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Some studies suggest increased susceptibilities to H. pylori infection in certain populations based on genetics and ethnicity; however, food sharing and housing habits may also have a role22,23,24. For example, in the Sumatra islands of Indonesia, the prevalence of H. pylori infection is very low in the Malay and Java populations, but is high in Batak populations, indicating that genetic factors may contribute to differential host susceptibility25. Gene and genome-wide association studies have identified that polymorphisms in IL-1B, Toll-like receptor 1 (TLR1) locus and the FCGR2A locus are associated with H. pylori seroprevalenceT polymorphism is associated with increased host susceptibility to Helicobacter pylori infection in Chinese. Helicobacter 12, 142–149 (2007)." href="/articles/s41572-023-00431-8#ref-CR26" id="ref-link-section-d933555e1154"26,27. However, a 2022 study has cast doubt on a role of the TLR1/6/10 locus in H. pylori seroprevalence28, and further studies are needed29./p>11% of individuals with the infection develop PUD compared with 1% of individuals without the infection45. In a prospective study, the lifetime risk of developing duodenal ulcer and gastric ulcer was respectively increased by 18.4-fold and 2.9-fold in individuals with infection with cagA-positive H. pylori strains46./p>

15% or unknown resistance rates42. Molecular genotypic testing enables the detection of resistance against frequently used antibiotics. Clarithromycin resistance conferred by mutations in the gene encoding 23S rRNA are predominantly related to A2143G, A2142G and A2142C193. Levofloxacin resistance is conferred by point mutations in the gyrase gene gyrA194,195. The accuracy of the molecular detection methods for predicting antibiotic resistance varies between antibiotics, favouring clarithromycin and quinolone resistance detection194,196. Formalin-embedded biopsy samples enable genotypical resistance testing at a later time point after endoscopy197,198,199,200./p>45 years or in the presence of alarm symptoms, endoscopy-based diagnosis is recommended to exclude mucosal changes207,208. H. pylori-associated dyspepsia is an independent entity that resembles but is distinct from functional dyspepsia1,208. A test-and-treat strategy is the most cost-effective approach in patients with H. pylori infection and dyspepsia if H. pylori prevalence in the population is >5%. This strategy is superior to alternative therapies including PPIs70,209,210, and the therapeutic gain of H. pylori eradication for symptom relief compared with other therapeutic options is substantial. A randomized, double-blind, placebo-controlled trial for primary prevention of peptic ulcer bleeding in older patients who were prescribed aspirin in primary care lends support to an H. pylori test-and-treat strategy in patients starting aspirin treatment. Gastrointestinal bleeding episodes within a 2-year period were reduced by 65% in the H. pylori eradication group211./p>

50 years or at any age in the presence of alarm symptoms. A patient with symptoms related to ulcerogenic drug (NSAIDs) use should also be considered for endoscopy70,392. Endoscopy-based investigations are the most reassuring and should be considered in patients with anxiety393./p>

45 years of age or earlier according to the age at which gastric cancer was diagnosed in the index patient394./p>

90%248,249 and, between 1997 and 2005, became the most widely recommended first-line therapy globally42,206,247,250. Treatment duration has since been recommended to be extended to 14 days owing to a substantially higher efficacy compared to the 7-day duration42,244,247. Antibiotics used in first-line PPI-TT are clarithromycin, amoxicillin and metronidazole or, more restrictive, levofloxacin and, in selected cases, furazolidone. Treatment failures with PPI-TT occur with increasing frequency and are primarily related to antibiotic resistance, insufficient acid suppression and inadequate adherence to medications10,251,252,253. Acid suppression with PPI (omeprazole, esomeprazole, lansoprazole, pantoprazole or rabeprazole in double standard dose) is essential and aims to raise intragastric pH to 6 or higher, which optimizes the stability, bioavailability and efficacy of antibiotics254,255. A modestly higher acid-inhibiting effect is shown for second-generation PPIs (esomeprazole, rabeprazole)256. Increased intragastric pH (optimum pH >6) enables bacterial replication, which increases the susceptibility of H. pylori to antibiotics. This is particularly important for amoxicillin, which is highly acid sensitive254,255. Less effective acid suppressants, such as histamine 2 receptor antagonists, are no longer considered in H. pylori eradication regimens246,257. PPI efficacy is further increased by doubling the PPI standard dose and should always be considered if first-line therapy fails258,259,260,261./p>15% and only used if individual AST or bismuth-based quadruple therapy (BiQT) are not locally available42,247,250. Levofloxacin as a component of PPI-TT is effective in first-line and second-line regimens in regions with low levofloxacin resistance284,285,286. However, levofloxacin resistance is now up to 20% in Europe and 18% in the Asia-Pacific region188,278,287. Although levofloxacin is not recommended as a first-line option, the high resistance restricts its use even in second-line regimens42,244,247. AST before using levofloxacin in empirical second-line regimens is advised189,244,278,287. Other quinolones, such as ciprofloxacin and moxifloxacin, which have reduced efficacy and/or less consistent results, are not an alternative to levofloxacin286,288. Sitafloxacin-based triple and dual regimens that have been successfully tested in Japan289 are not used as an alternative to levofloxacin in western countries42,244,247./p>25% in most areas of the world189,278 but has a minor effect on eradication efficacy when used in triple or quadruple regimens because of inconsistency between in vitro AST results and clinical efficacy and the synergism with co-administered drugs, in particular bismuth224,290,291. Resistance to amoxicillin and tetracycline is low (<2%) and these antibiotics remain a key component in standard PPI-TT and in BiQT, respectively, without the need for routine AST244,291. Rifabutin resistance is <1% and the H. pylori eradication rate of rifabutin-containing regimens is 73% according to a meta-analysis from 2020 (ref. 292). A rifabutin delayed-release preparation, combined with amoxicillin and omeprazole, obtained an eradication rate of 89%293 and FDA approval for use as a first-line therapy was granted in 2019 (ref. 294). Outside of the USA, rifabutin-containing regimens are recommended as rescue therapy only owing to the need of this drug for other critical infections and the risk of myelotoxicity in rare cases42,247. Furazolidone resistance is <5% and the drug is effective in triple and quadruple combinations; its use is limited to a few countries in Asia and South America195,295 and it may serve as rescue therapy in individual cases296./p>90% following previous treatment failures303,307,308./p>1% to 15% according to definitions applied, the population treated and type of therapy325. The non-recording of adverse effects as primary criteria in clinical trials accounts for the high variations. Darkening of the tongue and faeces is characteristic of bismuth salts326. Antibiotics affect gut microbiota and lead to mostly transient dysbiosis, bacterial resistance and overgrowth of opportunistic pathogens; however, rarely of Clostridioides difficile40,325,327./p>90% and continued acid inhibition with PPI is not required for uncomplicated duodenal ulcer42. Gastric ulcer requires prolonged acid inhibition for healing and endoscopic follow-up is needed to ensure complete ulcer healing and to exclude underlying gastric malignancy332. Management of bleeding peptic ulcers, both duodenal and gastric ulcers, requires immediate care by controlling and/or restoring cardiocirculatory and respiratory function and by performing emergency diagnostic endoscopic examination and endoscopic interventions according to standardized protocols333,334. PPI treatment is continued until complete healing is endoscopically documented44. H. pylori eradication should be initiated after the active bleeding phase is under control and oral nutrition can be resumed70,334. Patients with H. pylori infection exposed to ulcerogenic medications, in particular NSAIDs, are at an increased risk of complications56,335 and benefit from H. pylori testing and treatment42,70. Patients at high risk for rebleeding after H. pylori eradication, for example, those with continued NSAID use, require PPI maintenance therapy336./p>

T polymorphism is associated with increased host susceptibility to Helicobacter pylori infection in Chinese. Helicobacter 12, 142–149 (2007)./p>