[MALT lymphoma, stomach carcinoma--role of Helicobacter pylori. Are chances for prevention on the horizon?].

The pathogenesis of gastric carcinoma developing after infection with Helicobacter pylori now seems to be clear. The release of urease, alcohol dehydrogenase, enzymes and cytotoxin on the one hand, and chemotactic factors, PAF and heat-shock proteins on the other trigger chronic inflammation and epithelial metaplasia and dysplasia in the stomach. Under the influence of additional carcinogens, the epithelial changes progress to severe dysplasia and finally carcinoma. As a result of chronic inflammation, MALT lymphomas can also be induced. These can be made to regress by eradicating Hp. The possibility of being able to prevent up to 80% of the carcinomas of the stomach by eradicating Hp holds out good prospects, over the long-term, for the prevention of these tumors. Accurate identification of the patient groups carrying a high risk is now necessary.