2020, Number 5
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Rev Fac Med UNAM 2020; 63 (5)
Physiology of Hemostasis and its Alteration by Coagulopathy in COVID-19
González-Villalva A, de la Peña-Díaz A, Rojas-Lemus M, López-Valdez N, Ustarroz-Cano M, García-Peláez I, Bizarro-Nevares P, Fortoul TI
Language: Spanish
References: 63
Page: 45-57
PDF size: 568.13 Kb.
ABSTRACT
COVID-19 global pandemic caused by Sars-CoV-2 virus, has
worried to health care providers due to the high mortality
rate related to coagulopathy in many patients. COVID-19
coagulopathy is mainly thrombotic, first locally in lungs
but later on it becomes micro and macrovascular systemic
coagulopathy. It has been associated to endothelial damage,
inflammation, neutrophil-extracellular traps, monocyte
and macrophage activation, cytokines storm that induce
a vicious cycle of thrombosis and inflammation. The increased
levels of prothrombotic factors as tissue factor, Von
Willebrand factor, fibrinogen, VIII factor and the decreased
levels of antithrombotic factos, such as: antithrombin and
Protein S have been reported in COVID-19 patients. Insufficiency
of fibrinolysis because of the increased levels of PAI-1
(plasminogen activator inhibitor 1) have been reported also.
During this disease there are intraalveolar fibrin deposits
that needs to be degraded. Fibrinolysis of thrombus and
fibrin intraalveolar degradation are responsible for the high
increase of D-dimers levels that are an important predictor
of severity of the disease. In this report, the physiology of
hemostasis, thromboinflamation secondary to Sars-CoV-2
infection are reviewed, as well as the clinical evidence and
the physiopathology of COVID-19 coagulopathy from the
basic sciences point of view.
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