Related Experiment Video
Updated: Aug 11, 2026
Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance
Published on: March 7, 2025
Meta-Analysis: Prevalence of Non-Helicobacter pylori, Non-NSAID Peptic Ulcer Disease
Jun Watanabe1,2,3, Hiromi Sekiguchi4, Takeshi Kanno5,6
1Department of Surgery, Division of Gastroenterological, General and Transplant Surgery, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Background:
Non-Helicobacter pylori (H. pylori), non-nonsteroidal anti-inflammatory drug (NSAID) peptic ulcer disease (PUD) is increasingly recognized as a distinct subgroup, but its proportion across clinical presentations remains unclear.
Aim:
We aimed to estimate this proportion.
Methods:
We searched MEDLINE, Embase and CENTRAL from their inception to March 2026 for observational studies. The primary outcome was the proportion of non-H. pylori, non-NSAID PUD among adults with overall, bleeding and perforated PUD. Random-effects meta-analysis of logit-transformed proportions was performed using restricted maximum likelihood. Meta-regression assessed associations with study year, country-level H. pylori prevalence and region. Protocol registered in PROSPERO (CRD420251174202).
Results:
Overall, 92 studies (60,816 patients) from 32 countries were included. The pooled proportions of non-H. pylori, non-NSAID PUD cases were 13.0% (95% confidence interval [CI], 10.4-16.2) in overall PUD, 11.3% (95% CI, 8.8-14.4) in bleeding PUD, and 22.0% (95% CI, 13.1%-34.7%) in perforated PUD. In univariable meta-regression, a more recent study year was associated with a higher proportion of bleeding PUD (β = 0.076; 95% CI, 0.031-0.120). This association remained statistically significant after adjustment for country-level H. pylori prevalence (β = 0.070; 95% CI, 0.026-0.113). Lower H. pylori prevalence was also associated with a higher proportion after further adjustment for region (β = -0.025; 95% CI, -0.046 to -0.005).
Conclusion:
Non-H. pylori, non-NSAID PUD represents a non-negligible but heterogeneous component of PUD. In bleeding PUD, exploratory ecological analyses suggest a temporal increase, potentially reflecting evolving etiologic patterns beyond H. pylori infection and NSAID exposure.
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