Oussalah Abderrahim, Gleye Stanislas, Urmes Isabelle Clerc, Laugel Elodie, Barbé Françoise, Orlowski Sophie, Malaplate Catherine, Aimone-Gastin Isabelle, Caillierez Beatrice Maatem, Merten Marc, Jeannesson Elise, Kormann Raphaël, Olivier Jean-Luc, Rodriguez-Guéant Rosa-Maria, Namour Farès, Bevilacqua Sybille, Thilly Nathalie, Losser Marie-Reine, Kimmoun Antoine, Frimat Luc, Levy Bruno, Gibot Sébastien, Schvoerer Evelyne, Guéant Jean-Louis
Department of Molecular Medicine, Division of Biochemistry, Molecular Biology, and Nutrition, University Hospital of Nancy, F-54000 Nancy, France.
Faculty of Medicine of Nancy, University of Lorraine, INSERM UMR_S 1256, Nutrition, Genetics, and Environmental Risk Exposure (NGERE), F-54000 Nancy, France.
EClinicalMedicine. 2020 Oct;27:100554. doi: 10.1016/j.eclinm.2020.100554. Epub 2020 Sep 20.
In patients with severe COVID-19, no data are available on the longitudinal evolution of biochemical abnormalities and their ability to predict disease outcomes.
Using a retrospective, longitudinal cohort study design on consecutive patients with severe COVID-19, we used an extensive biochemical dataset of serial data and time-series design to estimate the occurrence of organ dysfunction and the severity of the inflammatory reaction and their association with acute respiratory failure (ARF) and death.
On the 162 studied patients, 1151 biochemical explorations were carried out for up to 59 biochemical markers, totaling 15,260 biochemical values. The spectrum of biochemical abnormalities and their kinetics were consistent with a multi-organ involvement, including lung, kidney, heart, liver, muscle, and pancreas, along with a severe inflammatory syndrome. The proportion of patients who developed an acute kidney injury (AKI) stage 3, increased significantly during follow-up (0·9%, day 0; 21·4%, day 14; <0·001). On the 20 more representative biochemical markers (>250 iterations), only CRP >90 mg/L (odds ratio [OR] 6·87, 95% CI, 2·36-20·01) and urea nitrogen >0·36 g/L (OR 3·91, 95% CI, 1·15-13·29) were independently associated with the risk of ARF. Urea nitrogen >0·42 g/L was the only marker associated with the risk of COVID-19 related death.
Our results point out the lack of the association between the inflammatory markers and the risk of death but rather highlight a significant association between renal dysfunction and the risk of COVID-19 related acute respiratory failure and death.
在重症新型冠状病毒肺炎(COVID-19)患者中,关于生化异常的纵向演变及其预测疾病结局能力的数据尚不可得。
采用回顾性纵向队列研究设计,针对连续的重症COVID-19患者,我们使用了包含系列数据的广泛生化数据集和时间序列设计,以评估器官功能障碍的发生情况、炎症反应的严重程度及其与急性呼吸衰竭(ARF)和死亡的关联。
在162例研究患者中,针对多达59种生化标志物进行了1151次生化检查,共获得15260个生化值。生化异常的范围及其动态变化与多器官受累一致,包括肺、肾、心、肝、肌肉和胰腺,同时伴有严重的炎症综合征。发生3期急性肾损伤(AKI)的患者比例在随访期间显著增加(第0天为0.9%;第14天为21.4%;P<0.001)。在20种更具代表性的生化标志物(>250次检测)中,只有CRP>90mg/L(比值比[OR]6.87,95%置信区间[CI],2.36 - 20.01)和尿素氮>0.36g/L(OR 3.91,95%CI,1.15 - 13.29)与ARF风险独立相关。尿素氮>0.42g/L是唯一与COVID-19相关死亡风险相关的标志物。
我们的结果指出炎症标志物与死亡风险之间缺乏关联,而是突出了肾功能障碍与COVID-19相关急性呼吸衰竭和死亡风险之间的显著关联。