pylori infection plays a significant role in gastric carcinogenesis. The risk of gastric

cancer increased threefold for the H. pylori-infected group compared with the non-infected group. In some studies, the incidence rate of metachronous gastric cancer decreased GSK-3 phosphorylation with H. pylori eradication after endoscopic resection of EGC.[27, 28] In a multicenter study of 544 patients with endoscopic resection of EGC, the incidence rate of metachronous gastric cancer was significantly reduced in the H. pylori eradication group compared with the non-eradication group. However, another retrospective study of 268 patients with endoscopic resection of EGC showed contradictory results, in that there was no significant difference in metachronous gastric cancer between the eradication group and the non-eradication group.[29, 30] Considering the high incidence of gastric cancer in Korea, H. pylori eradication is necessary to prevent metachronous gastric cancer after endoscopic resection of EGC. Information is lacking about the role learn more of H. pylori eradication in preventing metachronous gastric cancer after partial gastrectomy rather than endoscopic resection of EGC. Statement 4. H. pylori eradication is helpful for the prevention of gastric cancer in some patients with atrophic

gastritis/intestinal metaplasia. Level of evidence C, Grade of recommendation 2 Experts’ opinions: completely agree (14.8%), mostly agree (70.4%), partially agree (11.1%), mostly disagree (3.7%), completely disagree (0%), not sure (0%) H. pylori plays an important role in gastric carcinogenesis; in particular, it is an important cause of 71–95% of non-cardiac

gastric cancers.[31] H. pylori colonizes the gastric mucosa and triggers a series 2-hydroxyphytanoyl-CoA lyase of inflammatory reactions leading to cancer. The current model for gastric carcinogenesis begins with chronic gastritis, proceeds to mucosal atrophy, followed by intestinal metaplasia, dysplasia, and finally, carcinoma.[32] In H. pylori-positive patients with severe atrophic gastritis, the incidence rate of gastric cancer is 4.9 times higher than H. pylori-positive patients without atrophic gastritis and 14.5 times higher than H. pylori-negative patients without atrophic gastritis.[33, 34] In addition, in H. pylori-positive patients with intestinal metaplasia, the incidence of gastric cancer was 6.4 times greater than in H. pylori-positive patients without intestinal metaplasia, and 10.9 times greater in the Korean study.[10] Therefore, atrophic gastritis and intestinal metaplasia are considered important precancerous lesions in gastric carcinogensis.[33] In a Korean study, the mean prevalence of atrophic gastritis in the antrum and body was 42.5% and 20.1%, while the mean prevalence of intestinal metaplasia was 28.6% and 21.2%, respectively.[35, 36] In other studies, the age-adjusted prevalence of atrophic gastritis was 42.7% for men and 38.1% for women, and the prevalence of intestinal metaplasia was 42.5% for men and 32.