Covid-19: The Rollercoaster of Fibrin(Ogen), D-Dimer, Von Willebrand Factor, P-Selectin and Their Interactions with Endothelial Cells, Platelets and Erythrocytes
Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2), also known as coronavirus disease 2019 (COVID-19)-induced infection, is strongly associated with various coagulopathies that may result in either bleeding and thrombocytopenia or hypercoagulation and thrombosis. Thrombotic and bleeding or...
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Published in | International journal of molecular sciences Vol. 21; no. 14; p. 5168 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
MDPI AG
21.07.2020
MDPI |
Subjects | |
Online Access | Get full text |
ISSN | 1422-0067 1661-6596 1422-0067 |
DOI | 10.3390/ijms21145168 |
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Abstract | Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2), also known as coronavirus disease 2019 (COVID-19)-induced infection, is strongly associated with various coagulopathies that may result in either bleeding and thrombocytopenia or hypercoagulation and thrombosis. Thrombotic and bleeding or thrombotic pathologies are significant accompaniments to acute respiratory syndrome and lung complications in COVID-19. Thrombotic events and bleeding often occur in subjects with weak constitutions, multiple risk factors and comorbidities. Of particular interest are the various circulating inflammatory coagulation biomarkers involved directly in clotting, with specific focus on fibrin(ogen), D-dimer, P-selectin and von Willebrand Factor (VWF). Central to the activity of these biomarkers are their receptors and signalling pathways on endothelial cells, platelets and erythrocytes. In this review, we discuss vascular implications of COVID-19 and relate this to circulating biomarker, endothelial, erythrocyte and platelet dysfunction. During the progression of the disease, these markers may either be within healthy levels, upregulated or eventually depleted. Most significant is that patients need to be treated early in the disease progression, when high levels of VWF, P-selectin and fibrinogen are present, with normal or slightly increased levels of D-dimer (however, D-dimer levels will rapidly increase as the disease progresses). Progression to VWF and fibrinogen depletion with high D-dimer levels and even higher P-selectin levels, followed by the cytokine storm, will be indicative of a poor prognosis. We conclude by looking at point-of-care devices and methodologies in COVID-19 management and suggest that a personalized medicine approach should be considered in the treatment of patients. |
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AbstractList | Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2), also known as coronavirus disease 2019 (COVID-19)-induced infection, is strongly associated with various coagulopathies that may result in either bleeding and thrombocytopenia or hypercoagulation and thrombosis. Thrombotic and bleeding or thrombotic pathologies are significant accompaniments to acute respiratory syndrome and lung complications in COVID-19. Thrombotic events and bleeding often occur in subjects with weak constitutions, multiple risk factors and comorbidities. Of particular interest are the various circulating inflammatory coagulation biomarkers involved directly in clotting, with specific focus on fibrin(ogen), D-dimer, P-selectin and von Willebrand Factor (VWF). Central to the activity of these biomarkers are their receptors and signalling pathways on endothelial cells, platelets and erythrocytes. In this review, we discuss vascular implications of COVID-19 and relate this to circulating biomarker, endothelial, erythrocyte and platelet dysfunction. During the progression of the disease, these markers may either be within healthy levels, upregulated or eventually depleted. Most significant is that patients need to be treated early in the disease progression, when high levels of VWF, P-selectin and fibrinogen are present, with normal or slightly increased levels of D-dimer (however, D-dimer levels will rapidly increase as the disease progresses). Progression to VWF and fibrinogen depletion with high D-dimer levels and even higher P-selectin levels, followed by the cytokine storm, will be indicative of a poor prognosis. We conclude by looking at point-of-care devices and methodologies in COVID-19 management and suggest that a personalized medicine approach should be considered in the treatment of patients.Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2), also known as coronavirus disease 2019 (COVID-19)-induced infection, is strongly associated with various coagulopathies that may result in either bleeding and thrombocytopenia or hypercoagulation and thrombosis. Thrombotic and bleeding or thrombotic pathologies are significant accompaniments to acute respiratory syndrome and lung complications in COVID-19. Thrombotic events and bleeding often occur in subjects with weak constitutions, multiple risk factors and comorbidities. Of particular interest are the various circulating inflammatory coagulation biomarkers involved directly in clotting, with specific focus on fibrin(ogen), D-dimer, P-selectin and von Willebrand Factor (VWF). Central to the activity of these biomarkers are their receptors and signalling pathways on endothelial cells, platelets and erythrocytes. In this review, we discuss vascular implications of COVID-19 and relate this to circulating biomarker, endothelial, erythrocyte and platelet dysfunction. During the progression of the disease, these markers may either be within healthy levels, upregulated or eventually depleted. Most significant is that patients need to be treated early in the disease progression, when high levels of VWF, P-selectin and fibrinogen are present, with normal or slightly increased levels of D-dimer (however, D-dimer levels will rapidly increase as the disease progresses). Progression to VWF and fibrinogen depletion with high D-dimer levels and even higher P-selectin levels, followed by the cytokine storm, will be indicative of a poor prognosis. We conclude by looking at point-of-care devices and methodologies in COVID-19 management and suggest that a personalized medicine approach should be considered in the treatment of patients. Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2), also known as coronavirus disease 2019 (COVID-19)-induced infection, is strongly associated with various coagulopathies that may result in either bleeding and thrombocytopenia or hypercoagulation and thrombosis. Thrombotic and bleeding or thrombotic pathologies are significant accompaniments to acute respiratory syndrome and lung complications in COVID-19. Thrombotic events and bleeding often occur in subjects with weak constitutions, multiple risk factors and comorbidities. Of particular interest are the various circulating inflammatory coagulation biomarkers involved directly in clotting, with specific focus on fibrin(ogen), D-dimer, P-selectin and von Willebrand Factor (VWF). Central to the activity of these biomarkers are their receptors and signalling pathways on endothelial cells, platelets and erythrocytes. In this review, we discuss vascular implications of COVID-19 and relate this to circulating biomarker, endothelial, erythrocyte and platelet dysfunction. During the progression of the disease, these markers may either be within healthy levels, upregulated or eventually depleted. Most significant is that patients need to be treated early in the disease progression, when high levels of VWF, P-selectin and fibrinogen are present, with normal or slightly increased levels of D-dimer (however, D-dimer levels will rapidly increase as the disease progresses). Progression to VWF and fibrinogen depletion with high D-dimer levels and even higher P-selectin levels, followed by the cytokine storm, will be indicative of a poor prognosis. We conclude by looking at point-of-care devices and methodologies in COVID-19 management and suggest that a personalized medicine approach should be considered in the treatment of patients. |
Author | Maphumulo, Siphosethu C. Grobler, Corlia Lourens, Petrus J. Steenkamp, Janami Pretorius, Etheresia Laubscher, Gert J. Grobbelaar, L. Mireille Kell, Douglas B. Bredenkamp, Jhade C. |
AuthorAffiliation | 1 Department of Physiological Sciences, Faculty of Science, Stellenbosch University, Stellenbosch 7602, South Africa; 21069921@sun.ac.za (C.G.); 20825919@sun.ac.za (S.C.M.); 21074682@sun.ac.za (L.M.G.); 20006721@sun.ac.za (J.C.B.) 3 PathCare Laboratories, PathCare Business Centre, Neels Bothma Street, N1 City, Cape Town 7460, South Africa; janami.steenkamp@pathcare.org 5 The Novo Nordisk Foundation Centre for Biosustainability, Building 220, Kemitorve Technical University of Denmark, 2800 Kongens Lyngby, Denmark 2 Elsie du Toit Street, Stellenbosch MediClinic, Stellenbosch 7600, South Africa; laubscher911@gmail.com (G.J.L.); wodie22@icloud.com (P.J.L.) 4 Department of Biochemistry and Systems Biology, Institute of Systems, Molecular and Integrative Biology, Faculty of Health and Life Sciences, University of Liverpool, Crown St, Liverpool L69 7ZB, UK |
AuthorAffiliation_xml | – name: 4 Department of Biochemistry and Systems Biology, Institute of Systems, Molecular and Integrative Biology, Faculty of Health and Life Sciences, University of Liverpool, Crown St, Liverpool L69 7ZB, UK – name: 5 The Novo Nordisk Foundation Centre for Biosustainability, Building 220, Kemitorve Technical University of Denmark, 2800 Kongens Lyngby, Denmark – name: 1 Department of Physiological Sciences, Faculty of Science, Stellenbosch University, Stellenbosch 7602, South Africa; 21069921@sun.ac.za (C.G.); 20825919@sun.ac.za (S.C.M.); 21074682@sun.ac.za (L.M.G.); 20006721@sun.ac.za (J.C.B.) – name: 3 PathCare Laboratories, PathCare Business Centre, Neels Bothma Street, N1 City, Cape Town 7460, South Africa; janami.steenkamp@pathcare.org – name: 2 Elsie du Toit Street, Stellenbosch MediClinic, Stellenbosch 7600, South Africa; laubscher911@gmail.com (G.J.L.); wodie22@icloud.com (P.J.L.) |
Author_xml | – sequence: 1 givenname: Corlia surname: Grobler fullname: Grobler, Corlia – sequence: 2 givenname: Siphosethu C. orcidid: 0000-0002-2549-9763 surname: Maphumulo fullname: Maphumulo, Siphosethu C. – sequence: 3 givenname: L. Mireille surname: Grobbelaar fullname: Grobbelaar, L. Mireille – sequence: 4 givenname: Jhade C. surname: Bredenkamp fullname: Bredenkamp, Jhade C. – sequence: 5 givenname: Gert J. surname: Laubscher fullname: Laubscher, Gert J. – sequence: 6 givenname: Petrus J. surname: Lourens fullname: Lourens, Petrus J. – sequence: 7 givenname: Janami orcidid: 0000-0001-5838-7963 surname: Steenkamp fullname: Steenkamp, Janami – sequence: 8 givenname: Douglas B. orcidid: 0000-0002-9108-2384 surname: Kell fullname: Kell, Douglas B. – sequence: 9 givenname: Etheresia surname: Pretorius fullname: Pretorius, Etheresia |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32708334$$D View this record in MEDLINE/PubMed |
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SubjectTerms | Betacoronavirus Biomarkers Blood Platelets - metabolism Coronavirus Infections - pathology Coronaviruses COVID-19 Cytokine Release Syndrome - pathology Endothelial Cells - metabolism Erythrocytes - metabolism Fibrin Fibrinogen Degradation Products - metabolism Health risk assessment Humans P-Selectin - metabolism Pandemics Pneumonia, Viral - pathology Point-of-Care Systems Precision Medicine - methods Review SARS-CoV-2 Thrombocytopenia - pathology Thrombosis - pathology von Willebrand Factor - metabolism |
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Title | Covid-19: The Rollercoaster of Fibrin(Ogen), D-Dimer, Von Willebrand Factor, P-Selectin and Their Interactions with Endothelial Cells, Platelets and Erythrocytes |
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