Background: Autoimmune gastritis (AIG) and Helicobacter pylori gastritis are distinct etiologies of chronic gastritis, yet comparative data on their long-term progression remain limited. Objectives: We compared the evolution of precancerous gastric lesions in patients with AIG and H. pylori-associated gastritis. Methods: This retrospective single-center cohort included 116 patients (52 histologically defined AIG, 64 H. pylori-associated gastritis) who underwent two upper endoscopies with Sydney-protocol biopsies at least 12 months apart between 2013 and 2024 (median follow-up 60 and 49 months). The primary outcome was the development of glandular atrophy or intestinal metaplasia (IM) not present at baseline. Results: New atrophy or IM developed in 61.5% (32/52) of AIG and 34.4% (22/64) of H. pylori patients (adjusted odds ratio [OR] 3.81, 95% confidence interval [CI] 1.53–9.49). Incident atrophy was more frequent in AIG (65.1% vs. 31.5%), including in comparison with baseline H. pylori-positive patients only (adjusted OR 3.02, 95% CI 1.08–8.46), whereas differences in IM were less consistent. Progression occurred in 42.9% of patients who were H. pylori-negative after treatment and 55.6% of persistently infected patients (p = 0.70). Proton pump inhibitor (PPI) use, an exploratory clinical risk score, and symptom changes were not associated with progression. Conclusions: In this selected cohort with repeat endoscopy, histologically defined AIG was associated with more frequent histological progression, particularly glandular atrophy, than H. pylori-associated gastritis. Prospective studies with serologically confirmed AIG and neoplastic endpoints are needed to inform risk stratification.
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Filip et al. (2026) studied this question.
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