Department of Immunohaematology and Transfusion Medicine, "Papa Giovanni XXIII" Hospital, Bergamo, Italy.
Department of Biochemistry, CARIM, Maastricht University, Maastricht, the Netherlands.
Blood Transfus. 2022 Mar;20(2):143-151. doi: 10.2450/2021.0456-20. Epub 2020 Mar 30.
Polycythaemia vera is a myeloproliferative neoplasm characterised by a high incidence of thrombosis. The contribution of platelets, key players in haemostasis, in this setting is still unclear. So far, the majority of studies have been focussed on specific platelet abnormalities but not on their actual capacity to form thrombi. The aim of this study was to characterise, ex vivo under flow conditions, the capacity of platelets from patients with polycythaemia vera to adhere to collagen and induce thrombus formation.
Thirty-nine patients and 30 healthy controls were studied. Thrombus formation was induced by perfusing whole blood over a collagen-coated surface, in a parallel-plate flow chamber coupled to a fluorescent microscope. This dynamic system enables platelet adhesion and thrombus formation to be followed in real time and also allows measurements of the extent of the thrombus and platelet surface antigen expression. Laboratory data were analysed in the light of the patients' main haematological parameters and therapies.
Platelet adhesion was significantly greater in patients than in control subjects. Patient thrombi were usually larger and more complex than those formed by control platelets. A significant positive correlation was found between platelet adhesion and both the haematocrit and red blood cell count. These parameters remained significantly correlated with platelet adhesion also after multivariable analysis adjusted for gender, age, therapy and JAK2V617F allele burden. Furthermore, subjects with a haematocrit >45% had significantly greater platelet adhesion than subjects with a haematocrit <45%.
Our data indicate that increased platelet adhesion participates in the thrombotic diathesis of patients with polycythaemia vera, and that the haematocrit level can affect the adhesive and thrombus forming capacities of platelets.
真性红细胞增多症是一种骨髓增殖性肿瘤，其血栓形成的发生率较高。在这种情况下，血小板作为止血的关键参与者的作用仍不清楚。到目前为止，大多数研究都集中在血小板的特定异常上，而不是其形成血栓的实际能力上。本研究旨在描述真性红细胞增多症患者的血小板在流动条件下与胶原蛋白结合并诱导血栓形成的能力。
研究了 39 名患者和 30 名健康对照者。在与荧光显微镜耦合的平行板流动室中，通过将全血灌注在胶原蛋白涂层表面上诱导血栓形成。这种动态系统能够实时跟踪血小板的黏附和血栓形成，并允许测量血栓的程度和血小板表面抗原的表达。根据患者的主要血液学参数和治疗方法分析实验室数据。
患者的血小板黏附明显高于对照组。患者的血栓通常比对照血小板形成的血栓更大、更复杂。血小板黏附与血细胞比容和红细胞计数呈显著正相关。在多变量分析中，校正性别、年龄、治疗和 JAK2V617F 等位基因负担后，这些参数与血小板黏附仍然显著相关。此外，血细胞比容>45%的患者的血小板黏附明显高于血细胞比容<45%的患者。
我们的数据表明，血小板黏附增加参与了真性红细胞增多症患者的血栓形成倾向，并且血细胞比容水平可以影响血小板的黏附和血栓形成能力。
