Effects of nonsteroidal antiinflammatory drugs on platelet function and systemic hemostasis

J Clin Pharmacol. 1995 Mar;35(3):209-19. doi: 10.1002/j.1552-4604.1995.tb04050.x.


Aspirin and nonaspirin nonsteroidal antiinflammatory drugs (NSAIDs) inhibit platelet cyclooxygenase, thereby blocking the formation of thromboxane A2. These drugs produce a systemic bleeding tendency by impairing thromboxane-dependent platelet aggregation and consequently prolonging the bleeding time. Aspirin exerts these effects by irreversibly blocking cyclooxygenase and, therefore, its actions persist for the circulating lifetime of the platelet. Nonaspirin NSAIDs inhibit cyclooxygenase reversibly and, therefore, the duration of their action depends on specific drug dose, serum level, and half-life. The clinical risks of bleeding with aspirin or nonaspirin NSAIDs are enhanced by the concomitant use of alcohol or anticoagulants and by associated conditions, including advanced age, liver disease, and other coexisting coagulopathies.

Publication types

  • Comparative Study
  • Review

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / adverse effects
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Aspirin / adverse effects
  • Aspirin / pharmacology
  • Bleeding Time
  • Blood Platelets / drug effects*
  • Blood Platelets / metabolism
  • Blood Platelets / physiology
  • Cyclooxygenase Inhibitors / pharmacology
  • Gastrointestinal Hemorrhage / chemically induced
  • Hemorrhage / chemically induced
  • Hemostasis / drug effects*
  • Humans
  • Platelet Aggregation / drug effects
  • Risk Factors


  • Anti-Inflammatory Agents, Non-Steroidal
  • Cyclooxygenase Inhibitors
  • Aspirin