High acid secretion may protect the gastric mucosa from injury caused by ammonia produced by Helicobacter pylori in duodenal ulcer patients.

The aim of the present study was to investigate the mechanism by which gastric atrophy does not tend to occur in patients with duodenal ulcer despite frequent Helicobacter pylori infection. This investigation was performed in 60 patients with duodenal ulcer and 63 age-matched gastritis patients. Endoscopic findings in the antrum and corpus were classified as normal, atrophic and superficial changes. Biopsy specimens were taken from the antrum and corpus. Ninety per cent of patients with duodenal ulcer and 63.5% of patients with gastritis had H. pylori infection (P < 0.01). The incidence of normal findings in duodenal patients was 30% in antral regions and 50% in the corpus (P < 0.05). Atrophic change was observed in 21.7% of patients in the antrum and 3.3% of patients in the corpus (P < 0.01). The grade of inflammation in duodenal ulcer specimens was significantly higher in the antrum than in the corpus (P < 0.01). H. pylori density was significantly higher in the antrum than in the corpus in ulcer patients (P < 0.01). No significant difference in endoscopic findings, H. pylori density or the grade of inflammation was found between the antrum and corpus in patients with gastritis. The mean intragastric ammonia concentration was 10.3 mg/dL in duodenal ulcer patients and 6.2 mg/dL in gastritis patients (P < 0.01). The mean pH was 3.5 and 4.6 in ulcer and gastritis specimens, respectively (P < 0.01). Our data suggest that gastric mucosa injury is less frequently associated with duodenal ulcers than with gastritis due to the low H. pylori density in the corpus and to the higher acid output that neutralizes the ammonia produced by H. pylori.