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  1 / 2093 MEDLINE  
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[PMID]:29350259
[Au] Autor:Zhu X; Zhang J; Wang Q; Fu H; Chang Y; Kong Y; Lv M; Xu L; Liu K; Huang X; Zhang X
[Ad] Endereço:Peking University People's Hospital, Peking University Institute of Hematology, Beijing, 100044, China.
[Ti] Título:Diminished expression of ß2-GPI is associated with a reduced ability to mitigate complement activation in anti-GPIIb/IIIa-mediated immune thrombocytopenia.
[So] Source:Ann Hematol;97(4):641-654, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Anti-GPIIb/IIIa-mediated complement activation has been reported to be important in the pathogenesis of immune thrombocytopenia (ITP). However, the role of the complement system and the involved regulatory mechanism remain equivocal. Beta2-glycoprotein I (ß2-GPI), known as the main target for antiphospholipid autoantibodies, has been demonstrated as a complement regulator. Here, we investigated the complement-regulatory role of ß2-GPI in anti-GPIIb/IIIa-mediated ITP. Plasma complement activation and enhanced complement activation capacity (CAC) were found in ITP patients with anti-GPIIb/IIIa antibodies in vivo and in vitro. Diminished plasma levels of ß2-GPI were shown in patients of this group, which was inversely correlated with C5b-9 deposition. C5b-9 generation was inhibited by approximate physiological concentrations of ß2-GPI, in a dose-dependent manner. Inhibition of C3a generation by ß2-GPI and the existence of ß2-GPI/C3 complexes in plasma indicated a regulation on the level of the C3 convertase. Furthermore, ß2-GPI down-regulated the phosphorylation levels of c-Jun N-terminal kinase (JNK) and cleavage of BH3 interacting domain death agonist (Bid) and ultimately harbored platelet lysis. Our findings may provide a novel link between diminished plasma levels of ß2-GPI and enhanced complement activation, indicating ß2-GPI as a potential diagnostic biomarker and therapeutic target in the treatment of anti-GPIIb/IIIa-mediated ITP.
[Mh] Termos MeSH primário: Ativação do Complemento
Regulação para Baixo
Isoanticorpos/metabolismo
Complexo Glicoproteico GPIIb-IIIa de Plaquetas/antagonistas & inibidores
Púrpura Trombocitopênica Idiopática/metabolismo
beta 2-Glicoproteína I/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores/sangue
Plaquetas/imunologia
Plaquetas/metabolismo
Plaquetas/patologia
China/epidemiologia
Convertases de Complemento C3-C5/metabolismo
Complemento C3a/metabolismo
Feminino
Seres Humanos
Masculino
Meia-Idade
Complexo Glicoproteico GPIIb-IIIa de Plaquetas/metabolismo
Complexo Glicoproteico GPIb-IX de Plaquetas/antagonistas & inibidores
Complexo Glicoproteico GPIb-IX de Plaquetas/metabolismo
Púrpura Trombocitopênica Idiopática/imunologia
Púrpura Trombocitopênica Idiopática/patologia
Púrpura Trombocitopênica Idiopática/fisiopatologia
Risco
Trombocitopenia/sangue
Trombocitopenia/imunologia
Trombocitopenia/metabolismo
Trombose/epidemiologia
Trombose/etiologia
Adulto Jovem
beta 2-Glicoproteína I/sangue
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Isoantibodies); 0 (Platelet Glycoprotein GPIIb-IIIa Complex); 0 (Platelet Glycoprotein GPIb-IX Complex); 0 (beta 2-Glycoprotein I); 0 (glycoprotein receptor GPIb-IX); 80295-42-7 (Complement C3a); EC 3.4.21.- (Complement C3-C5 Convertases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180120
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-3215-3


  2 / 2093 MEDLINE  
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[PMID]:29049363
[Au] Autor:Raimondo MG; Pericleous C; Radziszewska A; Borghi MO; Pierangeli S; Meroni PL; Giles I; Rahman A; Ioannou Y
[Ad] Endereço:Centre for Rheumatology Research, UCL Division of Medicine, London, United Kingdom.
[Ti] Título:Oxidation of ß2-glycoprotein I associates with IgG antibodies to domain I in patients with antiphospholipid syndrome.
[So] Source:PLoS One;12(10):e0186513, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Domain I (DI) of beta-2-glycoprotein I (ß2GPI) contains the immunodominant epitope for pathogenic antiphospholipid antibodies (aPL). DI is exposed in the linear form of the molecule but not in the circular form that comprises 90% of serum ß2GPI. The majority of circulating ß2GPI is biochemically reduced with two free thiols in Domain V. However, increased levels of oxidised ß2GPI are found in patients with antiphospholipid syndrome (APS). It is not known whether oxidation of ß2GPI favours the linear form of the molecule and thus promotes development of anti-DI antibodies. We investigated whether the proportion of oxidised ß2GPI associates with the presence of anti-DI in APS patients. Serum samples from 44 APS patients were screened for IgG, IgM and IgA anti-DI, anti-ß2GPI, anti-cardiolipin (anti-CL) and biochemically reduced ß2GPI. A negative correlation was found between the proportion of ß2GPI in the biochemically reduced form and IgG anti-DI levels (r = -0.54, p = 0.0002), but not with IgM or IgA anti-DI. Moreover, the proportion of ß2GPI in the reduced form was lower in IgG anti-DI positive than anti-DI negative APS patients (p = 0.02). The relative amount of reduced ß2GPI was no different between patients who were positive or negative for IgG, IgM and IgA anti-ß2GPI or anti-CL. This study demonstrates that oxidised ß2GPI lacking free cysteine-thiol groups most closely associates with IgG anti-DI positivity compared to IgG anti-CL and anti-ß2GPI. Future studies are required to ascertain the directionality of this association to define causation.
[Mh] Termos MeSH primário: Síndrome Antifosfolipídica/imunologia
Autoanticorpos/imunologia
Imunoglobulina G/imunologia
beta 2-Glicoproteína I/metabolismo
[Mh] Termos MeSH secundário: Adulto
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Masculino
Meia-Idade
Oxirredução
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Immunoglobulin G); 0 (beta 2-Glycoprotein I)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171020
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186513


  3 / 2093 MEDLINE  
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[PMID]:28898362
[Au] Autor:Gupta A; Johnson DH; Nagalla S
[Ad] Endereço:Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas.
[Ti] Título:Antiphospholipid Antibodies.
[So] Source:JAMA;318(10):959-960, 2017 Sep 12.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Anticorpos Antifosfolipídeos/sangue
Síndrome Antifosfolipídica/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Síndrome Antifosfolipídica/complicações
Testes Hematológicos
Seres Humanos
Masculino
Embolia Pulmonar/etiologia
beta 2-Glicoproteína I/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Antiphospholipid); 0 (beta 2-Glycoprotein I)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.4854


  4 / 2093 MEDLINE  
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[PMID]:28755727
[Au] Autor:Yao K; Zhang L; Zhou H; Tang N; Li D
[Ad] Endereço:Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
[Ti] Título:Plasma Antiphospholipid Antibodies Effects on Activated Partial Thromboplastin Time Assays.
[So] Source:Am J Med Sci;354(1):22-26, 2017 Jul.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Activated partial thromboplastin time (aPTT) assays can be affected by plasma antiphospholipid antibodies (aPLs), but the degree of the interference is not easy to predict. This study aimed to investigate the effects on aPTT assay results of different types and combinations of aPLs, including anti-ß -glycoprotein I antibodies, anticardiolipin antibodies and lupus anticoagulant. MATERIALS AND METHODS: We retrospectively collected clinical information and laboratory tests from aPL-positive patients. The potential influence of aPLs on aPTT assays was assessed. RESULTS: The survey included 589 aPL-positive patients. No significant differences existed in basic characteristics such as sex, age, prothrombin time, fibrinogen and alanine aminotransferase among different cases with 1, 2 or 3 types of positive-aPL markers (P > 0.05). In 113 patients with abnormal aPTT values, multivariable linear regression analysis showed a significant correlation between an abnormal degree of aPTT values and dilute Russell viper venom time (dRVVT) or silica clotting time (SCT) with a correlation coefficient of 0.437 or 0.497 (P < 0.01), whereas age, anticardiolipin antibodies-immunoglobulin G, anticardiolipin antibodies-immunoglobulin M and anti-ß -glycoprotein I antibodies were of no significance (P > 0.05). Among blood samples with 3 types of aPLs positivity, the rate of abnormal aPTT detection values was 55.3%, which was significantly higher than that observed in patients with negative, single-positive or double-positive aPL markers (P < 0.05). Patients with a moderate to strong dRVVT or SCT had a higher proportion of abnormal aPTT assays than did patients with a low dRVVT or SCT (P < 0.05). CONCLUSIONS: When abnormal aPTT values are obtained, the influence of aPLs should be considered, especially in the presence of a moderate to strong dRVVT or SCT.
[Mh] Termos MeSH primário: Anticorpos Antifosfolipídeos/metabolismo
Tempo de Tromboplastina Parcial
beta 2-Glicoproteína I/metabolismo
[Mh] Termos MeSH secundário: Adulto
Anticorpos Anticardiolipina/metabolismo
Feminino
Seres Humanos
Inibidor de Coagulação do Lúpus/metabolismo
Masculino
Meia-Idade
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Anticardiolipin); 0 (Antibodies, Antiphospholipid); 0 (Lupus Coagulation Inhibitor); 0 (beta 2-Glycoprotein I)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170731
[St] Status:MEDLINE


  5 / 2093 MEDLINE  
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[PMID]:28727732
[Au] Autor:Tortosa C; Cabrera-Marante O; Serrano M; Martínez-Flores JA; Pérez D; Lora D; Morillas L; Paz-Artal E; Morales JM; Pleguezuelo D; Serrano A
[Ad] Endereço:Department of Immunology Instituto de Investigación, Hospital Universitario 12 de Octubre, Madrid, Spain.
[Ti] Título:Incidence of thromboembolic events in asymptomatic carriers of IgA anti ß2 glycoprotein-I antibodies.
[So] Source:PLoS One;12(7):e0178889, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The antiphospholipid syndrome (APS) is defined by simultaneous presence of vascular clinical events and antiphospholipid antibodies (aPL). The aPL considered as diagnostics are lupus anticoagulant and antibodies anticardiolipin (aCL) and anti-ß2 glycoprotein-I (aB2GP1). During recent years, IgA aB2GP1 antibodies have been associated with thrombotic events both in patients positive, and mainly negative for other aPL, however its value as a pro-thrombotic risk-factor in asymptomatic patients has not been well defined. OBJECTIVE: To test the role of IgA anti B2GP1 as a risk factor for the development of APS-events (thrombosis or pregnancy morbidity) in asymptomatic population with a 5-year follow-up. METHODS: 244 patients isolated positive for anti-beta2-glycoprotein I IgA (Group-1 study) and 221 negative patients (Group-2 control) were studied. All the patients were negative for IgG and IgM aCL. RESULTS: During the follow-up, 45 patients (9.7%) had APS-events, 38 positive for IgA-aB2GP1 and 7 negative (15.6% vs 3.2%, p<0.001). The incidence rate of APS-events was 3.1% per year in IgA-aB2GP1 positive patients and 0.6% per year in the control group. Arterial thrombosis were the most frequent APS-events (N = 25, 55%) and were mainly observed in Group-1 patients (21 vs 4, p = 0.001). Multivariate analysis were shown as independent risk-factors for the development of APS-events, age, sex (men) and presence of IgA-aB2GP1 (odds ratio 5.25, 95% CI 2.24 to 12.32). CONCLUSION: The presence of IgA-aB2GP1 in people with no history of APS-events is the main independent risk factor for the development of these types of events, mainly arterial thrombosis.
[Mh] Termos MeSH primário: Síndrome Antifosfolipídica/imunologia
Autoanticorpos/sangue
Tromboembolia/epidemiologia
beta 2-Glicoproteína I/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Síndrome Antifosfolipídica/sangue
Síndrome Antifosfolipídica/complicações
Feminino
Seres Humanos
Incidência
Masculino
Meia-Idade
Tromboembolia/sangue
Tromboembolia/complicações
Tromboembolia/imunologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (beta 2-Glycoprotein I)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178889


  6 / 2093 MEDLINE  
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[PMID]:28666081
[Au] Autor:Papalardo E; Romay-Penabad Z; Willis R; Christadoss P; Carrera-Marin AL; Reyes-Maldonado E; Rudrangi R; Alfieri-Papalardo S; Garcia-Latorre E; Blank M; Pierangeli S; Brasier AR; Gonzalez EB
[Ad] Endereço:University of Texas Medical Branch, Galveston.
[Ti] Título:Major Histocompatibility Complex Class II Alleles Influence Induction of Pathogenic Antiphospholipid Antibodies in a Mouse Model of Thrombosis.
[So] Source:Arthritis Rheumatol;69(10):2052-2061, 2017 Oct.
[Is] ISSN:2326-5205
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Both environmental and genetic factors are important in the development of antiphospholipid antibodies (aPL) in patients with antiphospholipid syndrome (APS). Currently, the only available data on predisposing genetic factors have been obtained from epidemiologic studies, without mechanistic evidence. Therefore, we studied the influence of major histocompatibility complex (MHC) class II alleles on the production of aPL in a mouse model of APS. METHODS: Three groups of mice, MHC class II-deficient (MHCII ) mice, MHCII mice transgenic for human HLA-DQ6 (DQ6), DQ8, or DR4 alleles, and the corresponding wild-type (WT) mouse strains were immunized; half were immunized with human ß -glycoprotein I (ß GPI), and the other half were immunized with control ovalbumin (OVA) protein. Thrombus formation in vivo, tissue factor activity in carotid and peritoneal macrophages, and serum levels of tumor necrosis factor (TNF), IgG anticardiolipin (aCL), antibodies, and anti-OVA antibodies were determined. RESULTS: Immunization with ß GPI induced significant production of aCL and anti-ß GPI in WT mice compared with control mice immunized with OVA (P < 0.001) but diminished aCL (P < 0.001) and anti-ß GPI (P = 0.016) production in MHCII mice. Anti-ß GPI production was fully restored in DQ6 and DQ8 mice, while levels of anti-ß GPI in DR4 mice and aCL in all transgenic lines were only partially restored (P < 0.001 to P < 0.046). Thrombus size in WT mice was twice that in MHCII mice (P < 0.001) but similar to that in all transgenic lines. Carotid and peritoneal macrophage tissue factor levels decreased by >50% in MHCII mice compared with wild-type B6 mice and were restored in DQ8 mice but not DR4 mice or DQ6 mice. TNF levels decreased 4-fold in MHCII mice (P < 0.001) and were not restored in transgenic mice. CONCLUSION: Our mechanistic study is the first to show that MHC class II alleles influence not only quantitative aPL production but also the pathogenic capacity of induced aPL.
[Mh] Termos MeSH primário: Anticorpos Antifosfolipídeos/imunologia
Genes MHC Classe II/genética
Antígenos HLA-DQ/genética
Antígeno HLA-DR4/genética
[Mh] Termos MeSH secundário: Alelos
Animais
Anticorpos Anticardiolipina/imunologia
Artérias Carótidas/imunologia
Modelos Animais de Doenças
Seres Humanos
Imunização
Imunoglobulina G/imunologia
Macrófagos/imunologia
Macrófagos Peritoneais/imunologia
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Ovalbumina/imunologia
Índice de Gravidade de Doença
Trombose
Fator de Necrose Tumoral alfa/imunologia
beta 2-Glicoproteína I/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Anticardiolipin); 0 (Antibodies, Antiphospholipid); 0 (HLA-DQ Antigens); 0 (HLA-DQ6 antigen); 0 (HLA-DQ8 antigen); 0 (HLA-DR4 Antigen); 0 (Immunoglobulin G); 0 (Tumor Necrosis Factor-alpha); 0 (beta 2-Glycoprotein I); 9006-59-1 (Ovalbumin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE
[do] DOI:10.1002/art.40195


  7 / 2093 MEDLINE  
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[PMID]:28641308
[Au] Autor:Sharma R; Huang X; Brekken RA; Schroit AJ
[Ad] Endereço:Hamon Center for Therapeutic Oncology Research, UT Southwestern Medical Center, Dallas, TX 75390, USA.
[Ti] Título:Detection of phosphatidylserine-positive exosomes for the diagnosis of early-stage malignancies.
[So] Source:Br J Cancer;117(4):545-552, 2017 Aug 08.
[Is] ISSN:1532-1827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: There has been increasing interest in the detection of tumour exosomes in blood for cancer diagnostics. Most studies have focussed on miRNA and protein signatures that are surrogate markers for specific tumour types. Because tumour cells and tumour-derived exosomes display phosphatidylserine (PS) in their outer membrane leaflet, we developed a highly sensitive ELISA-based system that detects picogram amounts of exosomal phospholipid in plasma as a cancer biomarker. METHODS: This report describes the development of a highly specific and sensitive ELISA for the capture of PS-expressing tumour exosomes in the blood of tumour-bearing mice. To monitor the relationship between tumour burden and tumour exosome plasma concentrations, plasma from one transplantable breast cancer model (MDA-MB-231) and three genetic mouse models (MMTV-PyMT; breast and KIC and KPC; pancreatic) were screened for captured exosomal phospholipid. RESULTS: We show that quantitative assessment of PS-expressing tumour exosomes detected very early-stage malignancies before clinical evidence of disease in all four model systems. Tumour exosome levels showed significant increases by day 7 after tumour implantation in the MDA-MB-231 model while palpable tumours appeared only after day 27. For the MMTV-PyMT and KIC models, tumour exosome levels increased significantly by day 49 (P⩽0.0002) and day 21 (P⩽0.001) while tumours developed only after days 60 and 40, respectively. For the KPC model, a significant increase in blood exosome levels was detected by day 70 (P=0.023) when only preinvasive lesions are microscopically detectable. CONCLUSIONS: These data indicate that blood PS exosome levels is a specific indicator of cancer and suggest that blood PS is a biomarker for early-stage malignancies.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/sangue
Neoplasias da Mama/sangue
Exossomos/química
Neoplasias Ovarianas/sangue
Neoplasias Pancreáticas/sangue
Fosfatidilserinas/sangue
[Mh] Termos MeSH secundário: Animais
Anticorpos/imunologia
Neoplasias da Mama/diagnóstico
Neoplasias da Mama/patologia
Estudos de Casos e Controles
Linhagem Celular Tumoral
Ensaio de Imunoadsorção Enzimática/métodos
Feminino
Seres Humanos
Camundongos
Estadiamento de Neoplasias
Transplante de Neoplasias
Neoplasias Ovarianas/diagnóstico
Neoplasias Pancreáticas/diagnóstico
Neoplasias Pancreáticas/patologia
Fosfatidilserinas/imunologia
Fatores de Tempo
Carga Tumoral
beta 2-Glicoproteína I/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Biomarkers, Tumor); 0 (Phosphatidylserines); 0 (beta 2-Glycoprotein I)
[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:170623
[St] Status:MEDLINE
[do] DOI:10.1038/bjc.2017.183


  8 / 2093 MEDLINE  
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[PMID]:28339096
[Au] Autor:Arachchillage DRJ; Laffan M
[Ad] Endereço:Department of Haematology, Imperial College Healthcare NHS Trust and Imperial College London, Hammersmith Hospital, London, UK.
[Ti] Título:Pathogenesis and management of antiphospholipid syndrome.
[So] Source:Br J Haematol;178(2):181-195, 2017 Jul.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Antiphospholipid antibodies are a heterogeneous group of autoantibodies that have clear associations with thrombosis and pregnancy morbidity, and which together constitute the 'antiphospholipid syndrome' (APS). However, the pathophysiology of these complications is not well understood and their heterogeneity suggests that more than one pathogenic process may be involved. Diagnosis remains a combination of laboratory analysis and clinical observation but there have been significant advances in identifying specific pathogenic features, such as domain I-specific anti-ß2-glycoprotein-I antibodies. This in turn has pointed to endothelial and complement activation as important factors in the pathogenesis of APS. Consequently, although anticoagulation remains the standard treatment for thrombotic APS and during pregnancy, the realisation that these additional pathways are involved in the pathogenesis of APS has significant implications for treatment: agents acting outside the coagulation system, such as hydroxychloroquine for pregnancy complications and sirolimus as an inhibitor of the mammalian target of rapamycin (mTOR) pathway, are now under evaluation and represent a radical change in thinking for haematologists. Conventional anticoagulation is also under challenge from new, direct acting anticoagulants. This review will provide a comprehensive overview of the evolving understanding of APS pathogenesis and how this and novel therapeutics will alter diagnosis and management.
[Mh] Termos MeSH primário: Síndrome Antifosfolipídica/etiologia
[Mh] Termos MeSH secundário: Anticoagulantes/uso terapêutico
Síndrome Antifosfolipídica/tratamento farmacológico
Autoanticorpos/imunologia
Proteínas Inativadoras do Complemento/uso terapêutico
Inibidores Enzimáticos/uso terapêutico
Feminino
Previsões
Seres Humanos
Hidroxicloroquina/uso terapêutico
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
Imunossupressores/uso terapêutico
Gravidez
Complicações na Gravidez/tratamento farmacológico
Complicações na Gravidez/etiologia
Rituximab/uso terapêutico
Sirolimo/uso terapêutico
Trombose/tratamento farmacológico
Trombose/etiologia
Trombose/imunologia
beta 2-Glicoproteína I/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anticoagulants); 0 (Autoantibodies); 0 (Complement Inactivator Proteins); 0 (Enzyme Inhibitors); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Immunosuppressive Agents); 0 (beta 2-Glycoprotein I); 4F4X42SYQ6 (Rituximab); 4QWG6N8QKH (Hydroxychloroquine); W36ZG6FT64 (Sirolimus)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14632


  9 / 2093 MEDLINE  
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[PMID]:28279839
[Au] Autor:Islam MA; Alam F; Wong KK
[Ad] Endereço:Human Genome Centre, School of Medical Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia.
[Ti] Título:Comorbid association of antiphospholipid antibodies and migraine: A systematic review and meta-analysis.
[So] Source:Autoimmun Rev;16(5):512-522, 2017 May.
[Is] ISSN:1873-0183
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Antiphospholipid antibodies (aPLs) namely anticardiolipin (aCL) antibody, anti-ß2-glycoprotein I (ß2GPI) antibody and lupus anticoagulant (LA) are autoantibodies produced against anionic phospholipids and proteins on plasma membranes. Migraine is a primary headache disorder which has growing evidences of autoimmune-mediated pathogenesis and previous studies suggested the presence of aPLs in migraine patients. AIMS: The aim of this study was to evaluate the comorbid association between aPLs (aCL, anti-ß2GPI and LA) and migraine compared to healthy controls. METHODS: Studies were searched through PubMed, ISI Web of Science and Google Scholar databases without restricting the languages and year (up to October 2016) and were selected based on the inclusion criteria. Two authors independently extracted data from the included studies. All analyses were conducted by using random effects model to calculate the odds ratio (OR) and 95% confidence interval (CI). Quality assessment was carried out by using the modified Newcastle-Ottawa Scale (NOS). Publication bias was evaluated via visualization of funnel plots, Begg's and Egger's tests. RESULTS: The database searches produced 1995 articles, 13 of which were selected (912 migraineurs and 822 healthy controls). 8.59%, 15.21% and 4.11% of the migraineurs exhibited aCL, anti-ß2GPI and LA which was 4.83, 1.63 and 3.03 times higher, respectively, than healthy controls. A significant presence of aCL (OR: 3.55, 95% CI: 1.59-7.95; p=0.002) or anti-ß2GPI antibodies (OR: 2.02, 95% CI: 1.20-3.42; p=0.008) was observed in migraine patients, however, LA was not significantly associated (OR: 2.02, 95% CI: 0.50-8.37; p=0.320). Majority of the studies (n=10 of 13) demonstrated NOS score of 7 or above and no significant publication bias was observed. CONCLUSION: Migraine might be an autoimmune-associated neurologic disorder. The presence of aCL or anti-ß2GPI antibodies was significant in migraine patients compared to healthy controls, suggesting an involvement of these autoantibodies in migraine attack.
[Mh] Termos MeSH primário: Anticorpos Antifosfolipídeos/efeitos adversos
Síndrome Antifosfolipídica/complicações
Autoanticorpos/sangue
Transtornos de Enxaqueca/complicações
[Mh] Termos MeSH secundário: Adolescente
Adulto
Anticorpos Antifosfolipídeos/imunologia
Síndrome Antifosfolipídica/imunologia
Estudos de Casos e Controles
Criança
Comorbidade
Feminino
Seres Humanos
Estudos Prospectivos
beta 2-Glicoproteína I/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Antiphospholipid); 0 (Autoantibodies); 0 (beta 2-Glycoprotein I)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170311
[St] Status:MEDLINE


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[PMID]:28274304
[Au] Autor:Zhu X; Zhou H; Wang X; Cai Q; He C; Xia L; Zhang G; Ouyang H
[Ad] Endereço:School of Medicine, Jiangsu University, Zhenjiang 212013, China.
[Ti] Título:[Anti-ß2GPI antibody promotes release of inflammatory and pro-thrombosis molecules from arteries in apolipoprotein E-deficient mice].
[So] Source:Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi;33(3):295-299, 2017 Mar.
[Is] ISSN:1007-8738
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Objective To investigate the roles of anti-beta 2 glycoprotein I antibodies (anti-ß2GPI Ab) in the expressions of atherosclerosis(AS)-related inflammatory factors and pro-thrombosis molecules in apolipoprotein E-deficient (ApoE ) mice. Methods ApoE mice were randomly divided into normal saline (NS) group, 100 µg anti-ß2GPI Ab group, 100 µg homologous antibody (rabbit-IgG) group and 100 µg ß2GPI/anti-ß2GPI Ab complex group after silastic collars were placed around their carotid arteries by surgery. All mice were fed a high fat diet and corresponding stimuli were given through intraperitoneal injection at 7-day intervals. Six weeks later, the mice were executed. The blockage of carotid arteries of the operated side was observed by HE staining. The expressions of TLR4, tissue factor (TF) and von Willebrand factor (vWF) were detected by immunohistochemistry. The mRNA levels of interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α) in aorta were tested by real-time quantitative PCR. Results HE staining showed that the blockage of carotid arteries in antibody group was the most obvious. The immunohistochemistry showed that the expressions of TLR4, TF and vWF in anti-ß2GPI Ab group increased remarkably. Furthermore, the mRNA levels of IL-1ß and TNF-α in anti-ß2GPI Ab group were higher than those in the other groups. Conclusion The anti-ß2GPI antibody promotes the formation of atherosclerotic plaques in mice by up-regulating the release of inflammatory cytokines IL-1ß, TNF-α and thrombosis-related molecules TF, vWF and TLR4, ultimately enhancing the development of AS.
[Mh] Termos MeSH primário: Anticorpos/administração & dosagem
Apolipoproteínas E/deficiência
Artérias/metabolismo
Aterosclerose/metabolismo
beta 2-Glicoproteína I/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos/efeitos adversos
Apolipoproteínas E/genética
Artérias/efeitos dos fármacos
Aterosclerose/etiologia
Aterosclerose/genética
Seres Humanos
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Masculino
Camundongos
Camundongos Knockout
Tromboplastina/genética
Tromboplastina/metabolismo
Receptor 4 Toll-Like/genética
Receptor 4 Toll-Like/metabolismo
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
Fator de von Willebrand/genética
Fator de von Willebrand/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Apolipoproteins E); 0 (Interleukin-1beta); 0 (Toll-Like Receptor 4); 0 (Tumor Necrosis Factor-alpha); 0 (beta 2-Glycoprotein I); 0 (von Willebrand Factor); 9035-58-9 (Thromboplastin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE



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