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3.
PLoS One ; 14(2): e0213073, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30818333

RESUMO

Research in rheumatoid arthritis (RA) is increasingly focused on the discovery of biomarkers that could enable personalized treatments. The genetic biomarkers associated with the response to TNF inhibitors (TNFi) are among the most studied. They include 12 SNPs exhibiting promising results in the three largest genome-wide association studies (GWAS). However, they still require further validation. With this aim, we assessed their association with response to TNFi in a replication study, and a meta-analysis summarizing all non-redundant data. The replication involved 755 patients with RA that were treated for the first time with a biologic drug, which was either infliximab (n = 397), etanercept (n = 155) or adalimumab (n = 203). Their DNA samples were successfully genotyped with a single-base extension multiplex method. Lamentably, none of the 12 SNPs was associated with response to the TNFi in the replication study (p > 0.05). However, a drug-stratified exploratory analysis revealed a significant association of the NUBPL rs2378945 SNP with a poor response to etanercept (B = -0.50, 95% CI = -0.82, -0.17, p = 0.003). In addition, the meta-analysis reinforced the previous association of three SNPs: rs2378945, rs12142623, and rs4651370. In contrast, five of the remaining SNPs were less associated than before, and the other four SNPs were no longer associated with the response to treatment. In summary, our results highlight the complexity of the pharmacogenetics of TNFi in RA showing that it could involve a drug-specific component and clarifying the status of the 12 GWAS-drawn SNPs.

4.
Arthritis Res Ther ; 21(1): 66, 2019 02 20.
Artigo em Inglês | MEDLINE | ID: mdl-30786913

RESUMO

BACKGROUND: The aim of our study was to investigate the influence of conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs) and body mass index (BMI) on circulating drug levels and clinical response to tumour necrosis factor inhibitor (TNFi) therapy in axial spondyloarthritis (axSpA) patients. METHODS: Prospective observational study during 1 year with 2 cohorts (Madrid and Amsterdam) including 180 axSpA patients treated with standard doses of infliximab or adalimumab. Patients were stratified by BMI, being 78 (43%) normal weight (18.5-24.9 kg/m2) and 102 (57%) overweight/obese (≥ 25.0 kg/m2). After the first year of treatment, TNFi trough levels were measured by capture ELISA. Clinical response to TNFi was defined as ∆BASDAI ≥ 2 and clinical remission as BASDAI < 2 and CRP ≤ 5 mg/L. Logistic regression models were employed to analyse the association between concomitant csDMARDs and BMI with drug levels and clinical response. RESULTS: Seventy-nine patients (44%) received concomitant csDMARDs. The administration of concomitant csDMARDs (OR 3.82; 95% CI 1.06-13.84) and being normal weight (OR 18.38; 95% CI 2.24-150.63) were independently associated with serum TNFi drug persistence. Additionally, the use of concomitant csDMARDs contributed positively to achieve clinical response (OR 7.86; 95% CI 2.39-25.78) and remission (OR 4.84; 95% CI 1.09-21.36) in overweight/obese patients, but no association was found for normal-weight patients (OR 1.10; 0.33-3.58). CONCLUSIONS: The use of concomitant csDMARDs with TNFi may increase the probability of achieving clinical response in overweight/obese axSpA patients. Further research studies including larger cohorts of patients need to be done to confirm it.

5.
Clin Rheumatol ; 2018 Nov 06.
Artigo em Inglês | MEDLINE | ID: mdl-30402698

RESUMO

To investigate the effect of concomitant conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs) with adalimumab or infliximab on maintaining serum drug and clinical outcomes after the first year of treatment in patients with rheumatoid arthritis (RA). Second, to assess the influence of methotrexate (MTX) dose on these outcomes. Ninety-two patients with RA starting infliximab (n = 67) or adalimumab (n = 25) tumor necrosis factor inhibitor (TNFi) with available drug levels and clinical improvement assessment (European League Against Rheumatism [EULAR] response) after 12 months were included. Patients were grouped according to concomitant csDMARD use: (i) TNFi monotherapy; (ii) TNFi+MTX; (iii) TNFi with csDMARDs other than MTX (TNFi+OD). Patients receiving MTX were also classified by dose as < 15 mg/week (TNFi+MTX<15) and ≥ 15 mg/week (TNFi+MTX≥15). Logistic regression analyses were employed. More TNFi+MTX patients had circulating serum TNFi at 12 months (71% TNFi+MTX vs. 20% TNFi+OD vs. 9% TNFi monotherapy). Of these, the probability of maintaining serum TNFi levels was twice (OR 2.3; p = 0.06) than that of patients without MTX. However, statistically significant results were observed only for the highest MTX dose (OR 4.9; p = 0.02). Most patients achieving good EULAR response were treated with TNFi+MTX (81%). The probability of achieving this response was three times higher in patients within the TNFi+MTX group (OR 3.4; p = 0.03); however, no differences were found with regard to MTX dose. The persistence of serum TNFi and the probability of achieving clinical response are influenced by MTX but not by OD in patients with RA treated with infliximab or adalimumab.

6.
Arthritis Rheumatol ; 2018 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-30277011

RESUMO

OBJECTIVES: The new RA-specific autoantibodies, the anti-carbamylated protein antibodies (ACarPA), provide an opportunity to improve management and understanding of RA. However, many questions remain about them, including their relationship with HLA-DRB1 alleles. MATERIAL AND METHODS: The samples of 1126 RA patients from three collections were obtained. Serum reactivity against in vitro carbamylated FCS proteins was determined by ELISA. HLA-DRB1 alleles were determined by either hybridization techniques or imputation from HLA dense genotypes. These results were combined by meta-analysis with data from three previously reported cohorts. The carrier frequencies of the common HLA-DRB1 alleles were compared between the antibody-positive subgroups and the double-negative subgroup in ACPA/ACarPA stratified patients, and between the four patient strata and the healthy controls. RESULTS: Meta-analysis was conducted with 3709 RA patients and 2305 healthy subjects. It revealed a significant increase of HLA-DRB1*03 carriers in the ACPA- /ACarPA+ subgroup in comparison with both ACPA- /ACarPA- patients and healthy controls that was consistent in the six sample collections. This association was independent of the SE and the analyzed confounders. No other allele was specifically associated with ACPA- /ACarPA+ patients. In contrast, the SE was significantly increased in the ACPA+ /ACarPA- and ACPA+ /ACarPA+ patient subgroups without distinction between them. Also, some alleles (including HLA-DRB1*03) were associated with protection from ACPA+ RA. CONCLUSION: A specific association of HLA-DRB1*03 with ACPA- /ACarPA+ RA has been identified that suggests preferential presentation of carbamylated peptides as a new mechanism for HLA contribution to RA susceptibility. This article is protected by copyright. All rights reserved.

8.
PLoS One ; 13(5): e0196793, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29734345

RESUMO

Genetic biomarkers are sought to personalize treatment of patients with rheumatoid arthritis (RA), given their variable response to TNF inhibitors (TNFi). However, no genetic biomaker is yet sufficiently validated. Here, we report a validation study of 18 previously reported genetic biomarkers, including 11 from GWAS of response to TNFi. The validation was attempted in 581 patients with RA that had not been treated with biologic antirheumatic drugs previously. Their response to TNFi was evaluated at 3, 6 and 12 months in two ways: change in the DAS28 measure of disease activity, and according to the EULAR criteria for response to antirheumatic drugs. Association of these parameters with the genotypes, obtained by PCR amplification followed by single-base extension, was tested with regression analysis. These analyses were adjusted for baseline DAS28, sex, and the specific TNFi. However, none of the proposed biomarkers was validated, as none showed association with response to TNFi in our study, even at the time of assessment and with the outcome that showed the most significant result in previous studies. These negative results are notable because this was the first independent validation study for 12 of the biomarkers, and because they indicate that prudence is needed in the interpretation of the proposed biomarkers of response to TNFi even when they are supported by very low p values. The results also emphasize the requirement of independent replication for validation, and the need to search protocols that could increase reproducibility of the biomarkers of response to TNFi.


Assuntos
Antirreumáticos/uso terapêutico , Artrite Reumatoide/tratamento farmacológico , Artrite Reumatoide/genética , Marcadores Genéticos/genética , Fator de Necrose Tumoral alfa/antagonistas & inibidores , Feminino , Genótipo , Humanos , Masculino , Pessoa de Meia-Idade , Reprodutibilidade dos Testes
9.
Clin Exp Rheumatol ; 36(1): 110-114, 2018 Jan-Feb.
Artigo em Inglês | MEDLINE | ID: mdl-28980904

RESUMO

OBJECTIVES: To investigate the association between serum golimumab (GLM) trough levels, clinical disease activity and treatment response during the first year of therapy in patients with axial spondyloarthritis (axSpA), as well as determining an optimal concentration range of GLM in axSpA. METHODS: This was an observational prospective study including 49 patients with axSpA monitored during 52 weeks (W52). Serum GLM trough levels were measured by capture ELISA and antidrug antibodies by bridging ELISA at baseline, W24 and W52. Disease activity was assessed by the Ankylosing Spondylitis Disease Activity Score (ASDAS) and clinical improvement by ΔASDAS. The association between serum GLM trough levels and disease activity was assessed using univariable and multivariable regression. In case of drop-out or missing data before W52, the last observation carried forward (LOCF) was performed. ASDAS values and GLM levels at W24 were available for 42 patients and 38 patients at W52. RESULTS: In the univariable analyses, serum GLM trough levels were inversely associated with ASDAS at W24 (n=42, r =-0.445; p<0.01), at W52 (n=38, r=-0.330; p<0.05) and W52LOCF (n=49, r=-0.309; p<0.05). In the multivariable analysis, this significant association remained. Serum trough GLM levels above the 0.7-1.4mg/L range did not contribute to additional clinical improvement. CONCLUSIONS: In patients with axSpA, serum GLM trough levels are associated with disease activity during the first year of treatment. A concentration range of 0.7-1.4mg/L appears to be useful to achieve clinical response to GLM.


Assuntos
Anticorpos Monoclonais/administração & dosagem , Antirreumáticos/administração & dosagem , Monitoramento de Medicamentos , Espondilite Anquilosante/tratamento farmacológico , Adulto , Anticorpos Monoclonais/sangue , Antirreumáticos/sangue , Artrite Psoriásica/sangue , Artrite Psoriásica/tratamento farmacológico , Distribuição de Qui-Quadrado , Monitoramento de Medicamentos/métodos , Ensaio de Imunoadsorção Enzimática , Feminino , Humanos , Modelos Lineares , Masculino , Pessoa de Meia-Idade , Análise Multivariada , Países Baixos , Valor Preditivo dos Testes , Estudos Prospectivos , Sistema de Registros , Índice de Gravidade de Doença , Espanha , Espondilite Anquilosante/sangue , Espondilite Anquilosante/diagnóstico , Fatores de Tempo , Resultado do Tratamento
10.
Thromb Res ; 162: 38-43, 2018 02.
Artigo em Inglês | MEDLINE | ID: mdl-29274563

RESUMO

OBJECTIVE: IgG and IgM antibodies directed at ß2-glycoprotein I are included in the classification criteria for the antiphospholipid syndrome (APS) while the IgA antibodies against ß2-glycoprotein I (IgA aß2GPI) are not. Conflicting data about the significance of IgA aß2GPI and APS manifestation can be found and more studies are necessary in order to define the diagnostic value of IgA aß2GPI. In the present article, we investigated the possible role of IgA aß2GPI as marker of APS. METHODS: A cohort of 314 patients with APS and systemic autoimmune disease was investigated for the presence of IgA aß2GPI and its association with clinical manifestation of APS. RESULTS: Eighty-nine patients presented IgA aß2GPI, 68 cases associated with others antiphospholipid antibodies (aPL) and in 21 cases being the only aPL present. In primary APS IgA aß2GPI are highly coincidental with other aPL (92,2%) while most of the isolated IgA aß2GPI were present in the SLE group (16/21). No association between IgA aß2GPI and APS manifestations: thrombosis and pregnancy morbidity was found, while a positive association between IgA aß2GPI and the presence of anti-nDNA, anti-RNP, anti-Sm, anti-SSA, anti-SSB antibodies was encountered. CONCLUSION: Our study does not show association between IgA aß2GPI and APS manifestations and does not support the inclusion of IgA aß2GPI as a classification criteria for APS.


Assuntos
Síndrome Antifosfolipídica/imunologia , Imunoglobulina A/imunologia , Trombose/complicações , beta 2-Glicoproteína I/imunologia , Feminino , Humanos , Masculino , Gravidez
11.
Clin Pharmacol ; 9: 101-111, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-29042821

RESUMO

Biopharmaceuticals directed against tumor necrosis factor-alpha, integrins, interleukins, interferons and their receptors have become key agents for the management of inflammatory diseases in the fields of gastroenterology, rheumatology, dermatology and neurology. However, response to these treatments is far from optimal. Therapeutic failure has been attributed in part to inadequate serum concentrations of the drug and the formation of antidrug antibodies (ADA). Therapeutic drug monitoring (TDM) based on drug concentrations and ADA represents a pharmacologically sound tool for guiding dosage adjustments to optimize exposure. Although becoming standard practice in tertiary care centers, the widespread accessibility and recognition of TDM is hindered by several hurdles, including a lack of education of health care providers on TDM. In this paper, the Monitoring of monoclonal Antibodies Group in Europe (MAGE) provides an introduction on the fundamental principles of the concept of TDM, aiming to educate clinicians and assist them in the process of implementing TDM of anti-inflammatory biopharmaceuticals.

12.
Sci Rep ; 7(1): 12023, 2017 Sep 20.
Artigo em Inglês | MEDLINE | ID: mdl-28931886

RESUMO

Classification of patients with rheumatoid arthritis (RA) as quickly as possible improves their prognosis. This reason motivates specially dedicated early arthritis (EA) clinics. Here, we have used 1062 EA patients with two years of follow-up to explore the value of anti-carbamylated protein (anti-CarP) antibodies, a new type of RA specific autoantibodies, for classification. Specifically, we aimed to determine whether the addition of anti-CarP antibodies to IgM rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies, which are helpful in RA classification, improves it or not. Our analysis showed that incorporation of the anti-CarP antibodies to combinations of the other two antibodies (all joint by the OR Boolean operator) produces a modest increase in sensitivity (2.2% higher), at the cost of decreased specificity (8.1% lower). The cost-benefit ratio was more favorable in the patients lacking the other autoantibodies. However, it did not improve by considering different titer levels of the anti-CarP antibodies, or after exhaustively exploring other antibody combinations. Therefore, the place in RA classification of these antibodies is questionable in the context of current treatments and biomarkers. This conclusion does not exclude their potential value for stratifying patients in joint damage, disease activity, disability, or mortality categories.

13.
Ther Drug Monit ; 39(4): 370-378, 2017 08.
Artigo em Inglês | MEDLINE | ID: mdl-28703718

RESUMO

Biopharmaceuticals have recently emerged as effective treatments for refractory pediatric autoimmune conditions. Several reports have shown a relationship between drug concentration, antidrug antibodies, and clinical response in these patients, strongly suggesting the potential interest, usefulness, and reliability of therapeutic drug monitoring (TDM) in children. This article reviews the current state of research in juvenile idiopathic arthritis, pediatric inflammatory bowel disease, and pediatric psoriasis from a TDM point of view. There is a remarkable lack of evidence-based data in pediatric patients, which is reflected throughout the article. Most investigations of TDM are focused on research of tumor necrosis factor alpha antagonists in inflammatory bowel disease, albeit preliminary publications are emerging from pediatric rheumatologists and dermatologists. To date, immunogenicity has been a primary concern, particularly regarding infliximab and adalimumab therapy in children, as it may lead to a loss of therapeutic response. Preliminary investigations show that adjusting the dose according to blood drug concentrations improves disease outcomes by overcoming antidrug antibodies, suggesting a crucial role for TDM. Patients who receive other drugs, such as etanercept, abatacept, or tocilizumab, could benefit from TDM because dosage can be optimized by adjusting it to the minimum effective dose.


Assuntos
Anticorpos Monoclonais Humanizados/uso terapêutico , Produtos Biológicos/uso terapêutico , Monitoramento de Medicamentos/métodos , Pediatria/métodos , Anticorpos Monoclonais Humanizados/sangue , Antirreumáticos/sangue , Antirreumáticos/uso terapêutico , Artrite Reumatoide/sangue , Artrite Reumatoide/tratamento farmacológico , Produtos Biológicos/sangue , Biofarmácia/métodos , Criança , Humanos , Doenças Inflamatórias Intestinais/sangue , Doenças Inflamatórias Intestinais/tratamento farmacológico , Psoríase/sangue , Psoríase/tratamento farmacológico
14.
Ther Drug Monit ; 39(4): 339-343, 2017 08.
Artigo em Inglês | MEDLINE | ID: mdl-28486309

RESUMO

Biopharmaceuticals bring together a number of specific characteristics as compared with other drugs. However, as it is done for most drugs, an individual adjustment of their dose may be necessary. Similar to "chemical" drugs, biopharmaceuticals used in immunoinflammatory diseases have a rather narrow therapeutic range, lack good early clinical or biological marker of response, have variable pharmacokinetics, and their serum concentrations are most often related with response. Monoclonal antibodies have additional specific sources of pharmacokinetic variability. Low concentrations may increase the risks of immunization, plasmapheresis may increase their elimination, and subcutaneous formulations may be associated with decreased adherence. For all these reasons, pharmacokinetic therapeutic drug monitoring may be useful. However, few randomized controlled therapeutic drug monitoring studies have been published. For monoclonal antibodies, a precise definition of the therapeutic concentrations is challenging because of the interindividual variability in their concentration-effect relationship.


Assuntos
Anti-Inflamatórios/sangue , Anti-Inflamatórios/uso terapêutico , Anticorpos Monoclonais/sangue , Anticorpos Monoclonais/uso terapêutico , Biofarmácia/métodos , Animais , Anticorpos Monoclonais/farmacologia , Monitoramento de Medicamentos/métodos , Humanos , Inflamação/sangue , Inflamação/tratamento farmacológico , Mediadores da Inflamação/antagonistas & inibidores , Mediadores da Inflamação/sangue
15.
Ann Rheum Dis ; 76(7): 1285-1288, 2017 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-28455438

RESUMO

OBJECTIVES: Controversy exists on the role of IgE antidrug antibodies (IgE-ADA) in infusion reactions (IR) on infliximab treatment, partly due to the lack of a positive control used for assay validation. We sought to (1) develop a robust assay to measure IgE-ADA, including a positive control, (2) determine the association between IgE-ADA and IR and (3) determine the incidence of IgE-ADA in infliximab treated patients. METHODS: A recombinant human IgE anti-infliximab monoclonal antibody was developed as standard and positive control. With this antibody, we set up a novel robust assay to measure IgE-ADA. IgE-ADA was determined in three retrospective cohorts (n=159) containing IR+ (n=37) and IR- (n=39), and longitudinal sera of 83 spondyloarthritis. RESULTS: IgE-ADA was found in 0/39 IR-, whereas 4/37 (11%) IR+ showed low levels (0.1-0.3 IU/mL, below the 0.35 IU/mL threshold associated with elevated risk of allergic symptoms). All patients who were IgE-ADA positive also had (very) high IgG-ADA levels. The incidence of IgE-ADA in patients with infliximab-treated spondyloarthritis was estimated at less than approximately 1%. CONCLUSIONS: IgE-ADA is rarely detected in infliximab-treated patients. Moreover, the absence of IgE-ADA in the majority of IR+ patients suggests that IgE-ADA is not associated with infusion reactions.


Assuntos
Anticorpos/imunologia , Antirreumáticos/efeitos adversos , Dispneia/induzido quimicamente , Rubor/induzido quimicamente , Imunoglobulina E/imunologia , Infliximab/efeitos adversos , Infusões Intravenosas/efeitos adversos , Prurido/induzido quimicamente , Artrite Reumatoide/tratamento farmacológico , Estudos de Coortes , Dispneia/imunologia , Rubor/imunologia , Humanos , Infliximab/imunologia , Prurido/imunologia , Espondilartrite/tratamento farmacológico , Espondiloartropatias/tratamento farmacológico , Urticária/induzido quimicamente
16.
J Dermatolog Treat ; 28(7): 606-612, 2017 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-28274164

RESUMO

PURPOSE: This study was conducted to examine the relationship between loss of clinical response to anti-tumor necrosis factor (TNF) therapy and the production of anti-drug antibodies (ADAs) and the potential effects of biologic immunogenicity. MATERIALS AND METHODS: This observational, non-interventional, cross-sectional study included patients with moderate-to-severe plaque psoriasis and secondary failure of adalimumab, etanercept and infliximab who were seen in the clinical practice setting. Clinical data and blood samples were collected after patient enrollment at the time that next doses of anti-TNF therapy were scheduled. ADA and serum drug concentrations were detected at a central reference laboratory using ELISA. RESULTS: Among 137 enrolled patients, ADA were identified in 31/65 (48%), 0/47 and 8/19 (42%) of patients treated with adalimumab, etanercept and infliximab, respectively. The presence of ADA was associated with a slightly worse clinical response in adalimumab-treated patients (Physician Global Assessment score: 3.7 vs. 3.2, ADA-positive vs. ADA-negative patients [p < .05]; correlation between serum ADA titer and body surface area: r = .292 [p = .019]). Concomitant DMARDs were not associated with anti-TNF immunogenicity in any treatment group. CONCLUSIONS: Additional evidence is needed from studies of anti-TNF therapy in psoriasis for clinicians to gain a better understanding of the impact of immunogenicity on clinical response.


Assuntos
Adalimumab/uso terapêutico , Antirreumáticos/uso terapêutico , Psoríase/tratamento farmacológico , Fator de Necrose Tumoral alfa/imunologia , Adalimumab/sangue , Adulto , Anticorpos Antinucleares/sangue , Antirreumáticos/sangue , Estudos Transversais , Etanercepte/sangue , Etanercepte/uso terapêutico , Feminino , Humanos , Imunoterapia , Infliximab/sangue , Infliximab/uso terapêutico , Masculino , Pessoa de Meia-Idade , Psoríase/patologia , Índice de Gravidade de Doença , Resultado do Tratamento
18.
Sci Rep ; 6: 31979, 2016 08 18.
Artigo em Inglês | MEDLINE | ID: mdl-27534721

RESUMO

Association between elevated C-reactive protein (CRP) serum levels and subclinical atherosclerosis and cardiovascular (CV) events was described in rheumatoid arthritis (RA). CRP, HNF1A, LEPR, GCKR, NLRP3, IL1F10, PPP1R3B, ASCL1, HNF4A and SALL1 exert an influence on elevated CRP serum levels in non-rheumatic Caucasians. Consequently, we evaluated the potential role of these genes in the development of CV events and subclinical atherosclerosis in RA patients. Three tag CRP polymorphisms and HNF1A, LEPR, GCKR, NLRP3, IL1F10, PPP1R3B, ASCL1, HNF4A and SALL1 were genotyped in 2,313 Spanish patients by TaqMan. Subclinical atherosclerosis was determined in 1,298 of them by carotid ultrasonography (by assessment of carotid intima-media thickness-cIMT-and presence/absence of carotid plaques). CRP serum levels at diagnosis and at the time of carotid ultrasonography were measured in 1,662 and 1,193 patients, respectively, by immunoturbidimetry. Interestingly, a relationship between CRP and CRP serum levels at diagnosis and at the time of the carotid ultrasonography was disclosed. However, no statistically significant differences were found when CRP, HNF1A, LEPR, GCKR, NLRP3, IL1F10, PPP1R3B, ASCL1, HNF4A and SALL1 were evaluated according to the presence/absence of CV events, carotid plaques and cIMT after adjustment. Our results do not confirm an association between these genes and CV disease in RA.


Assuntos
Artrite Reumatoide/sangue , Artrite Reumatoide/genética , Aterosclerose/sangue , Aterosclerose/genética , Proteína C-Reativa/genética , Doenças Cardiovasculares/sangue , Doenças Cardiovasculares/genética , Idoso , Artrite Reumatoide/epidemiologia , Aterosclerose/diagnóstico por imagem , Aterosclerose/epidemiologia , Doenças Cardiovasculares/diagnóstico por imagem , Doenças Cardiovasculares/epidemiologia , Grupo com Ancestrais do Continente Europeu , Feminino , Predisposição Genética para Doença , Genótipo , Humanos , Masculino , Pessoa de Meia-Idade , Polimorfismo Genético , Fatores de Risco
20.
Clin Exp Rheumatol ; 34(4): 655-62, 2016 Jul-Aug.
Artigo em Inglês | MEDLINE | ID: mdl-27214767

RESUMO

OBJECTIVES: The aim of this study is to compare clinical outcomes, incidence of flares and administered drug reduction between rheumatoid arthritis (RA) patients under TNF inhibitors (TNFi) tapering strategy and RA patients on standard regimen. METHODS: Two groups of RA patients on TNFi with DAS28<3.2 were compared: the tapering group (TG: 67 pts from Spain) and the control group with standard therapy regimen (CG: 77 pts from the Netherlands). DAS28 was measured at different time points: visit 0 (prior starting TNFi), visit 1 (prior to start tapering in TG and with DAS28<3.2 in TG and CG), visit 2 (6 months after visit 1), visit 3 (1 year after visit 1), visit 4 (the last visit available after visit 1) and visit-flare (visit with the worst flare between visit 1 and visit 4). RESULTS: Despite the reduction of administered drug at visit 4 in the TG (interval elongation of 32.8% in infliximab, 52.9% in adalimumab and 52.6% in etanercept), the DAS28 remained similar between groups at the end of the study (DAS28: 2.7±0.9 in TG vs. 2.5±1 in CG, p=0.1). No differences were seen in the number of patients with flares [26/67 (38.9%) in the TG vs. 30/77 (39%) in the CG, p=0.324] and only nineteen out of 136 patients (14%) had anti-drug antibodies at the end of the study. CONCLUSIONS: The tapering strategy of TNFi in RA patients result in a reduction of the drug administered, while the disease control is not worse than patients on the standard regimen.


Assuntos
Antirreumáticos/administração & dosagem , Artrite Reumatoide/tratamento farmacológico , Produtos Biológicos/administração & dosagem , Fator de Necrose Tumoral alfa/antagonistas & inibidores , Idoso , Antirreumáticos/sangue , Artrite Reumatoide/diagnóstico , Artrite Reumatoide/imunologia , Produtos Biológicos/sangue , Avaliação da Deficiência , Esquema de Medicação , Monitoramento de Medicamentos , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Países Baixos , Recidiva , Indução de Remissão , Estudos Retrospectivos , Índice de Gravidade de Doença , Espanha , Fatores de Tempo , Resultado do Tratamento , Fator de Necrose Tumoral alfa/imunologia
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