Department of Surgical Sciences, Anesthesiology and Intensive Care, Uppsala University, Uppsala, Sweden.
Department of Surgical Sciences, Anesthesiology and Intensive Care, Uppsala University, Uppsala, Sweden.
Cytokine. 2021 Feb;138:155389. doi: 10.1016/j.cyto.2020.155389. Epub 2020 Dec 14.
The infection caused by SARS CoV-2 has been postulated to induce a cytokine storm syndrome that results in organ failure and even death in a considerable number of patients. However, the inflammatory response in Corona virus disease-19 (Covid-19) and its potential to cause collateral organ damage has not been fully elucidated to date. This study aims to characterize the acute cytokine response in a cohort of critically ill Covid-19 patients.
24 adults with PCR-confirmed Covid-19 were included at time of admission to intensive care a median of eleven days after initial symptoms. Eleven adult patients admitted for elective abdominal surgery with preoperative plasma samples served as controls. All patients were included after informed consent was obtained. 27 cytokines were quantified in plasma. The expression of inflammatory mediators was then related to routine inflammatory markers, SAPS3, SOFA score, organ failure and 30-day mortality.
A general increase in cytokine expression was observed in all Covid-19 patients. A strong correlation between respiratory failure and IL-1ra, IL-4, IL-6, IL-8 and IP-10 expression was observed. Acute kidney injury development correlated well with increased levels of IL-1ra, IL-6, IL-8, IL-17a, IP-10 and MCP-1. Generally, the cohort demonstrated weaker correlations between cytokine expression and 30-day mortality out of which IL-8 showed the strongest signal in terms of mortality.
The present study found that respiratory failure, acute kidney injury and 30-day mortality in critically ill Covid-19 patients are associated with moderate increases of a broad range of inflammatory mediators at time of admission.
SARS-CoV-2 感染被推测会引发细胞因子风暴综合征，导致相当数量的患者发生器官衰竭甚至死亡。然而，迄今为止，冠状病毒病-19（Covid-19）中的炎症反应及其潜在的导致继发器官损伤的机制尚未完全阐明。本研究旨在描述一组重症 Covid-19 患者的急性细胞因子反应特征。
纳入 24 名经 PCR 确诊的 Covid-19 成年患者，于入住重症监护病房时纳入研究，中位时间为初始症状后 11 天。11 名因择期腹部手术而接受术前血浆样本的成年患者作为对照。所有患者均在获得知情同意后纳入研究。对血浆中的 27 种细胞因子进行定量分析。然后将炎症介质的表达与常规炎症标志物、SAPS3、SOFA 评分、器官衰竭和 30 天死亡率相关联。
所有 Covid-19 患者均表现出细胞因子表达的普遍增加。呼吸衰竭与 IL-1ra、IL-4、IL-6、IL-8 和 IP-10 表达之间存在强烈相关性。急性肾损伤的发生与 IL-1ra、IL-6、IL-8、IL-17a、IP-10 和 MCP-1 水平升高密切相关。总体而言，该队列中细胞因子表达与 30 天死亡率之间的相关性较弱，其中 IL-8 在死亡率方面显示出最强的信号。
本研究发现，重症 Covid-19 患者的呼吸衰竭、急性肾损伤和 30 天死亡率与入住时多种炎症介质的中度增加相关。
