Helicobacter pylori and gastric cancer—key statements relevant for prevention strategies
| Statement | Level of evidence | Grade of recommendation |
| Helicobacter pylori infection is the most consistent risk factor for gastric cancer. Its elimination is therefore the most promising strategy to reduce the incidence of gastric cancer | 1a | A |
| The influence of environmental factors is subordinate to the effect of H pylori infection | 1a | A |
| H pylori eradication abolishes the inflammatory response and slows or may arrest the progression of atrophy. In some cases it may reserve atrophy | 1a | A |
| There is strong evidence that H pylori eradication reduces the risk of gastric cancer development | 1c | A |
| The risk of gastric cancer can be reduced more effectively by employing eradication treatment before the development of preneoplastic conditions | 1a | A |
| H pylori eradication for gastric cancer prevention is cost-effective in certain communities with a high risk for gastric cancer | 3 | B |
| H pylori eradication offers additional clinical and financial benefits in addition to gastric cancer prevention | varies with disease (1a to 4) | A |
| A screen-and-treat strategy of H pylori should be explored in communities with a significant burden of gastric cancer | 2c | A |
| Validated serological tests for H pylori and markers of atrophy (ie, pepsinogens) are the best available non-invasive tests to identify subjects at high risk of gastric cancer | 1a | B |
| H pylori eradication to prevent gastric cancer should be undertaken in populations at high risk | 1c | A |
| Preneoplastic high-risk conditions require endoscopic follow- up. Prospective studies are needed to determine the correct timing of follow-up | 2c | A |