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World J Gastrointest Oncol. May 15, 2018; 10(5): 115-123
Published online May 15, 2018. doi: 10.4251/wjgo.v10.i5.115
Risk of gastric cancer development after eradication of Helicobacter pylori
Ka-Shing Cheung, Wai K Leung
Ka-Shing Cheung, Wai K Leung, Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China
Author contributions: All authors contributed equally to this paper with literature review and analysis, drafting and critical revision and editing, and approval of the final version of this article.
Conflict-of-interest statement: Wai K Leung has received honorarium for attending advisory board meetings of Boehringer Ingelheim and Takeda.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Wai K Leung, MB, ChB, MD, MRCP, Doctor, Professor, Department of Medicine, The University of Hong Kong, Queen Mary Hospital, 102 Pokfulam Road, Hong Kong, China. waikleung@hku.hk
Telephone: +86-852-22553348 Fax: +86-852-28162863
Received: February 7, 2018
Peer-review started: February 7, 2018
First decision: March 15, 2018
Revised: March 23, 2018
Accepted: April 15, 2018
Article in press: April 16, 2018
Published online: May 15, 2018
Abstract

Helicobacter pylori (H. pylori) infection is the most important risk factor for gastric cancer (GC) development through the Correa’s gastric carcinogenesis cascade. However, H. pylori eradication alone does not eliminate GC, as pre-neoplastic lesions (atrophic gastritis, intestinal metaplasia and dysplasia) may have already developed in some patients. It is therefore necessary to identify patients at high-risk for gastric cancer after H. pylori eradication to streamline the management plan. If the patients have not undergone endoscopy with histologic assessment, the identification of certain clinical risk factors and non-invasive testing (serum pepsinogen) can predict the risk of atrophic gastritis. For those with suspected atrophic gastritis, further risk stratification by endoscopy with histologic assessment according to validated histologic staging systems would be advisable. Patients with higher stages may require long-term endoscopic surveillance. Apart from secondary prevention to reduce deaths by diagnosing GC at an early stage, identifying medications that could potentially modify the GC risk would be desirable. The potential roles of a number of medications have been suggested by various studies, including proton pump inhibitors (PPIs), aspirin, statins and metformin. However, there are currently no randomized clinical trials to address the impact of these medications on GC risk after H. pylori eradication. In addition, most of these studies failed to adjust for the effect of concurrent medications on GC risk. Recently, large population-based retrospective cohort studies have shown that PPIs were associated with an increased GC risk after H. pylori eradication, while aspirin was associated with a lower risk. The roles of other agents in reducing GC risk after H. pylori eradication remain to be determined.

Keywords: Gastric adenocarcinoma, Stomach cancer, Helicobacter pylori, Chemoprevention, Intestinal metaplasia

Core tip: Although helicobacter pylori (H. pylori) infection is the most important risk factor for gastric cancer (GC) development, eradication of this bacteria does not guarantee the elimination of GC risk, as pre-neoplastic lesions may have already developed. It is therefore necessary to identify patients at high-risk for GC after H. pylori eradication by either endoscopy with histologic assessment or non-invasive testing. Long-term endoscopic surveillance is advisable for high-risk patients. Future studies are necessary to investigate medications that may modify the GC risk after H. pylori eradication.