PF4, Platelet factor 4

  • 文章类型: Journal Article
    UNASSIGNED:肝素诱导的血小板减少症(HIT)是一种免疫介导的并发症,发生在一小部分暴露于肝素的患者中。在接受需要体外循环的心脏手术的患者中,HIT的担忧尤其高,因为他们在术中接触高剂量的肝素。我们的目的是确定和评估在心脏手术后再次入院期间被诊断为HIT的患者的住院过程。
    UNASSIGNED:对2017年6月至2019年10月接受心脏直视手术的患者进行了回顾性回顾。其中,我们确定了重新入院后新诊断为HIT的患者.HIT阳性定义为抗PF4抗体筛查试验阳性,加上血清素释放试验阳性。
    未经证实:在确定的2496名患者中,13例患者入院时HIT阳性,被排除在外。在剩下的2483名患者中,351人在30天内再次入院。六人在重新入院期间被新诊断为HIT,其中5人出现血栓性并发症。一名患者因血小板减少症再次入院,并开始服用阿加曲班;其余5名患者在再次入院时血小板计数没有明显降低。在因静脉血栓栓塞再次入院的12例患者中,4检测为HIT阳性。
    未经证实:HIT在心脏直视手术后可能出现延迟。静脉血栓栓塞似乎是再入院期间HIT的重要指标,即使没有血小板减少症。这可能支持在确定HIT状态之前,再次接受血栓栓塞的心脏手术患者使用非肝素抗凝药物。
    UNASSIGNED: Heparin-induced thrombocytopenia (HIT) is an immune-mediated complication that occurs in a small percentage of patients exposed to heparin. Concerns of HIT are particularly high in patients undergoing cardiac procedures requiring cardiopulmonary bypass, as they are exposed to high doses of heparin intraoperatively. Our aim was to identify and assess the hospital courses of patients who were diagnosed with HIT during readmission following cardiac surgery.
    UNASSIGNED: A retrospective review of patients who underwent open cardiac surgical procedures from June 2017 through October 2019 was performed. Of these, we identified patients who were newly diagnosed with HIT upon readmission. HIT positivity was defined as a positive anti-PF4 antibody screening test, plus a positive serotonin release assay.
    UNASSIGNED: Of the 2496 patients identified, 13 patients were HIT positive on index admission and were excluded. Of the remaining 2483 patients, 351 were readmitted within 30 days. Six were newly diagnosed with HIT during readmission, 5 of whom presented with thrombotic complications. One patient was readmitted with thrombocytopenia and was started on argatroban; the remaining 5 did not have a significantly lower platelet count on readmission. Of the 12 patients readmitted for venous thromboembolism, 4 tested positive for HIT.
    UNASSIGNED: HIT can have a delayed appearance following open heart surgery. Venous thromboembolism appears to be a significant indicator for HIT during readmission, even in the absence of thrombocytopenia. This may support the use of non-heparin anticoagulation for cardiac surgery patients readmitted with thromboembolism until HIT status is determined.
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  • 文章类型: Journal Article
    对疫苗诱导的血栓性血小板减少症(VITT)的罕见但严重且可能致命的并发症的认识引起了人们对COVID-19疫苗安全性的担忧,并导致许多国家重新考虑疫苗接种策略。在描述腺病毒载体ChAdOx1疫苗的接受者中的VITT之后,Ad26后对类似病例的审查。COV2·S疫苗接种引起了一个问题,即该实体是否可能构成所有腺病毒载体疫苗的潜在类效应。大多数病例是女性,通常年龄小于60岁,在接种血小板减少症和血栓表现后不久(范围:5-30天)出现,偶尔在多个网站。在最初的不确定之后,指导诊断的具体建议(临床怀疑,初步实验室筛查,PF4-聚阴离子-抗体ELISA)和VITT(非肝素抗凝剂,皮质类固醇,静脉注射免疫球蛋白)已经发行。这种罕见综合征背后的机制目前是活跃研究的主题,包括以下内容:1)PF4-聚阴离子自身抗体的产生;2)腺病毒载体进入巨细胞中,随后在血小板表面表达刺突蛋白;3)腺病毒载体指导血小板和内皮细胞的结合和激活;4)PF4-聚阴离子自身抗体激活内皮细胞和炎性细胞;除了分析潜在的潜在机制外,这篇综述旨在概述VITT的临床和流行病学特征,提出当前关于VITT诊断和治疗工作的循证建议,并讨论描述该实体后出现的新困境和观点。
    The recognition of the rare but serious and potentially lethal complication of vaccine induced thrombotic thrombocytopenia (VITT) raised concerns regarding the safety of COVID-19 vaccines and led to the reconsideration of vaccination strategies in many countries. Following the description of VITT among recipients of adenoviral vector ChAdOx1 vaccine, a review of similar cases after Ad26.COV2·S vaccination gave rise to the question whether this entity may constitute a potential class effect of all adenoviral vector vaccines. Most cases are females, typically younger than 60 years who present shortly (range: 5-30 days) following vaccination with thrombocytopenia and thrombotic manifestations, occasionally in multiple sites. Following initial incertitude, concrete recommendations to guide the diagnosis (clinical suspicion, initial laboratory screening, PF4-polyanion-antibody ELISA) and management of VITT (non-heparin anticoagulants, corticosteroids, intravenous immunoglobulin) have been issued. The mechanisms behind this rare syndrome are currently a subject of active research and include the following: 1) production of PF4-polyanion autoantibodies; 2) adenoviral vector entry in megacaryocytes and subsequent expression of spike protein on platelet surface; 3) direct platelet and endothelial cell binding and activation by the adenoviral vector; 4) activation of endothelial and inflammatory cells by the PF4-polyanion autoantibodies; 5) the presence of an inflammatory co-signal; and 6) the abundance of circulating soluble spike protein variants following vaccination. Apart from the analysis of potential underlying mechanisms, this review aims to synopsize the clinical and epidemiologic features of VITT, to present the current evidence-based recommendations on diagnostic and therapeutic work-up of VITT and to discuss new dilemmas and perspectives that emerged after the description of this entity.
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