Abstract
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.
MeSH terms
-
Acute Kidney Injury / epidemiology
-
Acute Kidney Injury / therapy
-
Adult
-
Aged
-
Aged, 80 and over
-
Antithrombins / metabolism
-
Betacoronavirus
-
C-Reactive Protein / metabolism
-
COVID-19
-
Comorbidity
-
Coronavirus Infections / blood*
-
Coronavirus Infections / epidemiology
-
Coronavirus Infections / therapy
-
Critical Illness
-
Diabetes Mellitus / epidemiology
-
Dyslipidemias / epidemiology
-
Extracorporeal Membrane Oxygenation
-
Factor VIII / metabolism*
-
Female
-
Ferritins / metabolism
-
Fibrin Fibrinogen Degradation Products / metabolism
-
Fibrinogen / metabolism
-
Humans
-
Hypertension / epidemiology
-
International Normalized Ratio
-
Male
-
Middle Aged
-
Obesity / epidemiology
-
Pandemics
-
Partial Thromboplastin Time
-
Pneumonia, Viral / blood*
-
Pneumonia, Viral / epidemiology
-
Pneumonia, Viral / therapy
-
Protein C / metabolism*
-
Prothrombin Time
-
Renal Dialysis
-
Renal Insufficiency, Chronic / epidemiology
-
Respiration, Artificial
-
Respiratory Distress Syndrome / blood*
-
Respiratory Distress Syndrome / epidemiology
-
Respiratory Distress Syndrome / therapy
-
SARS-CoV-2
-
Thrombophilia / blood*
Substances
-
Antithrombins
-
Fibrin Fibrinogen Degradation Products
-
Protein C
-
fibrin fragment D
-
Factor VIII
-
Fibrinogen
-
C-Reactive Protein
-
Ferritins