Cilostazol

Phosphodiesterase III inhibitor, approved for the treatment of peripheral arterial occlusive disease ( AVK).

Inhibitor of phosphodiesterase (PDE) with high specificity for subtype III. inhibition of PDE leads to an increase in cyclo-AMP; this leads, among other things, to inhibition of platelet function as well as to vasodilating and antithrombotic effects. Furthermore, inhibition of proliferation and migration has been described in smooth muscle cells. In the heart, cilostazol induces a positive inotropic effect. Of the two main metabolites, dehydrocilostazole is a four to seven times more effective platelet aggregation inhibitor than the parent substance (4'-trans-hydroxy-cilostazole is only about 1/5 as effective). The elimination half-life is 10.5 hours, whereby the excretion of the starting substance and the metabolites takes place predominantly via the urine (74%).

Approved to extend the maximum and pain-free walking distance in patients with intermittent claudication who have no pain at rest and no signs of peripheral tissue necrosis. The phosphodiesterase III inhibitor relieves the symptoms and extends the pain-free walking distance.

Recommended dose: 2 times/day 100 mg p.o. tablets 30 minutes before or two hours after breakfast and dinner.

Frequent: headache (> 30%), diarrhoea and stool changes (> 15%).

Is mainly metabolized via cytochrome P-450 CYP3A4 and to a lesser extent via CYP2C19 and CYP1A2. Therefore, it is contraindicated in patients taking CYP3A4 or CYP2C19 inhibitors such as cimetidine, diltiazem, erythromycin, ketoconazole, lansoprazole, omeprazole and HIV-1 protease inhibitors.

Pletal

In patients who took cilostazol and aspirin simultaneously, there was no additive or synergistic effect on platelet aggregation compared to the administration of ASA alone. The daily dose should not exceed 80 mg ASA.