COVID-19 associated coagulopathy: Mechanisms and host-directed treatment
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, přehledy, práce podpořená grantem
PubMed
34752741
PubMed Central
PMC8576106
DOI
10.1016/j.amjms.2021.10.012
PII: S0002-9629(21)00403-1
Knihovny.cz E-zdroje
- Klíčová slova
- COVID-19, Coagulopathy, Endothelial dysfunction, Microangiopathy, SARS-CoV-2,
- MeSH
- COVID-19 * komplikace MeSH
- cytokiny MeSH
- endoteliální buňky MeSH
- heparin terapeutické užití MeSH
- koagulopatie * etiologie MeSH
- kritický stav MeSH
- lidé MeSH
- monoklonální protilátky terapeutické užití MeSH
- SARS-CoV-2 MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Názvy látek
- cytokiny MeSH
- heparin MeSH
- monoklonální protilátky MeSH
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.
Department of Clinical Hematology University Hospital of Ostrava Ostrava Czech Republic
Department of Internal Medicine and Cardiology University Hospital Ostrava Ostrava Czech Republic
Institute of Radiology University Hospital of Ostrava Ostrava Czech Republic
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