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Cellular and molecular mechanisms in COVID-19 coagulopathy: role of inflammation and endotheliopathy

INTRODUCTION: Coronavirus 2 (CoV-2) infection or coronavirus disease 2019 (COVID-19) is frequently associated with microvascular thrombosis.The microthrombosis in COVID-19 is the result of the interplay between inflammation and endotheliopathy. Elevated interleukin-6 (IL-6) characterizes COVID-19 in...

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Autores principales: Cacciola, Rossella, Gentilini Cacciola, Elio, Vecchio, Veronica, Cacciola, Emma
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8536904/
https://www.ncbi.nlm.nih.gov/pubmed/34687400
http://dx.doi.org/10.1007/s11239-021-02583-4
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author Cacciola, Rossella
Gentilini Cacciola, Elio
Vecchio, Veronica
Cacciola, Emma
author_facet Cacciola, Rossella
Gentilini Cacciola, Elio
Vecchio, Veronica
Cacciola, Emma
author_sort Cacciola, Rossella
collection PubMed
description INTRODUCTION: Coronavirus 2 (CoV-2) infection or coronavirus disease 2019 (COVID-19) is frequently associated with microvascular thrombosis.The microthrombosis in COVID-19 is the result of the interplay between inflammation and endotheliopathy. Elevated interleukin-6 (IL-6) characterizes COVID-19 inflammation resulting in endotheliopathy and coagulopathy marked by elevated D-dimer (DD). Aim of this study is to identify and to describe the coagulation changes in 100 moderate COVID-19 patients having lung involvement and to determine the association of coagulopathy with the severity and prognosis. METHODS: Inflammation, endothelial and coagulation molecules were measured in moderate and mild disease. RESULTS: IL-6 and tumor necrosis factor-α (TNF-α) and tissue factor (TF), von Willebrand factor (VWF), and tissue factor pathway inhibitor (TFPI) significantly increased in moderate disease as well as D-dimer, thrombin antithrombin complex (TAT), Fibrinogen (Fib), platelet factor-4 (PF4), β-thromboglobulin (β-TG), P-selectin, and platelet adhesion. Shortened clotting time (CT) and clot formation time (CFT), high maximum clot firmness (MCF) and low LY at 30 min were present in 100% of moderate COVID-19 patients compared with mild COVID-19 patients. CONCLUSIONS: These findings demonstrate that moderate COVID-19 has a profound inflammation associated with severee ndotheliopathy and intense coagulation activation uncontrolled by TFPI. Attention should be paid to coagulopathy in COVID-19. Closely monitoring of coagulation and application of appropriate anticoagulation may improve the prognosis of moderate COVID-19 and to prevent the progression to severe COVID-19 disease.
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spelling pubmed-85369042021-10-25 Cellular and molecular mechanisms in COVID-19 coagulopathy: role of inflammation and endotheliopathy Cacciola, Rossella Gentilini Cacciola, Elio Vecchio, Veronica Cacciola, Emma J Thromb Thrombolysis Article INTRODUCTION: Coronavirus 2 (CoV-2) infection or coronavirus disease 2019 (COVID-19) is frequently associated with microvascular thrombosis.The microthrombosis in COVID-19 is the result of the interplay between inflammation and endotheliopathy. Elevated interleukin-6 (IL-6) characterizes COVID-19 inflammation resulting in endotheliopathy and coagulopathy marked by elevated D-dimer (DD). Aim of this study is to identify and to describe the coagulation changes in 100 moderate COVID-19 patients having lung involvement and to determine the association of coagulopathy with the severity and prognosis. METHODS: Inflammation, endothelial and coagulation molecules were measured in moderate and mild disease. RESULTS: IL-6 and tumor necrosis factor-α (TNF-α) and tissue factor (TF), von Willebrand factor (VWF), and tissue factor pathway inhibitor (TFPI) significantly increased in moderate disease as well as D-dimer, thrombin antithrombin complex (TAT), Fibrinogen (Fib), platelet factor-4 (PF4), β-thromboglobulin (β-TG), P-selectin, and platelet adhesion. Shortened clotting time (CT) and clot formation time (CFT), high maximum clot firmness (MCF) and low LY at 30 min were present in 100% of moderate COVID-19 patients compared with mild COVID-19 patients. CONCLUSIONS: These findings demonstrate that moderate COVID-19 has a profound inflammation associated with severee ndotheliopathy and intense coagulation activation uncontrolled by TFPI. Attention should be paid to coagulopathy in COVID-19. Closely monitoring of coagulation and application of appropriate anticoagulation may improve the prognosis of moderate COVID-19 and to prevent the progression to severe COVID-19 disease. Springer US 2021-10-23 2022 /pmc/articles/PMC8536904/ /pubmed/34687400 http://dx.doi.org/10.1007/s11239-021-02583-4 Text en © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.
spellingShingle Article
Cacciola, Rossella
Gentilini Cacciola, Elio
Vecchio, Veronica
Cacciola, Emma
Cellular and molecular mechanisms in COVID-19 coagulopathy: role of inflammation and endotheliopathy
title Cellular and molecular mechanisms in COVID-19 coagulopathy: role of inflammation and endotheliopathy
title_full Cellular and molecular mechanisms in COVID-19 coagulopathy: role of inflammation and endotheliopathy
title_fullStr Cellular and molecular mechanisms in COVID-19 coagulopathy: role of inflammation and endotheliopathy
title_full_unstemmed Cellular and molecular mechanisms in COVID-19 coagulopathy: role of inflammation and endotheliopathy
title_short Cellular and molecular mechanisms in COVID-19 coagulopathy: role of inflammation and endotheliopathy
title_sort cellular and molecular mechanisms in covid-19 coagulopathy: role of inflammation and endotheliopathy
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8536904/
https://www.ncbi.nlm.nih.gov/pubmed/34687400
http://dx.doi.org/10.1007/s11239-021-02583-4
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