Villmow Torben, Kemkes-Matthes Bettina, Matzdorff Axel C
Department of Hematology/Oncology, Faculty of Internal Medicine, Justus-Liebig-University, Klinikstr. 36, 35385 Giessen, Germany.
Thromb Res. 2002 Nov 1;108(2-3):139-45. doi: 10.1016/s0049-3848(02)00354-7.
Changes in platelet count and function contribute to thrombo-hemorrhagic episodes in chronic myeloproliferative syndromes (MPS). We used flow cytometry to study platelet-leukocyte conjugates and markers of platelet activation in patients with MPS.
Whole blood from patients with chronic myelogenous leukemia (CML), polycythemia vera (PV), chronic myelofibrosis (MF), and essential thrombocythemia (ET) and from healthy volunteers was prepared for flow cytometry. Platelet microparticles and platelet microaggregates were identified with anti-CD42b and forward scatter, activated platelets with anti-CD62p. Anti-CD42b, anti-CD14, and anti-CD45 were used to study platelet-leukocyte conjugates.
The percentage of CD62p-positive platelets was elevated in all myeloproliferate syndrome subtypes. The median percentage of platelet microparticles was 5.2% in controls and significantly higher in PV (12.0%), MF (11.0%), and ET (11.0%, all p<0.05). There was an increased percentage of platelet-neutrophil conjugates in patients with PV (8.3%) and ET (10.4%) compared to normal controls (6.8%, all p<0.05). Platelet-monocyte conjugates were 8.0% in controls and elevated in PV (15.4%) and ET (15.0%, all p<0.05). Patients with a history of venous or arterial thrombotic events had slightly less platelet-leukocyte conjugates and slightly more microparticles than patients without thrombosis; however, this difference was not statistically significant.
These findings suggest that platelet-leukocyte conjugate formation occurs in myeloproliferative syndromes and indicates platelet activation. Also, platelet microparticles are elevated and might provide a catalytic surface for thrombin generation. This could explain the clinical observation that patients with myeloproliferative syndromes have an increased risk to experience arterial or venous thrombotic events.
血小板计数和功能的变化会导致慢性骨髓增殖性综合征（MPS）出现血栓形成-出血事件。我们运用流式细胞术研究MPS患者的血小板-白细胞结合物及血小板活化标志物。
制备慢性粒细胞白血病（CML）、真性红细胞增多症（PV）、慢性骨髓纤维化（MF）、原发性血小板增多症（ET）患者及健康志愿者的全血用于流式细胞术检测。用抗CD42b和前向散射光鉴定血小板微粒和血小板微聚集体，用抗CD62p鉴定活化血小板。用抗CD42b、抗CD14和抗CD45研究血小板-白细胞结合物。
在所有骨髓增殖综合征亚型中，CD62p阳性血小板的百分比均升高。对照组血小板微粒的中位数百分比为5.2%，在PV（12.0%）、MF（11.0%）和ET（11.0%，均p<0.05）中显著更高。与正常对照组（6.8%，均p<0.05）相比，PV（8.3%）和ET（10.4%）患者的血小板-中性粒细胞结合物百分比增加。对照组血小板-单核细胞结合物为8.0%，在PV（15.4%）和ET（15.0%，均p<0.05）中升高。有静脉或动脉血栓形成事件病史的患者比无血栓形成的患者血小板-白细胞结合物略少，微粒略多；然而，这种差异无统计学意义。
这些发现表明血小板-白细胞结合物的形成发生在骨髓增殖性综合征中，并提示血小板活化。此外，血小板微粒升高，可能为凝血酶生成提供催化表面。这可以解释临床上观察到的骨髓增殖性综合征患者发生动脉或静脉血栓形成事件的风险增加。
