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住院 COVID-19 患者的血浆组织型纤溶酶原激活物和纤溶酶原激活物抑制剂-1。

Plasma tissue plasminogen activator and plasminogen activator inhibitor-1 in hospitalized COVID-19 patients.

机构信息

Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.

Division of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.

出版信息

Sci Rep. 2021 Jan 15;11(1):1580. doi: 10.1038/s41598-020-80010-z.


DOI:10.1038/s41598-020-80010-z
PMID:33452298
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7810990/
Abstract

Patients with coronavirus disease-19 (COVID-19) are at high risk for thrombotic arterial and venous occlusions. However, bleeding complications have also been observed in some patients. Understanding the balance between coagulation and fibrinolysis will help inform optimal approaches to thrombosis prophylaxis and potential utility of fibrinolytic-targeted therapies. 118 hospitalized COVID-19 patients and 30 healthy controls were included in the study. We measured plasma antigen levels of tissue-type plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) and performed spontaneous clot-lysis assays. We found markedly elevated tPA and PAI-1 levels in patients hospitalized with COVID-19. Both factors demonstrated strong correlations with neutrophil counts and markers of neutrophil activation. High levels of tPA and PAI-1 were associated with worse respiratory status. High levels of tPA, in particular, were strongly correlated with mortality and a significant enhancement in spontaneous ex vivo clot-lysis. While both tPA and PAI-1 are elevated among COVID-19 patients, extremely high levels of tPA enhance spontaneous fibrinolysis and are significantly associated with mortality in some patients. These data indicate that fibrinolytic homeostasis in COVID-19 is complex with a subset of patients expressing a balance of factors that may favor fibrinolysis. Further study of tPA as a biomarker is warranted.

摘要

新型冠状病毒肺炎(COVID-19)患者存在发生血栓性动脉和静脉闭塞的高风险。然而,一些患者也出现了出血并发症。了解凝血和纤维蛋白溶解之间的平衡关系,有助于确定最佳的血栓预防策略,以及纤维蛋白溶解靶向治疗的潜在作用。研究纳入了 118 例住院 COVID-19 患者和 30 名健康对照者。我们测量了血浆组织型纤溶酶原激活物(tPA)和纤溶酶原激活物抑制剂-1(PAI-1)的抗原水平,并进行了自发血栓溶解试验。我们发现,住院 COVID-19 患者的 tPA 和 PAI-1 水平明显升高。这两种因子均与中性粒细胞计数和中性粒细胞激活标志物有很强的相关性。tPA 和 PAI-1 水平升高与呼吸状况恶化有关。特别是高水平的 tPA 与死亡率密切相关,并且显著增强了自发的体外血栓溶解。尽管 COVID-19 患者的 tPA 和 PAI-1 水平均升高,但极高水平的 tPA 增强了自发性纤维蛋白溶解,并且与某些患者的死亡率有显著相关性。这些数据表明,COVID-19 患者的纤维蛋白溶解平衡状态复杂,部分患者的一些因子可能有利于纤维蛋白溶解。需要进一步研究 tPA 作为生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8644/7810990/e6472121c259/41598_2020_80010_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8644/7810990/a30e49023b38/41598_2020_80010_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8644/7810990/1d91ff631878/41598_2020_80010_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8644/7810990/450f26f501ca/41598_2020_80010_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8644/7810990/e6472121c259/41598_2020_80010_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8644/7810990/a30e49023b38/41598_2020_80010_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8644/7810990/1d91ff631878/41598_2020_80010_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8644/7810990/450f26f501ca/41598_2020_80010_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8644/7810990/e6472121c259/41598_2020_80010_Fig4_HTML.jpg

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[4]
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[5]
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[9]
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[10]
Association Between Coagulation Fibrinolysis Markers and Severity in Patients with COVID-19.

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本文引用的文献

[1]
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Shock. 2021-6-1

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