骨髄増殖症候群の血小板機能に関する研究

第1編 骨髄増殖症候群の血小板凝集能に関する研究

抄録

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.