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Oxidative Status, Iron Plasma Levels in Venous Thrombosis Patients
Salvatore Santo Signorelli1, Andrea Barbagallo1, Gea Oliveri Conti2
1Department of Clinical and Experimental Medicine, University of Catania, Via Santa Sofia 80, 95123 Catania, Italy.
Antioxidants (Basel, Switzerland)
|June 27, 2024
Summary
Oxidative stress (OxS) and iron (Fe) dysregulation are linked to venous thrombosis (VTE). This study found elevated OxS markers, increased Fe, and higher hepcidin (Hep) in VTE patients, suggesting their role in VTE development.
Area of Science:
- Biochemistry
- Hematology
- Pathophysiology
Background:
- Venous thromboembolism (VTE) is a significant health concern.
- Oxidative stress (OxS) is increasingly recognized as a potential risk factor for VTE.
- The interplay between iron (Fe) metabolism, hepcidin (Hep) regulation, and OxS in VTE pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate the association between oxidative stress markers, plasma iron levels, and hepcidin protein levels in patients with venous thrombosis.
- To explore the potential role of iron dysregulation and oxidative stress in the development of VTE.
Main Methods:
- A case-control study was conducted with 20 hospitalized VTE patients and 20 healthy controls.
- Oxidative stress was assessed by measuring malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), and superoxide dismutase (SOD).
- Plasma iron (Fe) and hepcidin (Hep) levels were quantified in both groups.
Main Results:
- VTE patients exhibited significantly higher levels of MDA and 4-HNE, and lower SOD activity compared to controls, indicating activated OxS.
- Plasma iron levels were elevated, and hepcidin levels were significantly higher in VTE patients than in healthy individuals.
- Statistically significant differences were observed for all measured parameters between VTE patients and controls.
Conclusions:
- The findings suggest that activated oxidative stress, iron dysregulation, and overproduction of hepcidin are associated with venous thrombosis.
- Iron dysregulation appears to contribute to oxidative stress, potentially promoting inflammation and a pro-thrombotic state in VTE.
- Oxidative stress and iron metabolism, including hepcidin regulation, represent promising targets for VTE risk assessment and management.
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