Editing Helicobacter pylori (section)

==Prognosis==
''Helicobacter pylori'' colonizes the stomach for decades in most people, and induces chronic gastritis, a long-lasting inflammation of the stomach. In most 
cases symptoms are never experienced but about 10–20% of those infected will ultimately develop gastric and duodenal ulcers, and have a possible 1–2% lifetime risk of gastric cancer.<ref name="Debowski"/>

''H. pylori'' thrives in a high salt diet, which is seen as an environmental risk factor for its association with gastric cancer. A diet high in salt enhances colonization, increases inflammation, increases the expression of ''H. pylori'' virulence factors, and intensifies chronic gastritis.<ref name="Balendra">{{cite journal |vauthors=Balendra V, Amoroso C, Galassi B, Esposto J, Bareggi C, Luu J, Scaramella L, Ghidini M |title=High-Salt Diet Exacerbates H. pylori Infection and Increases Gastric Cancer Risks |journal=J Pers Med |volume=13 |issue=9 |date=August 2023 |page=1325 |pmid=37763093 |pmc=10533117 |doi=10.3390/jpm13091325 |doi-access=free }}</ref><ref name="Jaroenlapnopparat">{{cite journal |vauthors=Jaroenlapnopparat A, Bhatia K, Coban S |title=Inflammation and Gastric Cancer |journal=Diseases |volume=10 |issue=3 |date=June 2022 |page=35 |pmid=35892729 |pmc=9326573 |doi=10.3390/diseases10030035 |doi-access=free }}</ref> Paradoxically, extracts of [[kimchi]], a salted probiotic food, has been found to have a preventive effect on ''H. pylori''–associated gastric [[carcinogenesis]].<ref name="Park2021">{{cite journal |vauthors=Park JM, Han YM, Oh JY, Lee DY, Choi SH, Hahm KB |title=Transcriptome profiling implicated in beneficiary actions of kimchi extracts against Helicobacter pylori infection |journal=J Clin Biochem Nutr |volume=69 |issue=2 |pages=171–187 |date=September 2021 |pmid=34616109 |pmc=8482382 |doi=10.3164/jcbn.20-116 |url=}}</ref>

In the absence of treatment, ''H.&nbsp;pylori'' infection usually persists for life.<ref name="Brown">{{cite journal | vauthors = Brown LM | title = Helicobacter pylori: epidemiology and routes of transmission | journal = Epidemiologic Reviews | volume = 22 | issue = 2 | pages = 283–97 | year = 2000 | pmid = 11218379 | doi = 10.1093/oxfordjournals.epirev.a018040 | doi-access = free }}</ref> Infection may disappear in the elderly as the stomach's mucosa becomes increasingly atrophic and inhospitable to colonization. Some studies in young children up to two years of age have shown that infection can be transient in this age group.<ref name="Pacifico">{{cite journal |vauthors=Pacifico L, Osborn JF, Bonci E, Romaggioli S, Baldini R, Chiesa C |title=Probiotics for the treatment of Helicobacter pylori infection in children |journal=World J Gastroenterol |volume=20 |issue=3 |pages=673–83 |date=January 2014 |pmid=24574741 |pmc=3921477 |doi=10.3748/wjg.v20.i3.673 |doi-access=free |url=}}</ref><ref name=Goodman_2005>{{cite journal | vauthors = Goodman KJ, O'rourke K, Day RS, Wang C, Nurgalieva Z, Phillips CV, Aragaki C, Campos A, de la Rosa JM | title = Dynamics of Helicobacter pylori infection in a US-Mexico cohort during the first two years of life | journal = International Journal of Epidemiology | volume = 34 | issue = 6 | pages = 1348–55 | date = December 2005 | pmid = 16076858 | doi = 10.1093/ije/dyi152 | doi-access = free }}</ref>

It is possible for ''H.&nbsp;pylori'' to re-establish in a person after eradication. This recurrence can be caused by the original strain ([[recrudescence]]), or be caused by a different strain (reinfection). A 2017 meta-analysis showed that the global per-person annual rates of recurrence, reinfection, and recrudescence is 4.3%, 3.1%, and 2.2% respectively. It is unclear what the main risk factors are.<ref>{{cite journal |last1=Li |first1=R |last2=Zhang |first2=P |last3=Hu |first3=Z |last4=Yi |first4=Y |last5=Chen |first5=L |last6=Zhang |first6=H |title=Helicobacter pylori reinfection and its risk factors after initial eradication: A protocol for systematic review and meta-analysis. |journal=Medicine |date=14 May 2021 |volume=100 |issue=19 |pages=e25949 |doi=10.1097/MD.0000000000025949 |pmid=34106668 |pmc=8133036 |doi-access=free}}</ref>

Mounting evidence suggests ''H.&nbsp;pylori'' has an important role in protection from some diseases.<ref name="WJG2020"/> The incidence of [[gastroesophageal reflux disease|acid reflux disease]], [[Barrett's esophagus]], and [[esophageal cancer]] have been rising dramatically at the same time as ''H.&nbsp;pylori''{{'}}s presence decreases.<ref name = Blaser_2005 /> In 1996, [[Martin J. Blaser]] advanced the hypothesis that ''H.&nbsp;pylori'' has a beneficial effect by regulating the acidity of the stomach contents.<ref name="pmid14755326"/><ref name = Blaser_2005/> The hypothesis is not universally accepted, as several [[randomized controlled trials]] failed to demonstrate worsening of acid reflux disease symptoms following eradication of ''H.&nbsp;pylori''.<ref name="Graham 2007">{{cite journal | vauthors = Graham DY, Yamaoka Y, Malaty HM | title = Contemplating the future without Helicobacter pylori and the dire consequences hypothesis | journal = Helicobacter | volume = 12 | issue = Suppl 2 | pages = 64–8 | date = November 2007 | pmid = 17991179 | pmc = 3128250 | doi = 10.1111/j.1523-5378.2007.00566.x }}</ref><ref name="Delaney 2005">{{cite journal | vauthors = Delaney B, McColl K | title = Review article: Helicobacter pylori and gastro-oesophageal reflux disease | journal = Alimentary Pharmacology & Therapeutics | volume = 22 | issue = Suppl 1 | pages = 32–40 | date = August 2005 | pmid = 16042657 | doi = 10.1111/j.1365-2036.2005.02607.x | s2cid = 34921548 | type = Review }}</ref> Nevertheless, Blaser has reasserted his view that ''H.&nbsp;pylori'' is a member of the normal [[gastric microbiota]].<ref name="Blaser 2006">{{cite journal | vauthors = Blaser MJ | title = Who are we? Indigenous microbes and the ecology of human diseases | journal = EMBO Reports | volume = 7 | issue = 10 | pages = 956–60 | date = October 2006 | pmid = 17016449 | pmc = 1618379 | doi = 10.1038/sj.embor.7400812 }}</ref> He postulates that the changes in gastric physiology caused by the loss of ''H.&nbsp;pylori'' account for the recent increase in incidence of several diseases, including [[type 2 diabetes]], [[obesity]], and asthma.<ref name="Blaser 2006"/><ref name="Blaser 2008">{{cite journal | vauthors = Blaser MJ, Chen Y, Reibman J | title = Does Helicobacter pylori protect against asthma and allergy? | journal = Gut | volume = 57 | issue = 5 | pages = 561–7 | date = May 2008 | pmid = 18194986 | pmc = 3888205 | doi = 10.1136/gut.2007.133462 }}</ref> His group has recently shown that ''H.&nbsp;pylori'' colonization is associated with a lower [[incidence (epidemiology)|incidence]] of childhood asthma.<ref>{{cite journal | vauthors = Chen Y, Blaser MJ | title = Helicobacter pylori colonization is inversely associated with childhood asthma | journal = The Journal of Infectious Diseases | volume = 198 | issue = 4 | pages = 553–60 | date = August 2008 | pmid = 18598192 | pmc = 3902975 | doi = 10.1086/590158 }}</ref>