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 infecti on and preneoplastic and neoplastic changes. As far as biologic data a re concerned, some elements point to the role of H. pylori in the deve lopment of preneoplastic and neoplastic changes, such as intestinal me taplasia and dysplasia. The relationship with H. pylori would mainly b e due to an increased cellular proliferation with the presence of imma ture cells in the superficial layers, susceptible to metaplastic or dy splastic modifications. The subsequent passage toward cancer is probab ly caused by other factors inasmuch as H. pylori is not able to coloni ze metaplastic or dysplastic areas and hyperproliferation remains at c omparable levels, even in the absence of infection. In fact, available epidemiologic data show a high prevalence of H. pylori infection in s ome geographic areas with a high incidence of gastric cancer. It is al so true, however, that there are several populations in which a low ne oplastic risk is associated with a high prevalence of infection. We st ress the methodologic weaknesses of several studies that attempt to es tablish a strict association between cancer and H. pylori. Therefore, epidemiologic data are still contradictory and do not permit identifyi ng a precise role of H. pylori as a predominant causative agent in the onset of preneoplastic and neoplastic changes. We conclude that H. py lori 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 susceptib ility.