Relationship of Helicobacter pylori to gastric carcinogenesis

Abstract

The epidemiological evidence linking Helicobacter pylori infection to gastric carcinogenesis is reviewed. Only large geographical population studies have revealed a positive correlation between H. pylori infection and the incidence or mortality of gastric cancer.
In cace-control studies, the correlation varied in high-risk and low-risk countries, depending on the prevalence of H. pylori antibodies in the control group. In high-risk countries for gastric cancer, gastric atrophy is common in both the patient and control groups, and intestinal metaplasia is associated with a decrease of serum H. pylori antibody positivity. Both of these factors may be related to the negative correlation between gastric cancer and H. pylori infection.
In cohort studies, a significant positive correlation has been revealed between H. pylori infection and the risk of gastric cancer. Direct evidence on the progression of gastric atrophy in H. pylori-infected animal models and indirect evidence in clinical studies has been accumulated. H. pylori infection may be linked to gastric carcinogenesis via atrophy and intestinal metaplasia of the gastric mucosa, which accelerates cell proliferation and the exposure of epithelial cells to endogenous and exogenous mutagens. In addition, the secretion of ascorbic acid (anti-oxidant) into gastric juice is decreased.
As the WHO/IARC recently defined H. pylori as a group 1 carcinogen for gastric cancer based on these epidemiological studies, patients with H. pylori infection must be considered a high risk group for this cancer.