Clinical features of gastroduodenal injury associated with long-term low-dose aspirin therapy

World J Gastroenterol. 2013 Mar 21;19(11):1673-82. doi: 10.3748/wjg.v19.i11.1673.


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; Low-dose aspirin; Non-steroidal anti-inflammatory drugs; Upper gastrointestinal bleeding.

Publication types

  • Editorial
  • Review

MeSH terms

  • Animals
  • Anti-Bacterial Agents / therapeutic use
  • Anti-Inflammatory Agents, Non-Steroidal / administration & dosage
  • Anti-Inflammatory Agents, Non-Steroidal / adverse effects*
  • Aspirin / administration & dosage
  • Aspirin / adverse effects*
  • Cyclooxygenase 1 / metabolism
  • Cyclooxygenase 2 / metabolism
  • Dose-Response Relationship, Drug
  • Drug Administration Schedule
  • Gastric Mucosa / drug effects*
  • Gastric Mucosa / enzymology
  • Gastric Mucosa / microbiology
  • Gastric Mucosa / pathology
  • Gastrointestinal Hemorrhage / etiology
  • Helicobacter Infections / complications
  • Helicobacter Infections / microbiology
  • Helicobacter pylori / pathogenicity
  • Histamine H2 Antagonists / therapeutic use
  • Humans
  • Peptic Ulcer / chemically induced*
  • Peptic Ulcer / enzymology
  • Peptic Ulcer / microbiology
  • Peptic Ulcer / pathology
  • Peptic Ulcer / prevention & control
  • Prognosis
  • Proton Pump Inhibitors / therapeutic use
  • Risk Assessment
  • Risk Factors
  • Time Factors
  • Treatment Outcome


  • Anti-Bacterial Agents
  • Anti-Inflammatory Agents, Non-Steroidal
  • Histamine H2 Antagonists
  • Proton Pump Inhibitors
  • Cyclooxygenase 1
  • Cyclooxygenase 2
  • PTGS1 protein, human
  • PTGS2 protein, human
  • Aspirin