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Updated: Aug 19, 2026

Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia
Published on: February 16, 2024
Helicobacter pylori infection as a risk factor for gastric ulceration
Kenichiro Mitani1, Masaharu Tatsuta, Hiroyasu Iishi
1Department of Gastrointestinal Oncology, Osaka Medical Center for Cancer and Cardiovascular Disease, Osaka, Japan. k-mitani@ta2.so-net.ne.jp
Background/Aims:
Recent reports have shown that Helicobacter pylori infection is closely related to pathogenesis of gastric ulcers. But there have been no reports on the prospective follow-up study of the patients with H. pylori infection to determine whether H. pylori infection puts patients at high risk of developing gastric ulcers.
Methodology:
Fifty-two patients with H. pylori infection and 34 patients without H. pylori infection, who were found endoscopically not to have localized lesions in the esophagus, stomach, or duodenum, underwent endoscopy follow-ups during the average observation period of 52 months. During each endoscopy, biopsy specimens were obtained from the antrum and the middle corpus. The grade of atrophy and intestinal metaplasia in the biopsy specimens were assessed histologically in accordance with the guidelines of the Updated Sydney System.
Results:
Gastric ulcers developed in 8 (15%) of 52 patients with H. pylori infection, but not in patients without H. pylori infection: the difference was statistically significant (P<0.05). The development and the location of gastric ulcers was correlated to the development or progression of mucosal atrophy. In 8 (38%) of 21 patients in whom mucosal atrophy developed or progressed, gastric ulcers developed, but no ulcers developed in 31 patients without development or progression of gastric mucosal atrophy. Gastric ulcers developed in the gastric mucosa in which atrophy developed or progressed.
Conclusions:
H. pylori infection increases the risk for development of gastric ulcers and gastric ulcers developed through the progression of H. pylori-associated gastric mucosal atrophy.
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