| Literature DB >> 32773098 |
Agnès Ribes1, Fanny Vardon-Bounes2, Vincent Mémier3, Michael Poette2, Jonathan Au-Duong2, Cédric Garcia1, Vincent Minville4, Pierre Sié1, Alessandra Bura-Rivière5, Sophie Voisin1, Bernard Payrastre6.
Abstract
The novel Corona virus infection (Covid-19) first identified in China in December 2019 has rapidly progressed in pandemic leading to significant mortality and unprecedented challenge for healthcare systems. Although the clinical spectrum of Covid-19 is variable, acute respiratory failure and systemic coagulopathy are common in severe Covid-19 patients. Lung is an important target of the SARS-CoV-2 virus causing eventually acute respiratory distress syndrome associated to a thromboinflammatory state. The cytokinic storm, thromboinflammation and pulmonary tropism are the bedrock of tissue lesions responsible for acute respiratory failure and for prolonged infection that may lead to multiple organ failure and death. The thrombogenicity of this infectious disease is illustrated by the high frequency of thromboembolic events observed even in Covid-19 patients treated with anticoagulation. Increased D-Dimers, a biomarker reflecting activation of hemostasis and fibrinolysis, and low platelet count (thrombocytopenia) are associated with higher mortality in Covid-19 patients. In this review, we will summarize our current knowledge on the thromboembolic manifestations, the disturbed hemostatic parameters, and the thromboinflammatory conditions associated to Covid-19 and we will discuss the modalities of anticoagulant treatment or other potential antithrombotic options.Entities:
Keywords: Acute respiratory distress syndrome; Anticoagulants; Covid-19; Platelets; Thromboembolic events; Thromboinflammation
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Year: 2020 PMID: 32773098 DOI: 10.1016/j.jbior.2020.100735
Source DB: PubMed Journal: Adv Biol Regul ISSN: 2212-4926