Gastric Cancer — A Long-Term Consequence ofHelicobacter pyloriInfection?

Abstract

Chronic gastritis and chronic atrophic gastritis in particular are risk factors for gastric cancer. In Western societies, for example Finland, up to 70% of gastric cancer cases are associated with Helicobacter pylori-positive chronic non-atrophic or atrophic gastritis, approximately 15% appear in conjunction with autoimmune chronic corpus-limited H. pylori-negative atrophic gastritis, and 15% develop in individuals with a histologically normal stomach. The role of H. pylori infection in chronic gastritis has led to the hypothesis that this infection could be involved in the pathogenesis of gastric cancer. There are three main factors in support of this hypothesis: (i) H. pylori infection is the single causal aetiological agent in more than 80% of cases with chronic gastritis; (ii) H. pylori-positive chronic gastritis will develop into mucosal atrophy (atrophic gastritis) and intestinal metaplasia in a large proportion of affected individuals; (iii) the risk of gastric cancer is known to be high in people with chronic gastritis, and particularly in those with atrophic gastritis. In addition, there exists some correlation between the rates of H. pylori infection and gastric cancer mortality worldwide, and H. pylori infection relates to socioeconomic conditions known to associate with gastric cancer. Although H. pylori-positive gastritis cannot be considered a single and direct cause of gastric cancer, it is strongly associated with it and may trigger a cascade of events in the gastric mucosa that results in the development of gastric cancer in some patients.