Subject(s)
COVID-19/pathology , Fibrin Fibrinogen Degradation Products/metabolism , von Willebrand Factor/metabolism , Adult , Aged , COVID-19/complications , COVID-19/virology , Case-Control Studies , Factor VIII/metabolism , Female , Humans , Male , Middle Aged , Patient Discharge , Plasminogen Activator Inhibitor 1/metabolism , SARS-CoV-2/isolation & purification , Severity of Illness Index , Thrombosis/diagnosis , Thrombosis/etiology , Time FactorsABSTRACT
BACKGROUND: Abnormal coagulation parameters have been reported in COVID-19-infected patients. Although the underlying mechanism of COVID-19 coagulopathy remains unknown, it has been suggested to be a form of disseminated intravascular coagulation (DIC). OBJECTIVES: The aim of our study was to analyze the coagulation parameters of patients with COVID-19, determine whether coagulation factors consumption occurs and identify potential prognostic biomarkers of the disease. PATIENTS/METHODS: Blood samples from hospitalized patients with COVID-19 pneumonia were collected. We performed basic coagulation tests and quantification of coagulation factors and physiological inhibitor proteins. Laboratory data were compared with clinical data and outcomes. RESULTS: The study involved 206 patients (63.6% male). D-dimer was particularly elevated (median 450 ng/mL; IQR 222.5-957.3). Free protein S levels were below the normal range (median 56.6%; IQR: 43.6-68.9), and factor VIII showed an increasing trend (median 173.4%; IQR: 144.1-214.9). However, all coagulation factors were within normal limits. We found no correlation between abnormal coagulation parameters and thrombosis, except for higher D-dimer (HR 1.99; 95% CI 1.3-3.1; P = .002). CONCLUSIONS: COVID-19 is associated with coagulopathy that correlates with poor prognosis. However, we did not demonstrate a consumption of coagulation factors, as seen in DIC.
Subject(s)
Betacoronavirus/pathogenicity , Coronavirus Infections/complications , Cytokine Release Syndrome/complications , Disseminated Intravascular Coagulation/complications , Factor VIII/metabolism , Pneumonia, Viral/complications , Venous Thrombosis/complications , Aged , Aged, 80 and over , Biomarkers/blood , Blood Coagulation Tests , Blood Platelets/pathology , Blood Platelets/virology , COVID-19 , Coronavirus Infections/diagnosis , Coronavirus Infections/mortality , Coronavirus Infections/virology , Cytokine Release Syndrome/diagnosis , Cytokine Release Syndrome/mortality , Cytokine Release Syndrome/virology , Disseminated Intravascular Coagulation/diagnosis , Disseminated Intravascular Coagulation/mortality , Disseminated Intravascular Coagulation/virology , Female , Fibrin Fibrinogen Degradation Products/metabolism , Humans , Lung/blood supply , Lung/drug effects , Lung/pathology , Lung/virology , Male , Middle Aged , Pandemics , Pneumonia, Viral/diagnosis , Pneumonia, Viral/mortality , Pneumonia, Viral/virology , Prognosis , Protein S/metabolism , Retrospective Studies , SARS-CoV-2 , Severity of Illness Index , Survival Analysis , Venous Thrombosis/diagnosis , Venous Thrombosis/mortality , Venous Thrombosis/virologyABSTRACT
Critically ill patients with coronavirus disease 2019 (COVID-19) have been observed to be hypercoagulable, but the mechanisms for this remain poorly described. Factor VIII is a procoagulant factor that increases during inflammation and is cleaved by activated protein C. To our knowledge, there is only 1 prior study of factor VIII and functional protein C activity in critically ill patients with COVID-19. Here, we present a case series of 10 critically ill patients with COVID-19 who had severe elevations in factor VIII activity and low normal functional protein C activity, which may have contributed to hypercoagulability.