Chong B H, Pilgrim R L, Cooley M A, Chesterman C N
Department of Haematology, Prince of Wales Hospital, University of New South Wales, Sydney, Australia.
Blood. 1993 Feb 15;81(4):988-93.
Our previous finding that heparin-dependent antibodies in heparin-induced thrombocytopenia (HIT) bind to platelets via platelet IgG Fc receptors (FcRs) prompted this study. Platelet FcRs in 16 patients with HIT, 23 control patients, and 42 normal subjects were studied. Patients with HIT had substantially increased platelet FcRs during the acute illness. Those who suffered serious thrombotic complications or died shortly after diagnosis had significantly more FcRs per platelet than those with milder disease. Consistent with their increased FcRs, platelets of patients with HIT showed increased aggregation reactivity to aggregated IgG and heparin-dependent antibodies. Platelet FcRs in patients with HIT remained elevated for 1 to 3 months after the acute illness then stabilized to a mean value not significantly different from either control group. The increased expression of FcRs on HIT platelets and their increased reactivity to heparin-dependent antibodies may contribute to the pathogenesis of thrombocytopenia and thrombosis in HIT.
我们之前的发现，即肝素诱导的血小板减少症（HIT）中依赖肝素的抗体通过血小板IgG Fc受体（FcRs）与血小板结合，促使了本研究。我们研究了16例HIT患者、23例对照患者和42名正常受试者的血小板FcRs。HIT患者在急性疾病期间血小板FcRs显著增加。那些遭受严重血栓并发症或在诊断后不久死亡的患者，每血小板的FcRs明显多于病情较轻的患者。与FcRs增加一致，HIT患者的血小板对聚集的IgG和依赖肝素的抗体表现出增加的聚集反应性。HIT患者的血小板FcRs在急性疾病后1至3个月仍保持升高，然后稳定在一个与两个对照组均无显著差异的平均值。HIT血小板上FcRs表达的增加及其对依赖肝素抗体反应性的增加可能有助于HIT中血小板减少和血栓形成的发病机制。
