Helicobacter pylori and gastric cancer: what is the real risk?

Abstract

Some epidemiological data point to an association between infection from Helicobacter pylori (Hp) and gastric cancer, although several unresolved issues still cast doubts on the real weight of this association. These issues are as follows: the male-to-female ratio of gastric cancer ranges from 4:1 to 1.5:1 in all studies, whereas the prevalence of Hp infection is the same in both sexes; the prevalence of Hp infection is as high as 90% in several developing countries where the frequency of gastric cancer is very low; the acquisition of the infection at a young age, considered very important with regard to the risk for cancer, varies from 4.2% to 83% in several countries in which the mortality for stomach cancer is approximately 10 in 100,000; and the incidence of cancer in patients with a duodenal ulcer is half that of the general population, but Hp infects up to 100% of these patients. In the sequence of events that leads to gastric cancer, Hp appears to play a role only in the very initial steps, as a causative agent of chronic inflammation. The further events that cause gastric atrophy, intestinal metaplasia, dysplasia, and cancer are multifactorial, involving environmental agents and the host response. It is therefore inappropriate to consider Hp a direct carcinogen for humans. This also applies to specific strains of the bacterium such as the cagA gene. In fact, Hp infection is widespread in humans, and only a small minority will ever be affected by peptic ulcer and cancer.