Intestinal metaplasia, atrophic gastritis and stomach cancer: trends over time

Abstract

Background: The pathogenetic association of chronic atrophic gastritis and intestinal metaplasia with gastric cancer implies that the trends seen in these disorders over time should be similar. Both should similarly decrease in incidence with time, and a time-related relationship should occur between the incidence of gastric cancer and the rate of development of atrophic gastritis in the stomach of Helicobacter pylori-infected subjects.

Aims and methods: We reviewed some recent studies from Finland on the time trends seen in chronic gastritis, atrophic gastritis (and intestinal metaplasia) and gastric cancer over a period of 15 years (1977-1992). In addition, using results from earlier studies from Japan and Finland, we formed hypotheses on how the time-dependent evolution and extension of atrophic gastritis may accord with the occurrence of gastric cancer in the stomach.

Results: Our investigations showed that the incidence of gastric cancer and the prevalence of H. pylori-associated gastritis, atrophic gastritis and intestinal metaplasia have decreased similarly in outpatient series during the last 15 years. Correspondingly, gastric cancer, atrophic gastritis and intestinal metaplasia are cohort phenomena in the population, and the prevalence rate of atrophic gastritis is correlated with the cohort-specific incidence of gastric cancer; both are high in cohorts born near the beginning of the century but are quite low in those born in recent decades. Since antral and angular areas of the stomach are primary sites for gastric cancer tumours, the earlier investigations indicate that the time-dependent progression of gastritis in grade (development of atrophic gastritis and intestinal metaplasia) and extent (spreading of gastritis by pylorocardial extension) is well correlated with the rate and predisposition of gastric cancer tumours in the distal and angular stomach.

Conclusions: We conclude that atrophic gastritis (or intestinal metaplasia) and gastric cancer are very much alike in time trends and in course. This parallelism favours suggestions that H. pylori-associated gastritis with atrophic and metaplastic sequelae (atrophic gastritis) contribute to the pathogenesis of gastric cancer.