Department of Medical, Surgical and Advanced Technologies “G.F. Ingrassia”, University of Catania, Via Santa Sofia 87, 95123 Catania, Italy
Ilenia Nicolosi
Department of Medical, Surgical and Advanced Technologies “G.F. Ingrassia”, University of Catania, Via Santa Sofia 87, 95123 Catania, Italy
Pietro Zuccarello
Department of Medical, Surgical and Advanced Technologies “G.F. Ingrassia”, University of Catania, Via Santa Sofia 87, 95123 Catania, Italy
Luca Zanoli
Department of Clinical and Experimental Medicine, University of Catania, Via Santa Sofia 87, 95123 Catania, Italy
Agostino Gaudio
Department of Clinical and Experimental Medicine, University of Catania, Via Santa Sofia 87, 95123 Catania, Italy
Domenico Di Raimondo
Division of Internal Medicine and Stroke Care, Department of Promoting Health, Maternal-Infant, Excellence and Internal and Specialized Medicine (Promise) G. D’Alessandro, University of Palermo, 90127 Palermo, Italy
Margherita Ferrante
Department of Medical, Surgical and Advanced Technologies “G.F. Ingrassia”, University of Catania, Via Santa Sofia 87, 95123 Catania, Italy
Background: Hypercoagulative conditions play a key role in venous thromboembolism (VTE). Inflammation is currently linked to VTE, but the potential role of circulating microparticles and oxidative stress (OxS) must be elucidated. The aim of this study was to evaluate platelet-derived microparticles and surrogate OxS biomarkers in patients diagnosed with VTE through a case–control study. Methods: Platelet-derived microparticles (MPs), pro-thrombinase-induced clotting time assay (PiCT), phospholipids (PLPs), malondialdehyde (MDA), 4-hydroxynonenale (4-HNE), thiobarbituric acid reactive substances (TBARs), superoxide dismutase (SOD), and galectin-3 (Gal-3) were measured in VTE patients and in healthy controls. Results: PLPs, 4-HNE, TBARs, and Gal-3 were higher in VTE patients compared to controls; conversely, SOD was lower. A significant non-linear regression between OxS biomarkers and the markers of platelet degranulation was found. Conclusion: Our results suggest that OxS and platelet degranulation are concomitant pathophysiological mechanisms in VTE.
