Proliferation and apoptosis in gastric antral epithelial cells of patients infected with Helicobacter pylori

We measured cell proliferation and apoptosis in the antral epithelial cells of Helicobacter pylori-infected and H. pylori-uninfected persons, and examined these processes in relation to diagnosis and the histologic parameters of inflammation to investigate their role in cellular turnover in diseases of the upper gastrointestinal tract. The subjects were: 25 patients with antral gastric cancers, 20 with antral gastric ulcers, 18 with duodenal ulcers, and 28 with chronic gastritis, and 4 subjects with normal gastric mucosa. Seventy-two subjects were infected with H. pylori, and 23 subjects, including the 4 with normal gastric mucosa, were uninfected. H. pylori infection was associated with increased apoptosis and cell proliferation in the gastric mucosa, which correlated with the degree of acute inflammation and the density of H. pylori, and these latter two factors correlated with each other. Intestinal metaplasia and glandular atrophy were significantly higher in gastric cancers and gastric ulcers than in duodenal ulcers. Cell proliferation was significantly lower in gastric cancers than in gastric ulcers, but the apoptotic count did not show a significant differenence between these diseases. This decreased proliferation in the adjacent mucosa in gastric cancers compared with findings in the other diseases is thought to be closely related to the relatively decreased acute inflammation, which may, partly, contribute to glandular atrophy in the adjacent mucosa of gastric cancer.