2020
DOI: 10.1016/j.dib.2020.106519
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Prothrombotic hemostasis disturbances in patients with severe COVID-19: Individual daily data

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Cited by 21 publications
(16 citation statements)
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“…The changes in D-dimers levels over time can also help identify patients likely to develop thrombosis, as a D-dimers increment of 1.5-fold was strongly associated with the diagnosis of thrombosis in COVID-19 patients [33] . Progression curves of D-dimers also showed a rapid increase before the diagnosis of thrombotic events [14] , [34] .…”
Section: Methodsmentioning
confidence: 92%
“…The changes in D-dimers levels over time can also help identify patients likely to develop thrombosis, as a D-dimers increment of 1.5-fold was strongly associated with the diagnosis of thrombosis in COVID-19 patients [33] . Progression curves of D-dimers also showed a rapid increase before the diagnosis of thrombotic events [14] , [34] .…”
Section: Methodsmentioning
confidence: 92%
“…Hardy and colleagues demonstrated enhanced thrombin potential in patients being treated in ICU, using highly sensitive laboratory techniques. 64,65 Increased levels or activities of proteins involved in blood coagulation, such as factor VIII, accompanied by decreased coagulation inhibitors, very strongly suggest a prothrombotic state during COVID-19 disease manifestation. 28,[64][65][66] A feature of this COVID-19-associated prothrombotic state that remains unexplained is the reduction or absence of fibrinolytic variables in both TEG and TEM assays (LY30, LY60, and ML).…”
Section: Discussionmentioning
confidence: 99%
“…14 Differently, direct mechanisms are linked to the capacity of SARS-CoV-2 to infect endothelial cells through the angiotensin-converting enzyme 2 (ACE2) expressed on their cell membrane, 15,16 to proliferate within the cells and consequently to induce cell damage and apoptosis. 12 Once activated, endothelium reverts its anti-thrombotic phenotype to a prothrombotic one, 17 characterized by increased expression of cell surface adhesion molecules (i.e., ICAM-1, E-selectin, P-selectin, and VCAM-1) 18 ; downregulation of anticoagulant properties (i.e., thrombomodulin [TM], tissue factor pathway inhibitor [TFPI], and heparan sulfate) 19 ; increased expression of procoagulant (Tissue Factor, TF) and antifibrinolytic activities (plasminogen activator inhibitor 1, PAI-1). 20 The upregulation of TF and PAI-1, and downregulation of TM and TFPI, promote hypercoagulation and excessive fibrin formation.…”
Section: Introductionmentioning
confidence: 99%