肝素诱导的血小板减少症:诊断试验和生物学机制

PhD Jean Amiral (Scientific Director), MD, PhD Dominique Meyer (Professor)
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引用次数: 12

摘要

发现PF4在肝素依赖性抗体的发展和致病性中的作用,肝素依赖性抗体会引发肝素诱导的血小板减少症(HIT),这是肝素治疗的一种罕见但严重的不良反应,使我们能够重新审视这种并发症的诊断和涉及的病理机制。在这篇综述中,诊断测试可用于确认或预测HIT的分析,并讨论新的诊断策略。在一些肝素治疗的患者肝素依赖性免疫反应的发展所涉及的因素,然后提出。最后,假设抗体的存在是HIT的一个危险因素。讨论了导致并发症发生的机制和其他危险因素的作用,包括患者的临床状态和使用的肝素类型(Magnani, 1993)。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
12 Heparin-induced thrombocytopenia: diagnostic tests and biological mechanisms

The discovery of the role of PF4 in the development and pathogenicity of heparin-dependent antibodies which trigger heparin-induced thrombocytopenia (HIT), a rare but severe adverse effect of heparin therapy, has allowed us to revisit the diagnosis of this complication and the pathological mechanisms involved. In this review, diagnostic tests available for confirmation or prediction of HIT are analysed, and new diagnostic strategies are discussed. Factors involved in the development of the heparin-dependent immune response in some heparin-treated patients are then presented. Lastly, it is hypothesized that the presence of antibodies is a risk factor for HIT. The mechanisms which contribute to the development of complications and the role of additional risk factors, including the patient's clinical state and the type of heparin used, are discussed (Magnani, 1993).

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