Abstract

Introduction: Defecatory dysfunction is one of the most common gastrointestinal disorders. Recently, dysbiosis in the gut microbiota are well known to be associated with the development of defecatory dysfunction. Helicobacter pylori infection and its eradication therapy are possible factors leading to dysbiosis. In this study, we investigated the effects of H. pylori eradication on defecatory dysfunction using questionnaires and examined the relationship between the severity of gastric mucosal atrophy and the reversibility of defecatory dysfunction after eradication therapy. Methods: We recruited a total of 166 H. pylori—positive patients who performed H. pylorieradication therapy from August 2015 to June 2017. We evaluated severity of defecatory dysfunction between before therapy and after 2 months post—therapy using the gastrointestinal symptom rating scale (GSRS) and the Izumo scale. Patients were divided into two groups based on the outcome of H. pylori eradication treatment, a successful group (n = 142) and a failed group (n = 24). The severity of endoscopic atrophy was graded according to the Kimura—Takemoto classification. Results: The constipation—related and diarrhea—related cores in the GSRS before treatment were significantly improved after treatment, from 5.8 ± 3.3 and 5.2 ± 3.2 to 5.1 ± 2.7 (P < 0.01) and 4.6 ± 2.6 (P = 0.04), respectively. In patients with constipation before eradication, the constipation—related score in the Izumo scale improved from 5.1±2.7 to 3.4±2.5 (P=0.013). In the failed eradication group, scores of constipation—related symptoms before and after treatment were similar. In contrast, those in the successful group significantly improved after treatment, from 5.63 ± 3.06 to 5.11 ± 2.71 (P=0.02). The constipation—related score in patients with mild and moderate atrophy significantly decreased from 5.5±2.8 to 4.9±2.2 (P=0.024), but not in patients with severe atrophy. Conclusion: H. pylori eradication therapy has the potential to improve defecatory dysfunction in H. pylori—infected patients without severe gastric atrophy. We hypothesize that this difference is due to eradication—induced changes in the secondary gastrointestinal tract environment, such as improved gastric acid secretion, and in the homeostatic gut microbiota. Merits of H. pylori eradication therapy lie not only in the effect it has as a preventer of gastric cancer, but also in its potential to improve defecatory dysfunction.

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