Activation of coagulation and fibrinolysis in HIV-infected patients: relationship to oxidative stress

Various hemostatic dysfunctions usually considered as risk factors for thro mbotic events were reported in HIV infection, even in the absence of clinic ally-apparent thrombosis and correlation to the progression of the disease. Since oxidative stress has been suggested to promote a procoagulant activi ty, we carried out a study to investigate whether the apparently perturbed oxidative/antioxidant balance could contribute to an activation of the hemo static system in HIV infection. For that purpose, 49 consecutive HIV-infect ed 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 degrada tion products (D-dimer) were evaluated to investigate the degree of the act ivation of the hemostatic system. Plasma levels of malondialdehyde (MDA), t he main end product of lipid peroxidation, and erythrocyte glutathione pero xidase (GSH-Px), a key enzyme for protecting cells against hydroperoxides d erivates, were measured to investigate the oxidative/antioxidant balance. P lasma levels of F1+2 and D-dimer well correlated and were shown significant ly higher in HIV-infected patients when compared with the controls as was a PAI-activity. The index of peroxidation MDA and the antioxidant molecule G SH-Px was significantly higher in HIV-infected patients when compared to co ntrols. Furthermore, GSH-Px activity correlated with both F1+2 and D-dimer in HIV-infected patients, suggesting a relationship between perturbed antio xidant defenses and activation of the hemostatic system.