[Helicobacter pylori, a risk factor for stomach cancer and primary stomach lymphoma?]

Helicobacter pylori has been implicated as a possible etiologic factor in gastric cancer. Recent epidemiologic studies, in fact, have demonstrated that there is a significantly higher prevalence of H. pylori in patients with gastric cancer than in matched controls. In addition to these and other epidemiologic findings, there is evidence that several of the pathogenic consequences of H. pylori infection may be relevant to carcinogenesis. In accordance with the theory that the etiology of gastric cancer is likely to be multifactorial, it is believed that the overall risk is determined by dietary, genetic and other cofactors. A causal relationship between H. pylori and gastric cancer, however, remains to be proven by randomized intervention trials of the long-term effects of H. pylori eradication. Until conclusive results become available from these studies, bacterial eradication cannot be recommended as prophylactic measure to reducing the risk of gastric cancer. In patients with low-grade B-cell gastric lymphomas of the mucosa-associated lymphoid tissue type (MALT) a causal pathogenic association with H. pylori-associated gastritis was demonstrable not only in cell culture but also in preliminary clinical trials. Several investigators have reported that eradication of H. pylori results in complete regression of early stage gastric MALT lymphomas. Answers to the questions whether healing is permanent, whether lymphomas at a more advanced stage will respond as well, and how regression comes about will have to be established in future studies.