Talk:Helicobacter pylori/Archive 1

Broccoli

Broccoli works long term better than any drug-based treatment, IMHO.

The problem is that your HO needs supportive evidence before this can be mentioned in this article. If you can cite studies that compare broccoli with triple therapy, you are completely in your right to add this to the article. Otherwise, it will qualify as original research, something that's discouraged on Wikipedia. JFW | T@lk 07:30, 6 October 2005 (UTC)

Broccoli as a treatment is properly referenced in the article. My interpretation of the paper is that long term Broccoli consumption supresses H pylori activity but does not eliminate. GraemeLeggett 08:17, 6 October 2005 (UTC)

Harvard referencing

The Wikipedia guideline for non-numbered reference lists seems to be that the Harvard referencing system be used. I think it would be useful for the current reference list to be put in alphabetical order. --JWSchmidt 20:54, 18 December 2005 (UTC)

I personally think that numbered lists should be used when possible, but following guidelines if not makes sense - InvictaHOG 21:26, 18 December 2005 (UTC)

I think numbered references are nice because the hypertext links between citations and references in the list make it easy to keep going back-and-forth between the main text and the reference list. --JWSchmidt 02:05, 19 December 2005 (UTC)

I prefer numbered references.--FloNight 22:49, 19 December 2005 (UTC)

Acid good or bad?

The article states that before ulcers were known to be caused by bacteria, they were treated by medications which reduced stomach acid. But it also states that the bacteria itself releases enzymes to reduce stomach acid, to make its environment more hospitable to it. So is stomach acid helpful or harmful to the bacteria? 66.81.100.52 20:27, 30 August 2005 (UTC)

The levels of acidity that can be produced in the human stomach can be harmful to bacteria such as Helicobacter pylori, but Helicobacter pylori has mechanisms that protect it fromthe harsh acidic environment of the stomach. Once the stomach has been damaged (ulcer), the damaged tissue is itself less well protected against stomach acid, reducing acid production can help the ulcer to heal. --JWSchmidt 21:49, 30 August 2005 (UTC)

But presumably, even in the presence of an ulcer, the stomach acid is serving a purpose: to keep the H pylori population in check (its limited tolerance for acidic conditions notwithstanding), and in doing so prevent further ulcers from forming, which would happen if H pylori were allowed to reproduce and attack the stomach lining more heavily. So I still don't understand why intervening to decrease stomach acid is a good idea. It sounds like there should be a more detailed explanation. A5 05:36, 6 September 2005 (UTC)

H. pylori is not a thrifty organism and does not prolifically reproduce under any known circumstances. Temporarily reducing production of stomach acid helps ulcers heal to a degree largely without affecting H. pylori growth, as far as I know. --Bk0 (Talk) 19:25, 25 December 2005 (UTC)

It is thought that immune cell infiltration below the stomach epithelia may play some part in ulcer formation; H. pylori is thought to enhance inflamatory vs. antibody immune response (at least in some strains). Immune cell infiltration is, in fact, noted in even asymptomatic infection. Also, H. pylori is not particularly acid tolerant (the gastric mucosa being near neutral pH), and prolifically is very relative (it's doubling time is much faster than M. tuberculosis for example), and compare thrifty to some sucessful obligate intracellular organisms.

The gastric mucosa protects the stomach from the harsh environment it generates. An ulcer is essentially a wound to the stomach in which the mucosa can not protect as effectivley. Thus, reducing stomach acid helps the wound to heal.

Bacillus

I turned the characterization as "bacillus" back into "bacterium", because we already discuss the shape of the organism, and "bacillus" unfortunately has two meanings. To call it a "bacillus" seems to confuse more than it clarifies. AxelBoldt 19:07, 25 December 2005 (UTC)

I agree. It is classified as a spirochete in some publications, and as a "spiral bacillus" in others. --DocJohnny 17:41, 26 December 2005 (UTC)

Featured on biology portal

Congratulations! This article is the current Featured article on the Biology Portal. If you would like to help with the Biology Portal the best place to start is the portal talk page. --Cyde Weys _vote^talk 00:47, 29 December 2005 (UTC)

Version 0.5 nomination failed

This article is considered to fall outside the scope of the Version 0.5 test release, since this version only includes a limited number of articles. It is now held ready for a later version such as Version 1.0 nomination. Walkerma 04:07, 5 June 2006 (UTC)

Molecular hydrogen is the energy source

Molecular hydrogen is the energy source, not hydrogen methanogenesis. H. pylori is not a methanogen. For further reference, check this article in Science about metabolism. I've corrected it to reflect that.Antorjal 23:06, 21 August 2006 (UTC)

Does it use oxygen as electron acceptor? AxelBoldt 22:30, 9 September 2006 (UTC)

Thomas Borody

Dr. Borody certainly was one of the early pioneers of Helicobacter treatment, but was he the first to eradicate Helicobacter with triple therapy? I've always been taught that it was the Amsterdam group (PMID 1971318). -- Samir धर्म 03:32, 15 September 2006 (UTC)

spontaneous elimination

Recently, a colleague of mine, Dr. Karen Goodman, one of the leading epidemiologists studying H.pylori infection, changed this entry to correct the dogma that H.p is never spontaneously eliminated. Her research, among others, provides evidence that strongly suggests there is spontaneous elimination, and it might be quite frequent, at least among children. In any case, it is clear that there is no evidence that suggests H.p infection always persists. MarcoTolo (I don't know who s/he really is) deleted Dr. Goodman's correction, without explanation. MarcoTolo also added a reference that was presumably meant to support the dogmatic claim, but actually turned out to be a non sequitur (referencing the statement "It is widely believed...." with an article from 1992 obviously does not make sense, since the statement is about contemporary beliefs and the article is not contemporary and did not address beliefs). More important, on the issue of whether there is spontaneous elimination, a 1992 paper is of interest only for historical purposes since most (arguably, all) of the relevant research has taken place since then. Thus, when I added the accurate current information back, I removed the reference.

Dr. Goodman expressed skeptism about the value of trying to improve Wikipedia when I suggested she do so, and guessed that it would never keep up with the latest research, and thus her change would be replaced with the original dogma the very next day. Since her prediction of her contribution being trashed in a day was born out, I doubt she will bother to try to correct the mistake that was reintroduced or otherwise contribute to Wikipedia again. I am going to try to prove her wrong about the potential of Wikipedia by putting the correct information back into the article, and I hope it will not again be changed by someone who is not expert on the current literature. Carlvphillips 03:28, 22 September 2006 (UTC)

• Please, by all means, update the article if you have newer information - that's what Wikipedia is all about. But (and this is an important caveat), if you're an "expert in the literature", cite the literature when you update the article rather than making blanket, unreferenced statements. In general, the "because I said so" argument plays about as well in Wikipedia as it does elsewhere in science.

A quick read through the Goodman et al paper (I'm assuming you're referring to "Dynamics of Helicobacter pylori infection in a US-Mexico cohort during the first two years of life." (Goodman et al. Int J Epidemiol. 2005 Dec;34(6):1348-55. Epub 2005 Aug 2. (PMID 16076858)) looks promising, though I'd personally caution against claiming that Goodman 2005 has completely disproven the endemic and persistent nature of H. pylori infections with a study of children birth-to-24 months. As good as the study may be, the commentary by Perry & Parsonnet (Int J Epidemiol. 2005 Dec;34(6):1356-8. Epub 2005 Nov 22.) does have some good points. -- MarcoTolo 04:00, 22 September 2006 (UTC)

Ok, I get it. Thanks. I am going to guess that Dr. Goodman's original change was deleted because she did not cite references (though I will note that most of the rest of that entire section lacks references) and (if I am understanding how this works correctly) she did not sign in, so was not identifiable. Having reread what I wrote above, I wanted to apologize for it sounding so rude -- I should have been more careful about what I was writing "sounded" and I appreciate you responding more politely than I must have seemed to you. (I will also note that I am very impressed by how quickly you found the references and digested them -- it took you less time to do that than it took me to figure out how to format them). I have added two references -- the one you cite (which I am a coauthor on) and another Goodman reference. Those are the ones I happen to know off hand, but I can probably get her to add more when she sees this and realized that she can have an impact. FWIW, I have paper under review that shows that the Perry & Parsonnet commentary, while it looks convincing on its face, is actually mathematically completely wrong (based on some errors in their model, as well as further Bayesian analysis of the competing claims in light of the evidence). I suspect that that level of detail and debate is beyond the preferred scope for this forum. To clarify one point: The only thing that is 100% clear on this point is that no one should be confident that there is not widespread spontaneous elimination because we simply do not have enough data about enough populations (the belief comes from case-report-type observations of lack of spontaneous elimination in adults who are being treated for clinical symptoms, but such people are quite likely different from the average case). The actual evidence goes a step further (though is not necessary to make that point): There are several studies by several resarch teams that show what looks like spontaneous elimination, particularly in children. Thus, while there is no definitive proof (as is the case with a lot of things) there is actually more evidence to support the claim that there *is* spontaneous elimination (some evidence) rather than the historical dogma (very little generalisable evidence). I can make that more clear in the article if such expositions are appropriate -- I think Dr. Goodman had some of that point in her original entry. Carlvphillips 04:31, 22 September 2006 (UTC)

• Outstanding - thanks for adding the references. And don't worry about "sounding rude"; as you noted, electronic written communication has limitations in conveying tone and intent - I took no offense. I made some small, technical changes to the formatting of your references for continuity, but otherwise they were great.

The issue of "what level is appropriate on a given topic" is a tricky one on Wikipedia - and one for which there isn't likely to be a single answer. Some of the WP style guides (Wikipedia:Guide_to_writing_better_articles#Think_of_the_reader might be a good place to start) have some generally useful ideas to keep in mind.

Again, thanks for the excellent addition; I hope you'll continue editing at WP for a long time to come. -- MarcoTolo 20:46, 22 September 2006 (UTC)

Barry Marshall on this page

Just finished watching a roundtable discussion between this years Nobel prize laureates on the BBC, and during the discussion on information technology and the effects of the internet the subject of wikipedia came up. Dr. Marshall mentioned that he and Warren had been working on H. pylori for years and even they couldn't write a better article, and generally approved of the collaborative enterprise.

Do you have any idea of when that BBC discussion was recorded? --JWSchmidt 13:52, 18 December 2005 (UTC)

Ezeu just reported that this was on "Nobel Minds", a BBC/SVT produced forum discussion program. It was hosted by Nik Gowing, taped on 9 December ([1]) and aired on 17 December. I couldn't find an online video or transcript. AxelBoldt 22:58, 18 December 2005 (UTC)

That's awesome InvictaHOG 20:11, 18 December 2005 (UTC)

You can find the video here. "Interesting part" starts around 39:45. Barry Marshalls comment is around 43:00. --Avatar 09:13, 13 November 2006 (UTC)

Virulence factors

This is a great article but some of the major virulence factors of H. pylori are not mentioned in this acticle, e.g. VacA and HP-NAP. Would anyone mind if I fill in the gaps? Dabalk 14:30, 23 January 2007 (UTC)Dabalk

Conversion of urea into ammonia and bicarbonate

I've went through Image:H pylori ulcer diagram en.png and the main article about urease itself. Apparently, both show that the products are ammonia and carbon dioxide, which is different from what is written here (bicarbonate?) From what I understand, bicarbonate and carbon dioxide differs much. Is there by any chance that the urease in H.pylori converts urea into different products? Nevermind, I figured that out myself. — Yurei-eggtart 07:59, 1 February 2007 (UTC)

Role of pyrogenic (inflammatory) factors in invasion

Under the heading 'Structure of the Bacterium', a previous revision stated that 'It remains unknown how this mechanism is advantageous to the bacterium'. I reviewed the reference tag, and the discussion of the published article reads:

"Epithelial cells recognize and respond to an array of bacterial products, such as LPS, peptidoglycan and flagellin. These products are highly conserved among both pathogenic and commensal microorganisms. The precise 'cues' that are used by epithelial cells to discriminate between these different classes of microorganisms have yet to be clearly elucidated. One possibility is that pathogenic bacteria, by virtue of their virulence properties, are more likely to present such products to their cognate recognition molecules in target cells. For enteric pathogens, this is most likely to occur as a consequence of epithelial cell invasion by bacteria. Indeed, invasive enteropathogens, Shigella flexneri and enteroinvasive Escherichia coli trigger proinflammatory responses in epithelial cells via signaling by the intracellular host defense molecule, Nod1 (refs. 18,31). Here we have described a previously unknown mechanism by which an essentially noninvasive pathogen, H. pylori, is able to mediate proinflammatory responses from the outside of epithelial cells."

Which seems to indicate that the inflammatory response is beneficial to invasion. (This makes sense, as inflammation is often a factor in pathogenicity.) I have left the edit open-ended, so as not to be misleading in case it is incorrect.

For your point of view, this sentence (p.1172) would be better reference.

"The fact that the cagPAI has been retained by a proportion of H. pylori strains suggests that it is likely to be of benefit to the bacterium. Thus, the induction of Nod1-dependent signaling in host cells may actually facilitate bacterial survival and replication within the host. Alternatively, it is possible that the inflammatory responses triggered by the cagPAI represent one facet of a 'double-edged sword', the other of which is to promote host colonization via a mechanism independent of Nod1 signaling."

The author actually suggests that Nod1 induction (by peptidoglycan injection) may facilitate the bacterial survival in the host (though not "invade host tissue"). However previous revision is better yet, though your revision may be also acceptable later, I think. Because first principle of cellular Nod1 induction is the host defense, as described repetitively in the paper, it is natural to consider that most part of the inflammation act as host-defense response than as bacterial benefit. The beneficial role for the bacteria of "peptidoglycan injection", not whole cagPAI, seems to be rather speculative yet. --Y tambe 03:16, 6 February 2007 (UTC)

ACG guideline

doi:10.1111/j.1572-0241.2007.01393.x - new ACG guideline. JFW | T@lk 07:25, 7 August 2007 (UTC)

doi:10.1053/j.gastro.2007.05.008, 21-page free (because NIH-funded) review on Helicobacter vs the immune system. Potentially very useful in improving this article. JFW | T@lk 21:51, 9 August 2007 (UTC)

a short story:

my name is Brittany Mc Shea,( i wanted to try and add this ) the information i have is beneifical to your readers of Hplori. I'am 17 years old and i have Hyplori.October 28th 1998,I was having syptoms of Acid Reiflex.The diagnosed me with severe acid reflex .But growing up i was underweight ( due to uncomfortable severe pain when eating )i stopped seeing my gastrologest and tryed to live as normal as possibe. At the age of 15 i went into depression because i couldnt even look into the refidgreater without crying ( knowing i cant eat anything without severe pain) well my mom looked up another gastro doc.I went to see him and with a simple prodecure ( minor surgry)At the age of 16, he diagonosed me with , Acid Reflex and Hyplori .I had never heard of it .But since then i was on anttibiotics and it failed . and wilol be going back on them shortly .. I still cant eat what i want ( i weigh 122 pounds) but I'd like to think God will soon bless a man to find a cure. I hope my short story brang effect on you as-to how life struggling this bacteria is .—The preceding unsigned comment was added by 209.244.30.17 (talk • contribs) 22:46, 9 April 2007 (UTC).

Well, if antibiotics were ineffective then perhaps the pain is unrelated to H. pylori, or the eradication has been ineffective. To tell for sure, one would need further tests. Here in the UK we often use urease breath testing. A repeat endoscopy with another CLO test would be another option, but perhaps quite invasive.

There are still plenty of other possibilities for abdominal pain after eating. I would not ask this question on a public forum, where morons will sell you snake oil. Rather, I'd recommend discussing this with your own physician; a reasonable practicioner will be willing to revise the diagnosis and take your symptoms seriously. JFW | T@lk 22:01, 9 August 2007 (UTC)

Dead link in article of H pylori

reference item 21 is a dead URL link. It needs restated. I would think it would be more valid if a reference would quote the actual document not a URL first of all this particular URL is to JUSTOR which one has to have a membership to. a costly one at that. To make the references more valid I would think it would be good to reference the actual writing not a URL. I also believe that adds more credibility to the writing when a person reading the information can go to there referenced item and reasearch further on the subject.

Here is the dead link

^ http://www.jstor.org/cgi-bin/jstor/viewitem/09502688/ap070028/07a00130/0?frame=noframe&dpi=3&userID=ab4231b8@stanford.edu/01c0a834726f25118357f30dd&backcontext=page —Preceding unsigned comment added by Estone1000 (talk • contribs) 02:42, 5 April 2008 (UTC)

Question

Can we get some information or sources on the natural role of this bacterium in the human digestive tract. I've been reading up on it and it says that up tp 75% of people world wide have this 'infection' without actually suffering from gastric problems. Is there something in a specific lifestyle that can trigger a weakened immune system to something that could be completely normal in the stomach? I probably have it, my dad has it and my mom has it but never suffered any real stomach problems other than the usual 'I ate too many atomic sauced chicken wings and it gave me heart burn and diarrhea'. I was wondering about the concern people have that this bacterium could be an important element in the digestive enviornment and it seems to be unethical to force someone to treat this 'infection' by refusing to treat any other problem until the 'infection' is eradicated. Not enough is known about this just as nothing seem to be really understood about diseases such as Alzheimer's. So if anyone has any information about the possible importance of this bacterium as part of the digestive system then could you please either find reliable sources to post on the wikipedia article, or post it in the discussion page so I can review it. I would like to use this information on a complete and unbiased report and would like to adress all possibilities and uncertainties. Thank you for your help. Jean 75.15.214.103 (talk) 20:56, 31 July 2008 (UTC)

Cleanup tag

I added a title (Pathology) to, and somewhat otherwise revised, the segment with the cleanup tag. However, all the information in it is presented elsewhere in the article and I'm concerned that the section in question is completely unnecessary. I advise further revision, or removal, by a more experienced and knowledgable member of the Wikipedia medical community. 216.82.142.13 (talk) 01:47, 2 August 2008 (UTC)

U.S.A.

This form of the organism has not been cultured, but has been found in the water supply in the US. The source I found in an effort to remove the fact tag mentioned several areas other than the US in which H.pylori has been found in water supplies. Perhaps the reference to US should be expanded or perhaps "vagued" to something like "world-wide" Wouldn't want to leave out the Swedes or Japanese mentioned in the article! --JimmyButler (talk) 03:45, 4 August 2008 (UTC)

The same article states that there is no evidence of transmission via this route (water supply). Should that be incorporated in the sentence about US Water supply as well?--JimmyButler (talk) 03:48, 4 August 2008 (UTC)

The new source references Columbia, Lima, Peru, japan, and rural China along with a contaminated well in Pennsylvania as evidence that provides some support for water transmission; however, there seemed to be doubt regarding its ability to convert from coccoid form when in these water sources into the (bacillary) infectious form in humans. Just casually reading the sentence I thought perhaps the US water supply may be a risk source for transmission. Is there a reason to emphasize US water supply? --65.184.210.214 (talk) 14:32, 4 August 2008 (UTC)

Fixing this article

I've done some investigating, and we have to separate the bacteria (the pathogen) vs. the disease peptic ulcer. I've looked at several FA and GA articles on Wikipedia:WikiProject Medicine, such as Influenza vs. Orthomyxoviridae, Poliomyelitis vs. poliovirus, and chickenpox vs. Varicella zoster virus. This article does not describe the disease, peptic ulcers, but the pathogen that causes it. Unless there is an H. pylori disease that we're missing. Therefore, I'm going to do a bit of rearranging before tackling the article to format it close to other similar FA articles. OrangeMarlin ^{Talk• Contributions} 20:21, 30 August 2008 (UTC)

"Mucus" vs. "mucous"

I noticed that the spelling of "mucous" cells was changed to "mucus" cells. I looked up the spelling of mucous/mucus in my physiology textbook, and it states, "Both mucous surface cells and mucous neck cells secrete mucus." So I believe that "mucous" is used to describe the cell type, and "mucus" is used for the substance secreted from mucous cells. It's possible that this is a typo in my textbook, but there's a figure in it that also states that mucous cells secrete mucus. NighthawkJ (talk) 07:17, 5 September 2008 (UTC)

• That was me, I've just checked in my OED: Mucous 1. Containing, consisting of, or resembling mucus. Mucus 1. A viscid or slimy substance.... So I was wrong, but I would prefer Goblet cell. Graham Colm ^Talk 07:36, 5 September 2008 (UTC)

• • I thought it was one of the American vs. British English things. OrangeMarlin ^{Talk• Contributions} 17:51, 5 September 2008 (UTC)

• Not this time ;-) Graham Colm ^Talk 18:11, 5 September 2008 (UTC)

• I changed it back to "mucous" cells. I believe that the term "goblet" is reserved for mucus-secreting cells of the intestines(?). NighthawkJ (talk) 15:26, 6 September 2008 (UTC)

Secreted Urease?

One link in this article is to a rapid urease test that contains the following statement: 'The basis of the test is the ability of H. pylori to secrete the urease enzyme, which catalyzes the conversion of urea to ammonia and bicarbonate.' Does H. pylori SECRETE urease? The literature does not seem to have resolved this question and the urease protein does not have a predicted signal sequence. —Preceding unsigned comment added by Karin D. E. Everett (talk • contribs) 21:32, 8 January 2009 (UTC)

This article indicates that it does secrete urease, creating ammonia, which damages epithelial sells. I'm not sure I get what you're asking? OrangeMarlin ^{Talk• Contributions} 22:40, 8 January 2009 (UTC)

On this and this schematic images I made, you can see the urease localizing on surface of the bacteria. More strictly, urease is consider to associate from the outside to the plasma membrane ([2], [3]). So it localize between the plasma membrane and cell wall, so-called periplasm. Urease is once produced inside the bacterial cell, is released to outside, and then adsorbed onto the surface. I'm not sure, however, whether it is scientifically correct to call this process "secretion" because the mechanism of releasing is very unique on H. pylori. As described in this review article, H. pylori is consider to go "autolysis" (lyse its own plasma membrane) once to release the enzyme, and then reverts the bacterial form again. --Y tambe (talk) 01:37, 9 January 2009 (UTC)

So what would be the evolutionary advantage of it doing that? Interesting stuff however. OrangeMarlin ^{Talk• Contributions} 01:59, 9 January 2009 (UTC)

The question I have raised is: urease is outside of the H. pylori cell due either to LYSIS or a specific SECRETORY mechanism--do we have a conclusive opinion today (2009) on which is the mechanism? Specifically, Krishnamurthy et al. proposed in 1998[4] that some H. pylori die, altruistically spilling urease onto still living cells; Marcus & Scott (2001)[5] confirmed that lysis is responsible for extracellular urease; Kim et al., 2002[6] did an analysis for secretion (there are at least 5 known mechanisms) and showed that the UreB subunit of urease was neither secreted nor selectively released, but rather appeared in supernatants due to lysis; Ha & Oh (2001) (response to [7]) reported that intracellular urease effectively buffers H. pylori cytoplasm; Stingl & DeReuse (2005)[8] stated that it is 'widely accepted' that cytoplasmic urease protects H. pylori, and then they discussed the relative merits of periplasmic vs. cytoplasmic buffering. NOTE: in proteobacteria such as H. pylori, autolysis = cell death) —Preceding unsigned comment added by Karin D. E. Everett (talk • contribs) 20:50, 9 January 2009 (UTC)

Strange sentence

Even biopsy is dependent on the location of the biopsy. —Preceding unsigned comment added by 131.111.176.9 (talk) 16:45, 21 January 2009 (UTC)

International Phonetic Alphabet

I can understand the use of the international phonetic alphabet to define the pronounciation of common words, but scientific words that are generated according to strict rules governed by organizations such as The American Society for Microbiology, should be pronounced in the standard way they are developed to ensure proper communication. I have been a microbiologist for 34 years and I am unable to begin to decipher the given pronounciation guide for Helicobacter pylori, more correctly shown as hel' i ko' bak tir pi lor e (with the last three syllable vowels being long).Drhx (talk) 20:07, 23 January 2009 (UTC)

I agree with you. I think the IPA is the one of the dumber things we do on Wikipedia, I've never used it, can't decipher it, and find it quite useless. I think anyone who states the name of the bacteria in a clinical or research situation knows how to pronounce it. Of course, I always say "H pie-lore-ree" when describing it.  :) OrangeMarlin ^{Talk• Contributions} 23:02, 23 January 2009 (UTC)

Yes, thank-you. I would pronounce it as you show, except I would drop the 'r' in the last syllable. If the IPA is meant to be some sort of politically correct method of avoiding English as a standard language, it is a misplaced sentiment. I have talked to people from the mid-east, China, and other countries, who say 'of course English should be used, it is the language of commerce and science'. They take no offense in its predominance.Drhx (talk) 19:13, 26 January 2009 (UTC)

Honey treatment research

As for as I can tell, the external link to Honey Research Around the World leads to two relevant abstracts and this article: Causes of the antimicrobial activity of honey.

One of the two abstracts seems never to have led to a full publication. The other seems to have been followed up by: Osmotic effect of honey on growth and viability of Helicobacter pylori.

This is another reference for the action of honey on H. pylori: Susceptibility of Helicobacter pylori to the antibacterial activity of manuka honey.

It might be useful to have a section for research on non-antibiotic treatments for H. pylori. Unfortunately, this 2003 review indicates that no clinical trials for alternative therapies have shown positive results.

• Removed the external link on honey research as they are all 5-10 years old (1994-1999) and recent treatment guidelines do not mention them. The lastest link from Helicobacter journal Aug 2004 - The Year in Helicobacter pylori 2004 in the chapter [http:// www.blackwell-synergy.com/links/doi/10.1111/j.1083-4389.2004.00251.x/full/ Therapy of Helicobacter pylori] under Novel agents does include this "Bee glue propolis, has antimicrobial and anti-inflammatory effects and in vitro studies have shown its effectiveness in inhibiting H. pylori." [9] Other novel agents are also listed in the journal article include ginger root and essential oils. Petersam 08:22, 22 Dec 2004 (UTC)

Can you define the criterion that justifies the right to remove alternative content in light of the age of the research? Clearly a controlled agenda is at work here. —Preceding unsigned comment added by 68.150.124.54 (talk) 13:39, 11 March 2009 (UTC)

Important distinction, most alternative treatments including honey and gum are all in-vitro, which falls short of even Marshall's one man experiment. GraemeLeggett 11:32, 18 Feb 2005 (UTC)

Slanted/spammy content

Someone (i.e. TracyLW) thought it would be a good idea to add FUD and unsubstantiated claims about 'natural products' that are 'scientifically proven'. I've tried to revert it as best I can, but if I missed any obvious spammyness, please fix it 98.246.108.186 (talk) 05:32, 14 March 2009 (UTC)

Good job!!!!! Keep doing it. We have to watch over every medical article to keep out CAMmie woo, and we do it but being very strict with WP:MEDRS. OrangeMarlin ^{Talk• Contributions} 06:31, 14 March 2009 (UTC)

Tranmission unknown ?

"The route of transmission is unknown,"

http://www3.interscience.wiley.com/journal/120707988/abstract?CRETRY=1&SRETRY=0

"The route of person-to-person transmission of Helicobacter pylori may be either fecal–oral or oral–oral, because the bacterium is found in both dental plaque and feces" ? —Preceding unsigned comment added by 75.211.41.58 (talk) 16:42, 19 July 2009 (UTC)

Commercial links?

Both links at the end of this article are to a single website selling a 'natural treatment' for H. Pylori infection. I think these should be removed. LVehko (talk) 06:12, 25 October 2009 (UTC)

Urease-deficient H. Pylori

Urease deficient H. Pylori have been detected, and have been shown to cause peptic ulcers. (Sleisenger and Fordtran's Gastrointestinal and Liver Disease). Thus, the whole debate above about urease needs to be rectified, as does the article itself. However, the mechanisms through which such strains can survive is still being explored (most likely due to its other colonisation/adherence factors. —Preceding unsigned comment added by 60.240.34.106 (talk) 04:09, 6 November 2009 (UTC)

Triple Therapy?

The listed triple therapy only seems to have two components. One of the components of the triple therapy has gone missing. I tried looking back in the history to see when this happened, but I couldn't find it. Could someone fix this? 24.148.140.222 (talk) 00:33, 6 September 2009 (UTC)

Triple therapy involves two antibiotics (usually amoxicillan, metronidaxole or clarithromycin) and one adjunctive agent (Bismuth or Proton Pump inhibitor). --60.240.34.106 (talk) 04:12, 6 November 2009 (UTC)

Comment left on mainpage

Cause? Where does the bacterium originate? Through food or water? contact with other people? —Preceding unsigned comment added by 109.77.90.232 (talk • contribs) 13:17, 7 September 2010 - NB I moved this question over from the article and will direct 109.77.90.232 to this page Jebus989^★ 14:19, 7 September 2010 (UTC)

The Postman always knocks twice

Notes for the editor: Travelled around the world aged 24 - OK it was 1989. In India, contracted disentary, got it so bad that I lost 30lbs in six weeks, received emergency treatment including pottassium jab, ECG, and Xrays on the chest. Now it could be that I contracted H. Pylori before I left, as it was two Australian medics that discovered the connection some 30 years ago. Anyway symptoms ( and I do hope I can alert possible victims): Aged 25 commence work back in the City and take up rugby - very quickly I experience stomach bloating, a nervous disorder( playing rugby at weekends is a respite if I have a large Brandy before playing to ease stomach swelling and copius amounts of alchol thereafter), and gasping breath as the diaphram lifts rapidly into the chest. Swimming two miles a day is a little help (less gravity), but sprinting and high energy sports leaves you feeling like you have a terminal illness.

1998: still suffering, weighing 20lbs heavier, I seek help from gastro specialists ( bearing in mind I am mentally weak and fed up seeing several GP's) - diagonesd with gastro paraesis. I finally see a GP who sends me to a cancer hereditry specialist ( Mr Meliah based at Darenth Valley Hospital, Kent, England), where I was found to have pollops, but nothing serious. I begged, and I do mean beg, to see Mr Meliah private, as I was not concerned about terminal cancer, but what was in my stomach. He agreed, I had a stomach exploration, but I was also tested for H.Pylori. To my relief, it come back positive, how long had I had, I just don't know. I had the triple treatment, and was not allowed any alchol for six months, the treatment was enough to affect my liver count. I cannot express enough, how much it effected my daily life - commuting and twitching, walking many a mile after just a small lunch, and holding the bottom of my bloated abdoem like an 8 month pregnant woman, hanging from the ceiling from a deep sleep, feeling I could not breathe, trouble swallowing any fluids whilst having an attack, and feeling very low when I was generally an outgoing person. I never had another symptom until..

2010, working as a corporate broker, from nowhere, I started to get the same symptoms - and it always seemed to start whilst under pressure in a corporate meeting. This was folowed by bouts of fits on public transport, and late night sleeping patterns. I will let you know the outcome, but I intend to seek medical advice and asked to be screened again for H.Pylori, once bitten twice shy!! I know what I am feeling amd what to look out for, I really feel for the innocent victim of a bacteria that lives between the stomach wall and the stomach lining - where, the immune system can't attack it, the stomach acids can't kill it, and standard atibiotics without liver kill cannot contain it. Triple or quadruple treatment - have it done, the alternative is one flew over the cuckoo nest (a must watch film with Jack Nicholson). —Preceding unsigned comment added by 82.34.232.122 (talk) 21:15, 21 December 2010 (UTC)

Signs and symptoms

This page needs a section on signs and symptoms. Doc James (talk · contribs · email) 11:06, 8 February 2011 (UTC)

I completely agree. To make the article accessible to a normal person, it would be helpful to have a list of symptoms, rather than to have most people try to read a long article of medical language. I'll start adding some information from the rest of the article, although many of the symptoms associated with H. Pylori are vague and non-specific to this disease, so I'll add a warning to this effect.SuW (talk) 15:36, 16 February 2011 (UTC)

External/Internal references

Is there a reason why there is no "See also" and a blank "External links" section?

I propose adding a few serious external links, for example to the Helicobacter Foundation, as well as a summary of the other useful related pages in a "See also" section.

I understand that a user may just Google this subject, and that links like require maintenance. Adding External links does give some credibility, though. There are at least 3 sponsored links at the top of a current Google search, which are probably commercial, not unbiased information.SuW (talk) 18:11, 16 February 2011 (UTC)

Done SuW (talk) 15:42, 2 March 2011 (UTC)

I've added another, having had a look at the Helicobacter Foundation several of the pages are dated 2006 so some info there may be a bit dated. (possible Conflict of Interest - I work in testing for H pylori) GraemeLeggett (talk) 16:52, 2 March 2011 (UTC)

Parkinson's

I see two new mentions of the putative link to Parkinson's disease; would a short section commenting on the early correlative work and in-vivo experiments be appropriate at this stage? --Synaptophysin (talk) 19:26, 25 May 2011 (UTC)

No definitive link, animal study and not reviewed yet, so fails MEDRS. Any mention would fail UNDUE at this point as well, so have removed it. Yobol (talk) 19:30, 25 May 2011 (UTC)

And we don't predict the future. So if we put down every possible hypothesis for every medical condition, we'd have a bloated encyclopedia, filled with information that is out of date in a short period of time. We need to wait for solid clinical evidence. OrangeMarlin ^{Talk• Contributions} 19:32, 25 May 2011 (UTC)

Sounds good to me. Was asking because the page mentioned it, but with the mention removed there is no need to explain the correlative and animal research. --Synaptophysin (talk) 12:15, 26 May 2011 (UTC)

Etymology and the lead

When the article discusses microbiology, pathophysiology, diagnosis, treatment etc. it seems a bit mad to have the lead almost completely taken up with etymology. I suggest moving all that to a new "Etymology" section or the existing "History" section, and (if anybody feels up to it) writing a proper lead section. Scolaire (talk) 12:54, 31 August 2011 (UTC)

Looking at the Revision history I discovered that the etymology was in the History section at the time this article got FA. Well, it's back home now. Scolaire (talk) 12:22, 1 September 2011 (UTC)

What is it?

The History section tells us that "Helicobacter pylori was first discovered in the stomachs of patients with gastritis and stomach ulcers in 1982", and that "Marshall and Warren rewrote the textbooks with reference to what causes gastritis and gastric ulcers". The first sentence of Timeline of peptic ulcer disease and Helicobacter pylori is, "This is a timeline of the events relating to the discovery that peptic ulcer disease is caused by H. pylori." Now, I'm not a microbiologist or a clinician, so my question is, is this what h. pylori is or not? If it is, why is it watered down so much in the intro, with "strongly linked to the development of.." hedged around so much with talk of Gram-negative, microaerophilic, 80% asymptomatic etc. that it's barely visible. The whole article, but especially the intro, has the effect of making stomach ulcer sound like the elephant in the room instead of the main reason this article exists at all. Scolaire (talk) 12:23, 3 September 2011 (UTC)

I've always understood that if you have a peptic ulcer and h pylori then eliminating the latter improves the former. As to whether H pylori actually causes peptic ulcers seems uncertain which may explain the cautious tone and given there are asymptomatic people that give positive tests for H pylori that seems sensible. That said the intro seems clear enough - H pylori is a certain type of bacteria, its found in a certain place, it does a certain thing. Compare to "the Giant panda is a large mammal. It is found in China. It eats shoots and leaves.GraemeLeggett (talk) 13:33, 3 September 2011 (UTC)

But compare it with the 2005 Featured Article version: "Helicobacter pylori is a bacterium that infects the mucus lining of the human stomach. Many peptic ulcers and some types of gastritis are caused by H. pylori infection, although most humans who are infected will never develop symptoms." Your eyes don't glaze over before you get to the end of the sentence. If you have been involved in editing this article the current intro might well seem clear enough to you, but to me, a newcomer, quite honestly it's as clear as mud. There's nothing wrong with having a cautious tone after saying what it is. It's only when caution gets in the way of information that I have a problem with it. Scolaire (talk) 13:49, 3 September 2011 (UTC)

Signs and symptoms again

The "Signs and symptoms" section is all wrong. Diseases have signs and symptoms, organisms do not. If the section is to be retained, it needs to say something like "The chronic gastritis associated with H. pylori demonstrates symptoms such as x, y and z. Signs and symptoms suggestive of peptic ulcers or stomach cancer can also be associated with H. pylori infection." It also needs to be supported by reliable sources to avoid charming edits like this one. Failing that, I propose that the section just be removed again. Scolaire (talk) 18:17, 5 September 2011 (UTC)

having looked, I agree it could do with being removed. Much of the content is under pathophysiology already, though the latter is terminology heavy and therefor not as readable. GraemeLeggett (talk) 22:03, 5 September 2011 (UTC)

As you say, the Pathophysiology section is pretty heavy. I think having a readable, sourced Symptoms section is probably better after all. Scolaire (talk) 08:06, 6 September 2011 (UTC)

If the patho section was rewritten to make it clearer what symptoms are caused and by which mechanism, the overall symptoms would be mentioned in the lede as a summary. GraemeLeggett (talk) 10:54, 6 September 2011 (UTC)

I agree, that would be the ideal. Scolaire (talk) 11:01, 6 September 2011 (UTC)

Urea is really present in gastric juices?

The article states that H. pylori uses urea present in gastric juices. This struck me as very odd for I've never heard anything like this in all my biology classes, high-school or college. I have always learned that urea is merely a by-product of aminoacid or ammonia metabolism that is excreted in urine without any uses in the body. The article about gastric juices here in Wikipedia does not mention urea at all. I researched some websites and some claim there is really urea in the stomach, but many don't. Couldn't the urea be produced by the H. pylori's own metabolism? 200.145.73.222 (talk) 11:35, 19 October 2011 (UTC)

Helicobacter heilmannii?

Could someone please create a page for Helicobacter heilmannii (formely known as Gastrospirillum hominis)? It is a human pathogen causing gastritis very similar to H. pylori. 207.179.172.216 (talk) —Preceding undated comment added 20:26, 1 November 2011 (UTC).

Organization

I support that we keep this article organized similar to other articles on infectious diseases and per WP:MEDMOS Doc James (talk · contribs · email) 11:27, 27 December 2011 (UTC)

Also we typically summarize sources rather than quoting large bits of text.Doc James (talk · contribs · email) 09:30, 29 December 2011 (UTC)

Well, there's no standardised organisation of pathogenic organisms (compare trichomonas vaginalis and giardia), but I won't push to make a change in the section organization. What I don't understand, though, is why you reverted my edit including the quote? It's perfectly in line with Wikipedia:Quotations, it's reliably sourced ... and looking at the treatment/screening guidelines (e.g., only test for H.p. and only treat it if there's PUD etc. present) this article IMO needs to emphasize it a little more that colonalization per se is not a problem. Cheers, Mallexikon (talk) 10:58, 29 December 2011 (UTC)

Sure, so this is the quote in question. It was placed in the section on "signs and symptoms" but it does not mention anything regarding the signs and symptoms or lack thereof of the infection at hand. Also is the issue of WP:DUE. Why promote this single quote or these authors and this journal?

Colonization with H. pylori is not a disease in itself but a condition that affects the relative risk of developing various clinical disorders of the upper gastrointestinal tract ... Testing for H. pylori therefore has no relevance by itself but should be performed to find the cause of an underlying condition, such as peptic ulcer disease, or for the purpose of disease prevention, such as in subjects with familial gastric cancer.

— J. G. Kusters, A. H. M. van Vliet, and E. J. Kuipers −, "Pathogenesis of Helicobacter pylori Infection". Clin Microbiol Rev 19 (3): 449–90

--Doc James (talk · contribs · email) 11:07, 29 December 2011 (UTC)

WP:DUE? That deals with fringe theories. This quote we're talking about comes from a source which is already used twice in the article, it's derived from a respected journal, it's about "Pathogenesis of Helicobacter pylori Infection", and the view it expresses here is reflected in the current treatment guidelines. I can't see a conflict with WP:DUE. You have a point, though, about which section to place the quote in. Do you think "Prevention" is a more adequate location? Especially since it starts "H. pylori is a major cause of diseases of the upper gastrointestinal tract. Eradication of the infection improves symptoms including dyspepsia, gastritis and peptic ulcers, and may prevent gastric cancer..." (now if I read that it I get the impression we should all have empiric eradication therapy rather sooner than later). Mallexikon (talk) 03:39, 30 December 2011 (UTC)

This reference is already used in signs and symptoms when we state "Individuals infected with H. pylori have a 10 to 20% lifetime risk of developing peptic ulcers and a 1 to 2% risk of acquiring stomach cancer." We already state "Diagnosis of infection is usually made by checking for dyspeptic symptoms and by tests which can indicate H. pylori infection." which is similar to "Testing for H. pylori therefore has no relevance by itself but should be performed to find the cause of an underlying condition," but could be improved upon with this ref. This quote by itself does not fit anywhere but parts of the ideas within fit is a couple of spots.Doc James (talk · contribs · email) 11:29, 30 December 2011 (UTC)

... alright, I take that as a yes and will add the quote to the "Prevention" section. Cheers, Mallexikon (talk) 03:13, 31 December 2011 (UTC)

Hmm. Changed my mind. "Diagnosis" section seems to be more appropriate. Mallexikon (talk) 03:59, 31 December 2011 (UTC)

Have paraphrased. Much of it was stated already.Doc James (talk · contribs · email) 04:11, 1 January 2012 (UTC)

Sure. Thanks, Mallexikon (talk) 03:12, 2 January 2012 (UTC)

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Dyspepsia

I notice this edit by Mallexikon removed stuff about an association between Helicobacter pylori and Dyspepsia because it was only based on one source and other sources say other things.

I notice that the article on Dyspepsia says something similar. However, it also mentions the controversy, and a Cochrane review of the association, which found that it was there. Is that acceptable? Should it be mentioned in one article, or both, or none?

Yaris678 (talk) 16:11, 17 May 2012 (UTC)

Helicobacter and cancer

I propose to move this section to cancer bacteria, and expand it there, leaving behind a very short link. Thoughts? --Una Smith 17:00, 7 July 2007 (UTC)

No, cancer bacteria tries to generalise, while the strongest link between bacteria and cancer is in Helicobacter. I would prefer this content to remain here with necessarily some duplication on your new page. JFW | T@lk 21:57, 9 August 2007 (UTC)

MALT lymphoma

I felt like writing up MALT lymphoma. Comments there please :-) JFW | T@lk 09:18, 12 December 2005 (UTC)

Role in gastric cancer

According to doi:10.1111/j.1572-0241.2006.01109.x, Helicobacter is necessary for carcinogenesis of gastric cancer & lymphoma. They suggest long-term follow up for previous H pylori carriers. JFW | T@lk 14:31, 1 April 2007 (UTC)

Perhaps necessary, but not sufficient: only 1.4% of their patients infected with H pylori went on to develop one of these cancers. Very interesting, though. --Una Smith 17:00, 7 July 2007 (UTC)

Role in adenocarcinoma of the esophagus

Some attention should be brought to recent research that shows that absence of H. pylori increases the instance of adenocarcinoma of the esophagus. Journal of Infectious Diseases article on H pylori and asthma Its absence tying to the increasing instances of asthma and obesity are also important, but outside the scope of this cancer related discussion. 72.136.221.118 (talk) 12:25, 21 September 2008 (UTC)

Carcinogen / Cancer causing

Why put it in the carcinogen category, if no mention of it is made in the article? It's right, btw: it's on the WHO list of carcinogens 129.180.1.214 (talk) 07:39, 30 October 2012 (UTC)

Resistance

... depends on how heavily people use antibiotics doi:10.1136/gutjnl-2012-302254 JFW | T@lk 21:30, 11 December 2012 (UTC)

"In popular culture"

I notice this edit added the phrase "In popular culture" to "a number of foods may be useful to prevent colonization with H. pylori including: green tea, red wine..."

The phrase "In popular culture" implies that there is no scientific evidence.

How reliable do we think The Journal of Digestive Diseases is? It's published by the Chinese Society of Gastroenterology.

If we can rely on the source then we don't need "in popular culture". If we can't rely on the source then should the info even be there?

Yaris678 (talk) 20:42, 9 December 2012 (UTC)

I agree, this is not reputable reference or a useful contribution of the standard we expect. I shall remove it. SuW (talk) 19:16, 28 January 2013 (UTC)

Benefits of eradication

doi:10.1053/j.gastro.2015.01.040, from Gastroenterology JFW | T@lk 10:55, 26 March 2015 (UTC)

Prognosis

The third paragraph of prognosis, talking about Martin Blaser's work, is only about a single person's theories, therefore by WP:UNDUE, this paragraph should be shrunk, perhaps to a single sentence Hughperkins (talk) 15:54, 1 February 2013 (UTC)

I flagged the section 'Prognosis' for 'The Neutrality of This Section is Disputed'. This section suggests "mounting evidence" supports the view that H. Pyloris infection reduces the risks of various illnesses including cancer, and essentially might be a good thing. It appears this is misleading in that the view as to disease preventing characteristics of H. Pylori is a minority dissenting view in the medical profession proposed by a very small minority of researchers in the field. I think investigation of the footnotes supporting the dissenting view will show it is a very small closed group supporting the minority position. Dissenting views that are held by very few expert people should be identified as such rather than proposed to represent "mounting evidence". In particular unsubstantiated suggestions that infection is protective against cancer are of concern to me. My changes to alert this have been deleted, I'm not sure if my flag can be too, if it can be I suppose it will be. The full text of the paragraph I dispute the neutrality is as follows:

Mounting evidence suggests H. pylori has an important role in protection from some diseases. The incidence of acid reflux disease, Barrett's esophagus, and esophageal cancer have been rising dramatically at the same time as H. pylori's presence decreases.[78] In 1996, Martin J. Blaser advanced the hypothesis that H. pylori has a beneficial effect: by regulating the acidity of the stomach contents.[39][78] The hypothesis is not universally accepted as several randomized controlled trials failed to demonstrate worsening of acid reflux disease symptoms following eradication of H. pylori.[79][80] Nevertheless, Blaser has reasserted his view that H. pylori is a member of the normal flora of the stomach.[81] He postulates that the changes in gastric physiology caused by the loss of H. pylori account for the recent increase in incidence of several diseases, including type 2 diabetes, obesity, and asthma.[81][82] His group has recently shown that H. pylori colonization is associated with a lower incidence of childhood asthma.[83] — Preceding unsigned comment added by 121.54.54.223 (talk) 01:35, 5 June 2015 (UTC)

Consensus

Toronto consensus: doi:10.1053/j.gastro.2016.04.006 JFW | T@lk 13:57, 29 June 2016 (UTC)

Adding Small RNA paragraph

I am working on adding new non-coding RNAs to the Rfam database. I would like to update this article with information about new cag-pathogenicity island encoded ncRNA, under section Genes involved in virulence.... like this:

Small RNA

Small regulatory RNAs  are involved in many cellular processes. In H. pylori a cis-encoded 5'ureB sRNA regulates ureAB urease expression levels, and RepG sRNA is involved in the regulation of the TlpB chemotaxis receptor. The first sRNA encoded by the virulence-associated cag pathogenicity island (cag-PAI) called CncR1 (cag- non-coding RNA1) is an abundant and conserved sRNA which does not target  cag-PAI genes, but down-regulates bacterial motility and have positive role on the adhesion to host cells. 

— Preceding unsigned comment added by Joanna Argasinska (talk • contribs) 10:55, 10 August 2016 (UTC)

References

Genome

Is there more information regarding the "make-up" of the genome of this pathogen? — Preceding unsigned comment added by AmberRenea (talk • contribs) 18:48, 23 January 2017 (UTC)

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Recent edits / errors

I am hesitant to change anything in this article, because it's not my area, and recent edits have gone back and forth so much that maybe a reversion to a much older version is in order? I just wanted to point out that now the article contains a paragraph starting with "This pain typically occurs," this being the first mention of said pain. Paragraph could also use a period at the end. Jessicapierce (talk) 18:55, 9 October 2017 (UTC)

Above it says "Acute infection may appear as an acute gastritis with abdominal pain (stomach ache) or nausea." So not sure what you mean by first mention? Doc James (talk · contribs · email) 01:16, 10 October 2017 (UTC)

Oh, I see what you mean. There's that whole big paragraph in between the two mentions of "pain" (the first of which I somehow missed), and what with all the back and forth additions and removals of text, I thought some context had been removed. Thanks for the quick reply! Jessicapierce (talk) 01:58, 10 October 2017 (UTC)

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Criticism ?

Very long article with lots of information, but I was unable to find any criticism section or article. I know that there are different views among scientists and the relation between helicobacter and some of diseases is questioned. 93.185.28.234 (talk) 13:32, 16 December 2017 (UTC)

Can you point to any sources of criticism? Ruslik_Zero 20:34, 16 December 2017 (UTC)

North America

Wikipedia considers North America to be composed of Mexico, the US and Canada. This is also the concept that sustains areas such as the NAFTA. Therefore, the Epidemiology section should be consistent with that. Best, Jgsodre (talk) 16:26, 9 September 2018 (UTC)

Add material on frequency and source of H. pylori-induced gastric cancers

I would like to add the following material on the frequency and source of H. pylori-induced cancers. Is there any problem with this material?

Although the data varies between different countries, overall about 1% to 3% of people infected with Helicobacter pylori develop gastric cancer in their lifetime compared to 0.13% of individuals who have no H. pylori infection. Due to the prevalence of infection by H. pylori in middle-aged adults (74% in developing countries and 58% in developed countries), and 1% to 3% likelihood of infected individuals developing gastric cancer, H. pylori-induced gastric cancer is the third highest cause of worldwide cancer mortality as of 2018.

H. pylori-induced carcinogenic mutations and protein expression alterations are very often a result of initial H. pylori-induced epigenetic alterations. These epigenetic alterations include H. pylori-induced methylation of CpG sites in promoters of genes and H. pylori-induced altered expression of multiple microRNAs.

As reviewed by Santos and Ribeiro H. pylori infection is associated with reduced efficiency of the DNA repair machinery, which favors the accumulation of mutations and genomic instability as well as gastric carcinogenesis. In particular, after H. pylori infection, the DNA repair genes MLH1, PMS2 and MGMT are down-regulated due to an increase in epigenetic CpG methylation of their promoter regions. In further work, two DNA repair genes, ERCC1 and PMS2, were found to have severely epigenetically reduced protein expression once H. pylori infection had progressed to cause dyspepsia (which occurs in 20% of infected individuals). ERCC1 and PMS2 DNA repair proteins were virtually absent in tissue of gastric cancer cells. Bernstein0275 (talk) 23:32, 18 March 2020 (UTC)

References

The above linked site offers a wealth of information that could really help to solidify this article and make it more accurate and reliable. It is to available text of the journal Helicobacter pylori and has potentially better information than the 1994 NIH study. Specifically one of the articles has actual risk factor statistics for the increase in gastric cancer due to H. pylori. I am unfortunately not in the position to understand the details of the subject, so hopefully someone that is can make use of the articles from the above link to improve the article and its citation. - Taxman 23:43, Dec 22, 2004 (UTC)

As a side note, does anyone know about the prestige of the Helicobacter pylori journal or its peer review practices? - Taxman 23:43, Dec 22, 2004 (UTC)

I will do a Pubmed search and filter some useful references. The original discovery of the bug in the early 1980s will need to be refenced. As for the H. Pylori journal, this is a typical niche journal. The really relevant studies will have been published in the big core journals like The Lancet, NEJM, JAMA or the BMJ, or the core specialist journals (Am J Gastroenterol & Gut). JFW | T@lk 08:26, 23 Dec 2004 (UTC)

Go to GUT for that Journal GraemeLeggett 11:02, 18 Feb 2005 (UTC)

Organisms in the stomach

I have changed the text to show that Heicobacter thrives in the stomach rather than survives. Many organisism suvive a transit of the stomach including many bacteria and protozoan spores, Cryptospoidium, Giardia etc, many viruses, some parasitic platyhelminths, flukes, tape-worms, prions etc. I am also concerned about the authority for the statement that it "....can literally screw itself into the stomach lining." This implies some form of active burrowing activity which is not a characteristic of other helical bacteria. Is this referenced authoritatively somewhere ? It is probably also incorrect to refer to 'poor' people at being at highest risk. The epidemiology shows that affluent young Caucasions in the English speaking world are least at risk , but that doesn't equate to rich and poor. It is more a reflection of local customs and habits with the low incidence group adopting life-styles based on high standards of cleanliness and hygiene. Other life-styles may provide different but equally worth-while benefits not enjoyed by young white Americans.
Velela 13:27, 2 Mar 2005 (UTC)

Hp is a very active bacteria, those flagella do thrust it along. The stomach lining is question is the mucus layer rather than the flesh. GraemeLeggett 13:32, 2 Mar 2005 (UTC)

Weird ungrammaticality in "Infection and Diagnosis"

In er March 2nd edit, Velela deleted part of the sentence "Under poor sanitary conditions...", so that it is now ungrammatical; this change persisted subsequent edits. I about to edit it back, so that it is grammatical. I claim no knowledge of the subject material, and so hope that someone who is expert will audit this semi-reversion (semi- because this was not Velela's entire edit). --jholman 06:09, 26 Mar 2005 (UTC)

Microaerophilic

Does this term derive from aerophilism- an organism that can live in an enviroment that has extremly limited oxygen content? What is the format for adding in a term like this that doesn't quite deserve a full entry? Aerophilism doesn't exist in the Extremophile article, so one might add a new stub defining that. But what about microaerophilism- how could you make a stub of a stub? Would formating the article so that microaerophilic only has 'areophilic' linked?

I suggest a link through to aerobic organism GraemeLeggett 14:15, 28 Mar 2005 (UTC)

Microaerophilic is an accepted term in microbiology. The organism can *only* live in environments in which oxygen is limited (less than atmospheric), but present. Neither atmospheric nor anaerobic conditions are accepatable.

Incorrect statistic deleted

"The infection is also associated with the development of certain cancers occurring in less than 20% of cases." To avoid alarming people, I removed "occurring in less than 20% of cases". I think it might be a typo. The source cited makes no mention of such a statistic. Seems that cancer occurs in 1-3% of cases. Starlists (talk) 01:56, 16 January 2022 (UTC)

Helicobacter pylori

Is this cancer 2A00:23C4:801:1101:3C81:FFA0:6313:772F (talk) 10:42, 25 November 2022 (UTC)