COVID-19 Associated Coagulopathy: Mechanisms and Host-Directed Treatment
| Autor: | Jan Václavík, Jiří Plášek, V. Procházka, J. Škarda, J. Gumulec, T. Grézl, J. Máca |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Thrombotic microangiopathy
medicine.drug_class medicine.medical_treatment Critical Illness Review Article Monoclonal antibody Fibrinogen Von Willebrand factor Coagulopathy medicine Humans Endothelial dysfunction biology business.industry SARS-CoV-2 Heparin COVID-19 Antibodies Monoclonal Endothelial Cells General Medicine Blood Coagulation Disorders medicine.disease ADAMTS13 Cytokine Microangiopathy Immunology biology.protein Cytokines business medicine.drug |
| Zdroj: | The American Journal of the Medical Sciences |
| ISSN: | 1538-2990 0002-9629 |
| Popis: | Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) is associated with specific coagulopathy that frequently occurs during the different phases of coronavirus disease 2019 (COVID-19) and can result in thrombotic complications and/or death. This COVID-19-associated coagulopathy (CAC) exhibits some of the features associated with thrombotic microangiopathy, particularly complement-mediated hemolytic-uremic syndrome. In some cases, due to the anti-phospholipid antibodies, CAC resembles catastrophic anti-phospholipid syndrome. In other patients, it exhibits features of hemophagocytic syndrome. CAC is mainly identified by: increases in fibrinogen, D-dimers, and von Willebrand factor (released from activated endothelial cells), consumption of a disintegrin and metalloproteinase with thrombospondin type 1 motifs, member 13 (ADAMTS13), over activated and dysregulated complement, and elevated plasma cytokine levels. CAC manifests as both major cardiovascular and/or cerebrovascular events and dysfunctional microcirculation, which leads to multiple organ damage. It is not clear whether the mainstay of COVID-19 is complement overactivation, cytokine/chemokine activation, or a combination of these activities. Available data have suggested that non-critically ill hospitalized patients should be administered full-dose heparin. In critically ill, full dose heparin treatment is discouraged due to higher mortality rate. In addition to anti-coagulation, four different host-directed therapeutic pathways have recently emerged that influence CAC: (1) Anti-von Willebrand factor monoclonal antibodies; (2) activated complement C5a inhibitors; (3) recombinant ADAMTS13; and (4) Interleukin (IL)-1 and IL-6 antibodies. Moreover, neutralizing monoclonal antibodies against the virus surface protein have been tested. However, the role of antiplatelet treatment remains unclear for patients with COVID-19. |
| Databáze: | OpenAIRE |
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