Platelet aggregometry in the presence of PGE1 provides a reliable method for cilostazol monitoring

IntroductionCilostazol has been shown to be effective for prevention and treatment of cerebral infarction. However, there appears to be no widely accepted method appropriate for monitoring cilostazol. We attempted to establish an assay system for cilostazol monitoring, using platelet aggregation induced by arachidonic acid (AA) in the presence of PGE1 which upregulates intracellular cyclic AMP.MethodsBlood was drawn from stroke patients before and after cilostazol intake. AA-induced platelet aggregation after pretreatment with 0 ~ 30 nM PGE1 for 2 minutes was measured by light transmittance aggregometry.ResultsAA-induced platelet aggregation was 73.1 ± 2.2% in the absence of PGE1, and pretreatment with 30 nM PGE1 had virtually no inhibitory effect on platelet aggregation prior to cilostazol intake. In contrast, after cilostazol intake, 30 nM PGE1 significantly inhibited platelet aggregation to 12.7 ± 4.5% (p = 7.8 × 10(− 11)) , while in the absence of PGE1 platelet aggregation remained similar to that of prior-to-cilostazol value (70.6 ± 3.5%). The plasma concentration of cilostazol ranged from 0.55 to 3.51 μM. In the presence of 30 nM PGE1, all the patients with cilostazol concentrations exceeding 1 μM had their platelet aggregation inhibited almost completely. ROC analysis suggests that AA-induced platelet aggregation in the presence of 30 nM PGE1 had the excellent sensitivity (90.5%) and specificity (88.4%) for monitoring cilostazol.ConclusionsAA-induced platelet aggregation in the presence of 30 nM PGE1 could give good estimate on plasma concentrations of cilostazol. It is suggested that this system is a good tool for monitoring cilostazol.