Editorial
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World J Gastroenterol. Mar 21, 2013; 19(11): 1673-1682
Published online Mar 21, 2013. doi: 10.3748/wjg.v19.i11.1673
Clinical features of gastroduodenal injury associated with long-term low-dose aspirin therapy
Junichi Iwamoto, Yoshifumi Saito, Akira Honda, Yasushi Matsuzaki
Junichi Iwamoto, Yoshifumi Saito, Akira Honda, Yasushi Matsuzaki, Department of Gastroenterology, Tokyo Medical University, Ibaraki Medical Center, Ibaraki 300-0395, Japan
Author contributions: All the authors contributed equally to this work; all authors read and approved the final manuscript.
Correspondence to: Junichi Iwamoto, MD, Department of Gastroenterology, Tokyo Medical University, Ibaraki Medical Center, 3-20-1 Ami-machi Chuo, Inashiki-gun, Ibaraki 300-0395, Japan. junnki@dg.mbn.or.jp
Telephone: +81-298-871161 Fax: +81-298-883463
Received: September 14, 2012
Revised: December 3, 2012
Accepted: December 15, 2012
Published online: March 21, 2013
Processing time: 188 Days and 20.5 Hours
Abstract

Low-dose aspirin (LDA) is clinically used for the prevention of cardiovascular and cerebrovascular events with the advent of an aging society. On the other hand, a very low dose of aspirin (10 mg daily) decreases the gastric mucosal prostaglandin levels and causes significant gastric mucosal damage. The incidence of LDA-induced gastrointestinal mucosal injury and bleeding has increased. It has been noticed that the incidence of LDA-induced gastrointestinal hemorrhage has increased more than that of non-aspirin non-steroidal anti-inflammatory drug (NSAID)-induced lesions. The pathogenesis related to inhibition of cyclooxygenase (COX)-1 includes reduced mucosal flow, reduced mucus and bicarbonate secretion, and impaired platelet aggregation. The pathogenesis related to inhibition of COX-2 involves reduced angiogenesis and increased leukocyte adherence. The pathogenic mechanisms related to direct epithelial damage are acid back diffusion and impaired platelet aggregation. The factors associated with an increased risk of upper gastrointestinal (GI) complications in subjects taking LDA are aspirin dose, history of ulcer or upper GI bleeding, age > 70 years, concomitant use of non-aspirin NSAIDs including COX-2-selective NSAIDs, and Helicobacter pylori (H. pylori) infection. Moreover, no significant differences have been found between ulcer and non-ulcer groups in the frequency and severity of symptoms such as nausea, acid regurgitation, heartburn, and bloating. It has been shown that the ratios of ulcers located in the body, fundus and cardia are significantly higher in bleeding patients than the ratio of gastroduodenal ulcers in patients taking LDA. Proton pump inhibitors reduce the risk of developing gastric and duodenal ulcers. In contrast to NSAID-induced gastrointestinal ulcers, a well-tolerated histamine H2-receptor antagonist is reportedly effective in prevention of LDA-induced gastrointestinal ulcers. The eradication of H. pylori is equivalent to treatment with omeprazole in preventing recurrent bleeding. Continuous aspirin therapy for patients with gastrointestinal bleeding may increase the risk of recurrent bleeding but potentially reduces the mortality rates, as stopping aspirin therapy is associated with higher mortality rates. It is very important to prevent LDA-induced gastroduodenal ulcer complications including bleeding, and every effort should be exercised to prevent the bleeding complications.

Keywords: Gastroduodenal ulcer; Upper gastrointestinal bleeding; Low-dose aspirin; Non-steroidal anti-inflammatory drugs