Horne M K, Alkins B R
Clinical Pathology Department, Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda, MD 20892, USA.
J Lab Clin Med. 1996 May;127(5):435-42. doi: 10.1016/s0022-2143(96)90060-8.
Although heparin induces immune-mediated thrombocytopenia, it has been difficult to demonstrate heparin specificity of the putative immunoglobin. Recently, however, a body of data has indicated that platelet factor 4 (PF4) is required for heparin-induced thrombocytopenia (HIT) antibody to bind to heparin. Using viable platelets in a physiologic buffer, we have now documented specific and reversible platelet binding of iodine 125-labeled IgG from 5 patients with HIT and binding of 125I-labeled F(ab')2 from 2 of them. The binding requires the presence of both heparin and PF4 in a molar ratio of approximately 1:1. We have also shown that platelet activation increases HIT antibody binding. Our data suggest that the F(ab')2 domain of HIT antibody binds to heparin-PF4 complexes that accumulate on the platelet surface when equimolar concentrations of heparin and PF4 are present.
尽管肝素可诱发免疫介导的血小板减少症，但一直难以证明假定免疫球蛋白的肝素特异性。然而，最近有大量数据表明，肝素诱导的血小板减少症（HIT）抗体与肝素结合需要血小板因子4（PF4）。我们现在使用生理缓冲液中的活血小板，记录了5例HIT患者的125I标记IgG与血小板的特异性和可逆性结合，以及其中2例患者的125I标记F(ab')2与血小板的结合。这种结合需要肝素和PF4同时存在，摩尔比约为1:1。我们还表明，血小板活化会增加HIT抗体的结合。我们的数据表明，当存在等摩尔浓度的肝素和PF4时，HIT抗体的F(ab')2结构域会与积聚在血小板表面的肝素-PF4复合物结合。
