18 There is another noninvasive method to evaluate the risk of development of gastric cancer. The serum pepsinogen level is correlated with the extent

of chronic, atrophic fundic gastritis and is used for screening of EGC that arises from atrophic gastric mucosa.19–21 It detects the presence of atrophic gastritis and is therefore more applicable to intestinal-type Cell Cycle inhibitor gastric cancer that develops predominantly in post-ESD patients. A recent study has indicated that combination of H. pylori serology and pepsinogen level is good for predicting gastric cancer development.22 It has been demonstrated that those who had a pepsinogen level that indicated atrophic gastritis had a significantly higher risk (6–8 times increase) of developing gastric cancer, during a mean observation period of 4.7 years, than those with a normal pepsinogen level who were negative for H. pylori antibody. However, because the serum pepsinogen level is altered by H. pylori eradication,23 it cannot be used for patients who already have been treated by eradication therapy. Moreover, different cut-offs used in different studies might affect the sensitivity and specificity of the results. Recently, the prophylactic effect

of H. pylori eradication on the incidence of metachronous gastric cancer after endoscopic resection of EGC has been demonstrated in a randomized controlled trial.10 It has been shown that the odds ratio (OR) for developing metachronous cancer was 0.353 in favor of H. pylori eradication. In the present study, 12 (14.6%) metachronous EGCs developed during a mean find protocol follow up period of 55 months in patients who had undergone ESD for EGC after H. pylori eradication therapy. Although our

study was not designed to compare incidence of metachronous EGC in patients who received eradication therapy with those who did not, we could not find any association between H. pylori status and development of metachronous EGC. We speculated that when severe atrophy or intestinal metaplasia has already developed widely, the effect of H. pylori eradication for reducing development of EGC is limited. This is in line with the results of a large randomized study24 and other non-randomized studies.11,25,26 medroxyprogesterone They have suggested that H. pylori eradication is not beneficial in preventing cancer development in patients with precancerous lesions such as atrophy, intestinal metaplasia or dysplasia. Taking this into consideration, we would like to emphasize that surveillance endoscopy for early detection of metachronous EGC is essential for management of ESD patients, even if they received eradication therapy for H. pylori because a considerable number of metachronous EGCs would still develop. There are several limitations to consider in this study. First, the median observation period of this study was 55 months. Gastric cancer usually grows slowly, and it has been reported that the doubling time of EGC ranges from 2 to 10 years.