RESUMO
Fatal cerebral hemorrhage involving the left thalamus in a neonate was attributed to deep cerebral vein thrombosis. Although antithrombin levels were at the lower end of the normal range, family and genetic studies showed constitutional type I antithrombin deficiency related to a novel missense mutation in the antithrombin gene.
Assuntos
Antitrombinas/deficiência , Hemorragia Cerebral/genética , Mutação Puntual , Antitrombinas/genética , Evolução Fatal , Humanos , Recém-Nascido , Masculino , Trombose Venosa/complicaçõesRESUMO
Antithrombin is one of the main endogenous anticoagulants and its deficiency is associated with deep venous thrombosis. The aim of the present study was to evaluate the prevalence of antithrombin deficiency in patients with chronic lower extremity ulcers. Forty-eight patients with chronic lower limb ulcers for longer than 10 years, evaluated during 1997, were studied: 40 were female (83.3%) and eight were male (16.6%), with ages ranging from 43 to 73 years (mean, 55.2 years). Antithrombin was dosed by the coagulometric method, with evaluation of the functional activity. Measurement was repeated in those cases where deficiency was found to be present. The highest prevalence rate for antithrombin deficiency in the general population was one in every 2000 cases. Data analysis was performed by utilizing the odds ratio with a confidence interval of 95% and P < 0.05. Deficiency in antithrombin levels was recorded in two (4.1%) of the patients with chronic ulcer. These results indicate a higher prevalence rate of antithrombin deficiency in those patients with chronic leg ulcers, suggesting that an association may be present. Further studies with a larger number of patients are required to confirm this hypothesis.
Assuntos
Antitrombinas/deficiência , Úlcera da Perna/complicações , Adulto , Idoso , Antitrombina III/análise , Doença Crônica , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Razão de ChancesRESUMO
Hemostatic function was studied sequentially in 12 children receiving L-asparaginase, vincristine, and prednisone as remission induction chemotherapy for acute lymphoblastic leukemia. The three-week period of L-asparaginase therapy was characterized by progressive decreases in plasma antithrombin, plasminogen, and fibrinogen concentrations, and by progressive increases in plasma clotting times (prothrombin time, partial thromboplastin time, thrombin time). Platelet counts rose rapidly during the third and fourth weeks of therapy as bone marrow remission was achieved. Factor V levels increased steadily during a five-week period, perhaps related to vincristine or prednisone therapy. Recent reports of thrombosis and hemorrhage in children and adults receiving L-asparaginase may be explained by this complex set of abnormalities in coagulation and coagulation control.