situation genotyping would have been far superior to serotyping in terms of risk resolution. DQ2 serotyping by itself is a form biasing information, serotyping is not 'obsolete' but it must be followed up. The minimal definative serotype is DR-DQ for DQ2, but not DQ8.

DR3(17)-DQ2 = DRB1*0301-DQ2.5

DR7-DQ2 = DRB1*07-DQ2.2.

So this is the conundrum of being on the cutting edge. How to choose which information to use. If we want to be conservative we should focus on that which can be proven and that which can be proven without ambiguity is the HR genotyping based studies.

The pertinent argument here, IMHO, for the sake of an main-page general interest encyclopedia page should the information be abbreviated and complex discussions diverted elsewhere? I think other things are more important on this page than an complex understanding of the genetics, If this was simply an issue of genetic understanding and I would remove it an place it elsewhere.

Here is the delimna, the RCD issue will be followed up with thorough genetics and at that point I think the bulk of the issue and its complexity belongs here, RCD2 is a natural consequence of the direct progression of CD when certain facilitative genetics are present. When that point comes we will need the complex genetic background to introduce RCD1, RCD2/EATL relationships. Secondary diseases can be on another page, because these are spontaneous and chaotic associations, but RCD1 and RCD2, in terms of treatment, is the most severe form of celiac disease. The trend in the data has been to associate DQ2.5/DQ2 with higher risk in disease. There is a reason for that higher risk that are explained on the page, barely, but sufficient for introduction.

The critical issue here is target audiance, is this toward the general public with no specialized interest, if so the DQ2/DQ8 can suffice. While wiki may believe this is so I can say watching the latest cohort of college trainees, much of the interest in wiki is highly specialized as in 'what can I find on this subject in wikipedia'. If the audience has an HLA DQA1*:DQB1* typing in their hand, just out of the clinic and wants to know what it means then DQ2/DQ8 does not suffice. That person googles DQA1*0501 DQB1*0201 they are going to hit the HLA DR3-DQ2 page or some other page. Pdeitiker 05:38, 18 August 2007 (UTC)

A new page for HLA-DQ2 has been created. The discussion of transhaplotypes can be place here under a subsection for celiac disease, if that is desired.

Phil, for the purpose of this article we need a short but factual representation of this knowledge in a way that the informed layperson can understand. I am aware that this is frightfully difficult, given that the whole field seems to be in somewhat of a state of flux, with more DQ haplotypes being described. Could you perhaps compose such a paragraph and post it here for comments? We need to get this right. JFW | T@lk 09:43, 19 August 2007 (UTC)

I am working on it, right now the priority I have set is to correct the errors. I have not found anything that support CELIAC5 designation, so I am going to remove it. Also I have the full publications for the CELIAC2 to CELIAC4 loci so I will correct these. As far as CELIAC1 is concerned, the information is "right" but detailed explanations needs to be redirected. I have all ready altered the DQ page so that now the whole 'parental chromosome' thing is explained there in the same paragraph, there was more detailed explanation that it replaced, this is now on the discussion page for HLA-DQ. The problem with the DQ page is that in terms of information it is as much a editor's hair puller as CD is. Someone could help me out 'Wiki'ing the intro . . . . :^).

HLA-DQ2 page has been created and one can redirect basically to the associations portion on DQ2.5 and DQ2.2 (not completed). The DQ page has been markedly shortened and all DQ serotypes now have there own page. This will also be done to the HLA-DR page.

Short but factual is explaining that there are two ways to get DQ alpha-5 beta-2 without explaining in great detail how it is done.

I don't know of any new haplotypes being described for CD, its simply clarify the haplotypes that have been been described in other ways. For gluten sensitivity this is another story, new haplotypes are being described, but that description has little to no meaning. —The preceding unsigned comment was added by Pdeitiker (talk • contribs) 19:09:16, August 19, 2007 (UTC).

Genetics section has been modified, significantly shortened, errors in the CELIAC gene section were corrected. Links to detailed pages will be added later.Pdeitiker 20:47, 19 August 2007 (UTC)

Accolade

Prof David Adams (hepatology, Birmingham) refers to this article as "excellent quality [of] information" while reviewing a new edition of a textbook in Gut (Aug 2007 edition). He uses it as an example of how resources like Wikipedia may replace textbooks in the future. I have sent him an appreciative email. doi:10.1136/gut.2007.121533 JFW | T@lk 14:45, 17 August 2007 (UTC)

Wow. Praise indeed :) Fvasconcellos (t·c) 23:22, 17 August 2007 (UTC)

Good work, guys! -- Samir 23:24, 17 August 2007 (UTC)

More endo!

I have more pics! Classic cracked-mud nodular appearance WITH narrow-band imaging pics also, TTG just came back positive today, need patient to release images and we'll add them in -- Samir 23:21, 17 August 2007 (UTC)

Serology

doi:10.1111/j.1572-0241.2007.01360.x - these Finnish people are following up a cohort of genetically prone children. In those with a positive tTG antibody, they surveyed seroconversion of all other known antibodies (EMA, ARA, anti-Gliadin IgA and IgG). IgG-AGA is the first. I need to read the fulltext, because I don't understand the conclusion at all by just reading the abstract. JFW | T@lk 00:32, 24 August 2007 (UTC)

I saw this paper about a month ago. I understand the conclusions, its just not much is given as to why. What they are saying is that a subset of tTG+, an transient node in anti-tTG response, spontaneously revert to normal. The nodal state may be caused by viruses or infection, since they make no effort to assay for rotavirus titers, etc. I interpret this paper to mean that during the course of event(s) X of early childhood, titers rise to tTG, but then, as one expects, tolerance is regained to tTG. Whereas in the other 50% tolerance is lost and remains lost, resulting in coeliac disease. The way I look at this is that the revertants are demonstrating the way the immune system should work, its the 50% that fail to revert to the normal state that indicate a malfunction. Of course we do not know whether these may go on to have late-onset disease.

The critical issue involving triggers is why? We are pretty long in the tooth here with A. poor penetrance on DQ B. Weak genetics for all other sites C. lots of probable nasties that could cause a 'priming of the system' D. Lots of potential disease for early onset and yet we don't have the big environment factor X (besides wheat) that gets the immune system primed for autoimmune disease. This is important because in DQ2.5+ or DQ8+ children, if they have these diseases they could be asked to refrain from eating Triticeae and Oats for a 2 week period as too allow the 'priming' state to pass and heal.

Also, consider that these are the tTG+ non-CD that they catch, depending on the frequency of examination, if there is no-helper cell activity tTG can deplete excesses of antibodies from circulation rapidly, it could take less than 3 months to go from an ATA of 50 down to 8.Pdeitiker 08:18, 26 August 2007 (UTC)

The AGA IgA test is listed twice in the Blood antibody tests for coeliac disease chart. This is either a mistake, or correct but confusing. Epl (talk) 18:57, 8 February 2008 (UTC)

This error has been pointed out several times. Pdeitiker (talk) 14:16, 17 February 2008 (UTC)

Adding DR testing

Here is a practical one: adding HLA-DQ testing to serology makes it possible to say which negatives are true-negatives. JFW | T@lk 17:54, 4 September 2007 (UTC)

I know you meant to write DQ testing, but as a matter of fact, when it comes to serological testing I recommend DR and DQ. DR3-DR2 is specific for DQ2.5cis encoded isoform. DR3,DQ2 (homozygote) and DR3/DR7,DQ2/[DQ2] phenotypes are about 15 times more likely versus the DR7,DQ2 (homozygote) phenotype. With the genovision and dynal gene typing kits we are using it is possible to distinquish by control band/DQ-fragement band intensity homozygotes versus heterozygotes which can be added to the allele information (*0201 and *0202 are recognized). You cannot do this with serology, but with DR and DQ typing one can approach this level of identification. The DR5/DR7, DQ2/DQ7 phenotype is DQ2.5trans situation. DQB1* typing alone cannot positively provide linkage to the alpha *0505, but the genovision typing kit can predict either A1*0501-->B1*0201 and A1*0505-->*0301 with near 100% certainty. DQA1*0201 is associated with associated with B1*0202 (70%) and B1*0303 (30%) and therefore DQB1* typing is required. IOW there is no single definitive typing strategy. DQB1 typing is far better than DQ serology, DQA1 typing is far better except with DQ2.5trans. DR and DQ serology is better than DQB1* or DQA1* alone. The following pages have serological efficiency of DQ serotyping versus alleles. DQ2 serotyping is excellent, but other typing antibodies are not so good.

DQB1*0201 98%-DQ2 (2% that a true negative maybe a positive)

DQB1*0202 85%-DQ2 with DR5-DQ7 a 15% chance that a 'true negative' is a positive

DQB1*0301 85%-DQ7

DQB1*0302 66%-DQ8 33%-DQ3 (depends on assumption regarding DQ3)

DR3, but not DR7, is an additional risk factor for early onset type 1 diabetes. On additional advantage to DR-DQ serotyping. With DR4, gene typing has an advantage over serotyping for celiacs, certain DRB1*04 alleles add succeptibility for connective tissue autoimmunities which are common in late onset coeliac disease.

Also that paper only has _16_ positive celiacs.Pdeitiker 00:13, 9 September 2007 (UTC)

Anti-gliadin testing

There have been a few recent papers claiming now to have improved detection of coeliac associated antigliadin antibodies. This improvement has taken place with the enzymatic deamidation of gliadin. PMID 11673371- Aleanzi et al, PMID 17683995 They claim in the 2nd reference that the highest was for

sensitivity in childhood celiac disease
DGP/tTG IgA/G at 100% (119 of 119)
tTG IgA at 97% (115 of 119)
DGP IgG at 95% (113 of 119)
DGP IgA at 91% (108 of 119)
tTG IgG at 13% (15 of 119).

Specificity: (57 disease controls, 398 blood donors) DGP/tTG IgA/G at 89% (51 of 57), 97% (385 of 398)
tTG IgA at 96% (55 of 57), 98% (392 of 398)
DGP IgG at 86% (49 of 57), 99% (395 of 398)
DGP IgA at 91% (52 of 57), 92% (366 of 398)
tTG IgG at 100%

DGP = synthetic deamidated gliadin peptides With genetic testing provides now a very powerful noninvasive means of diagnosing early onset disease.Pdeitiker 20:47, 10 September 2007 (UTC)

Slight correction

Changed "diarrhoea" to "diarrhea" in first section of page.Flyboymb 22:34, 11 September 2007 (UTC)

No, this article uses British English, in which diarrhoea is spelled with an "o". Also note that there are numerous mentions of diarrhoea in the article. You only changed one of them; we need to be consistent. See this guideline for details. JFW | T@lk 15:12, 12 September 2007 (UTC)

Thrombosis risk

I would have thought that mild vitamin K malabsorption would lead to a gentle coagulopathy, but doi:10.1111/j.1365-2141.2007.06766.x found (in a 14,000 strong sample) that there is a mild prothrombotic tendency (HR 1.27, 95%CI 1.06–1.52). There are various explanations. Should probably included when I get hold of the fulltext. JFW | T@lk 15:09, 12 September 2007 (UTC)

Not sure why it occurred but I got an DOI does not exist error on the launch.

doi:10.1111/j.1365-2141.2007.06766.x works on Pubmed PMID 17854316

Idiopathic rise in anti-apolipoprotein antibodies in some celiac patients toward domain 4 is likely another cause.

CD is known to aggrevate thrombosis with Factor V leiden. Clotting abnormalities

Idiopathic rise in anti-apolipoprotein antibodies in some celiac patients toward domain 4 is likely another cause. DR4-DQ3, HLA-DR*0402-DQA1*0301-(DQB1*0302 shows almost 100% linkage with *0402 in Western Eurasians) so that thrombosis risk shares at least one Anti-ApoH genetic risk factor with CD.Pdeitiker 03:53, 16 September 2007 (UTC)

Oats - effects understated

When I was first diagnosed a few years ago, oats were mentioned as one of the grains that must be excluded from the diet. Now, some are doubting, but I believe, for the wrong reasons. Even if cross-contamination could be factored out, a sufferer will still risk the symptoms. The reason is that oats do contain some of the amino acids that will trigger the autoimmune response. —Preceding unsigned comment added by Maclilus (talk • contribs) 21:17, 17 September 2007 (UTC)

Amino acids do not cause celiac disease, peptides or proteins do. Oats have a known risk factor of about 2% of celiacs. One study has showed that one epitope (the only epitope so far) that can stimulate CD T-cells is strain specific. Another study showed that contamination or strain specific response while another strain (Langdon Oats, a northern variety) gave no response. The 2 CD stimulating strains are both derived, partially, from africa. The variety that I buy are grown in wyoming and the ones used in Finland that gave no response were locally grown. Of course there is more work to be done. At some point in time I expect to see very specifically defined parameters for oats that do not cause disease in any celiacs. CD is a T-cell defined disease, no T-cell response, no disease. This is the bottom line, reactive T-cells to oats have only been found in a few studies, and the response is generally weak compared to wheat and only found in a few individuals.

Oats are a valuable source of fiber and vitamins, things celiac generally need. As with any food a person can have allergies to oats, one of the most severe allergens in wheat is structurally similar to oat avenins. Therefore simply because one has a response to oats does not mean it is due to cellular immunity, and in the US getting Triticeae gluten free Oats is difficult. Starting next month BRM claims to be selling such oats.Pdeitiker 03:22, 18 September 2007 (UTC)

So, what is the parts per million (ppm) that these oats are tested for, and at what ppm does that a T-cell response is triggered in the average CD colon? —Preceding unsigned comment added by Maclilus (talk • contribs) 17:38, 21 September 2007 (UTC)

That is the big controversy. Some celiacs are sensitive to wheat at 1 mg/week level and therefore any level of contamination is not safe.

In fact, a study of three popular commercial oat products reported by Tricia Thompson, M.S., R.D.* found that none could be relied on to be gluten-free. In that assessment, oat samples were considered gluten-free if they contained 20 ppm or less. Nine of the twelve samples from these three brands of oats had gluten levels that ranged from 1807 to 23 ppm.http://www.glutenfreeoats.com/.

In a private communication one testing company said they found a major national brand was detected at one point as having 25% wheat contamination (i.e one grain in four was a wheat grain) in its Oats, and amazingly it is not required by the federal goverment to report as such on its label. Why are Americans getting so f-ed up? Anyway that particular company (gf-oats) is tested to 10 PPM. We can calculate that out. that is 1 part per 10,000. If you could tolerate gluten at 0.1 mg per day that would mean you could eat 1000 milligram or 1 gram of Oats per day safely. Some people however are that sensitive. Pdeitiker 9-21-2007 Pdeitiker 9-21-2007. BTW technically gluten is only the glue-proteins in wheat, but those in barley and rye can also make people sick, so who is testing and what is being tested in as important as the PPM values.

Errr, I should have rechecked the math. that is 1 part per 100,000 which translates to 10 grams per day. —Preceding unsigned comment added by Pdeitiker (talk • contribs) 04:06, 28 September 2007 (UTC)

I am concerned that newly diagnosed CD sufferers will be confused as to whether oats should be excluded from their diet as part of their initial adjustment and purging their digestive system, along with wheat, rye and barley. Given that gluten can have latent effects to other parts of a person's health - something as minor as teeth discoloration to something less defined but quite serious as depression, the sufferers may not have determined an adequate baseline without the effects of gluten. Should the reference about GF Oats be amended to state "after a year of strict dietary exclusions of wheat, rye, barley and oats, and the effects of gluten are minimized, the CD sufferer may try GF oats to determine if there are any adverse reactions.", or words to that effect? To put it another way, would you advise any newly diagnosed sufferer that they can use GF oats immediately? —Preceding unsigned comment added by Maclilus (talk • contribs) 04:31, 1 October 2007 (UTC)

It is strongly recommended by experts and including people who sell gluten free oats that newly diagnosed celiacs not eat oats. There are several reasons, but the primary reasons are that patients need to establish a baseline of recovery before challenging the system with a new potential aggrevant. The second reason is that newly diagnosed celiacs are more frequently glutened because they are not as familiar with what is contaminated with wheat, and their ability to read and cipher confusing packaging labels.Pdeitiker 13:12, 4 October 2007 (UTC) (!---someone please shoot the Auto sinebot!)