What is the role of Helicobacter pylori infection in the etiology of gastric cancer?

Updated: Feb 23, 2021
  • Author: Elwyn C Cabebe, MD; Chief Editor: N Joseph Espat, MD, MS, FACS  more...
  • Print

Chronic bacterial infection with H pylori is the strongest risk factor for stomach cancer.

H pylori may infect 50% of the world's population, but many fewer than 5% of infected individuals develop cancer. It may be that only a particular strain of H pylori is strongly associated with malignancy, probably because it is capable of producing the greatest amount of inflammation. In addition, full malignant transformation of affected parts of the stomach may require that the human host have a particular genotype of interleukin (IL) to cause the increased inflammation and an increased suppression of gastric acid secretion. For example, IL-17A and IL-17F are inflammatory cytokines that play a critical role in inflammation. Wu et al found that carriage of IL-17F 7488GA and GG genotypes were associated with an increased risk of gastric cancer. [17]

H pylori infection is associated with chronic atrophic gastritis, and patients with a history of prolonged gastritis have a sixfold increased risk of developing gastric cancer. Interestingly, this association is particularly strong for tumors located in the antrum, body, and fundus of the stomach but does not seem to hold for tumors originating in the cardia. [18]

A large-scale, long-term study from Korea—which along with China and Japan is a high-risk country for gastric cancer—concluded that in patients with a family history of gastric cancer, treatment of H pylori infection more than halves their risk of developing gastric cancer. In the study, which included 1676 patients ages 40 to 65 years with confirmed H pylori infection and at least one first-degree relative with gastric cancer, patients were randomized to triple antibiotic therapy or placebo and followed with surveillance endoscopy every 2 years. [19, 20]

Over a median follow-up of 9.2 years, gastric cancer developed in 1.2% of patients in the treatment group, versus 2.7% of those in the placebo group. Among patients with persistent infection (n = 979), gastric cancer developed in 2.9%, compared with 0.8% of those in whom the infection had been eradicated (hazard ratio, 0.27). [19, 20]

Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!