Navegando por Palavras-chave "Geração de trombina"

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    Efeito da suplementação vitamínica em parâmetros de geração de trombina, fibrinólise e função endotelial em pacientes com tromboembolismo venoso: Estudo duplo-cego, randomizado, controlado com placebo
    (Universidade Federal de São Paulo (UNIFESP), 2006-12-31) Rodrigues, Celso Arrais [UNIFESP]; Lourenco, Dayse Maria [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Background: Mild hyperhomocysteinemia is associated with an increased risk of venous thromboembolism (VTE) and other cardiovascular diseases. Previous studies suggest impaired endothelial function and increased thrombin generation in hyperhomocysteinemic patients. Whether decreasing homocysteine with B-vitamin supplementation interferes with its procoagulant effects is to be determined. Objectives: To evaluate the correlation between homocysteine and markers of thrombin generation and endothelial function and to evaluate the effect of lowering homocysteine by Bvitamin supplementation on these markers in patients with VTE. Patients/Methods: This study was a multicentre, randomized, double-blind, placebo-controlled trial. We randomized 105 patients with a first event of objectively confirmed VTE, aged between 18 and 70 years, to receive either vitamin supplementation (folic acid 5 mg, vitamin B6 50 mg and vitamin B12 0.4 mg) or placebo. Blood was collected at randomization and 8 weeks after the intervention period. Results: Ninety-nine (94.3%) completed the 8-week period of treatment. In patients treated with vitamins, there was a 29% decrease in the homocysteine levels and a significant increase in the tissue plasminogen activator (t-PA) levels (p=0.0008). Both t-PA and plasminogen activator inhibitor type 1 (PAI-1) levels significantly increased in the group of patients above the highest tertile of basal homocysteine (12.6 μmol/L) who received vitamin supplementation (p=0.0004 and p=0.014, respectively). There was no change in the levels of these two markers in patients with homocysteine levels below the lowest tertile or in patients who received placebo independently of the homocysteine level. All other markers (prothrombin fragment 1+2, thrombin-antithrombin complex, D-dimer, Factor VIII:C and von Willebrand factor antigen) were unaffected by both vitamins and placebo, even in patients above the highest tertile of homocysteine. There was no difference between patients with homocysteine above the highest tertile and those below the lowest tertile (9.9 μmol/L) in the levels of these markers. Conclusions: In patients with VTE, homocysteine reduction by B-vitamin supplementation significantly increased both t-PA and PAI-1 in patients with higher levels of homocysteine. However, there was no effect of homocysteine reduction by B-vitamin supplementation on other markers of endothelial function, fibrinolysis and thrombin generation.