Biomarkers Associated with Failure of Liberation from Oxygen Therapy in Severe COVID-19: A Pilot Study.

Oh Joo Kweon,Won-Young Kim,Moon Seong Baek,Seong-Ho Choi,Min Jae Cha

doi:10.3390/jpm11100974

Oh Joo Kweon, Won-Young Kim + Show 3 more

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https://doi.org/10.3390/jpm11100974

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Abstract

This study aimed to investigate whether clinical and laboratory biomarkers can identify patients with COVID-19 who are less likely to be liberated from oxygen therapy. This was a retrospective study comparing 18 patients in the weaning failure group with 38 patients in the weaning success group. Weaning failure was defined as death or discharge with an oxygen device before day 28 after hospital admission or requiring oxygen support as of day 28. The median quick Sequential Organ Failure Assessment (qSOFA) score was significantly higher and the median SpO2/FiO2 was significantly lower in the weaning failure group. The laboratory biomarkers, procalcitonin (PCT) and D-dimer, were significantly higher in the weaning failure group, as were the biomarkers of endothelial injury, such as angiopoietin-2 (Ang-2) and Ang-2/Ang-1, and tumor necrosis factor-α (TNF-α). Patients’ qSOFA scores, SpO2/FiO2, and PCT, D-dimer, Ang-2, Ang-2/Ang-1, endocan (4-day and 7-day increases), and TNF-α levels predicted weaning failure; 7-day endocan levels were the best predictor of weaning failure with an AUC of 0.81 (95% CI, 0.67–0.94). We identified clinical and laboratory parameters, including plasma biomarkers of endothelial injury, that may be considered as biomarkers for predicting failure of liberation from oxygen therapy in patients with severe COVID-19.

Highlights

Coronavirus disease 2019 (COVID-19) has spread to over 220 countries worldwide, approaching 224 million cumulative cases and reaching 4,627,540 deaths as of 14September 2021 [1]
We identified clinical and laboratory parameters, including plasma biomarkers of endothelial injury, that may be considered as biomarkers for predicting failure of liberation from oxygen therapy in patients with severe COVID-19
Activation of inflammatory cascades, endothelialitis, capillary leakage resulting in acute respiratory distress syndrome (ARDS), thromboembolism, and multiorgan failure are observed among patients with severe COVID-19 [3]

Summary

Introduction

Coronavirus disease 2019 (COVID-19) has spread to over 220 countries worldwide, approaching 224 million cumulative cases and reaching 4,627,540 deaths as of 14September 2021 [1]. Coronavirus disease 2019 (COVID-19) has spread to over 220 countries worldwide, approaching 224 million cumulative cases and reaching 4,627,540 deaths as of 14. Most patients develop a mild form of COVID-19, 5–10% may progress to more severe forms of the disease, often requiring intensive care [2]. Activation of inflammatory cascades, endothelialitis, capillary leakage resulting in acute respiratory distress syndrome (ARDS), thromboembolism, and multiorgan failure are observed among patients with severe COVID-19 [3]. Identification of laboratory predictors of progression to severe COVID-19 has been extensively studied, as valid predictors may help guide risk stratification and clinical management, allocate limited medical resources, and target patients for interventional studies. Recent meta-analyses of numerous studies worldwide have found significant associations between hematologic, biochemical, coagulation, and inflammatory biomarkers and COVID-19 severity [4,5]. Serum endothelial/epithelial molecules, such as endocan and soluble receptor for advanced glycation end-products (sRAGE), were found to predict mortality and to indicate the need for intensive care [6,7]

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