Various hemostatic dysfunctions usually considered as risk factors for thrombotic events were reported in HIV infection, even in the absence of clinically-apparent thrombosis and correlation to the progression of the disease. Since oxidative stress has been suggested to promote a procoagulant activity, we carried out a study to investigate whether the apparently perturbed oxidative/antioxidant balance could contribute to an activation of the hemostatic system in HIV infection. For that purpose, 49 consecutive HIV- infected outpatients and 43 matched HIV-negative healthy controls were studied at distance for any acute episode. Plasma levels of prothrombin fragment 1+2 (F1+2), plasminogen activator inhibitor (PAI-1) activity and fibrin degradation products (D-dimer) were evaluated to investigate the degree of the activation of the hemostatic system. Plasma levels of malondialdehyde (MDA), the main end product of lipid peroxidation, and erythrocyte glutathione peroxidase (GSH-Px), a key enzyme for protecting cells against hydroperoxides derivates; were measured to investigate the oxidative/antioxidant balance. Plasma levels of F1+2 and D-dimer well correlated and were shown significantly higher in HIV-infected patients when compared with the controls as was a PAI-activity. The index of peroxidation MDA and the antioxidant molecule GSH-Px was significantly higher in HIV- infected patients when compared to controls. Furthermore, GSH-Px activity correlated with both F1+2 and D-dimer in HIV-infected patients, suggesting a relationship between perturbed antioxidant defenses and activation of the hemostatic system.
|Number of pages||5|
|Journal||Fibrinolysis and Proteolysis|
|Publication status||Published - 1999|
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