Studies on platelet functions in myeloproliferative disorders Part 1. Studies on platelet aggregation in myeloproliferative disorders

Mechamisms of hemostatic abnormalities in myeloproliferative disorders are still questionable. In this study author examined platelet aggregation, platelet factor-3 availability (pf-3a) and bleeding time. Platelet aggregation was induced by epinephrine, collagen, ADP, bovine-fibrinogen (bf) and zymosan, respectively. Pf-3a was examined by Kaolin-Ca method and bleeding time was examined by Ivy method. Materials were 26 cases of chronic myelocytic leukemia and 5 cases of polycythemia vera. As results following were obtained. Namely, significant decreases of pf-3a and epinephrine-induced platelet aggregation were most frequently seen in these cases. Their incidences were 66.7% and 58.1% , respectively. Particularly decrease of epinephrine-induced platelet aggregation was recognized in all 4 cases which showed hemorrhagic tendencies. Prolongation of bleeding time and decrease of collagen-, ADP-, and bf-induced platelet aggregation were seen in 32.0%, 16.1%, 6.7% and 4.3%, respectively. Furthermore, it was recognized that two or more disturbances of platelet-functions were present in these myeloproliferative disorders. These results were thought to suggest that hemostatic abnormalities in myeloproliferative disorders might be mainly due to decreases of pf-3a and epinephrine-induced platelet aggregation.