Base de dados : MEDLINE
Pesquisa : C15.378.100.100.037 [Categoria DeCS]
Referências encontradas : 943 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 95 ir para página                         

  1 / 943 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29287725
[Au] Autor:Cates C; Rousselle T; Wang J; Quan N; Wang L; Chen X; Yang L; Rezaie AR; Li J
[Ad] Endereço:Department of Physiology and Biophysics, Mississippi Center for Heart Research, University of Mississippi Medical Center, Jackson, MS 39216, USA.
[Ti] Título:Activated protein C protects against pressure overload-induced hypertrophy through AMPK signaling.
[So] Source:Biochem Biophys Res Commun;495(4):2584-2594, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We found that the anticoagulant plasma protease, activated protein C (APC), stimulates the energy sensor kinase, AMPK, in the stressed heart by activating protease-activated receptor 1 (PAR1) on cardiomyocytes. Wild-type (WT) and AMPK-kinase dead (KD) transgenic mice were subjected to transverse aortic constriction (TAC) surgery. The results demonstrated that while no phenotypic differences can be observed between WT and AMPK-KD mice under normal physiological conditions, AMPK-KD mice exhibit significantly larger hearts after 4 weeks of TAC surgery. Analysis by echocardiography suggested that the impairment in the cardiac function of AMPK-KD hearts is significantly greater than that of WT hearts. Immunohistochemical staining revealed increased macrophage infiltration and ROS generation in AMPK-KD hearts after 4 weeks of TAC surgery. Immunoblotting results demonstrated that the redox markers, pShc , 4-hydroxynonenal and ERK, were all up-regulated at a higher extent in AMPK-KD hearts after 4 weeks of TAC surgery. Administration of APC-WT and the signaling selective APC-2Cys mutant, but not the anticoagulant selective APC-E170A mutant, significantly attenuated pressure overload-induced hypertrophy and fibrosis. Macrophage infiltration and pShc activation caused by pressure overload were also inhibited by APC and APC-2Cys but not by APC-E170A. Therefore, the cardiac AMPK protects against pressure overload-induced hypertrophy and the signaling selective APC-2Cys may have therapeutic potential for treating hypertension-related hypertrophy without increasing the risk of bleeding.
[Mh] Termos MeSH primário: Pressão Sanguínea
Cardiomegalia/fisiopatologia
Hipertensão/fisiopatologia
Proteína C/metabolismo
Proteínas Quinases/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Resistência à Proteína C Ativada
Animais
Cardiomegalia/patologia
Hipertensão/patologia
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Protein C); EC 2.7.- (Protein Kinases); EC 2.7.1.- (AMP-activated protein kinase kinase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171231
[St] Status:MEDLINE


  2 / 943 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29017215
[Au] Autor:Schuh T; Stöllberger C
[Ti] Título:[Pulmonary Embolism Despite Rivaroxaban in an Obese Patient].
[Ti] Título:Pulmonalembolie trotz Rivaroxaban bei einer adipösen Patientin..
[So] Source:Dtsch Med Wochenschr;142(20):1548-1551, 2017 Oct.
[Is] ISSN:1439-4413
[Cp] País de publicação:Germany
[La] Idioma:ger
[Ab] Resumo:Rivaroxaban, an oral factor Xa inhibitor, is approved for therapy of venous thromboembolism. It is unclear whether the standard dose for patients with a body mass index (BMI) > 40 kg/m is sufficient. The 45-year-old patient was admitted because of increasing respiratory distress. She had a history of pulmonary embolism 30 months before the admission, a factor V Leiden mutation and several hospitalisations due to dermatomycoses. The patient briefly took phenprocoumon which was changed to 20 mg rivaroxaban due to a lack of adherence. Six months before admission, the patient paused the rivaroxaban therapy because of dental surgery and suffered a recurrent pulmonary embolism. The patient presented with increasing difficulty of breathing, morbid obesity with a BMI of 59.3 kg/m and intertrigo of the lower extremities. The ECG showed a right axis deviation, a pulmonary P-wave and an incomplete right bundle branch block. Computed tomography showed pulmonary embolisms of the left lower lobe. The pulmonary artery was dilated, and the right atrium was enlarged. Venous thrombosis of the lower limb could not be certainly ruled out. The D-dimer was elevated with 5.895 mg/L (normal value up to 169 mg/L) and NT-pro-BNP was elevated at 5.580 ng/L (normal value up to 0.5 ng/L). Sixteen hours after the onset of symptoms, 22 hours after the last dose, the serum rivaroxaban level was 137 ng/ml. According to manufacturers, the therapeutic range of rivaroxaban after 2 - 4 hours is 22 - 535 ng/ml, and after 24 hours 6 - 239 ng/ml. After initiation of a therapy with low-molecular weight heparin and subsequent oral anticoagulation with phenprocoumon, the symptoms decreased. It is highly probable that the pulmonary embolism occurred at a time when the rivaroxaban level was in the therapeutic range. Since there are only few data about safety and efficacy of rivaroxaban and other non-vitamin K-oral anticoagulants (NOACs) in severely obese patients, the recommendations of the "International Society for Thrombosis and Haemostasis" should be followed: Rivaroxaban and other NOACs should not be used in patients with a BMI > 40 kg/m or weight > 120 kg, since only few data on this patient group are available. If NOACs are necessary in these patients, serum concentrations of NOACs should be measured.
[Mh] Termos MeSH primário: Obesidade Mórbida/complicações
Embolia Pulmonar/etiologia
Rivaroxabana/efeitos adversos
Rivaroxabana/uso terapêutico
Síndrome de Abstinência a Substâncias/etiologia
Tromboembolia Venosa/complicações
Tromboembolia Venosa/tratamento farmacológico
[Mh] Termos MeSH secundário: Resistência à Proteína C Ativada/complicações
Resistência à Proteína C Ativada/tratamento farmacológico
Contraindicações
Relação Dose-Resposta a Droga
Substituição de Medicamentos
Feminino
Produtos de Degradação da Fibrina e do Fibrinogênio/metabolismo
Heparina de Baixo Peso Molecular/uso terapêutico
Seres Humanos
Meia-Idade
Femprocumona/uso terapêutico
Embolia Pulmonar/diagnóstico por imagem
Embolia Pulmonar/tratamento farmacológico
Recidiva
Cirurgia Bucal
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fibrin Fibrinogen Degradation Products); 0 (Heparin, Low-Molecular-Weight); 0 (fibrin fragment D); 9NDF7JZ4M3 (Rivaroxaban); Q08SIO485D (Phenprocoumon)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171011
[St] Status:MEDLINE
[do] DOI:10.1055/s-0043-114547


  3 / 943 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28472350
[Au] Autor:Perez Botero J; Majerus JA; Strege AK; Johnson RD; Chen D; Pruthi RK
[Ad] Endereço:From the Division of Hematology, Department of Medicine.
[Ti] Título:Diagnostic Testing Approaches for Activated Protein C Resistance and Factor V Leiden: A Comparison of Institutional and National Provider Practices.
[So] Source:Am J Clin Pathol;147(6):604-610, 2017 Jun 01.
[Is] ISSN:1943-7722
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Objectives: To analyze the economic impact of testing for activated protein C resistance (APC-R) due to factor V Leiden (FVL) mutation with APC-R with reflexive FVL genotyping (algorithmic approach) or genotyping alone. Methods: OptumLabs Data Warehouse (OLDW) data were used to assess testing approaches. Insurance claims for APC-R and FVL in 2013 were compared with the Mayo Clinic database. Centers for Medicare & Medicaid Services diagnostic fee schedules were used to assign costs. Results: Of 19.3 million OLDW-covered individuals, 74,242 (0.385%) received 75,608 tests: APC-R, 2,265 (2.9%); FVL genotyping, 70,619 (90.1%); and both APC-R and FVL, 2,724 (7.0%). In total, 1,317 tests were performed at Mayo Clinic: APC-R with reflex FVL (1,256; 95.4%) and FVL alone (61; 4.6%). Costs per evaluated individual and per total population (person/year) in OLDW and algorithmic approach were $83.77 vs $36.38 and $0.32 vs $0.14, respectively. Conclusions: The cost-optimized algorithmic approach reduces health care costs.
[Mh] Termos MeSH primário: Resistência à Proteína C Ativada/diagnóstico
Fator V/genética
Trombofilia/diagnóstico
[Mh] Termos MeSH secundário: Resistência à Proteína C Ativada/genética
Algoritmos
Testes de Coagulação Sanguínea/economia
Redução de Custos
Feminino
Genótipo
Seres Humanos
Mutação
Trombofilia/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (factor V Leiden); 9001-24-5 (Factor V)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1093/ajcp/aqx033


  4 / 943 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28318106
[Au] Autor:Gessoni G; Valverde S; Valle L; Gessoni F; Caruso P; Valle R
[Ad] Endereço:Trasfusional Deptartment of Venetian District, Ospedale dell'Angelo, Mestre, Venice, Italy.
[Ti] Título:Lack of rivaroxaban influence on a prothrombinase-based assay for the detection of activated C protein resistance: an Italian ex vivo and in vitro study in normal subjects and factor V Leiden carriers.
[So] Source:Int J Lab Hematol;39(4):418-422, 2017 Aug.
[Is] ISSN:1751-553X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Activated protein C resistance (APCr) leads to hypercoagulability and is due, often but not exclusively, to Factor V Leiden (FVL). The aim of this study was to assess the ex vivo and in vitro interference of the direct factor Xa inhibitor rivaroxaban (RIV) on a prothrombinase-based assay for APCr detection. METHODS: An ex vivo study was performed on fresh plasma samples obtained from 44 subjects with FV wild-type and seven with FVL heterozygous, all treated with RIV. An in vitro study was performed on 15 plasma samples (six from normal subjects, six from heterozygous, and three from homozygous FVL carriers, all frozen specimens) spiked with RIV. RIV concentration was evaluated using a chromogenic assay, and APCr was evaluated by a prothrombinase-based assay. RESULTS: No significant interference of RIV on APCr results obtained by a prothrombinase-based assay was observed for drug concentrations up to 400 ng/mL in FV wild-type and FVL carriers (homozygous and heterozygous). These results were confirmed both ex vivo and in vitro. CONCLUSIONS: RIV did not significantly interfere with the prothrombinase-based assay used for the assessment of APCr, and this was observed to occur independently of FV status. However, only concentrations up to 400 ng/mL were tested and, therefore, what occurs in the presence of higher doses remains to be investigated.
[Mh] Termos MeSH primário: Resistência à Proteína C Ativada/genética
Coagulação Sanguínea/efeitos dos fármacos
Deficiência do Fator V/sangue
Deficiência do Fator V/genética
Fator V/genética
Heterozigoto
Rivaroxabana/farmacologia
Tromboplastina/metabolismo
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Testes de Coagulação Sanguínea
Monitoramento de Medicamentos
Deficiência do Fator V/diagnóstico
Deficiência do Fator V/tratamento farmacológico
Feminino
Homozigoto
Seres Humanos
Itália
Masculino
Rivaroxabana/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (factor V Leiden); 9001-24-5 (Factor V); 9035-58-9 (Thromboplastin); 9NDF7JZ4M3 (Rivaroxaban)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170321
[St] Status:MEDLINE
[do] DOI:10.1111/ijlh.12647


  5 / 943 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28196919
[Au] Autor:Kristoffersen AH; Petersen PH; Røraas T; Sandberg S
[Ad] Endereço:Laboratory of Clinical Biochemistry, Haukeland University Hospital, Bergen, Norway; ann.kristoffersen@helse-bergen.no.
[Ti] Título:Estimates of Within-Subject Biological Variation of Protein C, Antithrombin, Protein S Free, Protein S Activity, and Activated Protein C Resistance in Pregnant Women.
[So] Source:Clin Chem;63(4):898-907, 2017 Apr.
[Is] ISSN:1530-8561
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In pregnancy, interpretation of results from coagulation parameters can be difficult because of the procoagulant physiological changes. The aim of this study was to describe the course of 5 coagulation parameters (thrombophilia markers) in healthy pregnancies, and to estimate and compare the within-subject biological variation (CV ) of these parameters in healthy pregnant and nonpregnant women. METHODS: Blood samples were obtained every 4th week during pregnancy and 3 samples after delivery in 20 healthy women and every 4th week during 40 weeks in 19 healthy nonpregnant women. Protein C (PC), antithrombin (AT), protein S free (PS free), protein S activity (PS activity), and activated protein C resistance (with factor V-depleted plasma) (APCR) were analyzed. Before the calculation of CV , results were transformed into multiples of the median (MoM) and natural logarithm of MoM (lnMoM) to adjust for the physiological changes during pregnancy. RESULTS: During pregnancy, PC results showed large variability, AT decreased slightly, and PS free and PS activity decreased significantly. Both activated partial thromboplastin time tests used to calculate APCR decreased, and the APCR ratio was constant. The CV (lnMoM) in pregnancy were for PC 8.4%, for AT 3.8%, for PS free 11.5%, for PS activity 9.3%, and for APCR 0.5%, and similar to corresponding results in nonpregnant women. CONCLUSIONS: Transformation of coagulation parameters in healthy pregnancies to lnMoM is a tool to establish a kind of steady state. Although there is a physiological change in PC, AT, and PS free and PS activity during pregnancy, the CV was comparable with the CV of nonpregnant women.
[Mh] Termos MeSH primário: Resistência à Proteína C Ativada/sangue
Antitrombinas/sangue
Proteína C/análise
Proteína S/análise
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Gravidez
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antithrombins); 0 (Protein C); 0 (Protein S)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170601
[Lr] Data última revisão:
170601
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170216
[St] Status:MEDLINE
[do] DOI:10.1373/clinchem.2016.265900


  6 / 943 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28102772
[Au] Autor:Rimbas RC; Calin SI; Ionescu H; Dorobat B; Vinereanu D; Cinteza M
[Ad] Endereço:1 Cardiology Department, University and Emergency Hospital, Bucharest, Romania.
[Ti] Título:An extensive suprarenal inferior vena cava thrombosis successfully treated with catheter-directed thrombolysis in a postpartum 14-year-old girl.
[So] Source:Vasa;46(3):227-230, 2017 May.
[Is] ISSN:0301-1526
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:We report a case of extensive early postpartum acute suprarenal inferior vena cava thrombosis in a 14-year-old girl. Management included catheter-directed-thrombolysis, aiming to save renal function and prevent fatal pulmonary embolism. Treatment decisions were mostly based on adult guidelines, as guidelines for the paediatric population are not yet available.
[Mh] Termos MeSH primário: Cateterismo Venoso Central
Fibrinolíticos/administração & dosagem
Complicações Cardiovasculares na Gravidez/tratamento farmacológico
Terapia Trombolítica
Ativador de Plasminogênio Tecidual/administração & dosagem
Veia Cava Inferior/efeitos dos fármacos
Trombose Venosa/tratamento farmacológico
[Mh] Termos MeSH secundário: Resistência à Proteína C Ativada/complicações
Resistência à Proteína C Ativada/genética
Doença Aguda
Adolescente
Anticoagulantes/administração & dosagem
Angiografia por Tomografia Computadorizada
Fator V/genética
Feminino
Seres Humanos
Infusões Intravenosas
Mutação
Flebografia/métodos
Período Pós-Parto
Gravidez
Complicações Cardiovasculares na Gravidez/diagnóstico por imagem
Complicações Cardiovasculares na Gravidez/genética
Deficiência de Proteína S/complicações
Deficiência de Proteína S/genética
Fatores de Risco
Resultado do Tratamento
Veia Cava Inferior/diagnóstico por imagem
Trombose Venosa/diagnóstico por imagem
Trombose Venosa/genética
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticoagulants); 0 (Fibrinolytic Agents); 0 (factor V Leiden); 9001-24-5 (Factor V); EC 3.4.21.68 (Tissue Plasminogen Activator)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170619
[Lr] Data última revisão:
170619
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170120
[St] Status:MEDLINE
[do] DOI:10.1024/0301-1526/a000605


  7 / 943 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28063132
[Au] Autor:Sharma A; Singh K; Biswas A; Ranjan R; Kishor K; Kumar R; Pandey H; Kamal VK; Saxena R
[Ad] Endereço:Department of Haematology, All India Institute of Medical Sciences (AIIMS), New Delhi, 110029, India.
[Ti] Título:Evaluation of role of FV, FVIII and APLAs in the pathogenesis of APCR in FV Leiden negative DVT patients: a study in India.
[So] Source:J Thromb Thrombolysis;43(2):217-223, 2017 Feb.
[Is] ISSN:1573-742X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Resistance to APC (APCR) is a very important cause of thrombophilia and most frequently caused by the Leiden mutation. APCR is also seen in the absence of FV Leiden and associated with elevated levels of factor V (FV), factor VIII (FVIII) and antiphospholipid antibodies (APLAs). The aim of this prospective case control study was to find out the frequency and role of FV, FVIII and APLAs in the pathogenesis of APCR in FV Leiden negative deep vein thrombosis (DVT) patients in India. A total 30 APCR positive and FV Leiden negative patients with DVT and similar number of age and sex matched healthy controls were recruited. Significantly higher mean FVIII levels were observed in patients as compared to controls [patients: 132.3 ± 30.7 IU/ml, controls: 117.5 ± 17.7 IU/ml, p = 0.025]. A significant negative correlation was also observed between FVIII and APC ratio (Pearson correlation = 0.368, p = <0.001). Mean FV levels in patients [107.1 ± 13.1 IU/ml] and controls [102 ± 11.9 IU/ml] were not statistically significant (p = 0.119). Anti ß2 glycoprotein I (Anti-ß2-GPI, IgG) showed significant association with APCR phenotype (p = 0.050), unlike other factors such as protein C, protein S, lupus anticoagulant and anticardiolipin antibodies. The strong association of FVIII and anti-ß2 GPI (IgG) antibodies with APCR phenotype is suggestive of incorporation of these factors in APCR positive DVT patients in the absence of FV Leiden mutation in India. However more studies in large sample size are required for setting up the proper investigation protocol in these patients.
[Mh] Termos MeSH primário: Resistência à Proteína C Ativada/etiologia
Anticorpos Antifosfolipídeos/sangue
Fator VIII/análise
Fator V/genética
Trombose Venosa/etiologia
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Fator V/análise
Feminino
Seres Humanos
Índia
Masculino
Meia-Idade
Estudos Prospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Antiphospholipid); 0 (F8 protein, human); 0 (factor V Leiden); 9001-24-5 (Factor V); 9001-27-8 (Factor VIII)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170108
[St] Status:MEDLINE
[do] DOI:10.1007/s11239-016-1469-6


  8 / 943 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27986523
[Au] Autor:Tzoran I; Papadakis M; Brenner B; Fidalgo Á; Rivas A; Wells PS; Gavín O; Adarraga MD; Moustafa F; Monreal M; Registro Informatizado de Enfermedad TromboEmbólica Investigators
[Ad] Endereço:Department of Haematology and Bone Marrow Transplantation, Rambam Health Care Campus, Haifa, Israel. Electronic address: i_tzoran@rambam.health.gov.il.
[Ti] Título:Outcome of Patients with Venous Thromboembolism and Factor V Leiden or Prothrombin 20210 Carrier Mutations During the Course of Anticoagulation.
[So] Source:Am J Med;130(4):482.e1-482.e9, 2017 Apr.
[Is] ISSN:1555-7162
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Individuals with factor V Leiden or prothrombin G20210A mutations are at a higher risk to develop venous thromboembolism. However, the influence of these polymorphisms on patient outcome during anticoagulant therapy has not been consistently explored. METHODS: We used the Registro Informatizado de Enfermedad TromboEmbólica database to compare rates of venous thromboembolism recurrence and bleeding events occurring during the anticoagulation course in factor V Leiden carriers, prothrombin mutation carriers, and noncarriers. RESULTS: Between March 2001 and December 2015, 10,139 patients underwent thrombophilia testing. Of these, 1384 were factor V Leiden carriers, 1115 were prothrombin mutation carriers, and 7640 were noncarriers. During the anticoagulation course, 160 patients developed recurrent deep vein thrombosis and 94 patients developed pulmonary embolism (16 died); 154 patients had major bleeding (10 died), and 291 patients had nonmajor bleeding. On multivariable analysis, factor V Leiden carriers had a similar rate of venous thromboembolism recurrence (adjusted hazard ratio [HR], 1.16; 95% confidence interval [CI], 0.82-1.64), half the rate of major bleeding (adjusted HR, 0.50; 95% CI, 0.25-0.99) and a nonsignificantly lower rate of nonmajor bleeding (adjusted HR, 0.66; 95% CI, 0.43-1.01) than noncarriers. Prothrombin mutation carriers and noncarriers had a comparable rate of venous thromboembolism recurrence (adjusted HR, 1.00; 95% CI, 0.68-1.48), major bleeding (adjusted HR, 0.75; 95% CI, 0.42-1.34), and nonmajor bleeding events (adjusted HR, 1.10; 95% CI, 0.77-1.57). CONCLUSIONS: During the anticoagulation course, factor V Leiden carriers had a similar risk for venous thromboembolism recurrence and half the risk for major bleeding compared with noncarriers. This finding may contribute to decision-making regarding anticoagulation duration in selected factor V Leiden carriers with venous thromboembolism.
[Mh] Termos MeSH primário: Resistência à Proteína C Ativada/complicações
Anticoagulantes/uso terapêutico
Fator V/genética
Protrombina/genética
Tromboembolia Venosa/genética
[Mh] Termos MeSH secundário: Feminino
Hemorragia/induzido quimicamente
Hemorragia/etiologia
Hemorragia/genética
Heterozigoto
Seres Humanos
Masculino
Meia-Idade
Mutação/genética
Fatores de Risco
Resultado do Tratamento
Tromboembolia Venosa/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticoagulants); 0 (factor V Leiden); 9001-24-5 (Factor V); 9001-26-7 (Prothrombin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170510
[Lr] Data última revisão:
170510
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161218
[St] Status:MEDLINE


  9 / 943 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27323874
[Au] Autor:Hugon-Rodin J; Alhenc-Gelas M; Hemker HC; Brailly-Tabard S; Guiochon-Mantel A; Plu-Bureau G; Scarabin PY
[Ad] Endereço:a Inserm, UMR 1018 , Villejuif , France.
[Ti] Título:Sex hormone-binding globulin and thrombin generation in women using hormonal contraception.
[So] Source:Biomarkers;22(1):81-85, 2017 Feb.
[Is] ISSN:1366-5804
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: We investigated the impact of serum sex hormone-binding globulin (SHBG) on thrombin generation (TG) in women according to hormonal contraception. PATIENTS AND METHODS: A cross-sectional study of SHBG and TG measured via calibrated automated thrombography was conducted in 150 healthy women, including 75 users of combined oral contraceptives (COC), 22 users of progestin-only contraceptives (POC) and 53 nonusers. RESULTS: COC but not POC-users had significantly higher SHBG levels compared with nonusers. In hormonal contraceptive users, SHBG was positively associated with both activated protein C (APC) resistance and baseline TG, and protein S and prothrombin were important mediators. CONCLUSION: These data provide further evidence that SHBG may be used as a biomarker in assessing prothrombotic profile of hormonal contraception.
[Mh] Termos MeSH primário: Anticoncepcionais Orais Hormonais/efeitos adversos
Globulina de Ligação a Hormônio Sexual/análise
Trombina/biossíntese
[Mh] Termos MeSH secundário: Resistência à Proteína C Ativada/etiologia
Adulto
Biomarcadores/análise
Estudos de Coortes
Anticoncepcionais Orais Combinados/administração & dosagem
Anticoncepcionais Orais Hormonais/administração & dosagem
Estudos Transversais
Feminino
Seres Humanos
Progestinas/administração & dosagem
Progestinas/efeitos adversos
Trombose/induzido quimicamente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Contraceptives, Oral, Combined); 0 (Contraceptives, Oral, Hormonal); 0 (Progestins); 0 (Sex Hormone-Binding Globulin); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170203
[Lr] Data última revisão:
170203
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160622
[St] Status:MEDLINE
[do] DOI:10.1080/1354750X.2016.1204010


  10 / 943 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26102090
[Au] Autor:Florou E; Koukoulaki M; Theodoros T; Kalatzis V; Vougas V; Stamataki E; Kokkinou VC; Kostakis A; Drakopoulos S
[Ad] Endereço:From the First Department of Surgery Transplant Unit, Evangelismos General Hospital of Athens, Greece.
[Ti] Título:Successful Living-Related Renal Allograft in a Recipient With Factor V Leiden Deficiency: A Case Report.
[So] Source:Exp Clin Transplant;15(1):96-99, 2017 Feb.
[Is] ISSN:2146-8427
[Cp] País de publicação:Turkey
[La] Idioma:eng
[Ab] Resumo:Thrombophilia due to activated protein C resistance (Leiden mutation) is the most common inherited thrombophilic disorder with 5% incidence in whites. Renal transplant of these patients entails a risk of vascular thrombosis soon after the transplant; and acute rejection episodes and graft loss within the first year. We present a case of a successful living-related renal transplant in man with a recent history of repeat episodes of vascular access thrombosis attributed to inherited thrombophilia (heterozygosity for factor V mutation Q506 and homozygosity for mutation T677 for methylene-tetrahydrofolate reductase). Transplant recipient was administered anticoagulation therapy with low molecular weight heparin pre- and postoperatively. No thrombotic or hemorrhagic events occurred posttransplant. A high suspicion of thrombophilic disorders in patients with end-stage renal disease with vascular access thrombotic events should be screened further to prevent failure of a subsequent renal transplant. Inherited thrombophilic disorders may not exclude living-related kidney transplant provided that anticoagulation therapy is admin-istered perioperatively.
[Mh] Termos MeSH primário: Resistência à Proteína C Ativada/genética
Coagulação Sanguínea/genética
Fator V/genética
Falência Renal Crônica/cirurgia
Transplante de Rim/métodos
Doadores Vivos
Irmãos
[Mh] Termos MeSH secundário: Resistência à Proteína C Ativada/sangue
Resistência à Proteína C Ativada/diagnóstico
Resistência à Proteína C Ativada/tratamento farmacológico
Idoso
Aloenxertos
Anticoagulantes/uso terapêutico
Coagulação Sanguínea/efeitos dos fármacos
Feminino
Predisposição Genética para Doença
Heterozigoto
Homozigoto
Seres Humanos
Falência Renal Crônica/diagnóstico
Masculino
Metilenotetra-Hidrofolato Redutase (NADPH2)/genética
Meia-Idade
Fenótipo
Mutação Puntual
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticoagulants); 0 (factor V Leiden); 9001-24-5 (Factor V); EC 1.5.1.20 (MTHFR protein, human); EC 1.5.1.20 (Methylenetetrahydrofolate Reductase (NADPH2))
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150624
[St] Status:MEDLINE
[do] DOI:10.6002/ect.2014.0255



página 1 de 95 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde