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  1 / 1062 MEDLINE  
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[PMID]:28704253
[Au] Autor:Bauduer F; Poumier-Chabanier C
[Ad] Endereço:aUMR 5199 PACEA, Université de Bordeaux, Pessac bService d'Hématologie cService de Gynécologie-Obstétrique, Centre Hospitalier de la Côte Basque, Bayonne Cedex, France.
[Ti] Título:Preeclampsia in a factor XI deficient woman: discussion about one case.
[So] Source:Blood Coagul Fibrinolysis;28(5):423-424, 2017 07.
[Is] ISSN:1473-5733
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Fator XI
Pré-Eclâmpsia
[Mh] Termos MeSH secundário: Deficiência do Fator XI
Feminino
Seres Humanos
Gravidez
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
9013-55-2 (Factor XI)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE
[do] DOI:10.1097/MBC.0000000000000636


  2 / 1062 MEDLINE  
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[PMID]:28623485
[Au] Autor:Dimova D; Bajorath J
[Ad] Endereço:Department of Life Science Informatics, B-IT, LIMES Program Unit Chemical Biology and Medicinal Chemistry, Rheinische Friedrich-Wilhelms-Universität, Dahlmannstr. 2, 53113, Bonn, Germany.
[Ti] Título:Is scaffold hopping a reliable indicator for the ability of computational methods to identify structurally diverse active compounds?
[So] Source:J Comput Aided Mol Des;31(7):603-608, 2017 Jul.
[Is] ISSN:1573-4951
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Computational scaffold hopping aims to identify core structure replacements in active compounds. To evaluate scaffold hopping potential from a principal point of view, regardless of the computational methods that are applied, a global analysis of conventional scaffolds in analog series from compound activity classes was carried out. The majority of analog series was found to contain multiple scaffolds, thus enabling the detection of intra-series scaffold hops among closely related compounds. More than 1000 activity classes were found to contain increasing proportions of multi-scaffold analog series. Thus, using such activity classes for scaffold hopping analysis is likely to overestimate the scaffold hopping (core structure replacement) potential of computational methods, due to an abundance of artificial scaffold hops that are possible within analog series.
[Mh] Termos MeSH primário: 11-beta-Hidroxiesteroide Desidrogenase Tipo 1/química
Fator XI/química
Compostos Orgânicos/química
Receptor CB1 de Canabinoide/química
[Mh] Termos MeSH secundário: Interpretação Estatística de Dados
Estrutura Molecular
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Organic Chemicals); 0 (Receptor, Cannabinoid, CB1); 9013-55-2 (Factor XI); EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenase Type 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170618
[St] Status:MEDLINE
[do] DOI:10.1007/s10822-017-0032-7


  3 / 1062 MEDLINE  
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[PMID]:28615222
[Au] Autor:Asselta R; Paraboschi EM; Rimoldi V; Menegatti M; Peyvandi F; Salomon O; Duga S
[Ad] Endereço:Department of Biomedical Sciences, Humanitas University, Milan, Italy.
[Ti] Título:Exploring the global landscape of genetic variation in coagulation factor XI deficiency.
[So] Source:Blood;130(4):e1-e6, 2017 Jul 27.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Factor XI (FXI) deficiency is an autosomal bleeding disorder, usually posttrauma or postsurgery, characterized by reduced levels of coagulation FXI in plasma. The disease is highly prevalent in Ashkenazi Jews (heterozygote frequency, ∼9%), whereas it is considered a rare condition in most populations (prevalence of the severe deficiency, 1 in 10 in the white population). So far, >190 causative mutations have been identified throughout the gene. To have a global landscape of genetic variation of , we explored publicly available exome-based data obtained from >60 000 individuals belonging to different ethnicities (Exome Aggregation Consortium resource). This analysis revealed profound differences in heterozygote frequencies among populations (allele frequencies: African = 0.0016; East Asian = 0.0045; European = 0.0036; Finnish = 0.00030; Latino = 0.0021; South Asian = 0.0015), and a prevalence significantly higher than that reported so far (eg, the calculated prevalence of the severe deficiency in Europeans would be: 12.9 in 10 ). In addition, this analysis allowed us to evidence recurrent and ethnic-specific mutations: p.Phe223Leu in Africans (23.5% of all mutated alleles), p.Gln263X and p.Leu424CysfsX in East Asians (28.2% and 20.5%, respectively), and p.Ala412Thr in Latinos (25%).
[Mh] Termos MeSH primário: Alelos
Deficiência do Fator XI/genética
Fator XI/genética
Frequência do Gene
Mutação de Sentido Incorreto
[Mh] Termos MeSH secundário: Grupos de Populações Continentais/genética
Feminino
Seres Humanos
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
9013-55-2 (Factor XI)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-04-780148


  4 / 1062 MEDLINE  
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[PMID]:28445521
[Au] Autor:Martin-Fernandez L; Gavidia-Bovadilla G; Corrales I; Brunel H; Ramírez L; López S; Souto JC; Vidal F; Soria JM
[Ad] Endereço:Unit of Genomics of Complex Diseases, Biomedical Research Institute Sant Pau (IIB-Sant Pau), Barcelona, Spain.
[Ti] Título:Next generation sequencing to dissect the genetic architecture of KNG1 and F11 loci using factor XI levels as an intermediate phenotype of thrombosis.
[So] Source:PLoS One;12(4):e0176301, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Venous thromboembolism is a complex disease with a high heritability. There are significant associations among Factor XI (FXI) levels and SNPs in the KNG1 and F11 loci. Our aim was to identify the genetic variation of KNG1 and F11 that might account for the variability of FXI levels. The KNG1 and F11 loci were sequenced completely in 110 unrelated individuals from the GAIT-2 (Genetic Analysis of Idiopathic Thrombophilia 2) Project using Next Generation Sequencing on an Illumina MiSeq. The GAIT-2 Project is a study of 935 individuals in 35 extended Spanish families selected through a proband with idiopathic thrombophilia. Among the 110 individuals, a subset of 40 individuals was chosen as a discovery sample for identifying variants. A total of 762 genetic variants were detected. Several significant associations were established among common variants and low-frequency variants sets in KNG1 and F11 with FXI levels using the PLINK and SKAT packages. Among these associations, those of rs710446 and five low-frequency variant sets in KNG1 with FXI level variation were significant after multiple testing correction and permutation. Also, two putative pathogenic mutations related to high and low FXI levels were identified by data filtering and in silico predictions. This study of KNG1 and F11 loci should help to understand the connection between genotypic variation and variation in FXI levels. The functional genetic variants should be useful as markers of thromboembolic risk.
[Mh] Termos MeSH primário: Fator XI/genética
Fenótipo
Trombose/diagnóstico
Trombose/genética
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Criança
Pré-Escolar
DNA/química
DNA/metabolismo
Fator XI/análise
Feminino
Frequência do Gene
Loci Gênicos
Variação Genética
Genótipo
Seres Humanos
Masculino
Meia-Idade
Polimorfismo de Nucleotídeo Único
Análise de Sequência de DNA
Trombose/patologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 9007-49-2 (DNA); 9013-55-2 (Factor XI)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0176301


  5 / 1062 MEDLINE  
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[PMID]:28353616
[Au] Autor:Jiang J; Liu K; Zou J; Ma H; Yang H; Zhang X; Jiao Y
[Ad] Endereço:aDivision of Vascular Surgery, Department of General Surgery bDepartment of Nephrology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
[Ti] Título:Associations between polymorphisms in coagulation-related genes and venous thromboembolism: A meta-analysis with trial sequential analysis.
[So] Source:Medicine (Baltimore);96(13):e6537, 2017 Mar.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Recently, several studies showed that the polymorphisms in the coagulation-related genes might be associated with venous thromboembolism (VTE); however, the results were still controversial. We performed a meta-analysis with trial sequential analysis to investigate the associations between the endothelial cell-activated protein C receptor (EPCR) rs9574, F11 rs2289252, F11 rs2036914, FGG rs2066865, FGG rs1049636, CYP4V2 rs13146272, SERPINC1 rs2227589, and GP6 rs1613662 polymorphisms with the risk of VTE. METHODS: We searched both the common English-language databases and the Chinese literature databases. Two authors selected studies according to inclusion and exclusion criteria. Crude odds ratios with 95% confidence intervals (CI) were calculated to estimate the strength of this association. Between-study heterogeneity was assessed with the chi-square-based Q test and the I statistic. RESULTS: Overall, a total of 20 studies were included. The meta-analysis revealed that the F11 rs2289252, F11 rs2036914, FGG rs2066865, and CYP4V2 rs13146272 polymorphisms were closely related to the development of VTE in the white race under the best genetic models after multiple testing adjustments. The EPCR rs9574, FGG rs1049636, SERPINC1 rs2227589, and GP6 rs1613662 polymorphisms might be potential candidates in the pathogenesis of VTE, but trial sequential analyses and sensitivity analyses indicated that the evidences were limited. Larger scale studies were demanded to avoid false-positive outcomes. CONCLUSIONS: Finally, our study demonstrated the important role of rs2289252, rs2036914, rs2066865, and rs13146272 polymorphisms in the development of VTE in the white race. Rs9574, rs1049636, rs2227589 and rs1613662 polymorphisms might be risk factors of VTE. However, more studies involving diverse races are needed to probe the ethnic difference and the underlying mechanisms of significant associations.
[Mh] Termos MeSH primário: Família 4 do Citocromo P450/genética
Fator XI/genética
Fibrinogênio/genética
Tromboembolia Venosa/genética
[Mh] Termos MeSH secundário: Antígenos CD/genética
Antitrombina III/genética
Receptor de Proteína C Endotelial
Seres Humanos
Glicoproteínas da Membrana de Plaquetas/genética
Receptores de Superfície Celular/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Endothelial Protein C Receptor); 0 (PROCR protein, human); 0 (Platelet Membrane Glycoproteins); 0 (Receptors, Cell Surface); 0 (SERPINC1 protein, human); 0 (platelet membrane glycoprotein VI); 9000-94-6 (Antithrombin III); 9001-32-5 (Fibrinogen); 9013-55-2 (Factor XI); EC 1.14.13.- (CYP4V2 protein, human); EC 1.14.14.1 (Cytochrome P450 Family 4)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170330
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000006537


  6 / 1062 MEDLINE  
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[PMID]:27933406
[Au] Autor:Sylman JL; Daalkhaijav U; Zhang Y; Gray EM; Farhang PA; Chu TT; Zilberman-Rudenko J; Puy C; Tucker EI; Smith SA; Morrissey JH; Walker TW; Nan XL; Gruber A; McCarty OJT
[Ad] Endereço:Biomedical Engineering, School of Medicine, Oregon Health and Science University, 3303 SW Bond Ave, Portland, OR, 97239, USA. jsylman@gmail.com.
[Ti] Título:Differential Roles for the Coagulation Factors XI and XII in Regulating the Physical Biology of Fibrin.
[So] Source:Ann Biomed Eng;45(5):1328-1340, 2017 May.
[Is] ISSN:1573-9686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the contact activation pathway of the coagulation, zymogen factor XII (FXII) is converted to FXIIa, which triggers activation of FXI leading to the activation of FIX and subsequent thrombin generation and fibrin formation. Feedback activation of FXI by thrombin has been shown to promote thrombin generation in a FXII-independent manner and FXIIa can bypass FXI to directly activate FX and prothrombin in the presence of highly negatively charged molecules, such as long-chain polyphosphates (LC polyP). We sought to determine whether activation of FXII or FXI differentially regulate the physical biology of fibrin formation. Fibrin formation was initiated with tissue factor, ellagic acid (EA), or LC polyP in the presence of inhibitors of FXI and FXII. Our data demonstrated that inhibition of FXI decreased the rate of fibrin formation and fiber network density, and increased the fibrin network strength and rate of fibrinolysis when gelation was initiated via the contact activation pathway with EA. FXII inhibition decreased the fibrin formation and fibrin density, and increased the fibrinolysis rate only when fibrin formation was initiated via the contact activation pathway with LC polyP. Overall, we demonstrate that inhibition of FXI and FXII distinctly alter the biophysical properties of fibrin.
[Mh] Termos MeSH primário: Inibidores dos Fatores de Coagulação Sanguínea/química
Fator XII
Fator XI
Fibrina/química
Fibrinólise
[Mh] Termos MeSH secundário: Fator XI/antagonistas & inibidores
Fator XI/química
Fator XII/antagonistas & inibidores
Fator XII/química
Seres Humanos
Polifosfatos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Coagulation Factor Inhibitors); 0 (Polyphosphates); 9001-30-3 (Factor XII); 9001-31-4 (Fibrin); 9013-55-2 (Factor XI)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161210
[St] Status:MEDLINE
[do] DOI:10.1007/s10439-016-1771-7


  7 / 1062 MEDLINE  
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[PMID]:27780803
[Au] Autor:Fredenburgh JC; Gross PL; Weitz JI
[Ad] Endereço:Department of Medicine, McMaster University, Hamilton, ON, Canada.
[Ti] Título:Emerging anticoagulant strategies.
[So] Source:Blood;129(2):147-154, 2017 Jan 12.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Despite the introduction of direct oral anticoagulants (DOACs), the search for more effective and safer antithrombotic strategies continues. Better understanding of the pathogenesis of thrombosis has fostered 2 new approaches to achieving this goal. First, evidence that thrombin may be as important as platelets to thrombosis at sites of arterial injury and that platelets contribute to venous thrombosis has prompted trials comparing anticoagulants with aspirin for secondary prevention in arterial thrombosis and aspirin with anticoagulants for primary and secondary prevention of venous thrombosis. These studies will help identify novel treatment strategies. Second, emerging data that naturally occurring polyphosphates activate the contact system and that this system is critical for thrombus stabilization and growth have identified factor XII (FXII) and FXI as targets for new anticoagulants that may be even safer than the DOACs. Studies are needed to determine whether FXI or FXII is the better target and to compare the efficacy and safety of these new strategies with current standards of care for the prevention or treatment of thrombosis. Focusing on these advances, this article outlines how treatment strategies for thrombosis are evolving and describes the rationale and approaches to targeting FXII and FXI. These emerging anticoagulant strategies should address unmet needs and reduce the systemic underuse of anticoagulation because of the fear of bleeding.
[Mh] Termos MeSH primário: Anticoagulantes/farmacologia
Coagulação Sanguínea/fisiologia
Trombose/metabolismo
[Mh] Termos MeSH secundário: Animais
Coagulação Sanguínea/efeitos dos fármacos
Fator XI/antagonistas & inibidores
Fator XII/antagonistas & inibidores
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anticoagulants); 9001-30-3 (Factor XII); 9013-55-2 (Factor XI)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161027
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-09-692996


  8 / 1062 MEDLINE  
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[PMID]:27414984
[Au] Autor:Suchon P; Al Frouh F; Ibrahim M; Sarlon G; Venton G; Alessi MC; Trégouët DA; Morange PE
[Ad] Endereço:AIx Marseille Univ, INSERM, INRA, NORT, Marseille, France.
[Ti] Título:Genetic risk factors for venous thrombosis in women using combined oral contraceptives: update of the PILGRIM study.
[So] Source:Clin Genet;91(1):131-136, 2017 Jan.
[Is] ISSN:1399-0004
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Identifying women at risk of venous thrombosis (VT) under combined oral contraceptives (COC) is a major public health issue. The aim of this study was to investigate in COC users the impact on disease of genetic polymorphisms recently identified to associate with VT risk in the general population. Nine polymorphisms located on KNG1, F11, F5, F2, PROCR, FGG, TSPAN and SLC44A2 genes were genotyped in a sample of 766 patients and 464 controls as part of the PILGRIM (PILl Genetic Risk Monitoring) study. Cases were women who experienced an episode of documented VT during COC use, while controls were women with no history of VT using COC at the time of inclusion. Among the studied polymorphisms, only F11 rs2289252 was significantly associated with VT. The F11 rs2289252-A allele was associated with a 1.6-fold increased risk of VT (p < 0.0001). Besides, the combination of the rs2289252-A allele with non-O blood group, present in 52% of the cohort, was associated with an odds ratio of 4.00 (2.49-6.47; p < 10 ). The consideration of this genetic risk factor could help to better assess the risk of VT in COC users.
[Mh] Termos MeSH primário: Anticoncepcionais Orais Combinados/administração & dosagem
Predisposição Genética para Doença/genética
Polimorfismo de Nucleotídeo Único
Trombose Venosa/genética
[Mh] Termos MeSH secundário: Adulto
Alelos
Anticoncepcionais Orais Combinados/efeitos adversos
Monitoramento de Medicamentos/métodos
Fator XI/genética
Feminino
Frequência do Gene
Genótipo
Seres Humanos
Razão de Chances
Fatores de Risco
Trombose Venosa/etiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Contraceptives, Oral, Combined); 9013-55-2 (Factor XI)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170613
[Lr] Data última revisão:
170613
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160715
[St] Status:MEDLINE
[do] DOI:10.1111/cge.12833


  9 / 1062 MEDLINE  
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[PMID]:27710856
[Au] Autor:Kawankar N; Rathi J; Ghosh K; Shetty S
[Ad] Endereço:National Institute of Immunohaematology (ICMR), KEM Hospital, Parel, Mumbai 400 012, India.
[Ti] Título:Clinical and molecular epidemiology of factor XI deficiency in India.
[So] Source:Thromb Res;147:85-87, 2016 Nov.
[Is] ISSN:1879-2472
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Deficiência do Fator XI/epidemiologia
Deficiência do Fator XI/genética
Fator XI/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Sequência de Aminoácidos
Criança
Pré-Escolar
Sequência Conservada
Fator XI/análise
Fator XI/química
Deficiência do Fator XI/sangue
Deficiência do Fator XI/complicações
Feminino
Hemorragia/sangue
Hemorragia/etiologia
Hemorragia/genética
Seres Humanos
Índia/epidemiologia
Masculino
Meia-Idade
Epidemiologia Molecular
Mutação
Mutação de Sentido Incorreto
Adulto Jovem
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
9013-55-2 (Factor XI)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161007
[St] Status:MEDLINE


  10 / 1062 MEDLINE  
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[PMID]:27699729
[Au] Autor:Davies J; Kadir R
[Ad] Endereço:Department of Obstetrics and Gynaecology, The Royal Free Hospital, London, United Kingdom.
[Ti] Título:The Management of Factor XI Deficiency in Pregnancy.
[So] Source:Semin Thromb Hemost;42(7):732-740, 2016 Oct.
[Is] ISSN:1098-9064
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Management of factor XI (FXI) deficiency in pregnancy is complicated by lack of correlation between FXI level and bleeding risk. Clinicians should be vigilant about the potential for prolonged or excessive bleeding following miscarriage or termination of pregnancy, or postpartum hemorrhage (PPH). A multidisciplinary approach along with an individual care plan is recommended to prevent bleeding complications. Assessment of bleeding history, FXI level, and global tests of hemostasis can aid management decisions regarding hemostatic prophylaxis. The risk of PPH can be minimized by obstetric measures to avoid uterine atony and genital trauma, in addition to provision of appropriate hemostatic prophylaxis for labor and delivery. Women with FXI deficiency can be given the option of regional anesthesia, provided that prior consideration has been given to assessment of potential bleeding risk and appropriate treatment strategies are implemented. Antifibrinolytic agents are effective for the majority of women with FXI deficiency, but those with severe deficiency/phenotype require FXI concentrate. Recombinant activated factor VII (rFVIIa) has also been used successfully to prevent bleeding in FXI deficiency. However, all treatments should be used with caution in pregnancy due to thrombogenic potential. Neonatal bleeding complications are rare in FXI deficiency; however, hemostatic assessment and cover are important for invasive procedures such as circumcision.
[Mh] Termos MeSH primário: Fator VIIa/uso terapêutico
Deficiência do Fator XI
Hemostasia
Hemorragia Pós-Parto
Complicações Hematológicas na Gravidez
[Mh] Termos MeSH secundário: Fator XI/metabolismo
Deficiência do Fator XI/sangue
Deficiência do Fator XI/tratamento farmacológico
Feminino
Seres Humanos
Hemorragia Pós-Parto/sangue
Hemorragia Pós-Parto/etiologia
Hemorragia Pós-Parto/prevenção & controle
Gravidez
Complicações Hematológicas na Gravidez/sangue
Complicações Hematológicas na Gravidez/tratamento farmacológico
Proteínas Recombinantes/uso terapêutico
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Recombinant Proteins); 9013-55-2 (Factor XI); AC71R787OV (recombinant FVIIa); EC 3.4.21.21 (Factor VIIa)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170324
[Lr] Data última revisão:
170324
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161005
[St] Status:MEDLINE



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