ABSTRACT
Background: There are no data on circulating concentrations of sFas (proapoptotic protein of extrinsic pathway) and Bcl2 (antiapoptotic protein of intrinsic pathway) in COVID-19 patients. Thus, our objective study was to determine whether an association exists between serum concentrations of sFas and Bcl2 and COVID-19 patient mortality.
Methods: This observational and prospective study of COVID-19 patients was performed in eight Intensive Care Units (ICU) from Canary Islands (Spain). Serum levels of sFas and Bcl2 at ICU admission were determined. Mortality at 30 days was the end-point study.
Results: Surviving patients (n = 42) compared to non-surviving (n = 11) had lower APACHE-II (p < 0.001), lower SOFA (p = 0.004), lower serum sFas levels (p = 0.001) and higher serum Bcl2 levels (p < 0.001). Logistic regression showed an association between high serum sFas levels and mortality after controlling for APACHE-II (OR = 1.004; 95% CI = 1.101–1.007; p = 0.01) or SOFA (OR = 1.003; 95% CI = 1.101–1.106; p = 0.004), and between low serum Bcl2 levels and mortality after controlling for APACHE-II (OR = 0.927; 95% CI = 0.873–0.984; p = 0.01) or SOFA (OR = 0.949; 95% CI = 0.913–0.987; p = 0.01).
Conclusions: Thus, to the best of our knowledge, this is the first study reporting blood levels of sFas and Bcl2 in COVID-19 patients and its association with mortality.
KEYWORDS:
Article highlights
Non-surviving showed higher serum sFas levels and lower serum Bcl2 levels
There is an association between serum levels of sFas and Bcl2 and mortality
Serum levels of sFas and Bcl2 could be used as mortality biomarker
Abbreviations
APACHE II = Acute Physiology and Chronic Health Evaluation
aPTT = activated partial thromboplastin time
ARDS = acute respiratory distress syndrome
COPD = chronic obstructive pulmonary disease
FIO2 = fraction inspired oxygen
GCS = Glasgow Coma Scale
INR = international normalized ratio
NTproBNP = N-terminal prohormone of brain natriuretic peptide
PaO2 = pressure of arterial oxygen
SOFA = Sepsis-related Organ Failure Assessment
Acknowledgments
This study was supported by a grant from Instituto de Salud Carlos III (PI-18-00500) (Madrid, Spain) and co-financed with Fondo Europeo de Desarrollo Regional (FEDER). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Declaration of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.
Authors’ contributions
L Lorente conceived, designed and coordinated the study, participated in acquisition and interpretation of data, and drafted the manuscript. MM Martín, AF González-Rivero, A Pérez-Cejas, M Argueso, A Perez, L Ramos, JS Violán, JA Marcos y Ramos and N Ojeda participated in acquisition of data. A Jiménez participated in the interpretation of data. All authors revised the manuscript critically for important intellectual content, made the final approval of the version to be published, and were agreed to be accountable for all aspects of the work.