Abstract

AimAlthough proton pump inhibitors (PPIs) can prevent aspirin-induced upper gastrointestinal bleeding, a clinical dilemma exists as long-term use of PPI may also increase the risk of gastric cancer even after Helicobacter pylori (HP) eradication. We aimed to investigate the potential interaction between aspirin and PPIs on GC risk in patients who have HP eradicated.ResultsOf the 63,397 HP eradicated subjects (median follow-up 7.6 years), 153 (0.24%) developed GC. PPIs were associated with a higher GC risk among non-aspirin users (aHR: 3.73, 95% CI:2.11–6.60) but not among aspirin users (aHR: 0.35, 95% CI:0.04–2.74).Materials and MethodsThis is a post-hoc analysis based on a previously published territory-wide retrospective cohort study on the potential risk of PPIs on GC. Adults who had received an outpatient prescription of clarithromycin-based triple therapy for HP between 2003 and 2013 were identified. The adjusted hazard ratio (aHR) of GC with PPIs, stratified according to aspirin use, was calculated by Cox model with propensity score adjustment of other covariates.ConclusionsThe potential harmful effects of PPIs on GC development appear to be limited to non-aspirin users. Co-prescription of PPIs is therefore recommended for HP-eradicated patients who are at risk of aspirin-induced UGIB.

Highlights

  • Gastric cancer is the fifth commonest cancer and the third leading cause of cancer-related death [1]

  • The potential harmful effects of pump inhibitors (PPIs) on GC development appear to be limited to non-aspirin users

  • Co-prescription of PPIs is recommended for Helicobacter pylori (HP)-eradicated patients who are at risk of aspirin-induced upper gastrointestinal bleeding (UGIB)

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Summary

Introduction

Gastric cancer is the fifth commonest cancer and the third leading cause of cancer-related death [1]. Conclusions: The potential harmful effects of PPIs on GC development appear to be limited to non-aspirin users. Co-prescription of PPIs is recommended for HP-eradicated patients who are at risk of aspirin-induced UGIB.

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