Assuntos
Pressão Sanguínea , Braquidactilia/diagnóstico , Ossos da Mão/anormalidades , Hipertensão/congênito , Adulto , Pressão Sanguínea/genética , Braquidactilia/genética , Braquidactilia/fisiopatologia , Nucleotídeo Cíclico Fosfodiesterase do Tipo 3/genética , Análise Mutacional de DNA , Feminino , Predisposição Genética para Doença , Ossos da Mão/diagnóstico por imagem , Humanos , Hipertensão/diagnóstico , Hipertensão/genética , Hipertensão/fisiopatologia , Mutação , FenótipoAssuntos
Técnicas de Apoio para a Decisão , Produtos de Degradação da Fibrina e do Fibrinogênio/metabolismo , Papel do Médico , Embolia Pulmonar/diagnóstico , Diagnóstico Diferencial , Frequência Cardíaca , Hemoptise/etiologia , Humanos , Modelos Logísticos , Neoplasias/complicações , Países Baixos , Razão de Chances , Valor Preditivo dos Testes , Estudos Prospectivos , Embolia Pulmonar/sangue , Embolia Pulmonar/complicações , Embolia Pulmonar/etiologia , Medição de Risco , Fatores de Risco , Trombose Venosa/complicaçõesRESUMO
BACKGROUND AND OBJECTIVES: Clinical trials have demonstrated that initial outpatient treatment is safe and effective in patients with deep vein thrombosis (DVT). Considering the relative lack of literature-based evidence on outpatient low molecular weight heparin (LMWH) treatment in daily practice this study prospectively evaluated the implementation of a protocol for full outpatient treatment of DVT in a non-teaching hospital. DESIGN AND METHODS: Consecutive patients with objectively demonstrated DVT were treated on an outpatient basis with subcutaneous nadroparin injections for at least 5 days and oral anticoagulant treatment for at least 3 months. RESULTS: In 294 of 309 (95%) consecutive patients with proven DVT, nadroparin could be started on a fully outpatient basis. During initial LMWH treatment one patient had to be hospitalized because of objectively proven pulmonary embolism (PE), and one patient developed a major bleeding complication. Overall, during 3 months follow-up recurrent venous thromboembolism (VTE) occurred in nine patients (3.1%; 95 CI 1.1 to 5.1), four patients experienced a major non-fatal hemorrhage (1.4%; 95 CI 0.04 to 2.7) and ten patients died (3.4%; 95% CI 1.3 to 5.5) of whom seven with disseminated malignancy, but none of fatal PE. INTERPRETATION AND CONCLUSIONS: Out of hospital initiation of anticoagulant treatment with LMWH is safe and effective in the overall majority of patients (95%) with objectively proven DVT. We believe that these results are relevant to both clinicians and health care providers in view of the feasibility of home treatment in nearly all patients.
Assuntos
Heparina de Baixo Peso Molecular/uso terapêutico , Pacientes Ambulatoriais , Trombose Venosa/tratamento farmacológico , Doença Aguda , Adulto , Idoso , Anticoagulantes/administração & dosagem , Anticoagulantes/uso terapêutico , Feminino , Heparina de Baixo Peso Molecular/administração & dosagem , Humanos , Injeções Subcutâneas , Masculino , Pessoa de Meia-Idade , Gravidez , Complicações Hematológicas na Gravidez/tratamento farmacológico , Recidiva , Estudos Retrospectivos , Tromboembolia/epidemiologia , Resultado do Tratamento , Ultrassonografia , Trombose Venosa/diagnóstico por imagem , Trombose Venosa/fisiopatologiaRESUMO
Deep vein thrombosis (DVT) and pulmonary embolism (PE) are considered to be two forms of the same disease, however it is not fully understood what determines their clinical presentation. Proteins encoded by the FXIIIA and TAFI genes are involved in stabilizing the fibrin clot and in making it more lysis resistant. The FXIIIA 34Leu and TAFI -438A alleles might protect against DVT. Information on such an association with PE is either contradictory or missing. We hypothesized that both polymorphisms might influence the formation and fate of emboli and accordingly the risk of PE. We determined the frequencies of both polymorphisms in patients with objectively demonstrated PE. The frequency of FXIIIA Leu34Leu in PE patients and non-PE patients was 4.5% and 8.8%, [OR 0.5 (95% CI: 0.1 to 1.9)], respectively. For -438 A/A TAFI genotype the frequency was 1.5% and 8.1% [OR 0.1 (95% CI: 0.02 to 1.1)], respectively.