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肝素诱导的血小板减少症。

Heparin-induced thrombocytopenia.

作者信息

Greinacher A

机构信息

Institut für Immunologie und Transfusionsmedizin, Ernst-Moritz-Arndt-Universität Greifswald, Sauerbruchstr, Greifswald, Germany.

出版信息

J Thromb Haemost. 2009 Jul;7 Suppl 1:9-12. doi: 10.1111/j.1538-7836.2009.03385.x.

Abstract

Heparin-induced thrombocytopenia (HIT), typically occurring in the second week of heparin therapy, is an antibody-mediated adverse drug reaction associated with increased thrombotic risk. The most important antigens are located on platelet factor 4 (PF4)/heparin complexes. All HIT is caused by platelet-activating antibodies, but not all PF4/heparin-reactive antibodies cause HIT. Thus, tests have high negative, but only moderate, positive predictive value. Cessation of heparin requires substitution with an alternative anticoagulant, but as these drugs have increased bleeding risk, they should be used in therapeutic doses only if HIT is considered very likely. Avoiding/postponing coumarin is crucial in minimizing microthrombotic complications. Recent studies of HIT immunobiology suggest that HIT mimics immunity against repetitive antigens, as they are relevant in microbial defense. Thus, understanding HIT may help unravel why host defenses can trigger autoimmunity.

摘要

肝素诱导的血小板减少症(HIT)通常发生在肝素治疗的第二周,是一种抗体介导的药物不良反应,与血栓形成风险增加相关。最重要的抗原位于血小板因子4(PF4)/肝素复合物上。所有的HIT都是由血小板活化抗体引起的,但并非所有PF4/肝素反应性抗体都会导致HIT。因此,检测的阴性预测价值高,但阳性预测价值仅为中等。停用肝素需要用替代抗凝剂替代,但由于这些药物会增加出血风险,只有在认为很可能发生HIT时才应以治疗剂量使用。避免/推迟使用香豆素对于将微血栓形成并发症降至最低至关重要。最近关于HIT免疫生物学的研究表明,HIT模拟了针对重复抗原的免疫,因为它们在微生物防御中具有相关性。因此,了解HIT可能有助于揭示宿主防御为何会引发自身免疫。

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