What is the relationship between H. pylori infection and gastric malignancy?

Adenocarcinoma of the stomach is one of the most common malignancies in the world, although it is relatively uncommon in the United States (24,000 new cases and 14,000 deaths per year). There is evidence that H. pylori infection is associated with adenocarcinoma of the body and antrum of the stomach. However, gastric cancer occurs in some individuals with no evidence of H. pylori infection, and in the United States, fewer than 1 percent of H. pylori-infected individuals will ever develop gastric cancer. The effect of prevention or treatment of H. pylori infection on gastric cancer risk has not been studied adequately.

Descriptive epidemiologic data indicate that gastric cancer occurs more frequently in some populations that have higher rates of H. pylori infection. Rates of both H. pylori infection and gastric cancer correlate inversely with socioeconomic status, increase as a function of age, have declined in successive birth cohorts in developed countries, and occur less commonly in whites than in African Americans and Hispanics in the United States. A geographic correlation has been found between H. pylori infection and gastric cancer death rates. However, some clear examples exist of disparity in the epidemiology of the two diseases. Gastric cancer is more common in men than in women, whereas the rates of H. pylori infection are not different between the sexes. Some populations are reported to have a high rate of H. pylori infection but low rates of gastric cancer. These disparities indicate that factors other than H. pylori infection are also important in gastric cancer risk. 

Some but not all of the retrospective serologic studies have shown that patients with gastric cancer more frequently have H. pylori infection than do controls. The strongest evidence that H. pylori infection is associated with gastric cancer comes from three prospective cohort serologic studies which indicate that H. pylori-infected individuals have a significantly increased rate of gastric cancer. There is no association in any of these studies between H. pylori infection and cancer in the gastric cardia and gastroesophageal junction, which is increasing in incidence in the United States. 

Non-Hodgkin's lymphoma of the stomach is a rare disorder that accounts for only 3 percent of gastric malignancies. Mucosa-associated lymphoid tissue (MALT) lymphomas, which constitute a subset of Non-Hodgkin's lymphoma, are low-grade clonal neoplasms that are thought to arise from lymphoid aggregates in the lamina propria. Preliminary epidemiologic data suggest that H. pylori infection is associated with both non-Hodgkin's lymphoma and MALT lymphomas of the stomach. Further study of the relationship between H. pylori infection and gastric lymphomas is warranted. 

In summary, if there is any causal relationship between H. pylori infection and gastric cancer, clearly other factors are also important in gastric carcinogenesis. H. pylori eradication for the purpose of preventing gastric cancer cannot be recommended at this time.