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首页> 外文期刊>Chest: The Journal of Circulation, Respiration and Related Systems >So, does low-molecular-weight heparin cause less heparin-induced thrombocytopenia than unfractionated heparin or not?
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So, does low-molecular-weight heparin cause less heparin-induced thrombocytopenia than unfractionated heparin or not?

机译:那么,低分子量肝素引起的肝素诱导的血小板减少症是否比普通肝素引起的少?

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Heparin-induced thrombocytopenia (HIT) is a protlirombotic adverse effect of heparin caused by platelet-activating antibodies that recognize mul-timolecular complexes of the chemokine platelet factor 4 (PF4) when it is bound to heparin. The reduced risk of HIT and HIT-associated thrombosis (HITT) with low-molecular-weight heparin (LMWH) compared with unfractionated heparin (UFH) seems well established. It was demonstrated in a large randomized controlled trial (RCT),2 in several prospective nonrandomized comparisons, in metaanalyses of these (and other) studies, and also in several retrospective, but large-scale, population-based studies. Furthermore, in-study serologic investigations indicate much lower frequencies of anti-PF4/heparin antibody formation with LMWH compared with UFH. Finally, there is an underlying biological rationale, as larger, and presumably more immunogenic, PF4-polysacchari.de complexes are formed with UFH than with LMWH. The case in favor of LMWH vis-a-vis avoiding HIT would seemclosed. And yet, in this issue of CHEST (see page 1131),
机译:肝素诱导的血小板减少症(HIT)是由血小板活化抗体引起的肝素的多环血栓形成不良反应,当与肝素结合时,血小板活化抗体识别趋化因子血小板因子4(PF4)的多分子复合物。与普通肝素(UFH)相比,低分子量肝素(LMWH)降低HIT和HIT相关血栓形成(HITT)的风险似乎已经确立。在一项大型的随机对照试验(RCT)2中,在一些前瞻性非随机比较中,在这些(和其他)研究的荟萃分析中,以及在一些回顾性但大规模的基于人群的研究中,都证明了这一点。此外,研究中的血清学研究表明,与UFH相比,LMWH产生抗PF4 /肝素抗体的频率要低得多。最后,有一个潜在的生物学原理,因为UFH比LMWH形成更大且可能具有更大免疫原性的PF4-polysacchari.de复合物。 LMWH相对于避免HIT的案例似乎已经结束。但是,在本期的CHEST(请参阅第1131页)中,

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