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.
Our results do not support the notion that noninherited maternal antigens have a role in susceptibility to RA in the offspring.
BackgroundThe majority of patients with axial spondyloarthritis (SpA) response to anti-TNF therapy. However, discontinuation of this therapy due to different reasons is still a relevant problem. Currently, there is not enough data to know exactly which is the prevalence and causes of interruption of anti-TNF therapies in clinical practice.ObjectivesFirst, to evaluate the frequency and causes of discontinuating adalimumab or infliximab as the first anti-TNF in patients with axial SpA in clinical practice. Second, to investigate the influence of anti-drug antibodies (ADA) on these causes.MethodsA total of 326 patients with axial SpA who had received adalimumab (34%) or infliximab (66%) as a first anti-TNF therapy were included in this retrospective, observational study performed in a tertiary hospital. Disease activity (BASDAI, ASDAS, CRP and ESR) was measured before starting anti-TNF therapy, after 6 months and when interrupting the therapy to assess properly whether the reason for discontinuation was primary or secondary failure. Serum drug levels and/or ADA were measured at 6 months visit and at the end of anti-TNF treatment.ResultsA total of 99 (30.4%) patients discontinued treatment. Mean (SD) under anti-TNF therapy until discontinuation was 2.5 (2.9) years. Characteristics of these patients when initiating anti-TNF therapy are shown in Table 1. The reason to interrupt treatment was: primary failure in 22.2%, secondary failure in 36.4%, side effects 32.3%), and other reasons in 9.1%. Serum drug levels and ADA were available in 83 patients. In most patients with ADA positive (14/17), the reason for discontinuation was secondary failure. Out of those patients who discontinued due to secondary failure, 38.9% had ADA positive.ConclusionsIn our cohort of patients with axial SpA treated with adalimumab/infliximab, 30% of patients discontinued anti-TNF therapy. The main reason to discontinue treatment was secondary failure, which was related to the presence of ADA in almost 40% of patients.Disclosure of InterestE. Moral Grant/research support from: Funded by an unrestricted medical grant from Pfizer, C. Plasencia: None declared, V. Navarro-Compán: None declared, D. Pascual Salcedo: None declared, T. Jurado: None declared, C. Tornero: None declared, A. Pierens: None declared, M. B. Paredes: None declared, P. Bogas: None declared, I. Monjo: None declared, E. Martin Mola: None declared, A. Balsa: None declared
Background:There is great interest in the identification of prognostic biomarkers informing early therapeutic decisions for the improvement of rheumatoid arthritis (RA) evolution. Promising results in early arthritis (EA) patients indicate the anti-carbamylated protein antibodies (ACarPA) may serve this function. In effect, they are associated with high baseline disease activity and, in our patients, with less improvement in the first 6-months of follow-up. This association was independent of sex, age at diagnosis, time since symptoms onset, smoking and the year of onset. However, the influence of the treatment has not been explored yet.Objectives:We aimed to explore the influence of the initial treatment on the persistent high disease activity associated with the presence of ACarPA in EA patients.Methods:Samples were obtained at the first visit of two EA cohorts from Hospital Universitario La Paz and Hospital Universitario La Princesa, which recruit patients within one year from the clinical onset. Information on the initial treatment and the disease activity at the baseline and at 6-months of follow-up was available from 546 patients. Treatment was categorized according to the use of corticosteroids, methotrexate (MTX) and other DMARDs, and considering changes in the first 6 months. In addition, MTX dose was considered either quantitatively or as a dichotomous variable (≥ 12.5 mg and < 12.5 mg). Main effects general linear regression was used for analysis, including the treatment and the other confounders as covariates.Results:A large fraction (83%) of the EA patients received specific treatment from the initial visit. It comprised DMARD (50.1%), corticosteroids (10.6%), or a combination of both (39.3%). The most common DMARD was MTX (82.2%), whereas less frequently used medications included sulfasalazine (5.4%), leflunomide (3.2%), hydroxychloroquine (8.1%) and other (1.0%). The 35.5% of the treated patients maintained the treatment during the 6-month follow-up. The presence of ACarPA was associated with a 0.45 higher mean baseline DAS28 and with less decrease of DAS28 (ΔDAS28) from the baseline to 6 months of follow-up (β = 0.08, p = 0.016), as already communicated. This latter association persisted without modification after accounting for the initial treatment (DMARD, corticosteroids, and changes in treatment). In addition, it was independent of the consideration of all DMARDs in a single group, or separated into two categories: MTX and the other. Similarly, the association was independent on MTX dose, defined both as a categorical or a quantitative variable.Conclusion:The association of ACarPA with a persistently increased disease activity in EA patients is independent of the initial treatment. These results reinforce the possibility that ACarPA can be useful as prognostic biomarkers for the first 6 months of evolution and indicate the need for personalized management of the patients carrying ACarPA.Acknowledgement:Supported by grants PI17/01606 and RD16/0012/0014 of the Instituto de Salud Carlos III (Spain...
Background Spondyloarthropathies (SpA) include a heterogeneous group of rheumatic diseases that mainly affect the axial skeleton and entheses. Despite the anti-TNF therapy has been demonstrated effective in SpA patients, about 30% of them develop primary or secondary inefficacy. In rheumatoid arthritis (RA) has been shown that the development of antibodies (Ab) against the first anti-TNF determines the clinical response to a second anti-TNF. Objectives To assess if the effectiveness of second anti-TNF therapy is associated with the development of Ab against the first anti-TNF in SpA patients switching to a second anti-TNF. Methods We studied 33 SpA patients treated with a second anti-TNF after having an inadequate response to the first anti-TNF therapy. The diagnoses were: 23 (69.7%) Ankylosing Spondylitis (AS), 6 (18.2%) undifferentiated SpA, 2 (6.1%) psoriatic SpA, 1 (3%) SpA associated with inflammatory bowel disease and 1 (3%) reactive SpA. Clinical activity was measured by ASDAS-CRP at baseline to the 1st and 2nd anti-TNF treatment and after 6 months of the switching. Clinical improvement was assessed by the Delta-ASDAS (clinically important improvement ≥1.1). Drug through levels and anti-drug Ab were measured by ELISA at the end of the fist anti-TNF treatment. Statistical analysis was performed using SPSS 11.0. Results Our cohort included 33 patients, 18 (54.5%) male, mean age of 50.09±10 years and 21 (63.6%) HLA B27 positive. All of them were initially treated with an anti-TNF: 14 (42.4%) with infliximab (Ifx), 3 (9.1%) with adalimumab (Ada), 16 (48.5%) with etanercept (Eta). Nine out of 33 (27.3%) developed anti-drug Ab [8 anti-Ifx Ab (ATI) and 1 anti-Ada Ab (AAA)]. All patients switched to a 2nd anti-TNF, due to inefficacy: 7 (21.2%) to Ifx, 16 (48.5%) to Ada, 5 (15.2%) to Eta, 5 (15.2%) to golimumab. Clinical activity (ASDAS-CRP) was not different at baseline between first and second anti-TNF therapy (3.45±0.99 vs 3.22±0.96, p=0.24). No differences were observed between patients who developed or not anti-drug Ab at baseline to the first (3.34±0.87 with Ab vs 3.50±1.04 without Ab, p=0.93) and second (2.99±0.95 with Ab vs 3.31±0.96 without Ab, p=0.37) anti-TNF treatment. After 6 months of switching to a second anti-TNF, patients who had developed anti-drug Ab had lower clinical activity (ASDAS-CRP) than patients without anti-drug Ab (1.76±0.98 with Ab vs 2.79±1.10 without Ab, p=0.021). Moreover clinical improvement was higher in patients with anti-drug Ab (1.23±1.22 with Ab vs 0.52±1.08 without Ab, p=0.063). Most patients who had clinically important improvement had anti-drug Ab before switching [60% (6/10) vs 40% (4/10), p=0.010]. Conclusions Same as in RA, in SpA, the failure to a first anti-TNF therapy associated with the development of anti-drug Ab predicts a better clinical response to a second anti-TNF. The study of the immunogenicity in the biological treatment failure helps predict the response to a second biological treatment in SpA. Disclosure of Interest None Declared
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