Importance The COVID-19 pandemic saw one of the fastest developments of vaccines in an effort to combat an out-of-control pandemic. The 2 most common COVID-19 vaccine platforms currently in use, messenger RNA (mRNA) and adenovirus vector, were developed on the basis of previous research in use of this technology. Postauthorization surveillance of COVID-19 vaccines has identified safety signals, including unusual cases of thrombocytopenia with thrombosis reported in recipients of adenoviral vector vaccines. One of the devastating manifestations of this syndrome, termed vaccine-induced immune thrombotic thrombocytopenia (VITT), is cerebral venous sinus thrombosis (CVST). This review summarizes the current evidence and indications regarding biology, clinical characteristics, and pharmacological management of VITT with CVST.

Observations VITT appears to be similar to heparin-induced thrombocytopenia (HIT), with both disorders associated with thrombocytopenia, thrombosis, and presence of autoantibodies to platelet factor 4 (PF4). Unlike VITT, HIT is triggered by recent exposure to heparin. Owing to similarities between these 2 conditions and lack of high-quality evidence, interim recommendations suggest avoiding heparin and heparin analogues in patients with VITT. Based on initial reports, female sex and age younger than 60 years were identified as possible risk factors for VITT. Treatment consists of therapeutic anticoagulation with nonheparin anticoagulants and prevention of formation of autoantibody-PF4 complexes, the latter being achieved by administration of high-dose intravenous immunoglobin (IVIG). Steroids, which can theoretically inhibit the production of new antibodies, have been used in combination with IVIG. In severe cases, plasma exchange should be used for clearing autoantibodies. Monoclonal antibodies, such as rituximab and eculizumab, can be considered when other therapies fail. Routine platelet transfusions, aspirin, and warfarin should be avoided because of the possibility of worsening thrombosis and magnifying bleeding risk.

Conclusions and Relevance Adverse events like VITT, while uncommon, have been described despite vaccination remaining the most essential component in the fight against the COVID-19 pandemic. While it seems logical to consider the use of types of vaccines (eg, mRNA-based administration) in individuals at high risk, treatment should consist of therapeutic anticoagulation mostly with nonheparin products and IVIG.

重要性 COVID-19 大流行见证了疫苗的最快发展之一，以努力对抗失控的大流行。目前使用的 2 种最常见的 COVID-19 疫苗平台，信使 RNA (mRNA) 和腺病毒载体，是在先前使用该技术的研究的基础上开发的。COVID-19 疫苗的授权后监测已经确定了安全信号，包括在腺病毒载体疫苗接受者中报告的异常血小板减少症和血栓形成病例。这种综合征的破坏性表现之一，称为疫苗诱导的免疫血栓性血小板减少症(VITT) 是脑静脉窦血栓形成 (CVST)。本综述总结了有关 VITT 与 CVST 的生物学、临床特征和药理学管理的当前证据和适应症。

观察 VITT 似乎与肝素诱导的血小板减少症 (HIT) 相似，这两种疾病都与血小板减少症、血栓形成和血小板因子 4 (PF4) 自身抗体的存在相关。与 VITT 不同，HIT 是由最近接触肝素引发的。由于这两种情况的相似性和缺乏高质量证据，临时建议建议 VITT 患者避免使用肝素和肝素类似物。根据初步报告，女性和年龄小于 60 岁被确定为 VITT 的可能危险因素。治疗包括使用非肝素抗凝剂进行治疗性抗凝和预防自身抗体-PF4 复合物的形成，后者通过给予高剂量静脉内免疫球蛋白 (IVIG) 来实现。类固醇，理论上可以抑制新抗体的产生，已与 IVIG 联合使用。在严重的情况下，应使用血浆置换清除自身抗体。当其他疗法失败时，可以考虑使用单克隆抗体，如利妥昔单抗和依库珠单抗。应避免常规血小板输注、阿司匹林和华法林，因为可能会加重血栓形成和放大出血风险。

结论和相关性 尽管疫苗接种仍然是抗击 COVID-19 大流行的最重要组成部分，但已经描述了 VITT 等不良事件虽然不常见。虽然考虑在高危个体中使用不同类型的疫苗（例如基于 mRNA 的给药）似乎是合乎逻辑的，但治疗应包括主要使用非肝素产品和 IVIG 的治疗性抗凝治疗。