Navegando por Palavras-chave "Prothrombin"

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    Hypoprothrombinemia in the compensated form of hepatosplenic schistosomiasis: further studies
    (Instituto de Medicina Tropical, 1988-08-01) Forones, Nora Manoukian [UNIFESP]; Borges, Durval Rosa [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Coagulation abnormality is frequently observed in schistosomiasis patients but its pathophysiology has not been established. We measured, by immunodiffusion. the prothrombin-antigen concentration in 56 individuals; of these 19 with demonstrated compensated form of hepatosplenic schistosomiasis, 17 with cirrhosis and 20 were control subjects. Transaminases, albumin, transthyretin, prothrombin time, antithrombin III, factor VII, and fibrinogen were also evaluated. All parameters were altered in the cirrhotic group but only albumin, prothrombin and antithrombin III levels were altered in the schistosomiasis group. Ninety percent of the patients with cirrhosis and sixty percent of the patients with schistosomiasis had abnormal plasma levels of albumin, transthyretin, prothrombin-antigen, and/or antithrombin III; an impaired hepatic synthesis was responsible for these results. Conversely forty percent of the schistosomiasis patients with normal plasma concentrations of both albumin and transthyretin had decreased mean plasma levels of both prothrombin and antithrombin III. These results suggest that either proth rombin and antithrombin III are more sensitive markers of impaired hepatic synthesis in schistosomiasis than are levels of albumin and transthyretin combined, or a low grade chronic consumption of clotting proteins also occurs. Considering the latter hypothesis it is possible that the thrombin formed would be inhibited by antithrombin III with the complexed thrombin-antithrombin III being cleared by the liver. Consequently the plasma levels of both prothrombin and antithrombin would be decreased, but the level of fibrinogen would be preserved.
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    Thrombophilic mutations and risk of retinal vein occlusion
    (Conselho Brasileiro de Oftalmologia, 2007-12-01) Biancardi, Ana Luiza; Gadelha, Telma; Borges, Wander Inturias Sergillo; Moraes Jr., Haroldo Vieira De [UNIFESP]; Spector, Nelson; Universidade Federal do Rio de Janeiro; UFRJ Department of Internal Medicine Service of Hematology; Instituto Brasileiro de Oftalmologia; Universidade Federal de São Paulo (UNIFESP); Universidade Federal do Rio de Janeiro Department of Internal Medicine
    PURPOSE: The association of retinal vein occlusion and hereditary thrombophilia abnormalities is not established, with controversial results in the literature. This study investigates the association between retinal vein occlusion and three thrombophilic mutations: factor V 1691A (factor V Leiden), prothrombin 20210A (PT 20210A) and homozygous methylenetetrahydrofolate reductase 677T (MTHFR 677TT). METHODS: 55 consecutive retinal vein occlusion patients and 55 controls matched by age, gender and race, were tested for the presence of the following mutations: factor V Leiden, PT 20210A and MTHFR 677TT. The frequencies of the three mutations in cases and controls were compared. RESULTS: Factor V Leiden was found in 3.6% of patients and in 0% of controls; PT 20210A was found in 1.8% of patients and 3.6% of controls, (matched-pair odds ratio, 0.5; 95% confidence interval, 0.04 to 5.51); MTHFR 677TT was found in 9% of patients and 9% of controls (matched-pair odds ratio, 1; 95% confidence interval, 0.92 to 3.45). Arterial hypertension was more frequent in patients than controls (matched-pair odds ratio, 3.4; 95% confidence interval, 1.25 to 9.21). CONCLUSIONS: This study suggests that thrombophilic mutations are not risk factors for RVO. Routine investigation of hereditary thrombophilia in these patients is not justified.