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COVID-19: Not a thrombotic disease but a thromboinflammatory disease.
He, Shu; Blombäck, Margareta; Wallén, Håkan.
Afiliación
  • He S; Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden.
  • Blombäck M; Division of Coagulation Research, Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
  • Wallén H; Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden.
Ups J Med Sci ; 1292024.
Article en En | MEDLINE | ID: mdl-38327640
ABSTRACT
While Coronavirus Disease in 2019 (COVID-19) may no longer be classified as a global public health emergency, it still poses a significant risk at least due to its association with thrombotic events. This study aims to reaffirm our previous hypothesis that COVID-19 is fundamentally a thrombotic disease. To accomplish this, we have undertaken an extensive literature review focused on assessing the comprehensive impact of COVID-19 on the entire hemostatic system. Our analysis revealed that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection significantly enhances the initiation of thrombin generation. However, it is noteworthy that the thrombin generation may be modulated by specific anticoagulants present in patients' plasma. Consequently, higher levels of fibrinogen appear to play a more pivotal role in promoting coagulation in COVID-19, as opposed to thrombin generation. Furthermore, the viral infection can stimulate platelet activation either through widespread dissemination from the lungs to other organs or localized effects on platelets themselves. An imbalance between Von Willebrand Factor (VWF) and ADAMTS-13 also contributes to an exaggerated platelet response in this disease, in addition to elevated D-dimer levels, coupled with a significant increase in fibrin viscoelasticity. This paradoxical phenotype has been identified as 'fibrinolysis shutdown'. To clarify the pathogenesis underlying these hemostatic disorders in COVID-19, we also examined published data, tracing the reaction process of relevant proteins and cells, from ACE2-dependent viral invasion, through induced tissue inflammation, endothelial injury, and innate immune responses, to occurrence of thrombotic events. We therefrom understand that COVID-19 should no longer be viewed as a thrombotic disease solely based on abnormalities in fibrin clot formation and proteolysis. Instead, it should be regarded as a thromboinflammatory disorder, incorporating both classical elements of cellular inflammation and their intricate interactions with the specific coagulopathy.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Trombosis / Trastornos de la Coagulación Sanguínea / COVID-19 Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Ups J Med Sci Año: 2024 Tipo del documento: Article País de afiliación: Suecia Pais de publicación: Suecia

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Trombosis / Trastornos de la Coagulación Sanguínea / COVID-19 Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Ups J Med Sci Año: 2024 Tipo del documento: Article País de afiliación: Suecia Pais de publicación: Suecia