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与非COVID败血症相比,COVID-19中蛋白C通路活性下降:观察性和比较性队列研究

Heiko Rühl¹, Christian Bode², Tobias Becher³

¹Institute of Experimental Hematology and Transfusion Medicine, University Hospital Bonn, 53127 Bonn, Germany.

|September 28, 2024

概括

与非COVID败血症患者相比,COVID-19败血症患者表现出较低的抗凝剂反应,这与较低的活性蛋白C (APC) 水平相对于血栓标记物相对较低. 这种受损的蛋白C通路功能可能会导致COVID-19患者的凝血风险增加.

科学领域:

血液学血液学血液学
关键护理医学关键护理医学
传染性疾病传染性疾病

背景情况:

败血症相关的凝血病是死亡率的重要预测因素.
蛋白C (PC) 途径在抗凝中起着至关重要的作用.
PC通路的功能障碍可能是2019年冠状病毒病 (COVID-19) 败血症中观察到的前血栓状况的基础.

研究的目的:

评估COVID-19和非COVID败血症中蛋白C通路的功能.
为了比较关键酶,血栓素和活性蛋白C (APC) 的水平,在患者组和健康对照组之间.
为了研究凝血激活和败血症中抗凝剂反应之间的关系.

主要方法:

在30名COVID-19患者,47名非COVID败血症患者和40名健康对照人群中测量了血中血,活性蛋白C (APC),前列血片段1+2 (F1+2) 和血-抗血复合物 (TAT).
在健康对照组中,使用重组激活因子VII诱导了凝血激活和APC形成.
基于寡核酸的酶捕获试验用于测量血栓素和APC.

主要成果:

与受刺激的健康对照人群相比,患有COVID-19和非COVID败血症的患者表现出显著更高水平的血栓标记物 (血栓,F1+2,TAT).
与对照组相比,COVID-19和非COVID败血症组的APC水平都较高,但与血栓标记物相对的APC反应在COVID-19患者中较低.
与非COVID败血症组相比,在COVID-19组中APC/血素,APC/F1+2和APC/TAT的调整比率明显较低,并且刺激了健康对照.

结论:

COVID-19败血症的特征是相对较低的抗凝剂反应,特别是相对于血栓活性相对较低的活性蛋白C (APC) 生成.
在COVID-19败血症中,这种受损的APC反应可能是由于内皮功能障碍造成的,这有助于其独特的原血栓现象型.
了解这些途径差异对于管理败血症和COVID-19中的凝血病至关重要.

关键词:

在 COVID-19 疫情中,蛋白 C 是一种蛋白质.败血症是什么败血症是什么血栓激素血栓激素是一种血栓友爱症 (Thrombophilia) 是一种发生血栓友爱的疾病.

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