It remains unclear whether the Helicobacter pylori eradication may cause or provoke gastroesophageal reflux disease. Therefore, we aimed to elucidate the role of H. pylori eradication and other factors in the development of erosive esophagitis in patients with duodenal ulcer. Materials and methods. We enrolled 183 H. pylori-positive duodenal ulcer patients without erosive esophagitis. Final endoscopy was performed 12 months later or in case if ulcer relapse was suspected. H. pylori was diagnosed by the urease test and histology if the results of at least one of the tests were positive. A total of 142 patients were assigned to the eradication treatment. The control group included 41 volunteers – 20-mg omeprazole b.i.d. for 4 weeks was administered. Results. A total of 150 patients completed the study. Of the 119 patients, 70 (58.8%) were cured from H. pylori, and in 49 (41.2%) of patients, treatment of H. pylori was unsuccessful. All 31 controls remained H. pylori-positive. At the final endoscopy, erosive esophagitis was found in 19 (12.7%) patients. Erosive esophagitis developed in 8 (11.4%) successfully eradicated patients, in 9 (18.4%) unsuccessfully treated patients, and in 2 (6.5%) controls (P>0.05 comparing the groups). Multivariate logistic regression analysis revealed 3 factors at baseline, which were significant (P<0.05) in predicting the occurrence of erosive esophagitis: age more than 43 years (OR, 4.96; 95% CI, 1.47–16.71), nonerosive gastroesophageal reflux disease (OR, 3.96; 95% CI, 1.34–11.68), and smoking (OR, 3.17; 95% CI, 1.01–9.17). Conclusions. H. pylori eradication did not influence the incidence of erosive esophagitis in patients with duodenal ulcer during a one-year follow-up period. Pre-existing nonerosive gastroesophageal reflux disease, smoking, and older age are important predictors of de novo development of erosive esophagitis.
Efficacy and Safety of Vonoprazan in Patients With Nonerosive Gastroesophageal Reflux Disease
