Stomach (Gastric) Cancer Prevention (PDQ®): Prevention - Health Professional Information [NCI] - Description of the Evidence
H. pyloriinfection eradication
H. pylori infection is an accepted cause of gastric adenocarcinoma.[13,14] Questions remain concerning the natural history of H. pylori infection; the mechanism of transmission and the rates of reinfection or recrudescence for different populations are unknown.[15,16] A small randomized trial of antibiotic eradication in 140 H. pylori-infected people suggests the possibility of transmission among close family members. In 70 participants, only the participant received eradication therapy; in the other 70 participants, all H. pylori-infected family members living with the primary participant also received the eradication therapy. Nine months after the therapy, the positivity rates in the index participants in each group were 38.6% and 7.1%, respectively (odds ratio = 8.61; 95% confidence interval [CI], 2.91–22.84), suggesting the possibility of transmission from untreated, infected family members.
Since about half of the world population is infected with H. pylori, antibacterial treatment for all people who are chronically infected may be impractical and could trigger antimicrobial resistance. Vaccination against H. pylori has been shown effective in experimental animal models, but thus far, such efficacy has not been studied in humans.
A meta-analysis of seven randomized studies, all conducted in areas with high-risk gastric cancer populations, and all but one study conducted in Asia, suggests that treatment of H. pylori may reduce gastric cancer risk (from 1.7% to 1.1%; relative risk [RR] = 0.65; 95% CI, 0.43–0.98). Only two studies assessed gastric cancer incidence as the primary study outcome, and two different studies were double blinded. It is unclear how generalizable the results may be to the North American population. It would be useful to know which subgroups of persons with H. pylori are particularly likely to develop cancer in order to decide which subgroups might be appropriate to consider for targeted screening and eradication. However, studies in H. pylori-infected subjects have been underpowered for determining progression to invasive cancer. Even studies of associations between baseline characteristics (such as age, alcohol use, and well water used as the source of drinking water in rural China) and histologic progression of intestinal metaplasia to more severe grades of metaplasia show associations of insufficient magnitude to be useful in clinical decision making.
Interventions With Inadequate Evidence as to Whether They Reduce the Risk of Stomach (Gastric) Cancer or Evidence of No Effect
Excessive salt intake has been identified as a possible risk factor for gastric cancer in correlation and case-control studies.[20,21] The daily intake of salt has decreased drastically in most western countries and in Japan, in part due to public health campaigns to reduce hypertensive diseases. This may be at least partially responsible for declines in gastric cancer rates. There is a consistent association between high salt intake and the risk of gastric cancer.