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Drug DescriptionSide Effects & Drug InteractionsWarnings & Precautions
Clinical PharmacologyOverdosage & ContraindicationsIndications & DosagePatient Info

Pletal

[cilostazol]

• Vascular disorders

Very rare:

subacute thrombosis (These cases of subacute thrombosis occurred in patients treated with aspirin and “off label” use of cilostazol for prevention of thrombotic complication after coronary stenting.)

Text Continues Below




Drug Interactions:

Since PLETAL is extensively metabolized by cytochrome P-450 isoenzymes, caution should be exercised when PLETAL is coadministered with inhibitors of CYP3A4 such as ketoconazole and erythromycin or inhibitors of CYP2C19 such as omeprazole. Pharmacokinetic studies have demonstrated that omeprazole and erythromycin significantly increased the systemic exposure of cilostazol and/or its major metabolites.

Population pharmacokinetic studies showed higher concentrations of cilostazol among patients concurrently treated with diltiazem, an inhibitor of CYP3A4 (see CLINICAL PHARMACOLOGY, Pharmacokinetic and Pharmacodynamic Drug-Drug Interactions). PLETAL does not, however, appear to cause increased blood levels of drugs metabolized by CYP3A4, as it had no effect on lovastatin, a drug with metabolism very sensitive to CYP3A4 inhibition.

Use with other antiplatelet agents:

PLETAL inhibits platelet aggregation but in a reversible manner. Caution is advised in patients at risk of bleeding from surgery or pathologic processes. Platelet aggregability returns to normal within 96 hours of stopping PLETAL. Caution is advised in patients receiving both PLETAL and any other antiplatelet agent, or in patients with thrombocytopenia.

Cardiovascular Toxicity:

Repeated oral administration of cilostazol to dogs (30 or more mg/kg/day for 52 weeks, 150 or more mg/kg/day for 13 weeks, and 450 mg/kg/day for 2 weeks), produced cardiovascular lesions that included endocardial haemorrhage, hemosiderin deposition and fibrosis in the left ventricle, haemorrhage in the right atrial wall, haemorrhage and necrosis of the smooth muscle in the wall of the coronary artery, intimal thickening of the coronary artery, and coronary arteritis and periarteritis.

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