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World J Gastroenterol. Sep 7, 2014; 20(33): 11552-11559
Published online Sep 7, 2014. doi: 10.3748/wjg.v20.i33.11552
Metachronous gastric cancer after successful Helicobacter pylori eradication
Akiko Shiotani, Ken Haruma, David Y Graham
Akiko Shiotani, Ken Haruma, Department of Internal Medicine, Kawasaki Medical School, Kurashiki 701-0192, Japan
David Y Graham, Department of Medicine, Michael E DeBakey VAMC and Baylor College of Medicine, Houston, TX 77030, United States
Author contributions: Shiotani A mainly wrote the manuscript; Haruma K and Graham DY edited the manuscript.
Correspondence to: Akiko Shiotani, MD, PhD, Department of Internal Medicine, Kawasaki Medical School, 577 Matsushima, Kurashiki 701-0192, Japan. shiotani@med.kawasaki-m.ac.jp
Telephone: +81-86-4621111 Fax: +81-86-4641195
Received: October 25, 2013
Revised: December 30, 2013
Accepted: May 28, 2014
Published online: September 7, 2014
Abstract

The high incidence of gastric cancer in Japan initially resulted in establishment of a country-wide gastric cancer screening program to detect early and treatable cancers. In 2013 countrywide Helicobacter pylori (H. pylori) eradication was approved coupled with endoscopy to assess for the presence of chronic gastritis. Current data support the notion that cure of the infection in those with non-atrophic gastritis will prevent development of gastric cancer. However, while progression to more severe damage is halted in those who have already developed, atrophic gastritis/gastric atrophy remain at risk for subsequent development of gastric cancer. That risk is directly related to the extent and severity of atrophic gastritis. Methods to stratify cancer risk include those based on endoscopic assessment of the atrophic border, histologic grading, and non-invasive methods based on serologic testing of pepsinogen levels. Continued surveillance is required because those with atrophic gastritis/gastric atrophy retain considerable gastric cancer risk even after H. pylori eradication. Those who have already experienced a resectable early gastric cancer are among those at highest risk as metachronous lesions are frequent even after H. pylori eradication. We review the role of H. pylori and effect of H. pylori eradication indicating the incidence and the predictive factors on development of metachronous cancer after endoscopic therapy of early gastric cancer. Studies to refine risk markers to stratify for risk, surveillance methods, intervals, and duration after successful H. pylori eradication, and whether adjuvant therapy would change risk are needed.

Keywords: Atrophic gastritis, Pepsinogen, miRNA, Intestinal metaplasia, Cancer prevention

Core tip: For the patients with a history of endoscopic resection of early gastric cancer, Helicobacter pylori (H. pylori) eradication followed by continued surveillance for gastric cancer is generally required because those with severe gastric atrophy retain considerable gastric cancer risk even after H. pylori eradication. We review the role of H. pylori and effect of H. pylori eradication indicating the incidence and the predictive factors on development of metachronous cancer after endoscopic therapy of early gastric cancer.