RESUMEN
OBJECTIVE: Comparing the infection rates and density of Helicobacter pylori (H. pylori) and the patterns of gastritis in reflux esophagitis (RE) and non-erosive reflux disease (NERD) patients to investigate the role of H. pylori in the pathogenesis of RE. METHODS: Two hundred and twenty-three out-patients with typical gastroesophageal reflux symptoms who consecutively visited the hospital underwent ambulatory 24-hour pH monitoring and gastroscopy, and biopsy of the gastric mucosa. RE and NERD were diagnosed based on the presentation of endoscopy. Gastritis was divided into four different patterns: chronic non-atrophic antritis (CNAA); chronic non-atrophic pan-gastritis (CNAG); chronic atrophic antritis (CAA); and chronic atrophic pan-gastritis (CAG). H. pylori infection was evaluated by Warthin-Starry staining. DeMeester score > or = 15 was considered as pathological acid reflux. RESULTS: Sixty-two patients (27.8%) were found to have RE, 161 (72.2%) were found to have NERD. Totally, 67 patients had H. pylori infection (30.0%). There was no significant difference in H. pylori infection rate between the RE and NERD groups (25.8% vs. 31.5%, P > 0.05). 45 of the 223 patients were diagnosed as with CNAA (20.2%), 88 (39.5%) with CNAG, 65 (29.2%) with CAA, and 25 (11.2%) with CAG. The CAG rates in the RE and NERD groups were 6.5% and 13.0% respectively (P > 0.05). There were no differences in abnormal pH monitoring rate and DeMeester score among the different patterns of gastritis. In the sixty-seven H. pylori-positive GERD patients, the 24 h pH monitoring positive rate of the moderate-severe H. pylori colonization density group was 46.4%, significantly higher than that of the mild H. pylori colonization density group (73.5%, P < 0.05); and the mean intra-gastric pH value during 24 hours of the moderate-severe H. pylori colonization density group was 2.3 +/- 0.8, significantly higher than that of the mild H. pylori colonization density group (2.0 +/- 1.1, P < 0.05). CONCLUSION: H. pylori infection is associated with the pattern of gastritis, but shows no relationship to the incidence of RE. High density of H. pylori colonization in gastric corpus may reduce the esophageal acid exposure. Diffuse atrophic gastritis may protect the patients from RE.