Key result
Ibuprofen and flurbiprofen reduced the initial rate of thromboxane B2 production, with concentrations of about 3 and 0.2 micrograms/ml, respectively, inhibiting aggregation.
Why the study?
Does ibuprofen or flurbiprofen reduce thromboxane production and platelet aggregability?
Does ibuprofen or flurbiprofen reduce thromboxane production and platelet aggregability?
Ibuprofen and flurbiprofen inhibit platelet aggregation by reducing thromboxane B2 production, with specific serum concentration thresholds identified for efficacy.
Answers are grounded in this paper and cite their sources.
May inhibit platelet aggregation at achievable concentrations; leaves open clinical effects on bleeding or CV risk.
Arachidonate-induced ex vivo platelet aggregations were performed before and after subjects received various doses of either ibuprofen or flurbiprofen. Both ibuprofen and flurbiprofen reduced the initial rate of thromboxane B2 (TxB2) production, but about 10% of control TxB2 production was refractory to either drug. Aggregation was observed after TxB2 concentrations exceeded a threshold of about 40 ng/ml. Once the threshold was achieved, aggregation and TxB2 production occurred independently of either drug. Ibuprofen and flurbiprofen concentrations of about 3 and 0.2 micrograms/ml, respectively, inhibited aggregation during the 5-minute testing period. A pharmacodynamic model was developed that predicts TxB2 production, aggregation lag times, and percent aggregation as a function of the time course of drug concentrations in serum.
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Cox et al. (1987) studied this question. Ibuprofen or flurbiprofen vs. Baseline (before receiving drug) was evaluated on Thromboxane B2 (TxB2) production and platelet aggregation. Ibuprofen and flurbiprofen reduced the initial rate of thromboxane B2 production, with concentrations of about 3 and 0.2 micrograms/ml, respectively, inhibiting aggregation.
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