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Impact of Helicobacter pylori Infection on Progression of Nondysplastic Barrett’s Esophagus
Journal article   Open access

Impact of Helicobacter pylori Infection on Progression of Nondysplastic Barrett’s Esophagus

Vineeth Sadda, Jennifer M. Kolb, Ahmed E Aly, Ping Zheng and Shahin Ayazi
Journal of Gastrointestinal Surgery, Forthcoming
May 2026
DOI: https://doi.org/10.1016/j.gassur.2026.102457
Featured in Collection :   Research Supported by Drexel Libraries' OA Programs
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https://doi.org/10.1016/j.gassur.2026.102457View
Published, Version of Record (VoR) Open Access via Drexel Libraries Read and Publish Program 2026 Open CC BY V4.0

Abstract

Background Helicobacter pylori infection is associated with reduced risk of developing Barrett’s esophagus. However, its impact on progression of established non-dysplastic Barrett’s esophagus (NDBE) to dysplasia and esophageal adenocarcinoma (EAC) remains uncertain. Methods We queried a large U.S. clinical database to identify adults with NDBE between 2015–2023. The primary exposure was H. pylori infection; controls were uninfected NDBE patients. 1:1 propensity score matching was performed. The primary outcome was progression to dysplasia or EAC, defined as a new diagnosis during follow-up. Among H. pylori-infected patients, subgroup analyses examined the association between eradication therapy, esophagitis, sex, age, and smoking on progression. Results We identified 266,856 adults with NDBE, of whom 6,262 had H. pylori infection. After matching, progression to dysplasia or EAC was significantly higher in controls compared with the H. pylori cohort (8.3% vs 3.9%; p < 0.001; OR 2.23, 95% CI: 1.91-2.61), with a similar result for progression to HGD and EAC alone. Among H. pylori-infected patients, those who underwent eradication therapy had higher progression to dysplasia or EAC compared with untreated individuals (6.0% vs 3.5%; p < 0.001; OR 1.75, 95% CI: 1.35-2.26). Esophagitis prevalence was similar between treated and untreated H. pylori patients. Conclusion H. pylori infection was associated with a substantially lower risk of progression from NDBE to dysplasia or EAC. This association was attenuated following eradication therapy, but esophagitis was similar between cohorts, suggesting reflux severity did not explain the association. These findings support H. pylori as a potential risk-stratification marker in NDBE.

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