Markers of endothelial and in vivo platelet activation in patients with essential thrombocythemia and polycythemia vera

被引:29
作者
Karakantza, M [1 ]
Giannakoulas, NC
Zikos, P
Sakellaropoulos, G
Kouraklis, A
Aktypi, A
Metallinos, IC
Theodori, E
Zoumbos, NC
Maniatis, A
机构
[1] Univ Patras, Sch Med, Lab Hematol & Transfus Med, GR-26110 Patras, Greece
[2] Univ Patras, Sch Med, Dept Internal Med, Div Hematol, GR-26110 Patras, Greece
[3] Univ Patras, Sch Med, Dist Hosp, Dept Hematol, GR-26110 Patras, Greece
[4] Univ Patras, Sch Med, Dept Med Phys, GR-26110 Patras, Greece
[5] Univ Patras, Sch Med, Dept Neurol, GR-26110 Patras, Greece
关键词
platelet activation; endothelial activation; essential thrombocythemia; polycythemia vera; thrombosis;
D O I
10.1532/IJH97.E0316
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
We investigated endothelial and in vivo platelet activation in a cohort of 52 patients with essential thrombocythemia (ET) and polycythemia vera (PV) before and after cytoreductive treatment, 22 healthy controls, and 17 patients with acute cerebrovascular ischemia (ACVI) and normal platelet counts. We measured platelet expression of CD62P and CD63 antigens and levels of soluble vascular cell adhesion molecule 1 (sVCAM-1). We found increased in vivo platelet activation in all patients with ET and PV, both before and after cytoreductive treatment, compared with controls. In patients with arterial thrombosis, platelet expression of CD62P and in patients with erythromelalgia, expression of both markers was higher compared with expression in patients without thrombotic complications. In patients with ET and PV before and after treatment, sVCAM-1 expression was increased compared with expression in controls but also compared with expression in patients with ACVI and normal platelet counts. In patients with arterial thrombosis and erythromelalgia, in vivo platelet activation correlated with the level of sVCAM-1. Our findings indicated that in vivo platelet activation reflects intrinsic platelet defects in patients with ET and PV, persists after cytoreductive treatment, and results in endothelial damage, probably through release of angiogenic factors and/or activation of white blood cells. (C) 2004 The Japanese Society of Hematology.
引用
收藏
页码:253 / 259
页数:7
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