Minireviews
Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jul 7, 2015; 21(25): 7709-7717
Published online Jul 7, 2015. doi: 10.3748/wjg.v21.i25.7709
Geographic differences in low-dose aspirin-associated gastroduodenal mucosal injury
Katsunori Iijima, Tooru Shimosegawa
Katsunori Iijima, Tooru Shimosegawa, Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan
Author contributions: Iijima K drafted and edited this review; Shimosegawa T edited and approved the final version.
Conflict-of-interest statement: The authors declear no conflicts of interest.
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: Katsunori Iijima, MD, Division of Gastroenterology, Tohoku University Graduate School of Medicine, Seiryo-machi, Aobaku, Sendai 980-8574, Japan. kiijima@med.tohoku.ac.jp
Telephone: +81-22-7177171 Fax: +81-22-7177177
Received: April 7, 2015
Peer-review started: April 8, 2015
First decision: April 23, 2015
Revised: May 14, 2015
Accepted: June 10, 2015
Article in press: June 10, 2015
Published online: July 7, 2015
Processing time: 91 Days and 14.9 Hours
Abstract

Aspirin, even at low doses, has been known to cause upper gastro-intestinal complications, such as gastroduodenal ulcers, despite the definite benefits from its antithrombotic effects. Helicobacter pylori (H. pylori) is major pathogen responsible for gastroduodenal ulcer formation. There have been conflicting results about the potential interaction between these two ulcerogenic factors and the geographic areas involved. In Western countries, the prevalence of gastroduodenal ulcers is consistently higher in H. pylori-positive low-dose aspirin (LDA) users than in H. pylori-negative ones, suggesting that H. pylori infection exacerbates LDA-induced gastroduodenal mucosal injury in these geographic areas. Meanwhile, previous studies from Japan have generally reported a similar prevalence of LDA-induced gastroduodenal mucosal injury regardless of the presence of H. pylori infection, indicating that the infection is not an overall exacerbating factor for drug-induced injury. H. pylori infection could have a synergistic or antagonistic interaction with LDA use in adverse gastroduodenal events depending on gastric acid secretion. It is well-recognized that the net effect of H. pylori infection on gastric acid secretion shows considerable geographic variation at the population level. While gastric acid secretion levels were not decreased and were well-preserved in most patients with H. pylori infection from Western countries, the majority of Japanese patients with H. pylori infection exhibited decreased gastric acid secretion. Such large geographic differences in the net effect of H. pylori infection on gastric acid secretion could be at least partly responsible for the geographically distinct interaction between LDA use and H. pylori infection on adverse gastroduodenal lesions.

Keywords: Helicobacter pylori; Low-dose aspirin; Gastric acid secretion; Gastroduodenal ulcers; Geographic variation

Core tip: There have been conflicting results about the potential interaction between these low-dose aspirin (LDA) use and Helicobacter pylori (H. pylori) infection on the gastroduodenal ulcers and the geographic areas involved. H. pylori infection could have a synergistic or antagonistic interaction with LDA use in adverse gastroduodenal events depending on gastric acid secretion. Large geographic differences in the net effect of H. pylori infection on gastric acid secretion could be at least partly responsible for the geographically distinct interaction between LDA use and H. pylori infection on adverse gastroduodenal lesions.