PERSISTENT GASTRIC MUCOSAL INFLAMMATION AFTER HELICOBACTER PYLORI ERADICATION: MECHANISMS, CLINICAL SIGNIFICANCE AND MANAGEMENT

Abstract

Helicobacter pylori is a Group 1 carcinogen and a principal cause of chronic active gastritis and downstream premalignant lesions. Successful eradication reduces gastric cancer incidence at the population level, yet post-treatment mucosal recovery is frequently incomplete, with persistent inflammation reported during endoscopic follow-up. This narrative review integrates evidence from clinical follow-up cohorts, randomized trials, and mechanistic studies addressing post-eradication gastric mucosal inflammation, framed using the Updated Sydney System (activity vs chronic inflammation) and OLGA/OLGIM staging. Across longitudinal biopsy studies, neutrophilic activity declines earlier after eradication than chronic mononuclear inflammation, while atrophy and intestinal metaplasia regress slowly and may persist for years. Persisting inflammation after confirmed eradication may reflect residual immune activation, ongoing chemical/reactive injury (e.g., bile reflux, NSAIDs), or altered post-treatment microbial ecology. Dyspeptic symptoms may also persist despite cure, consistent with overlap with functional dyspepsia and non–H. pylori gastropathies. A practical approach emphasizes confirmation of eradication, identification of non–H. pylori drivers, and stage-based risk stratification to guide follow-up and surveillance