Abstract
BackgroundSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19) has infected over 112M patients and resulted in almost 2.5M deaths worldwide. The major clinical feature of severe COVID-19 patients requiring ventilation is acute respiratory distress syndrome (ARDS) possibly associated with a cytokine storm.ObjectivesTo elucidate serum levels of TNF-α and soluble TNF-Receptor 1 (sTNFR1) in patients with severe and mild COVID-19 disease as determinants of disease severity.MethodsWe determined serum TNF-α and sTNFR1 concentrations in 46 patients with laboratory-confirmed COVID-19 (17 patients with severe disease within the intensive care unit [ICU] and 29 non-severe, non-ICU patients) and 15 healthy controls upon admission using ELISA. Subjects were recruited between March-May 2020 at the Masih Daneshvari Hospital Tehran, Iran.ResultsSerum levels of sTNFRI were significantly higher in ICU patients (P<0.0001) and non-ICU patients (P=0.0342) compared with healthy subjects. Serum sTNFR1 were significantly higher in ICU patients than in non-ICU patients (P<0.0001). Serum TNF-α levels were greater in ICU and non-ICU patients than in the healthy subjects group (p<0.0001). The sTNFRI concentration in ICU (r=0.79, p=0.0002) and non-ICU (r=0.42, p=0.02) patients positively correlated with age although serum sTNFRI levels in ICU patients were significantly higher than in older healthy subjects. The sTNFRI concentration in ICU patients negatively correlated with ESR.ConclusionsThe study demonstrates higher sTNFRI in ICU patients with severe COVID-19 disease and this be a biomarker of disease severity and mortality. Future studies should examine whether lower levels of systemic sTNFR1 at admission may indicate a better disease outcome.
Highlights
Understanding the mechanism(s) and profiles of the cytokine storm observed in coronavirus disease 2019 (COVID-19) is crucial for the development of effective therapeutic interventions
Of the patients admitted to the intensive care unit (ICU), 76.5% were female and 23.5% male. 16/17 (94%) of severe COVID-19 patients admitted to ICU died
There were no significant differences in Erythrocyte sedimentation rate (ESR), C-Reactive protein (CRP), Creatine phosphokinase (CPK) and troponin between severe COVID-19 patients in ICU and milder patients not in ICU (Table 1)
Summary
Understanding the mechanism(s) and profiles of the cytokine storm observed in coronavirus disease 2019 (COVID-19) is crucial for the development of effective therapeutic interventions. COVID-19 is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) with symptoms such as fever, dry cough and shortness of breath [3]. Severe cases (approximately 15%) develop multi-organ failure due to a cytokine storm resulting in respiratory failure. These cases require admission to an intensive care unit (ICU) and the disease can lead to respiratory failure and death [4, 5]. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19) has infected over 112M patients and resulted in almost 2.5M deaths worldwide. The major clinical feature of severe COVID-19 patients requiring ventilation is acute respiratory distress syndrome (ARDS) possibly associated with a cytokine storm
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