Hashemi Tayer Akbar, Ranjbaran Reza, Kamravan Maryam, Abbasi Mojdeh, Zareian Reyhaneh
Research Center for Noncommunicable Diseases, Jahrom University of Medical Sciences, Jahrom, Iran.
Diagnostic Laboratory Sciences and Technology Research Center, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran.
Transfus Med Hemother. 2023 Mar 30;50(5):448-455. doi: 10.1159/000525640. eCollection 2023 Oct.
Thrombotic complication is one of the features of sickle cell disease (SCD), characterized by appearance of phosphatidylserine on the outer membrane of sickle-shaped red blood cells and most abundantly on membrane protrusions called microvesicles (MVs). However, the exact mechanism by which MVs may enhance coagulant activity in SCD patients has not been fully addressed. The aim of this study was to further investigate the procoagulant activity of circulating MVs in sickle cell crises.
Subjects included in this cross-sectional study were 47 patients with SCD and 25 normal subjects with written informed consent obtained from all the participants. MV analysis was conducted by using CD61, CD235α, and Annexin-V monoclonal antibodies. The coagulant activity of MVs was determined by an ELISA-based procoagulant activity assay.
The majority of MVs were originated from platelets (CD61+) and erythrocytes (CD235+). These MVs demonstrated significantly enhanced levels during the painful crisis when compared with the steady-state period ( < 0.001) and controls ( < 0.001). Also, the procoagulant activity of MVs was significantly higher in crisis compared to those of steady state ( < 0.001) and positively correlated with the number of Annexin-V+ MVs ( < 0.001). Significant correlations were found between erythrocyte-derived MVs with hemolysis marker ( = 0.51, < 0.001) and the hemoglobin level ( = -0.63, < 0.001).
The numbers of platelet- and erythrocyte-derived MVs are related to painful crisis, and their quantification in SCD may be helpful for identifying cases at increased risk of thrombotic complications.
血栓形成并发症是镰状细胞病（SCD）的特征之一，其特点是磷脂酰丝氨酸出现在镰状红细胞的外膜上，在称为微泡（MVs）的膜突起上最为丰富。然而，MVs可能增强SCD患者凝血活性的确切机制尚未完全阐明。本研究的目的是进一步研究镰状细胞危象中循环MVs的促凝活性。
本横断面研究纳入47例SCD患者和25名正常受试者，所有参与者均签署了书面知情同意书。使用CD61、CD235α和膜联蛋白-V单克隆抗体进行MV分析。通过基于酶联免疫吸附测定的促凝活性测定法测定MVs的凝血活性。
大多数MVs源自血小板（CD61+）和红细胞（CD235+）。与稳定期（<0.001）和对照组（<0.001）相比，这些MVs在疼痛危象期间水平显著升高。此外，与稳定期相比，MVs的促凝活性在危象时显著更高（<0.001），并且与膜联蛋白-V+MVs的数量呈正相关（<0.001）。发现红细胞衍生的MVs与溶血标志物（=0.51，<0.001）和血红蛋白水平（=-0.63，<0.001）之间存在显著相关性。
血小板和红细胞衍生的MVs数量与疼痛危象有关，对其在SCD中的定量分析可能有助于识别血栓形成并发症风险增加的病例。
