Abstract
Objective: We aimed to investigate the prognostic performances of oxidative stress (OS), inflammatory and cell activation biomarkers measured at admission in COVID-19 patients. Design: retrospective monocentric study. Setting: patients with suspected SARS-CoV-2 infection (COVID-19) admitted to the hospital. Patients: One hundred and sixty documented and unselected COVID-19-patients. Disease severity (from mild to critical) was scored according to NIH’s classification. Interventions: none. Measurements and main results: We measured OS biomarkers (thiol, advanced oxidation protein products (AOPP), ischemia-modified albumin (IMA)), inflammation biomarkers (interleukin-6 (IL-6), presepsin) and cellular activation biomarkers (calprotectin) in plasma at admission. Thiol concentrations decreased while IMA, IL-6, calprotectin and PSEP increased with disease severity in COVID-19 patients and were associated with increased O2 needs and ICU admission. The best area under the receiver-operating-characteristics curve (AUC) for the prediction of ICU admission was for thiol (AUC = 0.762). A thiol concentration <154 µmol/L was predictive for ICU admission (79.7% sensitivity, 64.6% specificity, 58.8% positive predictive value, 78.9% negative predictive value). In a stepwise logistic regression, we found that being overweight, having dyspnoea, and thiol and IL-6 plasmatic concentrations were independently associated with ICU admission. In contrast, calprotectin was the best biomarker to predict mortality (AUC = 0.792), with an optimal threshold at 24.1 mg/L (94.1% sensitivity, 64.9% specificity, 97.1% positive predictive value and 98.9% negative predictive value), and survival curves indicated that high IL-6 and calprotectin concentrations were associated with a significantly increased risk of mortality. Conclusions: Thiol measurement at admission is a promising tool to predict ICU admission in COVID-19-patients, whereas IL-6 and calprotectin measurements effectively predict mortality.
Highlights
Coronavirus Disease 19 (COVID-19) is caused by the new emerging severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), responsible for more than124,000,000 confirmed cases worldwide and 2,700,000 deaths [1]
For oxidative stress (OS) biomarkers, we found that thiol concentrations significantly decreased across severity in COVID-19-patients (from 272 (202–295) μmol/L in stage to 112 (79–140) μmol/L in stage 3, p < 0.001), while ischemia-modified albumin (IMA) concentrations increased from
Our results showed that IL-6, PSEP and calprotectin concentrations significantly increased with severity in COVID-19-patients (Figure 1D–F)
Summary
Coronavirus Disease 19 (COVID-19) is caused by the new emerging severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), responsible for more than124,000,000 confirmed cases worldwide and 2,700,000 deaths [1]. Coronavirus Disease 19 (COVID-19) is caused by the new emerging severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), responsible for more than. Disease severity ranges from asymptomatic to mild-to-moderate forms, and more rarely severe acute respiratory distress syndrome (ARDS). Many studies have reported the relationship between inflammation and the deterioration of the patient’s condition, and this ‘cytokine storm’ is considered to be a major factor for the development of ARDS and multiple organ dysfunction [2,3,4]. Deleterious action of ROS on alveolar epithelial and endothelial cell functions could be a major contributor for hypoxic respiratory failure observed in the most severe cases of COVID-19 [9]. SARS-CoV-2 infection can lead to cellular damage which can initiate toxic and inflammatory stress responses [10]. Antioxidant status can be evaluated by measuring total plasmatic thiol
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