PubMed · 16463234
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A Alkier. 2006-02-10. [What does the bleeding time predict?].. https://doi.org/10.1055/s-2006-932510
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Platelets constantly patrol the inner surface of blood vessels searching leaks to be sealed, in order to prevent blood loss. When they detect a vessel injury their action can be divided into three phases. ADHESION: The platelets adhere to the injured blood vessel wall via their receptors glycoprotein (GP) Ib and integrin alpha2bbeta3 (GPIIb/IIIa) mediated by the ligands von Willebrand factor (VWF), fibrinogen and others. AGGREGATION: Platelets stick to each other through fibrinogen bridging integrin alpha2bbeta3 (GPIIb/IIIa) on adjacent platelets. SECRETION: During activation the content of platelet granules is released by exocytosis, thus augmenting and propagating formation of a haemostatic plug or thrombus. Laboratory tests mimic one or several aspects of these three phases to obtain reliable data on a patients platelet function. In this overview assays, test principles, and pitfalls are presented.
Treatment of thrombotic disease requires a delicate balance between prevention of new thrombotic events and management of bleeding complications. Various antiplatelet and anticoagulant agents have been used to this end, with varying degrees of success. Among the antiplatelet agents tested so far, cilostazol, which selectively targets phosphodiesterase III (PDE-III), has unique features. Cilostazol is classified as an antiplatelet agent because it inhibits the platelet aggregation induced by collagen, 5'-adenosine diphosphate (ADP), epinephrine, and arachidonic acid. Unlike other antiplatelet agents cilostazol not only inhibits platelet function but also improves endothelial cell function. Platelets circulate throughout the body with continuous tethering on the surface of endothelial cells. When endothelial cells are stimulated, the number of activated, or pre-conditioned, platelets in circulation increases. These platelets enhance thrombus formation at the sites of endothelial disruption. Cilostazol effectively prevents the onset of thrombotic disease, not only by direct inhibition of platelet function, but also by reducing the number of activated or pre-conditioned platelets in circulation. Secondary prevention of stroke with modest increase in bleeding complications was achieved by administration of cilostazol in the Japanese Cilostazol Stroke Prevention Study done in Japan. These results suggest that cilostazol may reduce the risk of stroke without increasing the risk of bleeding complications.