University of Liverpool, UK.
Eur J Intern Med. 2010 Apr;21(2):79-83. doi: 10.1016/j.ejim.2009.11.007. Epub 2009 Dec 23.
Heparin-induced thrombocytopenia (HIT) is a prothrombotic disorder initiated by heparin administration. It is caused by the formation of pathogenic antibodies to complexes of platelet factor-4 (PF4) and heparin on platelet surfaces that cause platelet activation, aggregation and thrombosis. There has been intense research on this intriguing, drug-related thrombocytopenia explaining several characteristic aspects of this condition. However, prothrombotic potential of the key player, PF4 has not been investigated in many studies although it has been shown to be critical in monocyte chemotaxis, monocyte-platelet interaction, and megakaryocyte suppression, all of which can contribute to the pathophysiology of HIT. This article explains the important role of PF4 released during platelet activation with the administration of heparin in the pathogenesis of thrombocytopenia and thrombosis in HIT.
肝素诱导的血小板减少症（HIT）是一种由肝素给药引发的促血栓形成疾病。它是由血小板表面的血小板因子 4（PF4）和肝素形成的致病性抗体引起的，这些抗体导致血小板激活、聚集和血栓形成。人们对这种引人入胜的、与药物相关的血小板减少症进行了深入研究，解释了这种疾病的几个特征方面。然而，在许多研究中，尽管已经表明 PF4 在单核细胞趋化、单核细胞-血小板相互作用和巨核细胞抑制中至关重要，但关键参与者 PF4 的促血栓形成潜力尚未得到研究，所有这些都可能导致 HIT 的病理生理学。本文解释了肝素给药时血小板激活过程中释放的 PF4 在 HIT 血小板减少症和血栓形成发病机制中的重要作用。
