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In patients with rheumatoid arthritis (RA), the development of antibodies to infliximab (ATI) is associated with poor clinical response. 1 2-7 Nevertheless, there is no plausible explanation for why not all patients with ATI experience high disease activity. Table 1 Total: 11 patients with RA (%) Gender, female n (%) 11 (100) Age, mean (SD) 54.18±13.24 Autoantibodies: RF positive n (%) 9 (81.8) ACPA positive n (%) 9 (81.8) Disease duration (years), mean (SD) 14.20±6.42 Baseline DAS28, mean (SD) 5.45±1.13 Time under Ifx therapy in years, mean (SD) 8.00±2.75 ATI duration in years, mean (SD) 1.1±0.91 Concomitant treatment MTX alone 3 (27.2) OD 1 (9.0) MTX+OD 6 (54.8) Ifx monotherapy 1 (9.0) ACPA, Anticitrullinated protein antibody; ATI, antibodies to infliximab; DAS28, Disease Activity Score 28; Ifx, infliximab; MTX, Methotrexate; OD, Other DMARDs; RF, Rheumatoid Factor.

Background The use of anti-TNF therapy, as Etanercept (Etn), has proven to be effective in patients with rheumatoid arthritis (RA). However, a significant proportion of patients develop clinical inefficacy or adverse effects, resulting in treatment interruption. Recently, it has been reported that Etn serum trough levels are correlated with clinical activity in RA patients, so that, patients with low Eta serum trough levels had a worse clinical response. Objectives To evaluate whether Etn serum trough levels correlate with clinical activity and treatment discontinuation in RA patients treated with Etn. Methods In this ambispective study, 44 RA patients treated with Etn were included. Clinical activity was assessed using the Disease Activity Score 28 (DAS28), clinical improvement by the delta-DAS28 and response to treatment using EULAR criteria at baseline and at 1st, 2nd and > 3rd years of treatment. In every patient Etn was administered subcutaneously at a dose of 50 mg/week and Eta levels were assessed every 6 months by capture ELISA. Blood samples were obtained up to 24 hours before administration of Etn. Statistical analysis was performed using SPSS 11.0. For the statistical study, serum trough levels were divided into low levels (LL<1000 ng/ml) and high (HL ≥ 1000 ng/ml). Results Of the 44 RA patients treated with Etn, 34 (77.2%) were women. The mean age was 60.2 ± 12.7 years and the mean disease duration was 16.1 ± 9.9 years. The baseline clinical activity (DAS28) was 4.9 ± 1.0 and there were no differences between patients who later developed Etn LL and HL (5.3 ± 1.5 with LL vs 4.9 ± 0.8 with HL, p = 0.287). Clinical activity (DAS28) was higher in patients with Etn LL at all studied time points (4.3 ± 0.9 with LL vs 2.6 ± 0.6 with HL at 1st year, p = 0.003; 4.3 ± 1.2 with LL vs 2.5 ± 0.7 with HL at 2nd year, p = 0.002; 4.5 ± 0.9 with LL vs 2.7 ± 0.6 with HL at > 3rd year; p = 0.000). Clinical improvement (delta-DAS28) was lower in patients with Etn LL throughout the study (-0.7 ± 1.1 with LL vs 2.1 ± 0.9 with HL at 1 year, p = 0.006; 0.8 ± 2.1 with LL vs 2.4 ± 0.9 with HL at 2nd year, p = 0.036; 0.86 ± 1.4 with LL vs 2.2 ± 0.9 with HL at > 3rd year, p = 0.003). The drop-out of biological therapy during the study was more frequent in patients with Etn LL [7/13 (53.8%) vs 1/31 (3.2%) with HL, p = 0.000]. Etn serum trough levels (Mdn, P25-P75) were higher in patients with EULAR good (GR) and moderate response (MR) than in non-responders (NR) patients [2287.0; 1488.7-2625.0 classified as GR vs 821.5; 500.0-1143.0 with MR vs. 16.0; 16.0-16.0 with NR at 1st year, p = 0.026; 1379.2; 1190.5-3347.0 with GR vs 2225.0; 2225.0-2225.0 with MR vs 352.0; 0.0-973.0 with NR at 2nd year, p=0.154; 2300.0; 1812.0-3312.0 with GR vs 1274.0; 700.5-2605.0 with MR vs 37.0; 15.0-1200.0 with NR at >3rd year, p=0.007]. Conclusions The presence of low Etn serum trough levels correlates with a poor clinical response to Etn and a higher frequency of treatment discontinuation. However, patients classified as responders have higher Etn serum trough levels and a low frequency of treatment discontinuation. Disclosure of Interest None Declared

Background Biological therapy (BT) is very effective in patients with rheumatoid arthritis (RA). Although there are tools to measure treatment response, they have limitations making necessary to get more objective parameters to improve clinical evaluation. The immunogenicity of anti-TNF therapy has been associated with lack of efficacy, side effects and decreased survival. In our hospital, the monitoring of immunogenicity is considered as an additional tool to clinical practice since 2010, helping in treatment decisions as switching medication, dose reduction or even discontinuation. Objectives To asses the benefit of using the immunogenicity as a complementary tool in clinical practice of RA patients and to analyse differences in outcome measures before and after the use of immunogenicity. Methods We included 134 RA patients who started a 1st biologicbetween the years 2005-2012. The patients were divided into two time periods to analyze differences in clinical management after to monitor the BT immunogenicity: 1st period (1P) from 2005 to 2009 with 89 patients and 2nd period (2P) from 2010 to 2012 with 45 patients. The used drugs were infliximab, adalimumab, etanercept, rituximab, tocilizumab, abatacept and certolizumab. The clinical activity was measured by DAS28 and the clinical improvemet by delta-DAS28. The drug and anti-drug antibodies (ADA) serum levels were measured by ELISA. Statistical analysis was performed using SPSS 11.0. Results A similar control of disease activity is achieved in both periods, but in the 2P, where in addition to the usual measures we use immunogenicity monitoring, shows that we are more cost-effective, taking decisions earlier and more accurate. These data suggest that immunogenicity can help to improve and personalize the clinical manage of patients treated with biologicals. Conclusions A similar control of disease activity is achieved in both periods, but in the 2P, where in addition to the usual measures we use immunogenicity monitoring, shows that we are more cost-effective, taking decisions earlier and more accurate. These data suggest that immunogenicity can help to improve and personalize the clinical manage of patients treated with biologicals. Disclosure of Interest None Declared

Background The anti-TNF therapy has been a great progress in RA patients treatment. However, a proportion of patients develop primary inefficacy or loss of response, resulting in switching or treatment discontinuation. Recent studies correlate the antidrug antibodies (ADA) development with loss of efficacy. Objectives To asses in RA patients treated with infliximab (Ifx) or adalimumab (Ada) whether ADA development influences on the clinical efficacy and treatment duration. Methods We studied ambispectively 174 RA patients from La Paz University Hospital who received Ifx or Ada between years 2000-2012, both in combination with synthetic DMARDs or in monotherapy. The assessment of disease activity was performed by Disease Activity Score 28 (DAS28) and clinical improvement by delta-DAS28. Measurements were performed at baseline, 1, 2 and ≥ 3 years under the biological therapy (BT). ADA and drug levels were measured by ELISA. Statistical analysis was performed using SPSS 11.0. Results Of the 174 patients, 140 (80.5%) were women. The mean age was 57 ± 13.2 years and the disease duration was 14.7 ± 8.0 years. 128 patients (73.6%) were RF positive. The mean duration on BT was 5.0 ± 3.0 years. One hundred fifty patients (86.2%) received methotrexate, 98 other DMARDs (56.3%) and 11 (6.3%) were in monotherapy. The mean DAS28 at baseline was 5.28 ± 1.26 and there was no significant differences between DAS28 at baseline in patients with or without ADA ( 5,28±1,47 ADA+ vs 5,25±1,19 ADA-, p=0,918). Along the study, 62 patients (35.6%) developed ADA (47/105 patients (44.8%) to Ifx and 15/69 patients (21.7%) to Ada, p = 0.002). Ninety six (55.2%) patients dropped out the BT and this was more frequent in ADA positive patients [49/62 (79.0%) ADA+ vs. 47/112 (41.9%) ADA-, p <0.00001]. Most patients who discontinued by inefficacy had ADA [25/39 (64.1%) ADA+ vs 14/39 (35.9%) ADA-, p = 0.039]. Patients with ADA were more active in all studied point (at 1st year: 4.69 ± 1.15 ADA+ vs 3.43 ± 1.22 ADA-, p<0.0001; at 2nd year: 3.96 ± 1.40 ADA+ vs 3.08 ± 1.09 ADA-, p= 0.015; at 3rd year: 4.34 ± 1.26 ADA+ vs 3.21 ± 1.56 ADA-, p = 0.001). The clinical improvement was lower in ADA positive patients along this work (at 1st year: 0.94 ± 1.06 ADA+ vs 1.63 ± 1.32 ADA-, p = 0.045; at 2nd year: 0.72 ± 1,05 ADA+ vs. 1.83 ± 1.59 ADA-, p =0.021; at 3rd year: 0.44 ± 1.26 ADA+ vs 2,02 ± 1.87 ADA-, p<0.0001). Conclusions The ADA development in RA patients treated with Ifx or Ada is correlated with a clinical inefficacy and with the therapy survival, resulting in an earlier therapy discontinuation. Disclosure of Interest None Declared

Background The anti-TNF therapy is an effective treatment in RA patients, however a considerable percentage of patients develop clinical inefficacy (primary or secondary); part of which can be explained by the development of antibodies to infliximab (ATI). In some patients, a dose increase is often used to achieve a clinical improvement, mainly in patients with secondary inefficacy. However, there is no evidence that demonstrates if dose escalation is a good therapeutic option. Objectives To assess whether increasing the infliximab (Ifx) dose is an effective therapeutic option in RA patients who develop clinical inefficacy. Methods The present study included 36 RA patients treated since 2000 with Ifx at La Paz University Hospital, in whom a Ifx dose increase was implemented due to inefficacy [23/36 (64%) primary non-responders and 13/36 (36%) secondary non-responders]. All patients started to receive Ifx at 3 mg/kg i.v. at standard schedule. A therapeutic increase was defined as: Ifx dose higher than 3 mg/kg i.v. (until maximum of 5 mg/kg) or interval time between infusion 6-7 weeks. The clinical activity was measured by the Disease Activity Score 28 (DAS28) at baseline, before starting the dose escalation, at 6 months and at 1 year after the dose increase. The drug and ATI levels were measured by a capture and bridging ELISA, respectively. Statistical analysis was made using SPSS system 11.0. Results Thirty one out of 36 patients (86.1%) were female, with a mean age of 58±13.6 years. The disease duration was 19.2±10.5 years and the time under Ifx therapy was 6.6±3.8 years. Most patients received concomittant therapy with DMARDs [15 (41.7%) methotrexate, 22 (41.7%) other DMARDs and 8 (22.2%) in monotherapy] and 13 (38.2%) received prednisone. All patients were active (DAS28) at baseline and before starting the dose increase (5.4±1.0 at baseline and 4.2±1.2 just before dose escalation). ATI were detected in 13/34 (38.2%) patients at the moment of decision to increase (in 2 patients ATI were already present in the first available sample) and only 2 (5.5%) patients became negative after dose increase. The Ifx increment did not produce significant improvement in clinical activity (DAS28) in RA patients, independently on ATI status [ATI-negative: 4.25±1.4 at pre-increase vs 3.9 ±1.0 at 6 months after increase (p=0.311) and 4.04±1.1 vs 4.03 ±1.3 at 1 year after increase (p=0.970); ATI-positive: 4.09±0.9 at pre-increase vs 4.1±1.3 at 6 months after increase (p=0.945) 3.7 ±0.7 vs 3.0±0.8 at 1 year after increase (p=0.110)]. A total of 26 (76.5%) patients discontinued the Ifx therapy, not identifying differences between ATI-positive patients (15/21, 71.4%) and ATI-negative patients (11/13, 84.6%), p=0.378. Conclusions Infliximab dose escalation does not seem to be an effective therapeutic option in RA patients who develop primary and secondary inefficacy. Further studies are necessary to confirm these results. Disclosure of Interest None Declared

Background In psoriatic arthritis (PsA) with peripheral involvement classical DMARDs refractory, the anti-TNF therapy has proven to be effective. In recent years, there are some publications that demostrate the correlation between clinical activity and the anti-drug antibodies (ADA) development in rheumatic diseases such as rheumatoid arthritis (RA) and spondyloarthritis (SpA). To date, there is no studies that reveals theses findings in PsA patients treated with infliximab (Ifx) and adalimumab (Ada). Objectives To evaluate in PsA patients treated with Ifx and Ada wether the development of ADA correlate with clinical activity and biological treatment discontinuation. Methods We studied 37 patients with PsA treated with Ifx and Ada from La Paz University Hospital. Clinical activity was assessed using the Disease Activity Score 28 (DAS28), clinical improvement by the delta-DAS28 and treatment response by EULAR criteria at baseline, at 6 months, at 1 year and at > 2nd years of treatment. Ifx and Ada were administred at standard therapeutic schedule. Serum drug and ADA levels were measured by ELISA. Statistical analysis was performed using SPSS 11.0. Results Of the total of patients, 24/37 (64.9%) were treated with Ifx and 13/37 (35.1%) with Ada, being female 23 (62.1%). The mean age was 55.1 ± 12.3 years and the mean disease duration was 14.4 ± 9.9 years. The average time on biological therapy was 4.4 ± 3.2 years. Most patients received concomitantly classical DMARDs [29/37 (78.3%) with DMARDs vs 8/37 (21.7%) in monotherapy]. At baseline, clinical activity (DAS28) was higher in patients who subsequently not developed ADA (5.1 ± 0.9 without ADA vs 13.4 ± 0.6 with ADA, p = 0.021). Clinical activity (DAS28) tended to be higher in patients with ADA at all studied time points (5.4 ± 1.2 with ADA vs 2.8 ± 1.3 without ADA at 6 months, p = 0.007; 4.0 ± 1.2 with ADA vs 3.0 ± 1.3 without ADA at 1 year, p = 0.144; 2.9 ± 1.3 with ADA vs 2.4 ± 0.4 without ADA a> 2nd year, p = 0.169). Clinical improvement (delta-DAS28) was lower in patients with ADA throughout the study (-1.0 ± 1.6 with ADA vs 2.0 ± 1.4 without ADA at 6 months, p = 0.006, 0.3 ± 1.8 with ADA vs 2.1 ± 1.5 without ADA at 1 year, p = 0.052; 0.9 ± 1.5 with ADA vs 2.7 ± 0.8 without ADA a> 2nd year, p = 0.007). Patients without ADA were classified as responders more frequently based on criteria EULAR [2/5 (40%) with ADA vs. 27/30 (90%) without ADA, p = 0.006]. The median time to drug discontinuation was lower in patients with ADA (4.83 ± 1.6 years with ADA vs 7.93 ± 1.4 years without ADA, p = 0.061). The dose increase was more frequent in patients with ADA [3/6 (50%) with ADA vs 4/31 (12.9%) without ADA, p = 0.053], and in contrast, in patients without ADA was more often performed dose decrease of anti-TNF therapy [0/6 (0%) with ADA vs 15/31 (48.3%) without ADA, p = 0.053]. Conclusions The development of ADA correlates with poorer clinical response and more frequent treatment discontinuation in PsA patients in long-term treatment with Ifx and Ada. Disclosure of Interest None Declared

Background Limited data is currently available regarding the pharmacokinetics (PK) and –dynamics (PD) of tocilizumab (TCZ) in daily clinical practice. Objectives To assess the relationship between TCZ levels and clinical response in rheumatoid arthritis (RA) patients. Methods Observational cohort study of 46 consecutive RA patients treated with TCZ 8 mg/kg intravenously once every 4 weeks in the Netherlands (n=25) and Spain (n=21), monitored during 48 weeks. Samples and clinical data were collected at least at baseline, week (w) 24 and 48. TCZ trough levels and titres of anti-drug antibodies (ADA) against TCZ were determined using an ELISA and an Antigen Binding Test (ABT), respectively. Samples which were not trough level were excluded. Disease activity was assessed using the Disease Activity Score of 28 joints (DAS28) and response was defined as a DAS28 remission (DAS28 score <2.6). Values are reported in mean ± SD or median (IQR). Results At baseline patients had a DAS28 score of 5.5±1.4 and 8 patients were biological naive. Duration of follow-up varied between 12 to 48 weeks and 15 patients discontinued TCZ treatment before w48. At w24, 40% of the patients were in remission and at w48 44%. TCZ levels varied widely among patients, at w24 the median TCZ level (mg/L) was 9.6 (3.6-16.7). Figure 1 shows that patients with very low TCZ levels at w24, despite a dosage of 8 mg/kg per 4 weeks, had not improved (ΔDAS28) compared to baseline. Moreover, some patients had high TCZ levels without additional clinical benefit. No ADA against TCZ were detected. Non-parametric testing (not corrected for confounders) showed that TCZ levels at w24 (n=37) and w48 (n=26) were significantly higher in responders compared to non-responders, respectively, 20 (6.3-31.2) vs 6.9 (0.2-11.6) (p=0.004) and 15.5 (7.9-32.2) vs 6.8 (2.9-12.2) (p=0.025). Conclusions Although TCZ trough levels vary greatly, immunogenicity does not seem to be an important factor in the PK/PD of TCZ. However, it might be possible, that ADA were not detected due to drug interference. Another explanation for the variation of TCZ trough levels could be target-binding. Furthermore, this study shows that TCZ trough levels are associated with clinical outcome in RA and that some patients are currently over- or undertreated with TCZ 8 mg/kg per 4 weeks. Therefore, assessing TCZ levels may help to optimize treatment in patient treated with TCZ. Disclosure of Interest E. Kneepkens: None declared, I. Van Den Oever: None declared, C. Plasencia Grant/research support: Pfizer, D. Salcedo Pascual Grant/research support: Pfizer, Speakers bureau: Pfizer, M. Lopez-Casla: None declared, D. Van Der Kleij: None declared, M. Nurmohamed Consultant for: AbbVie, Roche, Pfizer, MSD, UCB, SOBI and BMS, Speakers bureau: AbbVie, Roche, Pfizer, T. Rispens Speakers bureau: AbbVie, A. Balsa Grant/research support: Pfizer, Speakers bureau: Pfizer, Roche, AbbVie, G. Wolbink Grant/research support: Pfizer, Speakers bureau: Pfizer, Amgen DOI 10.1136/annrheumdis-2014-eular.2915

Background Biological therapies have improved the treatment of Rheumatoid Arthritis (RA) in the last decade. The development of anti-TNF antibodies has been found crucial to drug efficacy and survival. All monoclonal antibodies are immunogenic, whereas the fusion proteins, like Etanercept, have proved to be less immunogenic in several studies. Objectives To assess the survival of 3 anti-TNF agents in a cohort of patients with RA, and to determine if there are differences in the survival of the 3 anti-TNF between patients who develop or not immunogenicity. Methods RA patients, who started Adalimumab (ADA), Infliximab (IFX) or Etanercept (ETN) as first biological treatment in a single center between 2002 to 2010 were included. Clinical and demographic data were collected: sex, age, rheumatoid factor, anti-CCP, disease duration, DMARD co-treatment, DAS28 at baseline, date of start and end of treatment and in the case of ADA and IFX, presence or absence of anti-drug antibodies. No patient with anti-ETN antibodies were identified. The reasons for drug discontinuation were classified as adverse event, administration reaction, inefficacy, remission and other (this included pregnancy, malignancies, lost of follow up, etc). The event was defined as drug discontinuation due to only the first 4 reasons. Cumulative incidence through competitive risk was performed to compare drug survival. Results We studied 177 patients with a mean age of 54,7±14,2 years, 83,1% were women. Out of them, 39% (69) started treatment with IFX, 40,7% (72) with ADA, and 20,3% (36) with ETN. The lowest survival was of IFX with a probability of drug discontinuation of 28,1% at 500 days, and 61,4% at 2000 days (about 5 years), compared to 10,2% at 500 days and 35,5% at 5 years of ADA, and versus 14% at 500 days and 31,5% at 5 years of ETN, which was statistically significant (p=0,0001). Inefficacy was the most common reason for discontinuing IFX and ADA with 32,7% and 31,6% respectively, while 41,2% of patients treated with ETN discontinued treatment for reasons that mainly encompassed pregnancy, malignancies, etc. Of the 69 patients treated with IFX, 43,3% developed anti-IFX antibodies (AIA). Anti-ADA antibodies (AAA) were observed in 15,2% of 72 patients who received ADA. In both drugs was found that drug survival was lower in the presence of anti-drug antibodies, as shown in the following table: Cumulative incidence through competitive risk (probability of drug discontinuation) 500 days 2000 days (5 years aprox.) >3000 days (9 years aprox.) p value Infliximab  No AIA 14,7% 47,6% 52,9% 0,016  With AIA 31,5% 68,5% 86,9% Adalimumab  No AAA 2,5% 11,4% 14,8% 0,006  With AAA 0,0% 57,1% 57,1% When survival was analyzed by subgroups of patients treated with IFX and ADA who had not developed antibodies compared with ETN, IFX still showed the lowest survival (probability of drug discontinuation at 5 years of 47,6%, versus 11,4% of ADA and 31,5% of ETN, p=0,003). Conclusions In our cohort, IFX has proven to be the anti-TNF with the lowest survival, even in patients who do not develop immunogenicity. The survival of ADA was slightly higher than ETN only in patients who did not develop AAA. The development of anti-drug antibodies is a very important factor in the survival of anti-TNF treatment. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.4543

[...]responders had a significantly higher golimumab trough level at 1 year of treatment. [...]the authors wish to thank the technicians of Sanquin Diagnostics Services for performing the assays, and Sanquin Reagents for the preparation of the biotinylated rabbit antigolimumab antibodies.

Background There is strong evidence that correlates the antibodies to infliximab appearance (ATI) with a poor clinical response, but for now sparse literature has demonstrated the predictive value of early serum infliximab (Ifx) levels monitoring with the ADA development Objectives To analize if serum Ifx levels at weeks 2, 6 and 14 can predict the ADA appearance at 6 months and 1 year in rheumatoid arthritis (RA) patients.and to define a predictive cutt-off Methods In this restrospective observational study, 83 RA patients (pts) under Ifx therapy were included. All patients fulfilled the 1987 ACR criteria to be included. The clinical activity was measured by DAS28. The drug and ATI levels were measured at baseline and before each infusion by capture and bridging ELISA, respectively. The data about ATI status were available in 44 patients at 6 months and 42 patients at 1 year. In the statistical study was used receiver-operator characteristics (ROC) analysis to obtain a representative cut-off value for Ifx levels between ATIpositive(+) and negative(−) patients at 6 months and 1 year Results Seventy four out of 83 RA patients were female and most of patients had positive rheumatoid factor (62/83, 74.7%) and ACPA (70/83, 84.3%).The mean of the disease duration was 15.46±8.96 years and the time on biological therapy 5.42±3.49 years. At baseline, all patients had active disease measured by DAS28 (5.49±1.35). Fourteen out of 44 (31.8%)patients were ATI+ at 6 months and 12 out of 42 (28.6%) at 1 year. The area under the curve to predict presence of ATI at 6 months was 0.790 (95%CI 0.624-0.957,p=0.002) at week 2, 0.885 (95%CI 0.766-1.000,p=0.001)at week 6 and 0.966 (95%CI 0.913-1.000,p=0.0001) at week 14. For the predictive value of ATI development at 1 year, the area under the curve was 0.773 (95%CI 0.604-0.942,p=0.002)at week 2, 0.853 (95%CI 0.725-0.982,p=0.001) at week 6 and 0.951 (95%CI 0.877-1.000,p=0.001) at week 14. The cut off of Ifx levels to predict ATI appearance at 6 months and 1 year are shown in Table Cutt off Sensitivity Specificity LR+ ATI status at 6 months  Ifx levels at week 2 26931 ng/ml 59% 88% 5.03  Ifx levels at week 6 9984 ng/ml 70% 94% 11.90  Ifx levels at week 14 392 ng/ml 93% 94% 15.86 ATI status at 1 year  Ifx levels at week 2 26931 ng/ml 57% 86% 4.00  Ifx levels at week 6 9984 ng/ml 68% 90% 7.15  Ifx levels at week 14 890 ng/ml 86% 95% 18.13 Conclusions The early Ifx levels monitoring has a high value to discriminate what RA patients on Ifx therapy will develop ATI during the treatment. These findings can help to know what patients are more likely to develop a secondary inefficacy associated to immunogenicity Disclosure of Interest P.-R. Chamaida Grant/research support: Pfizer, D. Pascual-Salcedo Grant/research support: Pfizer, Speakers bureau: Pfizer, M. Bonilla: None declared, A. Villalba: None declared, M. Lόpez-Casla: None declared, D. Peiteado: None declared, S. García-Carazo: None declared, S. Ramiro: None declared, K. Franco: None declared, D. Cajigas: None declared, E. Martín-Mola Speakers bureau: Pfizer, Roche, Abbvie, UCB, A. Balsa Grant/research support: Pfizer, Speakers bureau: Pfizer, Roche, Abbvie DOI 10.1136/annrheumdis-2014-eular.3237