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Effect of oral aspirin on plasma levels of vitamin K-dependent clotting factors--studies in healthy volunteers.

The rationale for the use of aspirin as an antithrombotic drug lies mainly in its inhibition of thromboxane A2-dependent platelet function (1). There is also clinical (2) and experimental evidence (3) that in some instances aspirin is antithrombotic at doses higher than those required to inhibit the platelet cyclooxygenase, suggesting that at high doses aspirin may also act through mechanism(s) other than its effects on platelet function. Among the mechanisms by which aspirin might be antithrombotic is inhibition of blood coagulation (3). Case reports of patients treated with aspirin for rheumatoid arthritis (4, 5) and non-controlled studies on healthy volunteers (5, 6) have shown that massive