Effects of nonsteroidal antiinflammatory drugs on platelet function and systemic hemostasis.
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.
Schafer
A I
AI
Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects / Q000494:pharmacology*; D001241:Aspirin / Q000009:adverse effects / Q000494:pharmacology; D001760:Bleeding Time; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D006471:Gastrointestinal Hemorrhage / Q000139:chemically induced; D006470:Hemorrhage / Q000139:chemically induced; D006487:Hemostasis / Q000187:drug effects*; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects; D012307:Risk Factors
D000894:Anti-Inflammatory Agents, Non-Steroidal; D016861:Cyclooxygenase Inhibitors; D001241:Aspirin