[Helicobacter pylori and gastric cancer]

Several unresolved issues still cast doubts on the epidemiological data which point to an association between infection from Helicobacter pylori (Hp) and gastric cancer. These are: a) the male/female ratio of gastric cancer ranges from 4 to 1.5 in all studies, whereas the prevalence of Hp infection is the same in both sexes; b) the prevalence of Hp infection is as high as 90% in several developing countries where the frequency of gastric cancer is very low; c) 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, on the average, 10/100,000; d) the incidence of cancer in patients with a duodenal ulcer is half of that of the general population but Hp infects up to 100% of these patients. In the sequence of events that lead 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 which lead to 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 ones expressing the cagA gene. In a study we conducted in an area with a low incidence of gastric cancer (Latina), the prevalence of Hp infection was equal to 78.6% and, among the positives, 81% resulted cagA positive. This data, if compared with a similar research that took place in another area with a high incidence of gastric cancer (San Marino) where the prevalence of Hp infection was 51% and cagA 69%, further demonstrates the inconsistency of associating Hp and cancer of the stomach.