摘要
肝素诱导的血小板减少症(heparin-induced thrombocytopenia,HIT)是肝素治疗引起的严重并发症,可导致血栓形成和栓塞。HIT的发病机制主要与肝素/血小板因子4抗体介导的免疫反应有关,IgG类是主要的致病抗体,能与肝素和血小板因子4结合形成复合物,引起血小板凝集和凝血反应增强,同时抗体还通过作用于血管内皮细胞和单核细胞参与HIT的形成。抗体相关的实验室检测包括功能性血小板试验和免疫学试验,临床表现结合实验室检测有助于本病的早期诊断和治疗,但是在检测方面目前尚没有理想的方法。本文就AHPF4抗体、HIT发病机制、临床实验室检测和免疫学试验检测等问题进行了综述。
Heparin-induced thrombocytopenia（HIT） is an antibody-mediated complication of heparin treatment that can lead to thrombosis and thromboembolism, HIT is mainly caused by immunoglobulin G （IgG） class among anti- heparin/platelet factor 4 antibodies that bind to epitopes on platelet factor 4 （PF4） released from activated platelets that developed when it forms complexes with heparin, Platelet aggregation and hypercoagulation status result from this process, Besides, the reactions between antibodies and vascular endothelial cells and monocytes are involved in HIT, Laboratory detection of anti-heparin/platelet factor 4 antibodies after heparin administration may help diagnose HIT early, Tests for detecting antibodies to the heparin/PF4 complex can be classified into functional platelet assays （ which rely on the demonstration of platelet activation） and immunoassays （ which detect the presence of an antibody without regard for its functional ability）, But there is no simple and effective test available currently. In this article the anti-heparin/platelet factor 4 antibodies, pathogenesis of HIT, clinical laboratory assays and immunoassays are reviewed,
出处
《中国实验血液学杂志》
CAS
CSCD
2008年第2期457-460,共4页
Journal of Experimental Hematology
