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

Abstract Introduction Cilostazol 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 PGE 1 which upregulates intracellular cyclic AMP. Methods Blood was drawn from stroke patients before and after cilostazol intake. AA-induced platelet aggregation after pretreatment with 0 ~ 30 nM PGE 1 for 2 minutes was measured by light transmittance aggregometry. Results AA-induced platelet aggregation was 73.1 ± 2.2% in the absence of PGE 1 , and pretreatment with 30 nM PGE 1 had virtually no inhibitory effect on platelet aggregation prior to cilostazol intake. In contrast, after cilostazol intake, 30 nM PGE 1 significantly inhibited platelet aggregation to 12.7 ± 4.5% (p = 7.8 × 10(− 11)) , while in the absence of PGE 1 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 PGE 1 , 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 PGE 1 had the excellent sensitivity (90.5%) and specificity (88.4%) for monitoring cilostazol. Conclusions AA-induced platelet aggregation in the presence of 30 nM PGE 1 could give good estimate on plasma concentrations of cilostazol. It is suggested that this system is a good tool for monitoring cilostazol.