Curing Helicobacter pylori infection in patients with duodenal ulcer does not provoke gastroesophageal reflux disease

Citation
R. Befrits et al., Curing Helicobacter pylori infection in patients with duodenal ulcer does not provoke gastroesophageal reflux disease, HELICOBACT, 5(4), 2000, pp. 202-205
Citations number
15
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
HELICOBACTER
ISSN journal
10834389 → ACNP
Volume
5
Issue
4
Year of publication
2000
Pages
202 - 205
Database
ISI
SICI code
1083-4389(200012)5:4<202:CHPIIP>2.0.ZU;2-Q
Abstract
Background. It has been suggested that the incidence of gastroesophageal re flux disease (GERD) increases after successful eradication of Helicobacter pylori infection. We present data on development of GERD from a controlled study of H. pylori eradication in 165 duodenal ulcer patients. Methods. Patients (mean age, 55 years; 102 men; current smokers; n = 74) we re randomly assigned 2 : 1 to receive omeprazole, 40 mg twice daily, in com bination with either amoxicillin, 750 mg twice daily, or placebo. Endoscopy and dyspeptic symptoms, including heartburn, were assessed at inclusion an d at 6, 12, and 24 months after treatment. In addition, symptoms were asses sed at 18 months. Patients with erosive esophagitis or reflux symptoms requ iring treatment at inclusion were not included in the study. Results. Fifty-one of 145 (35%) evaluable patients developed heartburn, and 13 of 145 (9%) developed esophagitis during follow-up. The life-table anal ysis of the cumulated risk of developing heartburn showed that patients who se H. pylori infection was eradicated had a significantly lower risk for de veloping heartburn than those with persistent H. pylori infection. The grou ps did not show any difference in cumulative risk of developing esophagitis . Conclusion. Our data show that successful eradication of H. pylori infectio n does not increase the incidence of GERD in duodenal ulcer patients.