[Analysis of inflammatory reaction and epithelial proliferation in corpus mucosa of the stomach. A contribution to carcinogenesis].

To elucidate conflicting evidence concerning the role of Helicobacter pylori (HP) in the evolution of gastric carcinoma, a retrospective analysis was performed on the corpus mucosa of gastric surgical specimens removed from patients with gastric carcinoma (n = 53) and pancreatic carcinoma (n = 45). Prevalence, activity and degree of chronic active gastritis (CAG) were investigated. Furthermore, proliferative activity was determined by the expression of the Ki67 antigen in epithelial cells of the neck region and the foveolae using immunohistochemistry. CAG and intestinal metaplasia were significantly more prevalent in patients with gastric than with pancreatic neoplasms. Degree and activity of CAG were higher in the group of patients with gastric carcinomas. Numbers of Ki67-positive nuclei were significantly higher in pronounced than in mild CAG. Our data are in keeping with the assumption that HP-associated CAG contributes to the development of gastric adenocarcinoma. As possible pathomechanism, it may be assumed that a conspicuously expressed inflammatory reaction triggers epithelial proliferation, with resulting higher vulnerability to mutagenic effects.