肝素诱导的血小板减少症:一个基于病例的重新评估

A. Kandoria, S. Rao, P. Negi, R. Bhardwaj, K. Mahajan, N. Gaur
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摘要

肝素诱导的血小板减少症(HIT)是一种免疫介导的药物不良反应,由肝素存在时激活血小板的抗体的出现引起。尽管血小板减少症,出血是罕见的。HIT与动脉和静脉系统的血栓栓塞性并发症密切相关。可进行若干实验室检查以确认诊断;然而,当临床怀疑HIT时,不应等待结果而不进行治疗。幸运的是,治疗策略已经得到了改进,新的有效的治疗药物已经出现。我们报告一例II型HIT。回顾HIT,检查重要的临床症状和诊断指标。然后讨论HIT的治疗,重点是当前的治疗方法。广泛的文献综述已经进行了目前的原因,病理生理和治疗HIT的全面审查。*通信:Somendra Rao,医学博士,印度西姆拉英迪拉甘地医学院心脏病学系高级住院医师,E-mail: sureshdev。rao@gmail.com收稿日期:2019年03月07日;录用日期:2019年3月26日;介绍介绍了两种类型的HIT。I型是一种非免疫的、介导的、无症状的、短暂的血小板计数下降,发生在一些肝素治疗的患者身上。其典型特征是在肝素治疗后的头两天内血小板计数下降较少,并经常在肝素治疗后恢复正常[1,2]。II型(HIT-II)是一种免疫介导的疾病,其特征是形成针对肝素-血小板因子4复合物的抗体。由于HIT的发生率根据所研究的患者人群的不同,在0.5%到5%之间变化[3]。一项荟萃分析指出,发病率为2.6%[4]。最近有人建议将“HIT I型”改为“非免疫性肝素相关性血小板减少症”,将“HIT II型”改为“HIT”,以避免两种综合征的混淆
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Heparin induced thrombocytopenia: A case-based re-appraisal
Heparin‐induced thrombocytopenia (HIT) is an immune mediated adverse drug reaction caused by the emergence of antibodies that activate platelets in the presence of heparin. Despite thrombocytopenia, bleeding is rare. HIT is strongly associated with thromboembolic complications involving both the arterial and venous systems. A number of laboratory tests are available to confirm the diagnosis; however, when HIT is clinically suspected, treatment should not be withheld pending the result. Fortunately, therapeutic strategies have been refined, and new and effective therapeutic agents are available. We present a case of HIT Type II. A review of HIT is presented, examining the important clinical symptoms and diagnostic indicators. The treatment of HIT is then discussed, with an emphasis on current therapies. An extensive literature review has been performed to present a comprehensive review of the causes, pathophysiology and treatment of HIT. *Correspondence to: Somendra Rao, MD Senior Resident, Department of Cardiology Indira Gandhi Medical College, Shimla, India, E-mail: sureshdev. rao@gmail.com Received: March 07, 2019; Accepted: March 26, 2019; Published: March 28, 2019 Introduction There are two types of HIT described. Type I is a non-immune, mediated, asymptomatic, transient drop in platelet count that occurs in some heparin treated patients. It is typically characterized by a lesser fall in platelet count within the first two days after heparin initiation and often returns to normal with continued heparin administration [1,2]. Type II (HIT-II) is an immune-mediated disorder characterized by the formation of antibodies against heparin-platelet factor 4 complexes. Since The frequency of HIT varies from 0.5% to 5%, depending on the patient population studied [3]. A meta-analysis noted an incidence of 2.6 percent [4]. It has recently been proposed that the term “HIT type I” be changed to “non‐immune heparin associated thrombocytopenia” and that the term “HIT type II” be changed to “HIT” to avoid confusion between the two syndromes
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