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[PMID]:29185959
[Au] Autor:Marchesoni A; Olivieri I; Salvarani C; Pipitone N; D'Angelo S; Mathieu A; Cauli A; Punzi L; Ramonda R; Scarpa R; Maccarone M; Lubrano E
[Ad] Endereço:Day Hospital of Rheumatology, ASST Gaetano Pini-CTO, Milano, Italy. antonio.marchesoni@asst-pini-cto.it.
[Ti] Título:Recommendations for the use of biologics and other novel drugs in the treatment of psoriatic arthritis: 2017 update from the Italian Society of Rheumatology.
[So] Source:Clin Exp Rheumatol;35(6):991-1010, 2017 Nov-Dec.
[Is] ISSN:0392-856X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To update the 2011 Italian Society of Rheumatology (SIR) recommendations for the use of biologics and other novel agents in the treatment of psoriatic arthritis (PsA). METHODS: To create this new set of recommendations, the SIR "Spondyloartritis and Psoriatic Arthritis study group - A. Spadaro" went through the following steps: literature search, identification of the items of interests for each of the four previously identified clinical domains of PsA and the different treatment phases, achievement of the consensus on all topics, and generation of the recommendations. RESULTS: An update on the available evidence on all of the biologics and new small molecules tested in PsA is reported, comprising the data for each of the individual articular manifestation. Indications for therapy inclusion criteria, choice of the drug, disease assessment, response definition, therapy failure management, and disease remission management for PsA peripheral joint arthritis, enthesitis, dactylitis, and spondylitis are provided. Suggestions for the treatment of patients with PsA and concomitant extra-articular manifestations are also given. CONCLUSIONS: These evidence-based recommendations may be used for guidance in the complex and fast-evolving field of the treatment of PsA.
[Mh] Termos MeSH primário: Antirreumáticos/uso terapêutico
Artrite Psoriásica/tratamento farmacológico
Produtos Biológicos/uso terapêutico
[Mh] Termos MeSH secundário: Abatacepte/uso terapêutico
Anticorpos Monoclonais Humanizados/uso terapêutico
Prática Clínica Baseada em Evidências
Seres Humanos
Interleucina-17/antagonistas & inibidores
Guias de Prática Clínica como Assunto
Fator de Necrose Tumoral alfa/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Antirheumatic Agents); 0 (Biological Products); 0 (Interleukin-17); 0 (Tumor Necrosis Factor-alpha); 0 (clazakizumab); 7D0YB67S97 (Abatacept)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE


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[PMID]:28975211
[Au] Autor:Wadström H; Frisell T; Askling J; Anti-Rheumatic Therapy in Sweden (ARTIS) Study Group
[Ad] Endereço:Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, 171 76 Stockholm, Sweden.
[Ti] Título:Malignant Neoplasms in Patients With Rheumatoid Arthritis Treated With Tumor Necrosis Factor Inhibitors, Tocilizumab, Abatacept, or Rituximab in Clinical Practice: A Nationwide Cohort Study From Sweden.
[So] Source:JAMA Intern Med;177(11):1605-1612, 2017 Nov 01.
[Is] ISSN:2168-6114
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: Considering the widespread and increasing use of biological immunomodulators (biological disease-modifying antirheumatic drugs [bDMARDs]) to treat chronic inflammatory conditions, and the concern that immunomodulation may alter cancer risk and progression, the limited available data on use of these therapies as used in clinical practice and cancer risks are a concern. Objective: To assess the risk of incident malignant neoplasms in patients with rheumatoid arthritis (RA) treated with bDMARDs. Design, Setting, and Participants: This was a national register-based prospective cohort study of the public health care system in Sweden from 2006 to 2015. Cohorts of patients with RA initiating treatment with tocilizumab (n = 1798), abatacept (n = 2021), and rituximab (n = 3586), a tumor necrosis factor inhibitor (TNFi) as first-ever (n = 10 782) or second-ever (n = 4347) bDMARD, a biologics-naive cohort treated with conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) (n = 46 610), and a general population comparator cohort (n = 107 491). Exposures: Treatment with tocilizumab, abatacept, rituximab, or TNFi. Main Outcomes and Measures: Outcomes included a first invasive solid or hematologic malignant neoplasm, or skin cancer. Hazard ratios were calculated using Cox-regression, adjusted for age, sex, disease and treatment characteristics, and educational level. Results: We identified a total of 15 129 initiations of TNFi as the first or second bDMARD, 7405 initiations of other bDMARDs, and 46 610 csDMARD users. The mean age varied from 58 to 64 years, and the proportion of female patients varied from 71% to 80%, across the 7 cohorts under study. The observed numbers of events (crude incidence per 100 000 person-years) for a first invasive solid or hematologic malignant neoplasm were 50 (959) for tocilizumab, 61 (1026) for abatacept, 141 (1074) for rituximab, 478 (978) for initiators of TNFi as first bDMARD, and 169 (917) for TNFi as second bDMARD. There were no statistically significant differences between initiators of a first or second TNFi, or other bDMARDs, and bDMARD-naive RA for any of a total of 25 drug- and outcome-specific comparisons, with 1 exception (abatacept and increased risk of squamous cell skin cancer). Conclusions and Relevance: The overall risk of cancer among patients with RA initiating TNFi as first or second bDMARD, tocilizumab, abatacept, or rituximab does not differ substantially from that of biologic drug-naive, csDMARD-treated patients with RA, although altered risks for specific cancer types, or those with longer latency, cannot be excluded.
[Mh] Termos MeSH primário: Abatacepte/uso terapêutico
Anticorpos Monoclonais Humanizados/uso terapêutico
Antirreumáticos/uso terapêutico
Artrite Reumatoide/tratamento farmacológico
Neoplasias/epidemiologia
Rituximab/uso terapêutico
Fator de Necrose Tumoral alfa/antagonistas & inibidores
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Incidência
Masculino
Meia-Idade
Estudos Prospectivos
Sistema de Registros
Medição de Risco
Fatores de Risco
Suécia/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Antirheumatic Agents); 0 (Tumor Necrosis Factor-alpha); 4F4X42SYQ6 (Rituximab); 7D0YB67S97 (Abatacept); I031V2H011 (tocilizumab)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1001/jamainternmed.2017.4332


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[PMID]:28800947
[Au] Autor:Samson M; Bonnotte B
[Ad] Endereço:Service de médecine interne et immunologie clinique, CHU François-Mitterrand, 2, boulevard Mal-de-Lattre-de-Tassigny, 21000 Dijon, France; Inserm U1098, université Bourgogne-Franche Comté, FHU Increase, 21000 Dijon, France. Electronic address: maxime.samson@chu-dijon.fr.
[Ti] Título:[From pathogenesis of giant cell arteritis to new therapeutic targets].
[Ti] Título:De la physiopathologie de l'artérite à cellules géantes aux nouvelles cibles thérapeutiques..
[So] Source:Rev Med Interne;38(10):670-678, 2017 Oct.
[Is] ISSN:1768-3122
[Cp] País de publicação:France
[La] Idioma:fre
[Ab] Resumo:Giant cell arteritis (GCA) is the most common vasculitis in adults. GCA is a granulomatous large-vessel vasculitis involving the aorta and its major branches in people>50 years. Glucocorticoids (GC) remain the cornerstone of GCA treatment. Prednisone is usually started at 0.7 or 1mg/kg/day depending on the occurrence of ischemic complications. Then, GC are progressively tapered and stopped after a mean duration of 18 months. GC are very efficient but relapses often occur during their tapering. Moreover, GC-related side effects are very common during this long term GC therapy. Thus, it can be assumed that GC are not the ideal treatment for GCA and that GC-sparing strategies have to be developed. The pathogenesis of GCA is not fully understood but major advances have been achieved in the recent years. If the trigger of GCA, which is suspected to be infectious, is still not identified, mechanisms triggering the granulomatous inflammation of the arterial wall and the progressive vascular remodeling leading to the occurrence of ischemic events have been better and better deciphered. Thanks to these advances in the knowledge of GCA pathogenesis, new therapeutic targets have emerged such as blockade of the activation of T cells or inhibition of the interleukin-6 (IL-6), IL-12/23 or IL-1ß pathways.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Drogas em Investigação/uso terapêutico
Arterite de Células Gigantes/tratamento farmacológico
Arterite de Células Gigantes/etiologia
[Mh] Termos MeSH secundário: Abatacepte/uso terapêutico
Anticorpos Monoclonais Humanizados/uso terapêutico
Arterite de Células Gigantes/genética
Glucocorticoides/uso terapêutico
Seres Humanos
Terapia de Alvo Molecular/métodos
Terapia de Alvo Molecular/tendências
Ustecinumab/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antibodies, Monoclonal, Humanized); 0 (Drugs, Investigational); 0 (Glucocorticoids); 7D0YB67S97 (Abatacept); FU77B4U5Z0 (Ustekinumab); I031V2H011 (tocilizumab)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170813
[St] Status:MEDLINE


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[PMID]:28774475
[Au] Autor:Keser G; Aksu K
[Ad] Endereço:Ege University School of Medicine, Department of Internal Medicine, Division of Rheumatology, Bornova, Izmir, Turkey. Electronic address: agkkeser@gmail.com.
[Ti] Título:What is new in management of Takayasu arteritis?
[So] Source:Presse Med;46(7-8 Pt 2):e229-e235, 2017 Jul - Aug.
[Is] ISSN:2213-0276
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Management of Takayasu arteritis (TAK) is challenging mostly due to difficulties in assessing actual disease activity. The rational of medical treatment is to suppress both vascular and systemic inflammation with appropriate systemic immunosuppression, including corticosteroids and conventional immunosuppressive (IS) agents. In case of refractory disease activity, biologic agents such as TNF inhibitors and tocilizumab may be tried. In selected cases, endovascular interventions and surgical procedures may be indicated and should be performed during inactive disease. Among conventional IS agents, new data is available for leflunomide. On the other hand, most of the new information in the management of TAK arises from the growing experience with biologic agents used in resistant cases. Besides, there are potential new therapeutic targets which may be promising in the future for medical treatment of TAK. Finally, new trends in endovascular interventions for management of TAK deserve attention.
[Mh] Termos MeSH primário: Arterite de Takayasu/terapia
[Mh] Termos MeSH secundário: Abatacepte/uso terapêutico
Anticorpos Monoclonais Humanizados/uso terapêutico
Procedimentos Endovasculares
Seres Humanos
Fatores Imunológicos/uso terapêutico
Imunossupressores/uso terapêutico
Radiologia Intervencionista
Rituximab/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Immunologic Factors); 0 (Immunosuppressive Agents); 4F4X42SYQ6 (Rituximab); 7D0YB67S97 (Abatacept); I031V2H011 (tocilizumab)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170805
[St] Status:MEDLINE


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[PMID]:28608166
[Au] Autor:Blair HA; Deeks ED
[Ad] Endereço:Springer, Private Bag 65901, Mairangi Bay, Auckland, 0754, New Zealand. demail@springer.com.
[Ti] Título:Abatacept: A Review in Rheumatoid Arthritis.
[So] Source:Drugs;77(11):1221-1233, 2017 Jul.
[Is] ISSN:1179-1950
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:The biological DMARD (bDMARD) abatacept (Orencia ), a recombinant fusion protein, selectively modulates a co-stimulatory signal necessary for T-cell activation. In the EU, abatacept is approved for use in patients with highly active and progressive rheumatoid arthritis (RA) not previously treated with methotrexate. Abatacept is also approved for the treatment of moderate to severe active RA in patients with an inadequate response to previous therapy with at least one conventional DMARD (cDMARD), including methotrexate or a TNF inhibitor. In phase III trials, beneficial effects on RA signs and symptoms, disease activity, structural damage progression and physical function were seen with intravenous (IV) or subcutaneous (SC) abatacept regimens, including abatacept plus methotrexate in methotrexate-naive patients with early RA and poor prognostic factors, and abatacept plus methotrexate or other cDMARDs in patients with inadequate response to methotrexate or TNF inhibitors. Benefits were generally maintained during longer-term follow-up. Absolute drug-free remission rates following withdrawal of all RA treatments were significantly higher with abatacept plus methotrexate than with methotrexate alone. Both IV and SC abatacept were generally well tolerated, with low rates of immunogenicity. Current evidence therefore suggests that abatacept is a useful treatment option for patients with RA.
[Mh] Termos MeSH primário: Abatacepte/uso terapêutico
Antirreumáticos/uso terapêutico
Artrite Reumatoide/tratamento farmacológico
[Mh] Termos MeSH secundário: Abatacepte/efeitos adversos
Abatacepte/farmacologia
Adulto
Antirreumáticos/administração & dosagem
Antirreumáticos/farmacocinética
Ensaios Clínicos como Assunto
Quimioterapia Combinada
Seres Humanos
Imunoconjugados/farmacologia
Imunoconjugados/uso terapêutico
Metotrexato/administração & dosagem
Metotrexato/efeitos adversos
Metotrexato/uso terapêutico
Resultado do Tratamento
Fator de Necrose Tumoral alfa/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antirheumatic Agents); 0 (Immunoconjugates); 0 (Tumor Necrosis Factor-alpha); 7D0YB67S97 (Abatacept); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE
[do] DOI:10.1007/s40265-017-0775-4


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[PMID]:28564491
[Au] Autor:Verstappen GM; Meiners PM; Corneth OBJ; Visser A; Arends S; Abdulahad WH; Hendriks RW; Vissink A; Kroese FGM; Bootsma H
[Ad] Endereço:University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
[Ti] Título:Attenuation of Follicular Helper T Cell-Dependent B Cell Hyperactivity by Abatacept Treatment in Primary Sjögren's Syndrome.
[So] Source:Arthritis Rheumatol;69(9):1850-1861, 2017 Sep.
[Is] ISSN:2326-5205
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To assess the effect of abatacept (CTLA-4Ig), which limits T cell activation, on homeostasis of CD4+ T cell subsets and T cell-dependent B cell hyperactivity in patients with primary Sjögren's syndrome (SS). METHODS: Fifteen patients with primary SS treated with abatacept were included. Circulating CD4+ T cell and B cell subsets were analyzed by flow cytometry at baseline, during the treatment course, and after treatment was completed. CD4+ effector T cell subsets and Treg cells were identified based on expression of CD45RA, CXCR3, CCR6, CCR4, CXCR5, programmed death 1, inducible costimulator (ICOS), and FoxP3. Serum levels of anti-SSA/anti-SSB and several T cell-related cytokines were measured. Expression of ICOS and interleukin-21 (IL-21) protein was examined in parotid gland tissue at baseline and after treatment. Changes in laboratory parameters and associations with systemic disease activity (EULAR Sjögren's Syndrome Disease Activity Index [ESSDAI]) over time were analyzed using generalized estimating equations. RESULTS: Abatacept selectively reduced percentages and numbers of circulating follicular helper T (Tfh) cells and Treg cells. Other CD4+ effector T cell subsets were unaffected. Furthermore, expression of the activation marker ICOS by circulating CD4+ T cells and expression of ICOS protein in parotid gland tissue declined. Reduced ICOS expression on circulating Tfh cells correlated significantly with lower ESSDAI scores during treatment. Serum levels of IL-21, CXCL13, anti-SSA, and anti-SSB decreased. Among circulating B cells, plasmablasts were decreased by treatment. After cessation of treatment, all parameters gradually returned to baseline. CONCLUSION: Abatacept treatment in patients with primary SS reduces circulating Tfh cell numbers and expression of the activation marker ICOS on T cells. Lower numbers of activated circulating Tfh cells contribute to attenuated Tfh cell-dependent B cell hyperactivity and may underlie the efficacy of abatacept.
[Mh] Termos MeSH primário: Abatacepte/farmacologia
Linfócitos B/efeitos dos fármacos
Imunossupressores/farmacologia
Síndrome de Sjogren/tratamento farmacológico
Linfócitos T Auxiliares-Indutores/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adulto
Linfócitos T CD4-Positivos/efeitos dos fármacos
Quimiocina CXCL13/sangue
Feminino
Citometria de Fluxo
Seres Humanos
Interleucinas/sangue
Ativação Linfocitária/efeitos dos fármacos
Masculino
Meia-Idade
Plasmócitos/efeitos dos fármacos
Estudos Prospectivos
Síndrome de Sjogren/imunologia
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL13 protein, human); 0 (Chemokine CXCL13); 0 (Immunosuppressive Agents); 0 (Interleukins); 0 (interleukin-21); 7D0YB67S97 (Abatacept)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170601
[St] Status:MEDLINE
[do] DOI:10.1002/art.40165


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[PMID]:28516880
[Au] Autor:Fukuyo S; Nakayamada S; Iwata S; Kubo S; Saito K; Tanaka Y
[Ad] Endereço:The First Department of Internal Medicine, University of Occupational and Environmental Health, Fukuoka, Japan.
[Ti] Título:Abatacept therapy reduces CD28+CXCR5+ follicular helper-like T cells in patients with rheumatoid arthritis.
[So] Source:Clin Exp Rheumatol;35(4):562-570, 2017 Jul-Aug.
[Is] ISSN:0392-856X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: The characteristics of T cells targeted by abatacept (ABT) in cases of rheumatoid arthritis (RA) are still unknown. The goal of the study was to determine the pathogenicity of T cells and the predictors of therapeutic effects of ABT. METHODS: We analysed the peripheral T cell phenotype of 34 RA patients via flow cytometry. The correlation of the phenotypes of CD4+ T cells with clinical disease activity and change in CD4+ T cell subsets at baseline and 24 weeks after ABT treatment were evaluated. RESULTS: RA patients showed an increase in the proportion of CD28- cells among CD4+ cells, which was significantly high in patients who had not achieved remission after ABT therapy. The proportions of CD4+CXCR5+ T follicular helper-like (Tfh-like) cells increased in RA patients compared to healthy donors. The proportions of Tfh-like cells among CD4+CD28+ cells were significantly higher than those among CD4+CD28- cells. The proportion of Tfh-like cells was higher in anti-cyclic citrullinated peptide antibody (ACPA)-positive patients. By contrast, the proportions of CD4+CXCR3+ T helper 1-like (Th1-like) cells and effector memory phase T cells among CD4+CD28- cells were significantly higher than those among CD4+CD28+ cells, and the proportion of these cells did not correlate with disease activity. After ABT therapy, the proportion of Tfh-like cells among CD4+CD28+ cells was significantly reduced. CONCLUSIONS: These results imply that CD4+ CD28+ Tfh-like cells could possibly be the targets of ABT. Conversely, CD4+ CD28- cells may be a potential predictor of treatment resistance.
[Mh] Termos MeSH primário: Abatacepte/uso terapêutico
Antirreumáticos/uso terapêutico
Artrite Reumatoide/tratamento farmacológico
Células Th1/imunologia
[Mh] Termos MeSH secundário: Idoso
Artrite Reumatoide/imunologia
Autoanticorpos/imunologia
Antígenos CD28/metabolismo
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/metabolismo
Feminino
Citometria de Fluxo
Seres Humanos
Masculino
Meia-Idade
Peptídeos Cíclicos/imunologia
Receptores CXCR3/metabolismo
Receptores CXCR5/metabolismo
Subpopulações de Linfócitos T/imunologia
Subpopulações de Linfócitos T/metabolismo
Linfócitos T Auxiliares-Indutores/imunologia
Linfócitos T Auxiliares-Indutores/metabolismo
Células Th1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antirheumatic Agents); 0 (Autoantibodies); 0 (CD28 Antigens); 0 (CXCR3 protein, human); 0 (CXCR5 protein, human); 0 (Peptides, Cyclic); 0 (Receptors, CXCR3); 0 (Receptors, CXCR5); 0 (cyclic citrullinated peptide); 7D0YB67S97 (Abatacept)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE


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[PMID]:28481462
[Au] Autor:Singh JA; Hossain A; Mudano AS; Tanjong Ghogomu E; Suarez-Almazor ME; Buchbinder R; Maxwell LJ; Tugwell P; Wells GA
[Ad] Endereço:Department of Medicine, Birmingham VA Medical Center, Faculty Office Tower 805B, 510 20th Street South, Birmingham, AL, USA, 35294.
[Ti] Título:Biologics or tofacitinib for people with rheumatoid arthritis naive to methotrexate: a systematic review and network meta-analysis.
[So] Source:Cochrane Database Syst Rev;5:CD012657, 2017 05 08.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Biologic disease-modifying anti-rheumatic drugs (biologics) are highly effective in treating rheumatoid arthritis (RA), however there are few head-to-head biologic comparison studies. We performed a systematic review, a standard meta-analysis and a network meta-analysis (NMA) to update the 2009 Cochrane Overview. This review is focused on the adults with RA who are naive to methotrexate (MTX) that is, receiving their first disease-modifying agent. OBJECTIVES: To compare the benefits and harms of biologics (abatacept, adalimumab, anakinra, certolizumab pegol, etanercept, golimumab, infliximab, rituximab, tocilizumab) and small molecule tofacitinib versus comparator (methotrexate (MTX)/other DMARDs) in people with RA who are naive to methotrexate. METHODS: In June 2015 we searched for randomized controlled trials (RCTs) in CENTRAL, MEDLINE and Embase; and trials registers. We used standard Cochrane methods. We calculated odds ratios (OR) and mean differences (MD) along with 95% confidence intervals (CI) for traditional meta-analyses and 95% credible intervals (CrI) using a Bayesian mixed treatment comparisons approach for network meta-analysis (NMA). We converted OR to risk ratios (RR) for ease of interpretation. We also present results in absolute measures as risk difference (RD) and number needed to treat for an additional beneficial or harmful outcome (NNTB/H). MAIN RESULTS: Nineteen RCTs with 6485 participants met inclusion criteria (including five studies from the original 2009 review), and data were available for four TNF biologics (adalimumab (six studies; 1851 participants), etanercept (three studies; 678 participants), golimumab (one study; 637 participants) and infliximab (seven studies; 1363 participants)) and two non-TNF biologics (abatacept (one study; 509 participants) and rituximab (one study; 748 participants)).Less than 50% of the studies were judged to be at low risk of bias for allocation sequence generation, allocation concealment and blinding, 21% were at low risk for selective reporting, 53% had low risk of bias for attrition and 89% had low risk of bias for major baseline imbalance. Three trials used biologic monotherapy, that is, without MTX. There were no trials with placebo-only comparators and no trials of tofacitinib. Trial duration ranged from 6 to 24 months. Half of the trials contained participants with early RA (less than two years' duration) and the other half included participants with established RA (2 to 10 years). Biologic + MTX versus active comparator (MTX (17 trials (6344 participants)/MTX + methylprednisolone 2 trials (141 participants))In traditional meta-analyses, there was moderate-quality evidence downgraded for inconsistency that biologics with MTX were associated with statistically significant and clinically meaningful benefit versus comparator as demonstrated by ACR50 (American College of Rheumatology scale) and RA remission rates. For ACR50, biologics with MTX showed a risk ratio (RR) of 1.40 (95% CI 1.30 to 1.49), absolute difference of 16% (95% CI 13% to 20%) and NNTB = 7 (95% CI 6 to 8). For RA remission rates, biologics with MTX showed a RR of 1.62 (95% CI 1.33 to 1.98), absolute difference of 15% (95% CI 11% to 19%) and NNTB = 5 (95% CI 6 to 7). Biologics with MTX were also associated with a statistically significant, but not clinically meaningful, benefit in physical function (moderate-quality evidence downgraded for inconsistency), with an improvement of HAQ scores of -0.10 (95% CI -0.16 to -0.04 on a 0 to 3 scale), absolute difference -3.3% (95% CI -5.3% to -1.3%) and NNTB = 4 (95% CI 2 to 15).We did not observe evidence of differences between biologics with MTX compared to MTX for radiographic progression (low-quality evidence, downgraded for imprecision and inconsistency) or serious adverse events (moderate-quality evidence, downgraded for imprecision). Based on low-quality evidence, results were inconclusive for withdrawals due to adverse events (RR of 1.32, but 95% confidence interval included possibility of important harm, 0.89 to 1.97). Results for cancer were also inconclusive (Peto OR 0.71, 95% CI 0.38 to 1.33) and downgraded to low-quality evidence for serious imprecision. Biologic without MTX versus active comparator (MTX 3 trials (866 participants)There was no evidence of statistically significant or clinically important differences for ACR50, HAQ, remission, (moderate-quality evidence for these benefits, downgraded for imprecision), withdrawals due to adverse events,and serious adverse events (low-quality evidence for these harms, downgraded for serious imprecision). All studies were for TNF biologic monotherapy and none for non-TNF biologic monotherapy. Radiographic progression was not measured. AUTHORS' CONCLUSIONS: In MTX-naive RA participants, there was moderate-quality evidence that, compared with MTX alone, biologics with MTX was associated with absolute and relative clinically meaningful benefits in three of the efficacy outcomes (ACR50, HAQ scores, and RA remission rates). A benefit regarding less radiographic progression with biologics with MTX was not evident (low-quality evidence). We found moderate- to low-quality evidence that biologic therapy with MTX was not associated with any higher risk of serious adverse events compared with MTX, but results were inconclusive for withdrawals due to adverse events and cancer to 24 months.TNF biologic monotherapy did not differ statistically significantly or clinically meaningfully from MTX for any of the outcomes (moderate-quality evidence), and no data were available for non-TNF biologic monotherapy.We conclude that biologic with MTX use in MTX-naive populations is beneficial and that there is little/inconclusive evidence of harms. More data are needed for tofacitinib, radiographic progression and harms in this patient population to fully assess comparative efficacy and safety.
[Mh] Termos MeSH primário: Antirreumáticos/uso terapêutico
Artrite Reumatoide/tratamento farmacológico
Produtos Biológicos/uso terapêutico
Metotrexato/uso terapêutico
Piperidinas/uso terapêutico
Pirimidinas/uso terapêutico
Pirróis/uso terapêutico
[Mh] Termos MeSH secundário: Abatacepte/uso terapêutico
Adalimumab/uso terapêutico
Adulto
Anticorpos Monoclonais/uso terapêutico
Teorema de Bayes
Etanercepte/uso terapêutico
Seres Humanos
Infliximab/uso terapêutico
Metilprednisolona/uso terapêutico
Metanálise em Rede
Ensaios Clínicos Controlados Aleatórios como Assunto
Rituximab/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antirheumatic Agents); 0 (Biological Products); 0 (Piperidines); 0 (Pyrimidines); 0 (Pyrroles); 4F4X42SYQ6 (Rituximab); 7D0YB67S97 (Abatacept); 87LA6FU830 (tofacitinib); 91X1KLU43E (golimumab); B72HH48FLU (Infliximab); FYS6T7F842 (Adalimumab); OP401G7OJC (Etanercept); X4W7ZR7023 (Methylprednisolone); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170803
[Lr] Data última revisão:
170803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD012657


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[PMID]:28473423
[Au] Autor:Mease PJ; Gottlieb AB; van der Heijde D; FitzGerald O; Johnsen A; Nys M; Banerjee S; Gladman DD
[Ad] Endereço:Swedish Medical Center and University of Washington, Seattle, Washington, USA.
[Ti] Título:Efficacy and safety of abatacept, a T-cell modulator, in a randomised, double-blind, placebo-controlled, phase III study in psoriatic arthritis.
[So] Source:Ann Rheum Dis;76(9):1550-1558, 2017 Sep.
[Is] ISSN:1468-2060
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To assess the efficacy and safety of abatacept, a selective T-cell costimulation modulator, in a phase III study in psoriatic arthritis (PsA). METHODS: This study randomised patients (1:1) with active PsA (~60% with prior exposure to a tumour necrosis factor inhibitor) to blinded weekly subcutaneous abatacept 125 mg (n=213) or placebo (n=211) for 24 weeks, followed by open-label subcutaneous abatacept. Patients without ≥20% improvement in joint counts at week 16 were switched to open-label abatacept. The primary end point was the proportion of patients with ≥20% improvement in the American College of Rheumatology (ACR20) criteria at week 24. RESULTS: Abatacept significantly increased ACR20 response versus placebo at week 24 (39.4% vs 22.3%; p<0.001). Although abatacept numerically increased Health Assessment Questionnaire-Disability Index response rates (reduction from baseline ≥0.35) at week 24, this was not statistically significant (31.0% vs 23.7%; p=0.097). The benefits of abatacept were seen in ACR20 responses regardless of tumour necrosis factor inhibitor exposure and in other musculoskeletal manifestations, but significance could not be attributed due to ranking below Health Assessment Questionnaire-Disability Index response in hierarchical testing. However, the benefit on psoriasis lesions was modest. Efficacy was maintained or improved up to week 52. Abatacept was well tolerated with no new safety signals. CONCLUSIONS: Abatacept treatment of PsA in this phase III study achieved its primary end point, ACR20 response, showed beneficial trends overall in musculoskeletal manifestations and was well tolerated. There was only a modest impact on psoriasis lesions. TRIAL REGISTRATION NUMBER: ClinicalTrials.gov number, NCT01860976 (funded by Bristol-Myers Squibb).
[Mh] Termos MeSH primário: Abatacepte/uso terapêutico
Antirreumáticos/uso terapêutico
Artrite Psoriásica/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Artrite Psoriásica/fisiopatologia
Método Duplo-Cego
Feminino
Seres Humanos
Hospedeiro Imunocomprometido
Masculino
Meia-Idade
Pneumonia por Pneumocystis/etiologia
Pneumonia por Pneumocystis/imunologia
Qualidade de Vida
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antirheumatic Agents); 7D0YB67S97 (Abatacept)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170506
[St] Status:MEDLINE
[do] DOI:10.1136/annrheumdis-2016-210724


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[PMID]:28403127
[Au] Autor:de Graav GN; Baan CC; Clahsen-van Groningen MC; Kraaijeveld R; Dieterich M; Verschoor W; von der Thusen JH; Roelen DL; Cadogan M; van de Wetering J; van Rosmalen J; Weimar W; Hesselink DA
[Ad] Endereço:1 Division of Nephrology and Kidney Transplantation, Department of Internal Medicine, Erasmus MC, University Medical Center, Rotterdam, the Netherlands. 2 Department of Pathology, Erasmus MC, University Medical Center, Rotterdam, the Netherlands. 3 Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, the Netherlands. 4 Department of Biostatistics, Erasmus MC, University Medical Center, Rotterdam, the Netherlands.
[Ti] Título:A Randomized Controlled Clinical Trial Comparing Belatacept With Tacrolimus After De Novo Kidney Transplantation.
[So] Source:Transplantation;101(10):2571-2581, 2017 Oct.
[Is] ISSN:1534-6080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Belatacept, an inhibitor of the CD28-CD80/86 costimulatory pathway, allows for calcineurin-inhibitor free immunosuppressive therapy in kidney transplantation but is associated with a higher acute rejection risk than ciclosporin. Thus far, no biomarker for belatacept-resistant rejection has been validated. In this randomized-controlled trial, acute rejection rate was compared between belatacept- and tacrolimus-treated patients and immunological biomarkers for acute rejection were investigated. METHODS: Forty kidney transplant recipients were 1:1 randomized to belatacept or tacrolimus combined with basiliximab, mycophenolate mofetil, and prednisolone. The 1-year incidence of biopsy-proven acute rejection was monitored. Potential biomarkers, namely, CD8CD28, CD4CD57PD1, and CD8CD28 end-stage terminally differentiated memory T cells were measured pretransplantation and posttransplantation and correlated to rejection. Pharmacodynamic monitoring of belatacept was performed by measuring free CD86 on monocytes. RESULTS: The rejection incidence was higher in belatacept-treated than tacrolimus-treated patients: 55% versus 10% (P = 0.006). All 3 graft losses, due to rejection, occurred in the belatacept group. Although 4 of 5 belatacept-treated patients with greater than 35 cells CD8CD28 end-stage terminally differentiated memory T cells/µL rejected, median pretransplant values of the biomarkers did not differ between belatacept-treated rejectors and nonrejectors. In univariable Cox regressions, the studied cell subsets were not associated with rejection-risk. CD86 molecules on circulating monocytes in belatacept-treated patients were saturated at all timepoints. CONCLUSIONS: Belatacept-based immunosuppressive therapy resulted in higher and more severe acute rejection compared with tacrolimus-based therapy. This trial did not identify cellular biomarkers predictive of rejection. In addition, the CD28-CD80/86 costimulatory pathway appeared to be sufficiently blocked by belatacept and did not predict rejection.
[Mh] Termos MeSH primário: Abatacepte/uso terapêutico
Rejeição de Enxerto/prevenção & controle
Sobrevivência de Enxerto/efeitos dos fármacos
Imunossupressão/métodos
Transplante de Rim
Tacrolimo/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Idoso
Biópsia
Relação Dose-Resposta a Droga
Feminino
Seguimentos
Rejeição de Enxerto/diagnóstico
Seres Humanos
Rim/patologia
Masculino
Meia-Idade
Estudos Prospectivos
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
7D0YB67S97 (Abatacept); WM0HAQ4WNM (Tacrolimus)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.1097/TP.0000000000001755



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