Gastric cancer and Helicobacter pylori: biologic and epidemiologic inconsistencies.

In this report we examine biologic and epidemiologic data with the aim of understanding any correlations between Helicobacter pylori infection and preneoplastic and neoplastic changes. As far as biologic data are concerned, some elements point to the role of H. pylori in the development of preneoplastic and neoplastic changes, such as intestinal metaplasia and dysplasia. The relationship with H. pylori would mainly be due to an increased cellular proliferation with the presence of immature cells in the superficial layers, susceptible to metaplastic or dysplastic modifications. The subsequent passage toward cancer is probably caused by other factors inasmuch as H. pylori is not able to colonize metaplastic or dysplastic areas and hyperproliferation remains at comparable levels, even in the absence of infection. In fact, available epidemiologic data show a high prevalence of H. pylori infection in some geographic areas with a high incidence of gastric cancer. It is also true, however, that there are several populations in which a low neoplastic risk is associated with a high prevalence of infection. We stress the methodologic weaknesses of several studies that attempt to establish a strict association between cancer and H. pylori. Therefore, epidemiologic data are still contradictory and do not permit identifying a precise role of H. pylori as a predominant causative agent in the onset of preneoplastic and neoplastic changes. We conclude that H. pylori behaves as a possible cofactor of other known damaging agents to the gastric mucosa, contributing to the risk of developing neoplastic modifications that may also be subject to individual genetic susceptibility.