ANZAC Research Institute, University of Sydney, Sydney, NSW, Australia.
Department of Haematology, Concord Repatriation General Hospital and NSW Health Pathology, Sydney, NSW, Australia.
Blood Adv. 2022 Jun 14;6(11):3494-3506. doi: 10.1182/bloodadvances.2021006698.
Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a severe prothrombotic complication of adenoviral vaccines, including the ChAdOx1 nCoV-19 (Vaxzevria) vaccine. The putative mechanism involves formation of pathological anti-platelet factor 4 (PF4) antibodies that activate platelets via the low-affinity immunoglobulin G receptor FcγRIIa to drive thrombosis and thrombocytopenia. Functional assays are important for VITT diagnosis, as not all detectable anti-PF4 antibodies are pathogenic, and immunoassays have varying sensitivity. Combination of ligand binding of G protein-coupled receptors (protease-activated receptor-1) and immunoreceptor tyrosine-based activation motif-linked receptors (FcγRIIa) synergistically induce procoagulant platelet formation, which supports thrombin generation. Here, we describe a flow cytometry-based procoagulant platelet assay using cell death marker GSAO and P-selectin to diagnose VITT by exposing donor whole blood to patient plasma in the presence of a protease-activated receptor-1 agonist. Consecutive patients triaged for confirmatory functional VITT testing after screening using PF4/heparin ELISA were evaluated. In a development cohort of 47 patients with suspected VITT, plasma from ELISA-positive patients (n = 23), but not healthy donors (n = 32) or individuals exposed to the ChAdOx1 nCov-19 vaccine without VITT (n = 24), significantly increased the procoagulant platelet response. In a validation cohort of 99 VITT patients identified according to clinicopathologic adjudication, procoagulant flow cytometry identified 93% of VITT cases, including ELISA-negative and serotonin release assay-negative patients. The in vitro effect of intravenous immunoglobulin (IVIg) and fondaparinux trended with the clinical response seen in patients. Induction of FcγRIIa-dependent procoagulant response by patient plasma, suppressible by heparin and IVIg, is highly indicative of VITT, resulting in a sensitive and specific assay that has been adopted as part of a national diagnostic algorithm to identify vaccinated patients with platelet-activating antibodies.
疫苗诱导的免疫性血栓性血小板减少症(VITT)是腺病毒疫苗(包括 ChAdOx1 nCoV-19[Vaxzevria]疫苗)的一种严重的促血栓形成并发症。推测的机制涉及形成病理性抗血小板因子 4(PF4)抗体,这些抗体通过低亲和力免疫球蛋白 G 受体 FcγRIIa 激活血小板,从而导致血栓形成和血小板减少。功能检测对于 VITT 的诊断很重要,因为并非所有可检测到的抗 PF4 抗体都是致病性的,而且免疫测定的敏感性也不同。G 蛋白偶联受体(蛋白酶激活受体-1)配体结合和免疫受体酪氨酸激活基序相关受体(FcγRIIa)的组合协同诱导促凝血血小板形成,这支持凝血酶生成。在这里,我们描述了一种基于流式细胞术的促凝血血小板检测方法,使用细胞死亡标志物 GSAO 和 P-选择素,通过在存在蛋白酶激活受体-1 激动剂的情况下将供体全血暴露于患者血浆中,来诊断 VITT。对使用 PF4/肝素 ELISA 进行筛选后进行确认性功能性 VITT 检测的连续患者进行了评估。在疑似 VITT 的 47 例患者的发展队列中,来自 ELISA 阳性患者(n=23)的血浆,但不是健康供体(n=32)或未发生 VITT 而暴露于 ChAdOx1 nCov-19 疫苗的个体(n=24),显著增加了促凝血血小板反应。在根据临床病理裁决确定的 99 例 VITT 患者的验证队列中,促凝血流式细胞术鉴定了 93%的 VITT 病例,包括 ELISA 阴性和 5-羟色胺释放试验阴性的患者。静脉注射免疫球蛋白(IVIg)和磺达肝素的体外作用与患者的临床反应趋势一致。患者血浆诱导的 FcγRIIa 依赖性促凝血反应可被肝素和 IVIg 抑制,高度提示 VITT,从而产生一种敏感且特异的检测方法,已被采用作为识别接种疫苗后具有血小板激活抗体的患者的国家诊断算法的一部分。