2020
DOI: 10.1515/dx-2020-0078
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COVID-19-associated coagulopathy

Abstract: Coronavirus disease 2019 (COVID-19), a viral respiratory illness caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been recently recognized as a systemic disorder inducing a prothrombotic state. The molecular mechanisms underlying the hypercoagulable state seen in patients with COVID-19 is still incompletely understood, although it presumably involves the close link between inflammatory and hemostatic systems. The laboratory coagulation monitoring of severely ill COVID-19 patients… Show more

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Cited by 53 publications
(54 citation statements)
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“…There are many publications showing thromboembolic complications of the virus. Although some patients receive anticoagulant therapy, thromboembolic complications may occur [27]. Thrombotic microangiopathy and widespread microthrombosis were observed in postmortem histopathological studies.…”
Section: Discussionmentioning
confidence: 99%
“…There are many publications showing thromboembolic complications of the virus. Although some patients receive anticoagulant therapy, thromboembolic complications may occur [27]. Thrombotic microangiopathy and widespread microthrombosis were observed in postmortem histopathological studies.…”
Section: Discussionmentioning
confidence: 99%
“…3,4,18,69,74 COVID-19-associated coagulopathy occurs proportional to disease severity and leads to treatment-resistant thrombotic and haemorrhagic events; characterised by d-dimer elevation with prothrombin prolongation and thrombocytopenia. [74][75][76][77] Furthermore, cytokine-and hypoxia-induced injury to the corpus callosum, particularly the splenium, has been reported within critical illness including acute respiratory distress syndrome and high-altitude cerebral oedema, potentially contributing to a vulnerability in COVID-19. 17,[78][79][80][81][82][83] Hypoxia directly induces chemical and hydrostatic endothelial cell disruption, promoting vascular permeability and hence contributing to neurological event pathogenesis.…”
Section: Neurological Events In White and Grey Mattermentioning
confidence: 99%
“…8 The molecular mechanisms responsible for the hypercoagulable state observed in patients with COVID-19 are still incompletely elucidated; however, there appears to be a close link between inflammatory and hemostatic systems ( Figure 1). 9,10 Current data suggest that COVID-19 can infect endothelial cells with an ensuing associated immune response and attendant activation of inflammatory pathways resulting in dysregulation of the endothelium, leukocyte activation, neutrophil extracellular traps (NET) generation (a matrix of DNA decorated with neutrophil granule proteins, such as myeloperoxidase, cathepsin G, and neutrophil elastase), complement deposition, and platelet activation and consumption. 10 It has been suggested that the virus instigates the process of pyroptosis, an inflammatory form of programmed cell death observed upon infection with intracellular pathogens, which could contribute to the endothelial cell death after COVID-19 infection and could increase proinflammatory cytokine releases, such as interleukin (IL)-1 beta and IL-18.…”
Section: Introductionmentioning
confidence: 99%