Banner Good Samaritan Medical Center, Medical Toxicology , Phoenix, AZ , USA.
Clin Toxicol (Phila). 2014 Jul;52(6):579-83. doi: 10.3109/15563650.2014.917181. Epub 2014 May 20.
Abstract A summary of heparin-induced thrombocytopenia (HIT) is presented. HIT is an adverse drug reaction characterized by thrombocytopenia and a high risk for venous or arterial thrombosis. The frequency of HIT ranges from 1 to 5% of patients receiving heparin with exact frequencies ranging between specific agents. Interestingly, this immune-mediated syndrome is ironically associated with thrombosis, not bleeding, with thrombin formation playing a major role. It is caused by heparin-dependent, platelet-activating antibodies that identifies a self-protein, PF4, bound to heparin that results in an antibody formation. The resulting platelet activation is associated with increased thrombin generation. Typically, the platelet count fall begins 5-10 days after starting heparin, although a rapid platelet count fall can occur in a patient who has antibodies from recent heparin use. Typical causes of HIT as well as the best diagnostic studies and treatment are discussed in this review. HIT was reviewed using a pubmed™ search; google scholar™ using key words: "Heparin-induced thrombocytopenia"; "heparin", and "drug AND thrombocytopenia."
介绍肝素诱导的血小板减少症（HIT）。HIT 是一种药物不良反应，其特征为血小板减少和发生静脉或动脉血栓的风险较高。HIT 的发生率在接受肝素治疗的患者中为 1%至 5%，具体频率因特定药物而异。有趣的是，这种免疫介导的综合征与血栓形成而不是出血有关，凝血酶形成起着重要作用。它是由肝素依赖性、血小板激活抗体引起的，该抗体可识别与肝素结合的自身蛋白 PF4，从而导致抗体形成。由此引起的血小板激活与凝血酶生成增加有关。通常，血小板计数下降始于开始使用肝素后 5-10 天，但最近使用肝素的患者中可能会出现血小板计数迅速下降。本文讨论了 HIT 的常见原因、最佳诊断研究和治疗方法。通过 pubmed™ 搜索和谷歌学术™ 使用关键词“肝素诱导的血小板减少症”、“肝素”和“药物和血小板减少症”进行了 HIT 综述。
