When sulphinpyrazone (either 200 mg q.d.s. for 7 days or 400 mg b.d.s. for 5 days) was administered to human volunteers, inhibition of platelet function was observed ex vivo. The inhibitory effect was measured by the increase in the concentration of sodium arachidonate required to cause platelet aggregation and a decrease in the biosynthesis by the platelets of malondialdehyde from added sodium arachidonate. ADP-induced primary platelet aggregation was statistically significantly inhibited only on 1 day of the two studies. The inhibitory effect did not correlate with the plasma concentrations of unchanged sulphinpyrazone nor with its sulphone metabolite but correlated with the plasma concentration of the thioether metabolite (r = 0.577, p < 0.001). Platelet count, plasma fibrinogen, β-thromboglobulin, urea and creatinine concentrations were not changed by the drug but there was a clinically insignificant increase in bleeding time in all but one subject.

Keywords:
Sulphinpyrazone, Platelet aggregation, Malondialdehyde
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© 1981 S. Karger AG, Basel
1981
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