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肝素诱导的血小板减少症:真实世界的问题。

Heparin-induced thrombocytopenia: real-world issues.

机构信息

Department of Medicine, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, Ontario, Canada.

出版信息

Semin Thromb Hemost. 2011 Sep;37(6):653-63. doi: 10.1055/s-0031-1291375. Epub 2011 Nov 18.

DOI:10.1055/s-0031-1291375
PMID:22102268
Abstract

Heparin-induced thrombocytopenia (HIT) is a prothrombotic drug reaction caused by platelet-activating antibodies. HIT sera often activate platelets without needing heparin-such heparin-"independent" platelet activation can be associated with HIT beginning or worsening despite stopping heparin ("delayed-onset HIT"). We address important issues in HIT diagnosis and therapy, using a recent cohort of HIT patients to illustrate influences of heparin type; triggers for HIT investigation; serological features of heparin-independent platelet activation; and treatment. In our cohort of recent HIT cases ( N = 13), low-molecular-weight heparin (dalteparin) was a common causative agent ( N = 8, 62%); most patients were diagnosed after HIT-thrombosis had occurred; and danaparoid was the most frequently selected treatment. Heparin-independent platelet activation was common (7/13 [54%]) and predicted slower platelet count recovery (>1 week) among evaluable patients (5/5 vs 1/6; P = 0.015). In our experience with argatroban-treated patients, HIT-associated consumptive coagulopathy confounds anticoagulant monitoring. Our observations provide guidance on practical aspects of HIT diagnosis and management.

摘要

肝素诱导的血小板减少症(HIT)是一种由血小板激活抗体引起的促血栓形成药物反应。HIT 血清通常在不需要肝素的情况下激活血小板 - 这种肝素“非依赖性”血小板激活可能与肝素停用后 HIT 的开始或恶化有关(“迟发性 HIT”)。我们使用最近的 HIT 患者队列来阐明肝素类型的影响、HIT 调查的触发因素、肝素非依赖性血小板激活的血清学特征以及治疗方法,解决了 HIT 诊断和治疗中的重要问题。在我们最近的 HIT 病例队列中(N=13),低分子量肝素(达肝素)是常见的致病药物(N=8,62%);大多数患者在 HIT 血栓形成后被诊断;而达那肝素是最常选择的治疗药物。肝素非依赖性血小板激活很常见(7/13 [54%]),在可评估患者中预测血小板计数恢复较慢(>1 周)(5/5 比 1/6;P=0.015)。在我们对阿加曲班治疗患者的观察中,HIT 相关的消耗性凝血病使抗凝监测变得复杂。我们的观察结果为 HIT 诊断和管理的实际方面提供了指导。

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