Low-Dose Aspirin-Induced Gastroduodenal Mucosal Injury in Japanese Patients with Arteriosclerotic Disease

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Background We aimed to elucidate the risk factors and preventive factors associated with chronic low-dose aspirin (L-ASA)-induced gastroduodenal mucosal injury in Japanese patients with arteriosclerotic disease. Methods This retrospective observational study included 400 L-ASA users who underwent upper gastrointestinal endoscopy. We investigated patients clinical characteristics, including age, peptic ulcer history, concomitant drugs [i.e. gastric agents, antiplatelet drugs, anticoagulants, non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids], abdominal symptoms, endoscopic findings, and interruption of L-ASA before endoscopy. The severity of gastroduodenal mucosal lesions was evaluated using the modified LANZA score (MLS). Results Of 400 patients, 249 (62%) and 41 (10%) had gastroduodenal mucosal lesions (MLS ≥1) and gastroduodenal ulcers, respectively. Peptic ulcer history, abdominal symptoms, proton pump inhibitor (PPI), histamine type 2-receptor antagonists (H2RA), and the cessation of L-ASA before endoscopy were significantly associated with L-ASA-induced gastroduodenal ulcers; the odds ratio (OR) (confidence interval (CI)) was 5.49 (1.82-16.55), 4.56 (1.93-10.75), 0.12 (0.03-0.42), 0.13 (0.04-0.40) and 0.11 (0.04-0.29), respectively. Moreover, patients having two or more of five factors [i.e. advanced age (≥75), anticoagulants, antiplatelet drugs, NSAIDs and corticosteroids] had a significantly higher prevalence of L-ASA-induced gastroduodenal ulcers [OR (CI): 2.39 (1.002-5.69)]. Conclusion Peptic ulcer history, abdominal symptoms and the summation of risk factors increased the risk for L-ASA-induced gastroduodenal ulcers. H2RAs and PPIs were effective for the prevention of L-ASA-induced gastroduodenal ulcers. The cessation of L-ASA before endoscopy might lead to the underestimation of L-ASA-induced gastroduodenal injury.

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