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[PMID]:29267496
[Au] Autor:Wu L; Wang X; Chen F; Lv X; Sun W; Guo Y; Hou H; Ji H; Wei W; Gong L
[Ad] Endereço:Department of Ultrasonography, Tianjin Medical University General Hospital, Tianjin, China.
[Ti] Título:T cell subsets and immunoglobulin G levels are associated with the infection status of systemic lupus erythematosus patients.
[So] Source:Braz J Med Biol Res;51(2):e4547, 2017 Dec 11.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Systemic lupus erythematosus (SLE) is a chronic, autoimmune disorder that affects nearly all organs and tissues. As knowledge about the mechanism of SLE has increased, some immunosuppressive agents have become routinely used in clinical care, and infections have become one of the direct causes of mortality in SLE patients. To identify the risk factors indicative of infection in SLE patients, a case control study of our hospital's medical records between 2011 and 2013 was performed. We reviewed the records of 117 SLE patients with infection and 61 SLE patients without infection. Changes in the levels of T cell subsets, immunoglobulin G (IgG), complement C3, complement C4, globulin, and anti-double-stranded DNA (anti-ds-DNA) were detected. CD4+ and CD4+/CD8+ T cell levels were significantly lower and CD8+ T cell levels were significantly greater in SLE patients with infection than in SLE patients without infection. Additionally, the concentrations of IgG in SLE patients with infection were significantly lower than those in SLE patients without infection. However, complement C3, complement C4, globulin, and anti-ds-DNA levels were not significantly different in SLE patients with and without infection. Therefore, clinical testing for T cell subsets and IgG is potentially useful for identifying the presence of infection in SLE patients and for distinguishing a lupus flare from an acute infection.
[Mh] Termos MeSH primário: Imunoglobulina G/sangue
Infecção/sangue
Infecção/patologia
Lúpus Eritematoso Sistêmico/sangue
Lúpus Eritematoso Sistêmico/patologia
Subpopulações de Linfócitos T/patologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Anticorpos Antinucleares/sangue
Complemento C3/análise
Complemento C4/análise
Ensaio de Imunoadsorção Enzimática
Feminino
Citometria de Fluxo
Seres Humanos
Infecção/imunologia
Lúpus Eritematoso Sistêmico/imunologia
Masculino
Meia-Idade
Nefelometria e Turbidimetria
Reação em Cadeia da Polimerase
Fatores de Risco
Soroglobulinas/análise
Estatísticas não Paramétricas
Subpopulações de Linfócitos T/imunologia
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Antinuclear); 0 (Complement C3); 0 (Complement C4); 0 (Immunoglobulin G); 0 (Serum Globulins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


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[PMID]:27778395
[Au] Autor:Michailidou I; Naessens DM; Hametner S; Guldenaar W; Kooi EJ; Geurts JJ; Baas F; Lassmann H; Ramaglia V
[Ad] Endereço:Department of Genome Analysis, Academic Medical Center, Meibergdreef 9, Amsterdam, 1105, The Netherlands.
[Ti] Título:Complement C3 on microglial clusters in multiple sclerosis occur in chronic but not acute disease: Implication for disease pathogenesis.
[So] Source:Glia;65(2):264-277, 2017 02.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microglial clusters with C3d deposits are observed in the periplaque of multiple sclerosis (MS) brains and were proposed as early stage of lesion formation. As such they should appear in the brain of MS donors with acute disease but thus far this has not been shown. Using postmortem brain tissue from acute (n = 10) and chronic (n = 15) MS cases we investigated whether C3d+ microglial clusters are part of an acute attack against myelinated axons, which could have implications for disease pathogenesis. The specificity of our findings to MS was tested in ischemic stroke cases (n = 8) with initial or advanced lesions and further analyzed in experimental traumatic brain injury (TBI, n = 26), as both conditions are primarily nondemyelinating but share essential features of neurodegeneration with MS lesions. C3d+ microglial clusters were found in chronic but not acute MS. They were not associated with antibody deposits or terminal complement activation. They were linked to slowly expanding lesions, localized on axons with impaired transport and associated with neuronal C3 production. C3d+ microglial clusters were not specific to MS as they were also found in stroke and experimental TBI. We conclude that C3d+ microglial clusters in MS are not part of an acute attack against myelinated axons. As such it is unlikely that they drive formation of new lesions but could represent a physiological mechanism to remove irreversibly damaged axons in chronic disease. GLIA 2017;65:264-277.
[Mh] Termos MeSH primário: Complemento C3/metabolismo
Microglia/metabolismo
Esclerose Múltipla/patologia
[Mh] Termos MeSH secundário: Doença Aguda
Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Autopsia
Doença Crônica
Complemento C3/genética
Citocinas/metabolismo
Proteínas de Ligação a DNA/metabolismo
Modelos Animais de Doenças
Feminino
Traumatismos Cranianos Fechados/patologia
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Meia-Idade
Proteínas da Mielina/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Neurônios/patologia
Acidente Vascular Cerebral/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (AIF1 protein, human); 0 (C3 protein, human); 0 (Complement C3); 0 (Cytokines); 0 (DNA-Binding Proteins); 0 (Myelin Proteins); 0 (Nerve Tissue Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1002/glia.23090


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[PMID]:28470643
[Au] Autor:Habibi I; Sfar I; Kort F; Bouraoui R; Chebil A; Limaiem R; Ayed S; Ben Abdallah T; El Matri L; Gorgi Y
[Ad] Endereço:Research Laboratory of renal Transplantation and Immunopathology (LR03SP01), University Tunis El Manar, Charles Nicolle Hospital, Tunis, Tunisia (Chairmen: Prof. Yousr Gorgi).
[Ti] Título:Complement Component C3 Variant (R102G) and the Risk of Neovascular Age-Related Macular Degeneration in a Tunisian Population.
[Ti] Título:Komplementkomponente C3-Variante (R102G) und das Risiko für exsudative altersbedingte Makuladegeneration in der tunesischen Bevölkerung..
[So] Source:Klin Monbl Augenheilkd;234(4):478-482, 2017 Apr.
[Is] ISSN:1439-3999
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:To explore the association between the polymorphism (S/F) p.R102G in the C3 gene and age-related macular degeneration (AMD) in a Tunisian population. The molecular study was performed by polymerase chain reaction using sequence-specific primers (PCR-SSP) in 207 control subjects free of any eye disease (fundus normal) and 145 patients with exudative AMD. The activity and quantification of and have been made by technical home method and nephelometry, respectively. The prevalence of GG genotype polymorphism was significantly higher in AMD patients compared to controls (OR: 2.41, IC 95% [1.90-3.05], p = 0.0007). However, no correlation was found between this allelic variant and the type of neovascularization. Similarly, there is no association between this polymorphism and the presence of functional and/or quantitative hypocomplementemia. The GG genotype of the gene could be a susceptibility factor for AMD in the Tunisian population. However, it does not seem to influence the clinical profile of the disease.
[Mh] Termos MeSH primário: Complemento C3/genética
Estudos de Associação Genética
Predisposição Genética para Doença/epidemiologia
Predisposição Genética para Doença/genética
Degeneração Macular/epidemiologia
Degeneração Macular/genética
Polimorfismo de Nucleotídeo Único/genética
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Feminino
Marcadores Genéticos/genética
Seres Humanos
Incidência
Degeneração Macular/diagnóstico
Masculino
Meia-Idade
Mutação/genética
Reprodutibilidade dos Testes
Medição de Risco/métodos
Sensibilidade e Especificidade
Tunísia/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (C3 protein, human); 0 (Complement C3); 0 (Genetic Markers)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1055/s-0043-104419


  4 / 12103 MEDLINE  
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[PMID]:27777179
[Au] Autor:Colombo G; Clerici M; Altomare A; Rusconi F; Giustarini D; Portinaro N; Garavaglia ML; Rossi R; Dalle-Donne I; Milzani A
[Ad] Endereço:Department of Biosciences, Università degli Studi di Milano, Milan, Italy. Electronic address: graziano.colombo@unimi.it.
[Ti] Título:Thiol oxidation and di-tyrosine formation in human plasma proteins induced by inflammatory concentrations of hypochlorous acid.
[So] Source:J Proteomics;152:22-32, 2017 01 30.
[Is] ISSN:1876-7737
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:In this study, we assessed the oxidative damage occurring in plasma proteins when human blood was exposed to inflammatory concentrations of hypochlorous acid (HOCl). We used specific thiol labelling and Western blot analyses to determine protein thiol oxidation, as well as analytical gel filtration HPLC coupled to fluorescence detection to explore formation of high molecular weight (HMW) protein aggregates. Thiol-containing proteins oxidized by HOCl were identified by redox proteomics. Mass spectrometry (MS) analysis was performed to elucidate the protein composition of HMW aggregates. α1-antitrypsin, transthyretin, and haptoglobin showed thiol oxidation at HOCl concentrations higher than those causing complete oxidation of albumin. At the highest HOCl concentrations, formation of carbonylated and di-tyrosine cross-linked HMW protein aggregates also occurred. MS analysis identified fibrinogen, complement C3 and apolipoprotein A-I as components of HMW protein aggregates. These results could be relevant for human diseases characterized by inflammatory conditions in which myeloperoxidase and HOCl are involved. BIOLOGICAL SIGNIFICANCE: In this study we evaluated the oxidative damage occurring on plasma proteins when reconstituted human blood was exposed to inflammatory concentrations of hypochlorous acid (HOCl). Pathophysiological concentrations of HOCl are able to induce different modifications on plasma proteins such as carbonylation, sulfhydryl oxidation and formation of high molecular weight (HMW) protein aggregates characterized by di-tyrosine fluorescence. There are two relevant aspects emerging from this paper. The first one consists on identifying low abundant proteins undergoing sulfhydryl oxidation by biotin-maleimide derivatization followed by MALDI-TOF mass spectrometry. This approach suggests three low-abundant proteins undergoing HOCl-induced oxidation: transthyretin, α1-antitrypsin, and haptoglobin. In addition, we analysed HMW protein aggregates forming after HOCl exposure. These aggregates are characterized by carbonylation, intra- and/or intermolecular di-tyrosine bridges. After their isolation from SDS-PAGE gel electrophoresis, using electrospray tandem mass spectrometry coupled to reversed-phase nanoscale capillary liquid chromatography, we identified some protein constituents of these HMW aggregates such as α, ß, γ fibrinogen chains, apolipoprotein A-I and complement C3. In particular, our work highlights how fibrinogen is an important constituent of HOCl-induced HMW protein aggregates validating the mass spectrometry result with additional experiments. Further investigations are required in order to evaluate the possibility to use carbonylated and di-Tyr cross-linked HMW protein aggregates as (early) biomarkers for disease progression in inflammatory conditions in which myeloperoxidase and HOCl are involved.
[Mh] Termos MeSH primário: Proteínas Sanguíneas/metabolismo
Ácido Hipocloroso/farmacologia
Inflamação/induzido quimicamente
Estresse Oxidativo/efeitos dos fármacos
Compostos de Sulfidrila/metabolismo
Tirosina/metabolismo
[Mh] Termos MeSH secundário: Apolipoproteína A-I/metabolismo
Biomarcadores/sangue
Coleta de Amostras Sanguíneas/métodos
Complemento C3/metabolismo
Fibrinogênio/metabolismo
Seres Humanos
Espectrometria de Massas
Oxirredução
Peroxidase/metabolismo
Agregados Proteicos/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (APOA1 protein, human); 0 (Apolipoprotein A-I); 0 (Biomarkers); 0 (Blood Proteins); 0 (Complement C3); 0 (Protein Aggregates); 0 (Sulfhydryl Compounds); 42HK56048U (Tyrosine); 712K4CDC10 (Hypochlorous Acid); 9001-32-5 (Fibrinogen); EC 1.11.1.7 (Peroxidase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


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[PMID]:27772636
[Au] Autor:Fogo AB; Lusco MA; Najafian B; Alpers CE
[Ad] Endereço:Department of Pathology, Microbiology and Immunology, Vanderbilt University, Nashville, TN. Electronic address: agnes.fogo@vanderbilt.edu.
[Ti] Título:AJKD Atlas of Renal Pathology: Anti-Glomerular Basement Membrane Antibody-Mediated Glomerulonephritis.
[So] Source:Am J Kidney Dis;68(5):e29-e30, 2016 Nov.
[Is] ISSN:1523-6838
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Doença Antimembrana Basal Glomerular/patologia
Membrana Basal Glomerular/patologia
Rim/patologia
[Mh] Termos MeSH secundário: Doença Antimembrana Basal Glomerular/metabolismo
Cápsula Glomerular/metabolismo
Cápsula Glomerular/patologia
Cápsula Glomerular/ultraestrutura
Complemento C3/metabolismo
Membrana Basal Glomerular/metabolismo
Membrana Basal Glomerular/ultraestrutura
Seres Humanos
Imunoglobulina A/metabolismo
Imunoglobulina G/metabolismo
Imunoglobulina M/metabolismo
Rim/metabolismo
Rim/ultraestrutura
Microscopia
Microscopia Eletrônica
Microscopia de Fluorescência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Complement C3); 0 (Immunoglobulin A); 0 (Immunoglobulin G); 0 (Immunoglobulin M)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171205
[Lr] Data última revisão:
171205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  6 / 12103 MEDLINE  
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[PMID]:28745692
[Au] Autor:Yurova VA; Bobrova LA; Kozlovskaya NL; Korotchaeva YV; Serova AG; Kozlov LV; Andina SS; Demyanova KA; Kuchieva AM; Roshchupkina SV
[Ad] Endereço:I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow, Russia.
[Ti] Título:[Changes in the complement system in membranoproliferative glomerulonephritis].
[Ti] Título:Izmeneniia v sisteme komplementa pri membranoproliferativnom glomerulonefrite..
[So] Source:Ter Arkh;89(6):69-77, 2017.
[Is] ISSN:0040-3660
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:AIM: To compare the clinical manifestations membranoproliferative glomerulonephritis (MPGN) in its idiopathic variant, lupus nephritis (LN), and C3 glomerulopathy (C3-GP), by comparing them with changes in the complement system. SUBJECTS AND METHODS: The clinic of nephrology followed up 42 patients with different types of MPGN in 2013 to 2015. The study included 35 patients divided into 3 groups: 1) 8 patients with C3-GP, 2) 13 with idiopathic MPGN; 3) 14 with Class IV LN. The investigators studied the blood and urine levels of components and markers for activation of the classical and alternative pathways (C3 and C4, С3а, C5a, CFH, CFB, and CFD) of the terminal complement complex (TCC). RESULTS: The detection rate of C3-GP was 19%. The patients with C3-GP were noted to have the lowest blood concentration of S3 and the highest urinary level of С3а, C5a, TCC, CFH, CFB, and CFD. C3 nephritic factor was detected in 2 patients from the C3-GP (dense deposit disease) group. CONCLUSION: Alternative complement pathway dysregulation caused by genetic or autoimmune factors plays a leading role in the pathogenesis of C3-GP.
[Mh] Termos MeSH primário: Complemento C3/metabolismo
Proteínas do Sistema Complemento/metabolismo
Glomerulonefrite Membranoproliferativa
Nefrite Lúpica
[Mh] Termos MeSH secundário: Adulto
Complemento C3/urina
Proteínas do Sistema Complemento/urina
Feminino
Glomerulonefrite Membranoproliferativa/sangue
Glomerulonefrite Membranoproliferativa/urina
Seres Humanos
Nefrite Lúpica/sangue
Nefrite Lúpica/urina
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Complement C3); 9007-36-7 (Complement System Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171129
[Lr] Data última revisão:
171129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.17116/terarkh201789669-77


  7 / 12103 MEDLINE  
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[PMID]:27772633
[Au] Autor:Heybeli C
[Ad] Endereço:Sarikamis State Hospital, Sarikamis, Turkey.
[Ti] Título:C4 Deposition in Glomerular Disease.
[So] Source:Am J Kidney Dis;68(5):817, 2016 11.
[Is] ISSN:1523-6838
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Complemento C4
Complemento C4b
[Mh] Termos MeSH secundário: Complemento C3
Seres Humanos
Glomérulos Renais
[Pt] Tipo de publicação:LETTER; COMMENT
[Nm] Nome de substância:
0 (Complement C3); 0 (Complement C4); 80295-50-7 (Complement C4b)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171129
[Lr] Data última revisão:
171129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:27772631
[Au] Autor:Sethi S; Fervenza FC
[Ad] Endereço:Mayo Clinic, Rochester, Minnesota.
[Ti] Título:In Reply to 'C4 Deposition in Glomerular Disease'.
[So] Source:Am J Kidney Dis;68(5):817, 2016 11.
[Is] ISSN:1523-6838
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Complemento C4
Complemento C4b
[Mh] Termos MeSH secundário: Complemento C3
Seres Humanos
Glomérulos Renais
[Pt] Tipo de publicação:LETTER; COMMENT
[Nm] Nome de substância:
0 (Complement C3); 0 (Complement C4); 80295-50-7 (Complement C4b)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171129
[Lr] Data última revisão:
171129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:28457114
[Au] Autor:Sthoeger Z; Lorber M; Tal Y; Toubi E; Amital H; Kivity S; Langevitz P; Asher I; Elbirt D; Agmon Levin N
[Ad] Endereço:Department of Internal Medicine B and Clinical Immunology, Allergy and Neve-Or AIDS Center, Kaplan Medical Center, Rehovot, Israel.
[Ti] Título:Anti-BLyS Treatment of 36 Israeli Systemic Lupus Erythematosus Patients.
[So] Source:Isr Med Assoc J;19(1):44-48, 2017 Jan.
[Is] ISSN:1565-1088
[Cp] País de publicação:Israel
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Anti-BLyS treatment with the human belimumab monoclonal antibody was shown to be a safe and effective therapeutic modality in lupus patients with active disease (i.e., without significant neurological/renal involvement) despite standard treatment. OBJECTIVES: To evaluate the "real-life" safety and efficacy of belimumab added to standard therapy in patents with active lupus in five Israeli medical centers. METHODS: We conducted a retrospective open-labeled study of 36 lupus patients who received belimumab monthly for at least 1 year in addition to standard treatment. Laboratory tests (C3/C4, anti dsDNA autoantibodies, chemistry, urinalysis and complete blood count) were done every 3-4 months. Adverse events were obtained from patients' medical records. Efficacy assessment by the treating physicians was defined as excellent, good/partial, or no response. RESULTS: The study group comprised 36 lupus patients (8 males, 28 females) with a mean age of 41.6 } 12.2 years. Belimumab was given for a mean period of 2.3 } 1.7 years (range 1-7). None of the patients discontinued belimumab due to adverse events. Four patients (11.1%) had an infection related to belimumab. Only 5 patients (13.9%) stopped taking belimumab due to lack of efficacy. The response was excellent in 25 patients (69.5%) and good/partial in the other 6 (16.6%). Concomitantly, serological response (reduction of C3/C4 and anti-dsDNA autoantibodies) was also observed. Moreover, following belimumab treatment, there was a significant reduction in the usage of corticosteroids (from 100% to 27.7%) and immunosuppressive agents (from 83.3% to 8.3%). CONCLUSIONS: Belimumab, in addition to standard therapy, is a safe and effective treatment for active lupus patients.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/uso terapêutico
Imunossupressores/uso terapêutico
Lúpus Eritematoso Sistêmico/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Autoanticorpos/sangue
Complemento C3/análise
Complemento C4/análise
DNA/imunologia
Feminino
Seres Humanos
Israel/epidemiologia
Lúpus Eritematoso Sistêmico/imunologia
Masculino
Infecções Oportunistas/epidemiologia
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Autoantibodies); 0 (Complement C3); 0 (Complement C4); 0 (Immunosuppressive Agents); 73B0K5S26A (belimumab); 9007-49-2 (DNA)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


  10 / 12103 MEDLINE  
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[PMID]:27777195
[Au] Autor:Chen S; Ma BL; Cao MQ; Yu HJ; Ma XM
[Ad] Endereço:1School of Basic Medicine, Lanzhou University, Lanzhou 730030, China; 2Second Hospital of Lanzhou University, Lanzhou 730030, China. E-mail: lncsi@126.com.
[Ti] Título:[Correlation among serum MBL, MASP-2, HsCRP and C levels in rheumatoid arthritis].
[So] Source:Nan Fang Yi Ke Da Xue Xue Bao;36(10):1340-1344, 2016 Oct 20.
[Is] ISSN:1673-4254
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To investigate the correlation among serum levels of manning-binding lectin (MBL), MBL-associated serine proteases-2 (MASP-2), complement C and high-sensitive C reactive protein (HsCRP) in patients with rheumatoid arthritis (RA). METHODS: Fasting venous blood were collected from 50 RA patients (25 in active stage and 25 in remission) and 40 healthy subjects for detecting serum levels of MBL, MASP-2, complement C and HsCRP using enzyme-linked immunosorbent assay (ELISA) and immune turbidity assay. RESULTS: The serum levels of MBL and MASP-2 were significantly lower and HsCRP level was significantly higher in patients with RA (in both acute stage and remission) than in the healthy control group (P<0.05), but complement C level was similar between the RA patients and control group. Bivariate Pearson correlation analysis showed that in RA patients, MBL was positively correlated with MASP-2 level (r=0.550, P=0.001) and negatively with HsCRP (r=-0.323, P=0.022) but not correlated with C (r=-0.022, P=0.882); MASP-2 was negatively correlated with HsCRP (r=0.453, P=0.453) and was not correlated with C (r=0.049, P=0.738). ROC curve analysis revealed the largest area under curve (AUC) of HsCRP (0.844, P=0.001) and smaller AUCs of MBL (0.025, P=0.001) and MASP-2 (0.266, P=0.001). HsCRP had a much higher sensitivity (84%) than MBL (10%) and MASP-2 (40%) in the diagnosis of RA. CONCLUSION: In RA patients, MBL and MASP-2 are negatively correlated with HsCRP level. Serum MBL and MASP-2 levels decrease with the progression of joint injury in RA patients, suggesting their involvement in the pathological process of RA; but due to their low sensitivity, they are not appropriate indicators for evaluating the disease activity of RA.
[Mh] Termos MeSH primário: Artrite Reumatoide/sangue
Proteína C-Reativa/análise
Complemento C3/análise
Lectina de Ligação a Manose/sangue
Serina Proteases Associadas a Proteína de Ligação a Manose/análise
[Mh] Termos MeSH secundário: Estudos de Casos e Controles
Ensaio de Imunoadsorção Enzimática
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (C3 protein, human); 0 (Complement C3); 0 (Mannose-Binding Lectin); 9007-41-4 (C-Reactive Protein); EC 3.4.21.- (MASP2 protein, human); EC 3.4.21.- (Mannose-Binding Protein-Associated Serine Proteases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE



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