Abstract

Background/Aim: Rifaximin is a gut-selective antibiotic with minimal systemic absorption that exerts its effects primarily within the gastrointestinal tract. Beyond its antimicrobial activity, rifaximin has been shown to possess anti-inflammatory and immunomodulatory properties. Gastric intestinal metaplasia (GIM) is a premalignant lesion associated with chronic gastric inflammation and Helicobacter pylori infection and is considered an important step in gastric carcinogenesis. Given the regulatory effects of rifaximin on the gut microbiota and mucosal inflammation, its potential impact on gastric histopathological alterations remains poorly understood. This study aimed to evaluate the effects of rifaximin therapy on gastric histopathological findings, particularly gastric intestinal metaplasia. Methods: In this retrospective single-center study, patients who received rifaximin therapy for various gastrointestinal indications and underwent upper gastrointestinal endoscopy with gastric biopsies both before and after treatment were included. Demographic characteristics, rifaximin treatment data, and histopathological findings were obtained from hospital records. Pre- and post-treatment biopsy findings were compared with respect to gastric intestinal metaplasia, dysplasia, and Helicobacter pylori positivity. Results: A total of 80 patients (mean age: 62.4 ± 11.9 years; 58.8% male) were included. Following rifaximin therapy, gastric intestinal metaplasia demonstrated significant regression (p < 0.001). Complete regression was observed in 45 patients (56.2%), partial regression in 12 patients (15.0%), stable disease in 14 patients (17.5%), and progression in 9 patients (11.3%). Helicobacter pylori positivity decreased from 42.5% to 31.2% (p = 0.041), whereas no significant change was observed in dysplasia rates (p = 0.564). No significant correlation was found between biopsy interval and the degree of intestinal metaplasia regression (Spearman’s r = −0.057, p = 0.617). Conclusions: Rifaximin therapy was associated with regression in both the presence and severity of gastric intestinal metaplasia. These findings provide preliminary evidence supporting further investigation of rifaximin in gastric intestinal metaplasia. However, the results should be considered hypothesis-generating, and larger prospective controlled studies are required to establish a causal relationship and further elucidate the underlying mechanisms.

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