Increased Thrombopoiesis and Platelet Activation in Hantavirus-Infected Patients
Increased Thrombopoiesis and Platelet Activation in Hantavirus-Infected Patients
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DOI：
10.1093/infdis/jiv161
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发表时间：
2015-10-01
影响因子：
6.4
通讯作者：
Nilsson, Sofie
中科院分区：
文献类型：
--
作者：
Connolly-Andersen, Anne-Marie;Sundberg, Erik;Nilsson, Sofie
背景资料。血小板减少是病毒性出血热的常见表现，包括肾综合征出血热(HFRS)。血小板减少的两个主要原因是血小板生成受损和/或血小板外周破坏增加。此外，肾综合征出血热期间血管内凝血的风险增加，这可能是由于血小板的激活。在肾综合征出血热期间，通过量化血小板计数、血小板生成素、未成熟血小板分数和平均血小板体积来确定血栓生成。测定血浆中可溶性P-选择素(sP-选择素)和糖蛋白VI(SGPVI)的含量。通过体外刺激、流式细胞仪分析血小板表面结合的纤维蛋白原和P-选择素的暴露来测定循环血小板的功能。通过对弥散性血管内凝血(DIC)评分和血栓栓塞症并发症的记录来判断疾病期间的血管内凝血情况。在肾综合征出血热期间，血小板生成素、未成熟血小板分数和平均血小板体积的水平都表明血小板生成增加。与随访相比，疾病期间循环血小板的体外功能降低。最有趣的是，我们观察到有血管内凝血(DIC和血栓栓塞症并发症)的HFRS患者体内血小板活化显著增加，如sP-选择素和sGPVI水平所示。肾综合征出血热患者的血小板生成和活化增加，从而导致血管内凝血。
Background. Thrombocytopenia is a common finding during viral hemorrhagic fever, which includes hemorrhagic fever with renal syndrome (HFRS). The 2 main causes for thrombocytopenia are impaired thrombopoiesis and/or increased peripheral destruction of platelets. In addition, there is an increased intravascular coagulation risk during HFRS, which could be due to platelet activation.Methods. Thrombopoiesis was determined by quantification of platelet counts, thrombopoietin, immature platelet fraction, and mean platelet volume during HFRS. The in vivo platelet activation was determined by quantification of soluble P-selectin (sP-selectin) and glycoprotein VI (sGPVI). The function of circulating platelets was determined by ex vivo stimulation followed by flow cytometry analysis of platelet surface-bound fibrinogen and P-selectin exposure. Intravascular coagulation during disease was determined by scoring for disseminated intravascular coagulation (DIC) and recording thromboembolic complications.Results. The levels of thrombopoietin, immature platelet fraction, and mean platelet volume all indicate increased thrombopoiesis during HFRS. Circulating platelets had reduced ex vivo function during disease compared to follow-up. Most interestingly, we observed significantly increased in vivo platelet activation in HFRS patients with intravascular coagulation (DIC and thromboembolic complications) as shown by sP-selectin and sGPVI levels.Conclusions. HFRS patients have increased thrombopoiesis and platelet activation, which contributes to intravascular coagulation.