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大剂量静脉注射免疫球蛋白治疗和预防肝素诱导的血小板减少症:综述。

High-dose intravenous immunoglobulin for the treatment and prevention of heparin-induced thrombocytopenia: a review.

机构信息

a Department of Pathology and Molecular Medicine, McMaster University , Hamilton , Ontario , Canada.

b McMaster Centre for Transfusion Research, McMaster University , Hamilton , Ontario , Canada.

出版信息

Expert Rev Hematol. 2019 Aug;12(8):685-698. doi: 10.1080/17474086.2019.1636645. Epub 2019 Jul 5.

Abstract

: Heparin-induced thrombocytopenia (HIT) is known for its strong association with thrombosis and distinct pathogenesis involving anti-PF4/polyanion antibodies that activate platelets strongly through clustering of platelet FcγIIa receptors. Autoimmune HIT (aHIT) refers to a subgroup of patients whose HIT antibodies have both heparin-dependent and heparin-independent platelet-activating properties. aHIT patients have atypical clinical presentations including delayed-onset HIT, persisting (refractory) HIT, heparin 'flush' HIT, fondaparinux-associated HIT, severe thrombocytopenia (platelet count <20 × 10/L) with overt disseminated intravascular coagulation, and spontaneous HIT syndrome. : This article reviews all available literature describing the use of high-dose intravenous immunoglobulin (IVIG) as an adjunct treatment to anticoagulation in HIT patients. IVIG is usually effective in interrupting platelet activation by aHIT antibodies, manifesting as a rapid platelet count increase after starting IVIG (usual dose, 1g/kg × 2 days). Experience to date suggests IVIG de-escalates HIT and likely reduces thrombotic risk. A new case of aHIT successfully treated with IVIG is presented. Use of IVIG to prevent acute HIT with planned heparin reexposure in antibody-positive patients is also discussed. : High-dose IVIG appears to rapidly inhibit HIT antibody-induced platelet activation and has the potential to become an important treatment adjunct for HIT, particularly in patients with aHIT.

摘要

肝素诱导的血小板减少症(HIT)与血栓形成密切相关,其发病机制独特,涉及抗 PF4/多阴离子抗体,这些抗体通过血小板 FcγIIa 受体的聚集强烈激活血小板。自身免疫性 HIT(aHIT)是指一组患者的 HIT 抗体具有肝素依赖性和肝素非依赖性血小板激活特性。aHIT 患者具有非典型的临床表现,包括迟发性 HIT、持续性(难治性)HIT、肝素“冲洗”HIT、磺达肝素相关 HIT、伴有明显弥散性血管内凝血的严重血小板减少症(血小板计数 <20×10/L)和自发性 HIT 综合征。本文综述了所有可用的文献,描述了在 HIT 患者中使用大剂量静脉注射免疫球蛋白(IVIG)作为抗凝治疗的辅助治疗。IVIG 通常可有效阻断 aHIT 抗体引起的血小板激活,表现为开始 IVIG 后血小板计数迅速增加(常用剂量为 1g/kg×2 天)。迄今为止的经验表明,IVIG 可减轻 HIT 并可能降低血栓形成风险。报告了一例成功用 IVIG 治疗的 aHIT 新病例。还讨论了在抗体阳性患者中计划重新使用肝素时使用 IVIG 预防急性 HIT 的情况。大剂量 IVIG 似乎可迅速抑制 HIT 抗体诱导的血小板激活,有可能成为 HIT 的重要治疗辅助手段,特别是在 aHIT 患者中。

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