Assuntos
Arteriopatias Oclusivas/sangue , Coagulação Sanguínea , Monitorização Transcutânea dos Gases Sanguíneos , Endotélio Vascular/fisiopatologia , Exercício Físico , Perna (Membro)/irrigação sanguínea , Ativação Plaquetária , Idoso , Antifibrinolíticos/metabolismo , Biomarcadores/sangue , Fatores de Coagulação Sanguínea/metabolismo , Endotélio Vascular/lesões , Feminino , Fibrinolíticos/metabolismo , Humanos , Hipóxia/sangue , Isquemia/sangue , Perna (Membro)/fisiopatologia , Contagem de Leucócitos , Masculino , Pessoa de Meia-Idade , Contagem de PlaquetasRESUMO
Hyperhomocysteinaemia is a risk factor for premature atherosclerosis and venous thromboembolic disease. Supplementation with folic acid and vitamin B6 has been shown to decrease plasma homocysteine but data fail to assess an effect on the progression of vascular disease. We measured plasma homocysteine and two markers of endothelial injury (plasma soluble thrombomodulin and von Willebrand factor) at baseline and after 3 months of treatment with folic acid and vitamin B6. After this treatment there was a significant decrease in fasting soluble thrombomodulin (-15 ng/ml, 95%CI 5-22.2). Von Willebrand factor was significantly raised after methionine load at baseline but did not significantly rise after supplementation.
Assuntos
Ácido Fólico/administração & dosagem , Hiper-Homocisteinemia/dietoterapia , Piridoxina/administração & dosagem , Doenças Vasculares/etiologia , Adulto , Endotélio Vascular , Feminino , Homocisteína/sangue , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de Risco , Trombomodulina/sangue , Fator de von Willebrand/análiseRESUMO
Hyperhomocysteinaemia has been associated with arterial and venous thrombosis possibly by causing damage to the endothelium. We hypothesised that an oral load in methionine, that increases plasma homocysteine, would also result in an increase in biological markers of endothelial or platelet dysfunction. Then we investigated two groups of patients with arterial or venous occlusive disease: 17 with hyperhomocysteinemia and 12 without hyperhomocysteinemia. We measured in both groups plasma soluble thrombomodulin, von Willebrand factor, P-selectin and tissue factor plasma inhibitor before and 6 hours after a load with 100 mg/kg oral methionine. Methionine load resulted in a significant increase in von Willebrand factor in both groups (P<0.02), suggesting that endothelial dysfunction occurs during the load.
Assuntos
Arteriosclerose/etiologia , Arteriosclerose/metabolismo , Endotélio Vascular/metabolismo , Hiper-Homocisteinemia/complicações , Administração Oral , Adolescente , Adulto , Idoso , Biomarcadores/análise , Endotélio Vascular/efeitos dos fármacos , Feminino , Humanos , Hiper-Homocisteinemia/diagnóstico , Masculino , Metionina/administração & dosagem , Pessoa de Meia-Idade , Selectina-P/sangue , Valores de Referência , Sensibilidade e Especificidade , Estatísticas não Paramétricas , Trombomodulina/sangue , Fator de von Willebrand/análise , Fator de von Willebrand/efeitos dos fármacosRESUMO
Patients infected with HIV are at increased risk of atherosclerosis, and have evidence of endothelium dysfunction. The hypothesis was tested that HIV-related endothelium dysfunction is related to loss of antioxidants. This was done by the supplementation of the antioxidants selenium and beta-carotene. We supplemented the diet of 10 HIV-seropositive subjects with 100 microg selenium daily, 11 subjects with 30 mg beta-carotene twice daily while 15 subjects were not supplemented. Plasma was obtained at outset and after a year, and tested by ELISA for endothelial cell, platelet and inflammatory markers. The non-supplemented patients experienced increases in von Willebrand factor and soluble thrombomodulin (both p <0.01). There were no changes in any of the indices in the patients taking selenium or beta-carotene. Increased von Willebrand factor and soluble thrombomodulin in the non-supplemented patients imply increased damage to the endothelium over the year of the study. Therefore we interpret the lack of increase in the patients taking antioxidants as evidence of the protection of the endothelium by these agents.
