与炎症相关的颈静脉血栓形成的神经学表现可能是长期COVID的后遗症

Neuroprotection Pub Date : 2023-11-09 DOI:10.1002/nep3.24
Elizabeth Mendoza‐Portillo, Estefania Aleman‐Navarro, G. Aleph Prieto, Yvonne Rosenstein, Jose J. Lozano‐Nuevo, Araceli Perez‐Lopez
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引用次数: 0

摘要

自严重急性呼吸综合征冠状病毒2 (SARS - CoV - 2)大流行开始以来的三年中,全球已记录了超过6.7亿例冠状病毒病2019 (COVID - 19)。约45%的COVID - 19幸存者会出现一种称为长期COVID的综合征,在急性感染后症状甚至持续数月。约76%的长期COVID患者出现神经系统症状。此外,幸存的患者发生脑静脉血栓形成的风险增加。本病例报告描述了一名41岁女性,在接种牛津-阿斯利康(ChAdOx1 nCoV - 19)疫苗(阿斯利康-印度血清研究所)24小时后出现与颈静脉血栓相关的神经系统症状。她在接种疫苗前三个月感染了SARS - CoV - 2。尽管考虑到她最近接种了疫苗,最初怀疑是疫苗诱导的免疫性血栓性血小板减少症(VITT),但该患者没有任何VITT的特征,如血小板减少症、d -二聚体水平升高或抗血小板因子- 4抗体。此外,神经系统表现与高浓度的炎症细胞因子(包括白细胞介素(IL) - 6、IL - 17A和IL - 21)以及脑脊液中中性粒细胞水平升高有关,这表明炎症免疫成分在血栓形成事件的发展中起作用,并指向另一种诊断。在本例中,实验室结果显示与颈静脉血栓形成相关的神经学表现与VITT无关。因此,我们认为左颈静脉血栓形成是SARS - CoV - 2感染的后遗症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neurological manifestations with jugular vein thrombosis linked to an inflammatory profile may be a sequela of long COVID
Abstract More than 670 million cases of coronavirus disease 2019 (COVID‐19) have been recorded worldwide in the 3 years since the start of the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) pandemic. About 45% of survivors of COVID‐19 develop a syndrome known as long‐term COVID, in which symptoms persist even months after the acute infection. About 76% of patients with long COVID experience neurological manifestations. Moreover, patients who have survived COVID‐19 have an increased risk of cerebral venous thrombosis. This case report describes a 41‐year‐old woman who developed neurological manifestations associated with jugular vein thrombosis 24 h after administration of the Oxford–AstraZeneca (ChAdOx1 nCoV‐19) vaccine (AstraZeneca‐Serum Institute of India). She had been infected with SARS‐CoV‐2 three months before vaccination. Although initially suspected to be a case of vaccine‐induced immune thrombotic thrombocytopenia (VITT) in view of her recent vaccination, the patient did not have any hallmarks of VITT, such as thrombocytopenia, an increased d ‐dimer level, or antibodies against platelet factor‐4. Moreover, the neurological manifestations were associated with a high concentration of inflammatory cytokines, including interleukin (IL)‐6, IL‐17A, and IL‐21, and elevated neutrophil levels in cerebrospinal fluid, suggesting that inflammatory immune components had a role in the development of thrombotic events and pointing to an alternative diagnosis. In this case, the laboratory results indicated that the neurological manifestations associated with jugular vein thrombosis were not associated with VITT. Therefore, we propose that the thrombosis of the left jugular vein was a sequela of SARS‐CoV‐2 infection.
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