PubMed · 15658393
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Chisato Shimazu. 2004. [Bleeding time, capillary resistance test].. https://pubmed.ncbi.nlm.nih.gov/15658393/
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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.
Thrombocytosis is frequently observed in pediatric patients. Among them the secondary thrombocytosis are the most frequent and result from several causes. The rarely primary thrombocytosis can be either constitutive (and often familial) or acquired (essential thrombocythemia). The purpose of this article is to give diagnostic orientation and to suggest which biological tests should be performed.
The bleeding tendency in von Willebrand disease (VWD) is heterogeneous and some patients with the mildest form of the disease have no significant bleeding symptoms throughout their lives. In some cases, the most difficult task for a clinician is to decide whether any treatment is actually required. However, cases with moderate to severe factor VIII (FVIII) and von Willebrand factor (VWF) deficiency usually require treatment to stop or prevent bleeding. Increasing autologous FVIII/VWF by desmopressin administration or providing normal allogeneic VWF through the infusion of plasma-derived concentrates can correct FVIII and VWF deficiencies and normalize or shorten bleeding time (BT). FVIII levels are the best predictors of soft tissue or surgical bleeding, while BT normalization, reflecting the correction of platelet-dependent functions of VWF, is considered a reliable indicator of an effective treatment of mucosal bleeding. Recombinant concentrates of FVIII are not indicated (apart from cases with alloantibodies against exogenous VWF), since they are devoid of VWF and lack its stabilizing effect on circulating FVIII. A very-high-purity concentrate of VWF has recently been made available, but its advantages over conventional concentrates containing both FVIII and VWF moieties are not obvious. The best way to select the appropriate treatment is to perform a test infusion with desmopressin in any patient with clinically significant VWD, provided that he/she has no contraindication to the compound or belongs to subtype with an anticipated lack of response (for example, type 3 VWD with FVIII/VWF lower than 5%).