| Autor: |
Martinelli N; Department of Medicine, University of Verona, 37129 Verona, Italy., Rigoni AM; Angiology Unit, Department of Cardiovascular and Thoracic, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy., De Marchi S; Department of Medicine, University of Verona, 37129 Verona, Italy., Osti N; Department of Medicine, University of Verona, 37129 Verona, Italy., Donini M; Department of Medicine, University of Verona, 37129 Verona, Italy., Montagnana M; Section of Clinical Biochemistry, University of Verona, 37129 Verona, Italy., Castagna A; Department of Medicine, University of Verona, 37129 Verona, Italy., Pattini P; Department of Medicine, University of Verona, 37129 Verona, Italy., Udali S; Department of Medicine, University of Verona, 37129 Verona, Italy., De Franceschi L; Department of Medicine, University of Verona, 37129 Verona, Italy., Tinazzi E; Department of Medicine, University of Verona, 37129 Verona, Italy., Mazzi F; Department of Medicine, University of Verona, 37129 Verona, Italy., Moruzzi S; Department of Medicine, University of Verona, 37129 Verona, Italy., Argentino G; Department of Medicine, University of Verona, 37129 Verona, Italy., Delfino L; Department of Medicine, University of Verona, 37129 Verona, Italy., Sartori G; Department of Medicine, University of Verona, 37129 Verona, Italy., Azzini AM; Department of Diagnostics and Public Health, University of Verona, 37129 Verona, Italy., Tacconelli E; Department of Diagnostics and Public Health, University of Verona, 37129 Verona, Italy., Van Dreden P; Clinical Research Department, Diagnostica Stago, 92230 Gennevilliers, France., Lippi G; Section of Clinical Biochemistry, University of Verona, 37129 Verona, Italy., Girelli D; Department of Medicine, University of Verona, 37129 Verona, Italy., Olivieri O; Department of Medicine, University of Verona, 37129 Verona, Italy., Friso S; Department of Medicine, University of Verona, 37129 Verona, Italy., Pizzolo F; Department of Medicine, University of Verona, 37129 Verona, Italy. |
| Abstrakt: |
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causal agent of coronavirus disease 2019 (COVID-19), in which coagulation abnormalities and endothelial dysfunction play a key pathogenic role. Tissue factor (TF) expression is triggered by endothelial dysfunction. Activated factor VII-antithrombin (FVIIa-AT) complex reflects indirectly FVIIa-TF interaction and has been proposed as a potential biomarker of prothrombotic diathesis. FVIIa-AT plasma concentration was measured in 40 patients (30 males and 10 females; 64.8 ± 12.3 years) admitted with SARS-CoV-2 pneumonia during the first pandemic wave in Italy. Two sex- and age-matched cohorts without COVID-19, with or without signs of systemic inflammation, were used to compare FVIIa-AT data. The FVIIa-AT plasma levels in COVID-19 patients were higher than those in non-COVID-19 subjects, either with or without inflammation, while no difference was observed among non-COVID-19 subjects. The association between COVID-19 and FVIIa-AT levels remained significant after adjustment for sex, age, C-reactive protein, renal function, fibrinogen, prothrombin time and activated partial thromboplastin time. Our results indicate that SARS-CoV-2 infection, at least during the first pandemic wave, was characterized by high FVIIa-AT levels, which may suggest an enhanced FVIIa-TF interaction in COVID-19, potentially consistent with SARS-CoV-2-induced endotheliopathy. |
