Related Experiment Video
Updated: Nov 30, 2025
Author Spotlight: Deciphering Coagulation Disorders in Traumatic Brain Injury Patients
Published on: August 4, 2023
COVID-19 and Sepsis Are Associated With Different Abnormalities in Plasma Procoagulant and Fibrinolytic Activity
Emma G Bouck1, Frederik Denorme2, Lori A Holle1
1Department of Pathology and Laboratory Medicine and UNC Blood Research Center, University of North Carolina, Chapel Hill (E.G.B., L.A.H., A.S.W.).
Insights
Coronavirus disease 2019 (COVID-19) and sepsis activate coagulation differently. COVID-19 shows increased thrombin generation and altered fibrinolysis, unlike sepsis, with severe COVID-19 paradoxically showing delayed coagulation initiation.
Area of Science:
- Hematology
- Critical Care Medicine
- Infectious Diseases
Background:
- Coronavirus disease 2019 (COVID-19) shares similarities with sepsis-induced coagulopathy.
- Key differences in clinical laboratory metrics suggest distinct pathophysiological mechanisms.
- Understanding these differences is crucial for managing thrombotic complications in COVID-19.
Purpose of the Study:
- To compare plasma coagulation and fibrinolytic potential in COVID-19 patients versus sepsis patients and healthy donors.
- To elucidate the distinct impacts of COVID-19 and sepsis on hemostatic pathways.
- To investigate the relationship between disease severity and coagulation dynamics in COVID-19.
Main Methods:
- Comparative cross-sectional study of 99 hospitalized patients (46 COVID-19, 53 sepsis) and 18 healthy donors.
- Measurement of endogenous coagulation and fibrinolytic biomarkers using immunoassays.
- Assessment of thrombin and plasmin generation potential via fluorescence assays; fibrin formation and lysis measured by turbidity.
Main Results:
- Both COVID-19 and sepsis groups exhibited elevated fibrinogen, d-dimer, soluble thrombomodulin, and plasmin-antiplasmin complexes compared to healthy donors.
- COVID-19 patients demonstrated increased thrombin generation potential despite anticoagulation, whereas sepsis patients did not.
- COVID-19 plasma showed enhanced endogenous plasmin potential, while sepsis patients had delayed plasmin generation; severe COVID-19 correlated with prolonged lag times for thrombin, plasmin, and fibrin formation.
Conclusions:
- COVID-19 and sepsis both involve endogenous activation of coagulation and fibrinolysis but differentially affect plasma procoagulant and fibrinolytic potentials.
- Distinct dysregulation of procoagulant and fibrinolytic pathways contributes uniquely to the pathophysiology of COVID-19 and sepsis.
- Severe COVID-19 may be associated with a paradoxical loss of coagulation-initiating mechanisms.
Objective:
Coronavirus disease 2019 (COVID-19) is associated with derangement in biomarkers of coagulation and endothelial function and has been likened to the coagulopathy of sepsis. However, clinical laboratory metrics suggest key differences in these pathologies. We sought to determine whether plasma coagulation and fibrinolytic potential in patients with COVID-19 differ compared with healthy donors and critically ill patients with sepsis. Approach and Results: We performed comparative studies on plasmas from a single-center, cross-sectional observational study of 99 hospitalized patients (46 with COVID-19 and 53 with sepsis) and 18 healthy donors. We measured biomarkers of endogenous coagulation and fibrinolytic activity by immunoassays, thrombin, and plasmin generation potential by fluorescence and fibrin formation and lysis by turbidity. Compared with healthy donors, patients with COVID-19 or sepsis both had elevated fibrinogen, d-dimer, soluble TM (thrombomodulin), and plasmin-antiplasmin complexes. Patients with COVID-19 had increased thrombin generation potential despite prophylactic anticoagulation, whereas patients with sepsis did not. Plasma from patients with COVID-19 also had increased endogenous plasmin potential, whereas patients with sepsis showed delayed plasmin generation. The collective perturbations in plasma thrombin and plasmin generation permitted enhanced fibrin formation in both COVID-19 and sepsis. Unexpectedly, the lag times to thrombin, plasmin, and fibrin formation were prolonged with increased disease severity in COVID-19, suggesting a loss of coagulation-initiating mechanisms accompanies severe COVID-19.
Conclusions:
Both COVID-19 and sepsis are associated with endogenous activation of coagulation and fibrinolysis, but these diseases differently impact plasma procoagulant and fibrinolytic potential. Dysregulation of procoagulant and fibrinolytic pathways may uniquely contribute to the pathophysiology of COVID-19 and sepsis.
More Related Videos
Related Concept Videos
01:30Anticoagulant Drugs: Low-Molecular-Weight Heparins
01:24Disorders of Hemostasis
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
01:20Extrinsic and Intrinsic Pathways of Hemostasis
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
01:16Clot Retraction and Fibrinolysis
01:09Coagulation
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
01:06Coagulation