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Editorial: the never‐ending story—Helicobacter pylori and peptic ulcer disease

Peptic ulcer is the most important cause of nonvariceal upper gastrointestinal bleeding (NVUGIB). Helicobacter pylori infection and medications including nonsteroidal antiinflammatory drugs (NSAIDs) and antithrombotic drugs are the two major culprits.1 Patients with H. pylori infection who take such medications have a further increased risk of bleeding.2 To prevent bleeding from H. pyloripositive peptic ulcers, eradication of H. pylori is the primary strategy. Coadministration of an acidsuppressing drug— notably a proton pump inhibitor— is the mainstay for reducing gastroduodenal injury from mucosal damaging medications. Eradication therapy has reduced peptic ulcer disease and bleeding.3 However, realworld data have not confirmed that eradication of H. pylori significantly reduces the incidence of ulcer bleeding.4 Guo et al analysed a large medical database in Hong Kong and found that, among middleaged to elderly patients, a longterm increased risk of NVUGIB persisted after H. pylori eradication (HR 1.7; 95% CI 1.531.89).5 A shortcoming of their study was that eradication success was not routinely confirmed. However, they did demonstrate an eradication success rate of around 85% in small samples extracted from the cohort.5 As is inherent to retrospective, aetiological studies, residual confounding factors such as the use of NSAIDs still posed a concern, even although they performed an extensive propensity matching for prescribed medications. Aside from them, what might be the other causes of increased risk of NVUGIB after eradication of H. pylori? Aggravation of preexisting oesophagitis may be a possibility; acid hypersecretion after eradication therapy has been reported in Asian countries.6 However, this seems unlikely since the increased risk of bleeding occurred 2 years after eradication therapy,5 and acid hypersecretion subsides within 6 months.6 MalloryWeiss tears, Cameron erosions, Dieulafoy lesions and gastric antral vascular ectasia are all possible causes of bleeding, but detailed analyses on their possible contribution were not provided in this study. It is noteworthy that a separate group of investigators has reported that idiopathic ulcers (i.e., those not due to H. pylori infection or NSAID use) were increasing in Hong Kong.7 Alarming features among patients with idiopathic ulcers include high rates of recurrence, increased risk of complications, and high mortality due to serious comorbidity. Indeed, patients with serious comorbidity were higher in the eradication cohort in this study,5 a feature shared with those with idiopathic ulcers. Thus, H. pylori eradication might simply have uncovered such idiopathic ulcers in some patients. However, recent molecular methods have consistently identified the presence of H. pylori and other gastric bacteria in subjects considered to be H. pylorinegative by multiple conventional diagnostic methods.810 Therefore, we need to redefine stringent criteria for eradication success and the categorisation of idiopathic ulcer for evaluating the risk of ulcer bleeding after eradication, wherein the roles of other gastric bacteria might also be addressed. Until then, the tale of H. pylori and peptic ulcer will continue.