Gastric carcinogenesis is related to inflammatory reaction induced by Helicobacter pylori infection. Infection is involved in pathogenesis of both histological types of gastric cancer, intestinal or diffuse. In the first type, cancer is the last step of successive alterations of the gastric mucosa (atrophy, intestinal metaplasia, dysplasia). In the second type, cancer occurs faster due to chromosomic alterations related to oxidative stress. Inflammation and consequently cancer risk are modulated by bacterial virulence and by the immunologica responsiveness of the host. Helicobacter pylori eradication should be proposed to high risk patients: first degree relatives of patients having gastric cancer, patients with preneoplastic lesions. Cancer prevention is more effective when eradication is performed before occurrence of preneoplastic lesions. When preneoplastic lesions are present, eradication decreases but not suppresses the risk of cancer. Therefore periodic follow up with gastroscopy and biopsies should be planned in these patients.

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