Helicobacter pylori infection and gastric cancer

Abstract

Gastric cancer is the second most common fatal malignancy in the world. Prospective case-control studies have shown that subjects with H. pylori infection have an increased (by 2 to 4 folds) risk of development of gastric cancer. Animal studies have confirmed that infection with H. pylori results in the development of gastric cancer in Mongolian gerbils. H. pylori infection leads to changes of many factors that are important in the pathogenesis of gastric cancer, such as decrease in the ascorbic acid (vitamin C) level in gastric juice, increase in reactive oxygen metabolites, and imbalance between epithelial cell proliferation and apoptosis. Specific virulent strain and host factors may both contribute to the carcinogenesis of gastric cancer. Eradication of H. pylori infection may provide a powerful strategy in the prevention of gastric cancer. Whereas studies of patients with precancerous lesions have produced conflicting results regarding whether these lesions are reversible after eradication of the infection, chemoprevention trials on asymptomatic subjects are cautiously carried out in high risk populations. Vaccination may be proven to be the optimal strategy in humans in the management of H. pylori infection and thus prevention of gastric cancer.