Published online Sep 15, 2016. doi: 10.4251/wjgo.v8.i9.663
Peer-review started: March 24, 2016
First decision: May 23, 2016
Revised: June 8, 2016
Accepted: July 14, 2016
Article in press: July 18, 2016
Published online: September 15, 2016
Helicobacter pylori (H. pylori) infection was thought to be the main cause of gastric cancer, and its eradication showed improvement in gastric inflammation and decreased the risk of gastric cancer. Recently, a number of studies reported the occurrence of gastric cancer after successful eradication. Patients infected with H. pylori, even after eradication, have a higher risk for the occurrence of gastric cancer when compared with uninfected patients. Metachronous gastric cancer occurs frequently following the endoscopic removal of early gastric cancer. These data indicate that metachronous cancer leads to the occurrence of gastric cancer even after successful eradication of H. pylori. The pathogenesis of this metachronous cancer remains unclear. Further research is needed to identify biomarkers to predict the development of metachronous gastric cancer and methods for gastric cancer screening. In this article, we review the role of the H. pylori in carcinogenesis and the histological and endoscopic characteristics and risk factors for metachronous gastric cancer after eradication. Additionally, we discuss recent risk predictions and possible approaches for reducing the risk of metachronous gastric cancer after eradication.
Core tip: Helicobacter pylori (H. pylori) eradication and endoscopic resection appeared to reduce the risk of gastric cancer. However, recent studies show that the risk of metachronous gastric cancer increases in the background of gastric mucosal atrophy even after successful eradication. Thus, curing H. pylori infections may not prevent metachronous gastric cancer in background mucosa with intestinal metaplasia. We review the risk factors and possible approaches for reducing the risk of metachronous gastric cancer.