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Wiki Education Foundation-supported course assignment

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This article was the subject of a Wiki Education Foundation-supported course assignment, between 29 August 2018 and 14 December 2018. Further details are available on the course page. Peer reviewers: Sgmcalpi.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 00:30, 17 January 2022 (UTC)[reply]

Helminthic therapy

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I have significantly shortened the section on helminthic therapy. This is still in its experimental stages, and Wikipedia does not need to tell the public how a German company is trying to market this. When it hits the shelves, we'll see.

I have also replaced the news links with an actual scientific report in a peer-reviewed journal. The BBC link quoted the New Scientist, and the latter got its information from the article. This is much more direct. JFW | T@lk 23:17, 27 Nov 2004 (UTC)

Please note the link is broken for the scientific report (reference #19). This should be fixed. — Preceding unsigned comment added by 71.7.239.165 (talk) 13:27, 2 January 2012 (UTC)[reply]

Life events

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Life events may herald onset of Crohn's but not IBD as a whole - doi:10.1111/j.1572-0241.2006.00931.x. JFW | T@lk 16:59, 11 March 2007 (UTC)[reply]

Clustering with immune conditions

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doi:10.1111/j.1572-0241.2007.01215.x JFW | T@lk 06:23, 29 April 2007 (UTC)[reply]

Review on diagnostics

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doi:10.1053/j.gastro.2007.09.001 JFW | T@lk 01:52, 23 November 2007 (UTC)[reply]

Rollback feature

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I have been reverting a vandal, but I made a mistake the first time and I think I corrected it the second time. Just started using this so please if I still made any mistakes please bring it to my attentions and I will fix it or always feel free to fix anything I should do. Thank you, --CrohnieGalTalk 11:39, 25 April 2008 (UTC)[reply]

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I've pruned the external links section. I removed:

  • a dead link (no content),
  • a blog,
  • a link to an organization that provides face-to-face meetings in two cities, and
  • an online support group.

The first three are pretty obvious to most people: for example, Wikipedia is a worldwide encyclopedia, and something that happens half a world a way does you no good. The last one sometimes surprises people, so let me explain. Wikipedia's external links policy and the specific guidelines for medicine-related articles do not generally permit the inclusion of external links to non-encyclopedic material, particularly including internet chat boards and e-mail discussion groups. Here's some specific information from the guidelines:

  • This page, which applies to all articles in the entire encyclopedia, says that links "to social networking sites (such as MySpace or Fan sites), discussion forums/groups (such as Yahoo! Groups), USENET newsgroups or e-mail lists" are to be avoided.
  • This page deprecates ""helpful" external links, such as forums, self-help groups and local charities."
  • This medical-specific page reinforces the pan-Wiki rules, with a note that "All links must meet Wikipedia's external links guidelines, which in particular exclude discussion forums."

Wikipedia is an encyclopedia, and while it may occasionally be useful to patients or their families, it is not a web directory.  Please do not re-insert links that do not conform to the standard rules.  Any editor, BTW, is welcome to read all of the rules and perform another "audit" in the remaining links.  Thanks, WhatamIdoing (talk) 03:36, 28 April 2008 (UTC)[reply]

Pred of death

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doi:10.1111/j.1572-0241.2008.01836.x - steroids increase mortality, thiopurines do not. JFW | T@lk 10:11, 26 May 2008 (UTC)[reply]

HLA - B27

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add info about HLA-B27 please! —Preceding unsigned comment added by 128.125.28.127 (talk) 01:39, 1 June 2008 (UTC)[reply]

Thrombosis

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Risk of thrombosis increased, especially during flare. I can hear a trial approaching, especially with one of the oral antithrombotics. In fact, perhaps this might also show a disease modifying effect! doi:10.1016/S0140-6736(09)61963-2 JFW | T@lk 10:04, 21 February 2010 (UTC)[reply]

What kind of inflammatory bowel disease is this?

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Before any reinsertion, I think it needs to be specified what kind of inflammatory bowel disease (if even IBD) is referred to in the following study, since it appears to consist of multiple types with different pathogenesis. Mikael Häggström (talk) 16:20, 25 October 2010 (UTC)[reply]

Research[1] has shown that IL-23 is overexpressed in tissues taken from mouse models of IBD. The group showed that knocking out IL-23 (heterodimer of IL-12p40 and IL-23p19) sharply reduced inflammation of the bowel, both in terms of cells and proinflammatory cytokine production. Also, they found that a novel group of CD4+ T lymphocytes, Th17 T cells, are highly unregulated in bowels of diseased mice. Taken together, the group shows that IL-23 but not IL-12 (a heterodimer of IL-12p40 and IL-12p35) drives innate and T cell mediated intestinal inflammation.
  1. ^ Hue S, Ahern P, Buonocore S; et al. (2006). "Interleukin-23 drives innate and T cell-mediated intestinal inflammation" ([dead link]Scholar search). J. Exp. Med. 203 (11): 2473–83. doi:10.1084/jem.20061099. PMC 2118132. PMID 17030949. {{cite journal}}: Explicit use of et al. in: |author= (help); External link in |format= (help)CS1 maint: multiple names: authors list (link)

Pregnancy

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doi:10.1136/gut.2010.222893 - large cohort of pregnancy on thiopurines; they seem to be safe. JFW | T@lk 12:51, 5 January 2011 (UTC)[reply]

Evolutionary Considerations

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Prototype to material that should be considered when discussing causes of IBD

The low incidence of pathogens within modern societies are thought to have contributed to Inflammatory Bowel Disease vulnerability[1] . This has been known as the Hygiene Hypothesis[1] . Humanity has been exposed to a wide range of bacteria and viruses with the practice of agriculture in the Neolithic Revolution[1] . This was due to an increase in population density and a sedentary lifestyle that accompanied agricultural practice[1] . In the post Neolithic Revolution, humans adapted to the high rate of pathogens through developing a more active immune system[1] . In the modern society, improved sanitation and medicine has lowered pathogen exposure[1] . This leads to an evolutionary mismatch between adaptation and environment where the low pathogen exposure increases susceptibility to Inflammatory Bowel Disease[1] . This is a result of an inappropriate response from the immune system that has not been exposed to many pathogens[1] . Several lines of evidence have proven supportive of this hypothesis[1] . Helminthic infection, which was common in a pre-modern setting, is shown to modulate a strong Th2 response[1]. The increase in Th2 decreases the Th1 response which is associated with auto-immune and Crohn's Disease. Patients with IBD are shown to have lower prevalence of Helicobacter pylori, common in third world countries, to matched controls and disease controls.[1] This observation suggests a protective role of H. pylori in the development of IBD[1] . Taken together, these suggest that the active immune system is mismatched in the modern, low pathogen setting and may be a reason for vulnerability to IBD.[1]

References

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1. Koloski, Natasha; Laurel Bret, Graham Radford-Smith (1/14/08). "Hygiene Hypothesis in Inflammatory Bowel Disease: A Critical Review of the Literature". World Journal of Gastroenterology: 185–173. doi:10.3748/wjg.14.165.

LiZhang1312 (talk) 14:30, 14 October 2013 (UTC)[reply]

I am unable to glean useful text from the content above, but have copied it to User:LiZhang1312/sandbox so the original editor can continue work there. SandyGeorgia (Talk) 14:47, 24 October 2013 (UTC)[reply]
One needs to be very careful about WP:RECENTISM and WP:MEDRS here. "New research" might not yet be suitable for inclusion into an encyclopedia article. Artices and studies on the evolutionary aspects of disease are almost without exception highly speculative, and of course cannot be confirmed experimentally. JFW | T@lk 11:47, 25 October 2013 (UTC)[reply]
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Proposal ?

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This might represent a copyedited version of the proposal above. It lacks wikilinking, and there are undefined terms. It also lacks analysis of why this hypothesis has not gained wide traction, and it is based entirely on one source which is a review limited specifically to one theory, not a broad overview of IBD (in other words, WP:UNDUE missing-- what weight should be assigned to this theory, if any). If something along these lines were to be included, it would not be under "Evolutionary considerations", it would be under "Causes" (See WP:MEDMOS). Perhaps User:Jfdwolff will have a look to opine on the due weight aspects, as well as the proposed text. SandyGeorgia (Talk) 17:19, 11 November 2013 (UTC)[reply]

The "Hygiene hypotheis" says that low incidence of pathogens within modern societies may have contributed to IBD vulnerability.[1] Due to an increase in population density and a sedentary lifestyle that accompanied agricultural practice, humanity was exposed to a wide range of bacteria and viruses.[1] In the post-Neolithic Revolution, humans adapted to the high rate of pathogens by developing a more active immune system; in modern society, improved sanitation and medicine has lowered pathogen exposure, leading to an evolutionary mismatch between adaptation and environment where the low pathogen exposure increases susceptibility to IBD as a result of an inappropriate immune response.[1] Several lines of evidence have proven supportive of this hypothesis:[1]

  • Helminthic infection, which was common in a pre-modern setting, is shown to modulate a strong Th2 response.[1]
  • The increase in Th2 decreases the Th1 response which is associated with auto-immune and Crohn's Disease. Patients with IBD are shown to have lower prevalence of Helicobacter pylori, common in third world countries, to matched controls and disease controls.[1] This observation suggests a protective role of H. pylori in the development of IBD.[1]
  1. ^ a b c d e f g h i j k l m n o p q r s t Koloski, Natasha (1/14/08). "Hygiene Hypothesis in Inflammatory Bowel Disease: A Critical Review of the Literature". World Journal of Gastroenterology: 185–173. doi:10.3748/wjg.14.165. {{cite journal}}: Check date values in: |date= and |year= / |date= mismatch (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)CS1 maint: unflagged free DOI (link) Cite error: The named reference "Hygiene Hypothesis" was defined multiple times with different content (see the help page).

The source is (correctly formatted as):

LiZhang1312, by altering your previous post here on talk, you make it harder for other editors to discuss your proposed text. You might instead say that you have proposed text in your sandbox, link to your sandbox, and ask for commentary there. SandyGeorgia (Talk) 17:22, 11 November 2013 (UTC)[reply]

It is not a secret that WJG is a journal that is known for doubtful editorial practices. The above version attempts to summarise the hygiene hypothesis and to cite it to Koloski et al. Nowhere in Koloski et al is there any mention of a Neolithic Revolution. The content is very much not ready for inclusion. JFW | T@lk 20:55, 12 November 2013 (UTC)[reply]

Updated Sandbox with two more review articles on the hygiene hypothesis LiZhang1312 (talk) 05:00, 3 December 2013 (UTC) https://en.wikipedia.org/wiki/User:LiZhang1312/sandbox LiZhang1312 (talk) 05:03, 3 December 2013 (UTC) Also thank you JFdwolff and Bluerasberry for your comments LiZhang1312 (talk) 05:07, 3 December 2013 (UTC)[reply]

Causes - 'Concentrated milk fats' ?

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Anybody know what that's supposed to mean? Isn't milk fat just butter? How can you concentrate it? Looks like anti processed food POV pushing to me. --Ef80 (talk) 22:09, 19 December 2013 (UTC)[reply]

The intent may be to include both cheese and butter.187.210.137.17 (talk) 17:17, 20 December 2013 (UTC)[reply]

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1st and most important sentence in the article, 2nd word "medicine" links to the wikipedia article on "medicine" which I think is ridiculous. As if "inflammatory bowel disease" might also apply to some other area, such as astronomy or economics.Jonny Quick (talk) 18:58, 27 July 2014 (UTC)[reply]

recent reverts/post wikiproject Med

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  • no need to add Irritable bowel syndrome is excluded when there are inflammatory changes.[30] Celiac disease can't be excluded if specific antibodies (anti-transglutaminase antibodies) are negative,[31][32] nor in absence of intestinal villi atrophy.[33]...IMO--Ozzie10aaaa (talk) 20:01, 15 March 2016 (UTC)[reply]

Hi, Ozzie10aaaa and Jrfw51.

The World Gastroenterology Organisation believes that the warning about irritable bowel disease (IBS) is necessary:

World Gastroenterology Organisation Global Guidelines. Inflammatory Bowel Disease. Update August 2015 (page 16)

Table 4 - Main differential diagnoses for ulcerative colitis and Crohn’s disease

UC: Acute self-limiting colitis (ASLC), Amebic colitis, Schistosomiasis, CD, Colon cancer, IBS (if there are inflammatory changes, it is not IBS), Intestinal TB, NSAID enteropath

CD: Intestinal TB, Behçet’s disease, UC, NSAID enteropathy, IBS, Celiac disease

Crohn's disease and celiac disease may present associated, overlaped, or be confused, and sometimes Crohn's disease develops secondary to a pre-existing celiac disease. Also, they share genetic risk factors. Evaluate the association of both diseases and / or make a correct differential diagnosis is very important for the prognosis and treatment of the patient. Nevertheless, about 85% cases of celiac disease are unrecognized and undiagnosed.[1] Among main problems for diagnosis are frequent errors in the interpretation of serology and biopsies.

  1. ^ Lionetti E, Gatti S, Pulvirenti A, Catassi C (Jun 2015). "Celiac disease from a global perspective". Best Pract Res Clin Gastroenterol (Review). 29 (3): 365–79. doi:10.1016/j.bpg.2015.05.004. PMID 26060103. The ratio of known (previously diagnosed) to undiagnosed CD cases was as high as 1-7

Int J Colorectal Dis. 2005 Jul;20(4):376-80. Epub 2004 Dec 1. Association of Crohn's disease and latent celiac disease: a case report and review of the literature. Schedel J1, Rockmann F, Bongartz T, Woenckhaus M, Schölmerich J, Kullmann F. (Review) PMID 15578194

in most cases, Crohn's disease develops secondary to a pre-existing celiac disease (Note: when they present associated)

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4009516/ World J Gastroenterol. 2014 May 7;20(17):4846-56. doi: 10.3748/wjg.v20.i17.4846. Inflammatory bowel disease and celiac disease: overlaps and differences. Pascual V, Dieli-Crimi R, López-Palacios N, Bodas A, Medrano LM, Núñez C.(Review) PMID 24803796

The present review summarizes the current knowledge of different features related to the two major clinical forms of IBD, Crohn’s disease (CD) and ulcerative colitis (UC), and CeD, paying special attention to the overlaps and differences between them. These two diseases share genetic risk factors, and it would be interesting to know whether this overlap also extend to other disease characteristics in order to gain knowledge about common pathogenic mechanisms and possible shared treatments.

Best regards. --BallenaBlanca (talk) 22:53, 15 March 2016 (UTC)[reply]

We already state that coeliac disease is in the differential diagnosis. Your WGGO Guidelines recommend coeliac antibody testing and we already talk about histological testing. A large study PMID 19786375 found coexisting IBD and coeliac to be less common than the general population. We need to retain a balance. Jrfw51 (talk) 09:06, 16 March 2016 (UTC)[reply]
You cited a 2010 primary source PMID 19786375, and I cited a 2004 review, secondary source per WP:MEDRS that doesn't support the conclusions of your 2010 primary source PMID 15578194. Recent reviews show a definite association between celiac disease and IBD in adults and in some children. Let's see another secondary source of January 2016:
Pol Merkur Lekarski. 2016 Jan 28;40(235):53-5. Coexistence of coeliac disease and inflammatory bowel disease in children. Krawiec P1, Pawłowska-Kamieniak A1, Pac-Kożuchowska E1, Mroczkowska-Juchkiewcz A1, Kominek K1. (Review) PMID 26891438

Coeliac disease and inflammatory bowel disease are chronic inflammatory conditions of gastrointestinal tract with complex aetiology with genetic, environmental and immunological factors contributing to its pathogenesis. It was noted that immune-mediated disorders often coexist. There is well-known association between coeliac disease and type 1 diabetes and ulcerative colitis and primary sclerosing cholangitis. However, growing body of literature suggests the association between coeliac disease and inflammatory bowel disease, particularly ulcerative colitis. This is an extremely rare problem in paediatric gastroenterology. To date there have been reported several cases of children with coexisting coeliac disease and inflammatory bowel disease. Herewith we present review of current literature on coexistence of coeliac disease and inflammatory bowel disease in children.

I agree in this edit removing detail of quotations, but there is no reason to withdraw the references nor to modify the text. It seems an attempt to bias the information. WP:NEU So I will correct to neutrality.
Best regards. --BallenaBlanca (talk) 11:01, 16 March 2016 (UTC)[reply]

I've been looking at this and scratching my head for a while. What exactly is the point of this information about celiac? Is the point to say that if you diagnose IBS, that it might actually be CD instead? WhatamIdoing (talk) 22:35, 16 March 2016 (UTC)[reply]

WhatamIdoing, it is "simple": IBD may present associated, overlapped, or be confused with celiac disease. Evaluate the association of both diseases and / or make a correct differential diagnosis is very important for the prognosis and treatment of the patient. The only treatment available for celiac disease is a longlife strict gluten-free diet. Celiac disease may affect any organ of the body. If remain untreated, people may have severe disease symptoms, may develope associated disorders (such autoimmune diseases) and are exposed to the risk of other long-term complications, which include cancers -lymphoma, small bowel adenocarcinoma, and other malignancies (gastric, oesophageal, bladder, breast, brain)- and greater mortality.[1][2][3][4][5][6] But in everyday medical practice, celiac disease is often not correctly evaluated and most patients (85%) remain unrecognized, undiagnosed and untreated.[7]
Best regards. --BallenaBlanca (talk) 13:09, 17 March 2016 (UTC)[reply]

References

  1. ^ Vriezinga SL, Schweizer JJ, Koning F, Mearin ML (Sep 2015). "Coeliac disease and gluten-related disorders in childhood". Nat Rev Gastroenterol Hepatol (Review). 12 (9): 527–36. doi:10.1038/nrgastro.2015.98. PMID 26100369.
  2. ^ Ciccocioppo R, Kruzliak P, Cangemi GC, Pohanka M, Betti E, Lauret E, Rodrigo L (Oct 22, 2015). "The Spectrum of Differences between Childhood and Adulthood Celiac Disease". Nutrients (Review). 7 (10): 8733–51. doi:10.3390/nu7105426. PMC 4632446. PMID 26506381.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  3. ^ Elli L, Branchi F, Tomba C, Villalta D, Norsa L, Ferretti F, Roncoroni L, Bardella MT (Jun 21, 2015). "Diagnosis of gluten related disorders: Celiac disease, wheat allergy and non-celiac gluten sensitivity". World J Gastroenterol (Review). 21 (23): 7110–9. doi:10.3748/wjg.v21.i23.7110. PMC 4476872. PMID 26109797.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  4. ^ Lebwohl B, Ludvigsson JF, Green PH (Oct 2015). "Celiac disease and non-celiac gluten sensitivity". BMJ (Review). 5: 351:h4347. doi:10.1136/bmj.h4347. PMC 4596973. PMID 26438584.
  5. ^ Levy J, Bernstein L, Silber N (Dec 2014). "Celiac disease: an immune dysregulation syndrome". Curr Probl Pediatr Adolesc Health Care (Review). 44 (11): 324–7. doi:10.1016/j.cppeds.2014.10.002. PMID 25499458.
  6. ^ Hourigan CS (Jun 2006). "The molecular basis of coeliac disease". Clin Exp Med (Review). 6 (2): 53–9. PMID 16820991.
  7. ^ Lionetti E, Gatti S, Pulvirenti A, Catassi C (Jun 2015). "Celiac disease from a global perspective". Best Pract Res Clin Gastroenterol (Review). 29 (3): 365–79. doi:10.1016/j.bpg.2015.05.004. PMID 26060103.
Ballena, I know all that. What I'm trying to figure out is the purpose of this paragraph:

Irritable bowel syndrome is excluded when there are inflammatory changes.[30] Celiac disease can't be excluded if specific antibodies (anti-transglutaminase antibodies) are negative,[31][32] nor in absence of intestinal villi atrophy.

The paragraph appears to be about IBS (not IBD). Does the second sentence mean "If you think that you have IBSyndrome rather than Celiac because these two tests turned up negative, then you might still have Celiac instead of IBSyndrome"? WhatamIdoing (talk) 15:10, 17 March 2016 (UTC)[reply]
I agree. Our current entry is about Inflammatory Bowel Disease (IBD), and although Irritable Bowel Syndrome (IBS) and Celiac Disease can produce some similar symptoms, apart from including them in the list of differential diagnoses, I still feel this amount of detail is not appropriate for the IBD entry. We are writing an encyclopedia and not a diagnostic textbook. In reality this is a very small footnote when diagnosing IBD and of only some relevance for celiac disease. Jrfw51 (talk) 08:56, 18 March 2016 (UTC)[reply]
That is exactly my concern. This is not the page to explain how to diagnose IBSyndrome correctly. WhatamIdoing (talk) 03:01, 19 March 2016 (UTC)[reply]
yep(as noted on my first two points)--Ozzie10aaaa (talk) 13:51, 30 March 2016 (UTC)[reply]

Environmental risk factors

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Meta-meta-analysis if there is such a thing doi:10.1053/j.gastro.2019.04.016 JFW | T@lk 21:21, 26 August 2019 (UTC)[reply]

Nutritional and dietetic therapies

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I added more information about the significance of B vitamins in nutrient absorption and lipid metabolism [1] JewelSciComm (talk) 23:00, 19 October 2020 (UTC)[reply]

References

  1. ^ Lloyd-Price, Jason (2019). "Multi-omics of the gut microbial ecosystem in inflammatory bowel diseases". Nature. 569 (7758): 655–662. Bibcode:2019Natur.569..655L. doi:10.1038/s41586-019-1237-9. PMC 6650278. PMID 31142855. Retrieved 16 October 2020.

Microbiome

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I added information about the significance of short-chain fatty acids and secondary bile acids and how metabolomics can help us identify bacterial species that produce secondary bile acids. [1] JewelSciComm (talk) 23:00, 19 October 2020 (UTC)[reply]

References

  1. ^ Lloyd-Price, Jason (2019). "Multi-omics of the gut microbial ecosystem in inflammatory bowel diseases". Nature. 569 (7758): 655–662. Bibcode:2019Natur.569..655L. doi:10.1038/s41586-019-1237-9. PMC 6650278. PMID 31142855. Retrieved 16 October 2020.

Sulfasalazine

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Anyone can add information on this drug: Sulfasalazine ? AXONOV (talk) 19:16, 23 November 2021 (UTC)[reply]