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Background Discordance between baseline patient’s and evaluator’s global assessment of disease activity is common1 and may reduce the likelihood of remission following tumor necrosis factor inhibitor (TNFi) treatment in patients with psoriatic arthritis (PsA).2 However, the impact of such discordance on retention rates of TNFi in PsA patients remains unexplored. Objectives To explore the impact of discordance, defined as patient’s minus evaluator’s global assessment (ΔPEG), on retention rates and remission rates (DAS28(3)CRP (which does not include patient’s global) and DAS28(4)CRP (which includes patient’s global)) in PsA patients initiating their first TNFi treatment. We used pooled data from the European Spondyloarthritis Research Collaboration (EuroSpA). Methods TNFi naive PsA patients from 11 European registries in EuroSpA were included. Kaplan-Meier analyses were used to estimate TNFi retention rates after 6/12/24 months, with comparison between baseline ΔPEG quartiles using the log rank test, stratified by gender. Remission rates were compared between different ΔPEG quartiles with Chi-square test, stratified by gender. Results A total of 5422 PsA patients were included. Mean (SD) age for women(n=2988)/men(n=2867) were 49.3(12.5)/47.4(11.7) years, disease duration 6.6(7.3)/6.7(7.2) years, median(25-75 percentiles) baseline ΔPEG 17(0-38)/10(0-30) mm. Retention rates and DAS28(4)CRP but not DAS28(3)CRP remission rates were lower for higher quartiles of baseline ΔPEG (table, figure). Conclusion High baseline discordance (ΔPEG) was associated with lower TNFi retention rates and with DAS28(4)CRP but not DAS28(3)CRP remission rates after 6, 12 and 24 months’ follow-up in both male and female PsA patients. The choice of remission criteria in the follow-up of PsA patients may affect important treatment decisions, and may be of particular impact in patients with high baseline ΔPEG. References [1] Lindstrom, et al., J Rheumatol 2015;42:1781-5; 2 Michelsen, et al. Ann Rheum Dis 2016;76:708-11. Acknowledgement Novartis Pharma AG and IQVIA for supporting the EuroSpA collaboration.: Disclosure of Interests Brigitte Michelsen Grant/research support from: Unrestricted grant: Novartis, Consultant for: Novartis, UCB, Lykke Ornbjerg Grant/research support from: Unrestricted grant: Novartis, Heřman Mann Consultant for: Pfizer, Eli Lilly, Sanofi, Speakers bureau: AbbVie, Roche, Pfizer, MSD, Eli Lilly, Sanofi, Joseph Sexton: None declared, Michael Nissen Consultant for: AbbVie, Lilly, Novartis, and Pfizer, Maria Jose Santos: None declared, Dan Nordstrom Grant/research support from: MSD, Pfizer, Consultant for: AbbVie, BMS, MSD, Novartis, Roche, Pfizer, UCB, Speakers bureau: Novartis, UCB, Lennart T.H. Jacobsson Consultant for: LJ has received lecture and consulting fees from Pfizer, Abbvie, Novartis, Eli-Lily and Janssen, Ziga Rotar: None declared, Bjorn Gudbjornsson: None declared, Suleyman Serdar Koca: None declared, Catalin Codreanu: None declared, Manuel Pombo-Suarez: None declared, Irene van der Horst-Bruinsma Grant/research support from: MSD, Pfizer, AbbVie, Consultant for: Abbvie, UCB, MSD, Novartis, Speakers bureau: BMS, AbbVie, Pfizer, MSD, Anne Gitte Loft: None declared, Karel Pavelka: None declared, Eirik kristianslund: None declared, Burkhard Moeller Consultant for: Swissmedic Human Medicines Expert Committee Member (regulatory agency), Elsa Vieira-Sousa Grant/research support from: MSD, Novartis, Anna-Mari Hokkanen: None declared, Ulf Lindstrom: None declared, Matija Tomsic: None declared, Thorvardur Jon Love Consultant for: Received reimbursment from Celgene for speaking about guidelines for the treatment of psoriatic arthritis, Berna Goker: None declared, Ruxandra Ionescu: None declared, Carlos Sanchez-Piedra: None declared, Marleen van de Sande Grant/research support from: van Janssen, Novartis, Eli Lily, Consultant for: Novartis and Abbvie, Gary Macfarlane Grant/research support from: Have received research grants (not current) from Abbvie and Pfizer. Have received research grants (not current) from the British Society for Rheumatology, who received the funds from Abbive, Pfizer and UCB. Have received research grant (current) from the British Society for Rheumatology, who received the funds from Celgene., Florenzo Iannone: None declared, Lise Hyldstrup: None declared, Niels Steen Krogh: None declared, Mikkel Ǿstergaard Grant/research support from: Abbvie, Celgene, Centocor, Merck, Novartis, Consultant for: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis

Background The use of ultrasound (US) as a tool for assessing disease activity in patients with rheumatoid arthritis (RA) has increased in recent years and its value is supported by studies showing that US provides more accurate assessment of joint inflammation than clinical examination at time of diagnosis and in clinical state of remission. Various scoring systems have been proposed for monitoring of synovitis. Among these are the novel consensus-based Global OMERACT-EULAR Synovitis Score (GLOESS) was developed applying the highest score of grey-scale (GS) or Doppler as the final score for the joint. Different joint sets have been proposed for optimal and feasible evaluation of patients with inflammatory arthritis but currently there is no agreement on a specific reduced set of joints that should be evaluated by US to acquire the best information about clinical and subclinical activity when monitoring patients with RA. Objectives To evaluate if synovitis assessment of hands only is enough (testing GS, Doppler and GLOESS sum scores) for assessing changes during treatment in order to increase clinical feasibility of US in daily clinical practice. Methods US and clinical assessment for tender/swollen joint count (TJC/SJC) were performed in 19 patients fulfilling ACR 1987 criteria for RA initiating treatment with TNF inhibitor (TNFi) (week 0), and after 6 and 16 weeks of follow up. Forty-six joints were evaluated by US (sternoclavicular, acromioclavicular, glenohumeral, elbow, wrist, MCP1-5, PIP1-5, hip, knee, ankle and MTP 1-5 bilaterally) using a GE Logiq E9 machine with a linear array transducer. Joint inflammation was graded 0-3 on GS and Colour Doppler (CD) and synovitis was defined as a GS score >1 with or without Doppler score >1. Doppler settings for slow flow was applied according to guidelines. GS, CD and GLOESS sum scores were obtained for the total joint set and different joint subsets: hands as joint set (wrist, 1-5 MCP, 1-5 PIP bilaterally), 28 conventional joints evaluated for DAS and the 9-joint set suggested for the GLOESS (shoulder, elbow, wrist, MCP1 and 4, PIP2, MTP 3 and 5, knee). Data from the different joint sets were analyzed applying Spearman’s correlation coefficient. Results Mean change in GS sum score between week 0 and 16 was of 2.58, 1.35, 1.47 and 1.11 for 46-joint set, hands, 28-joint set and 9-joint set, respectively. Compared to the 46 joint set the GS and CD sums core had a high correlation coefficient (>0.78) for 28 joint set and the hand as joint set for all time points - table 1. The 9 joint set GS sum score had low correlation when compared to the 46 joint set at baseline and during follow up – table 1. GLOESS for the hands performed equally well with a correlation coefficient (>0.70) for all joint sets at all time points – table 1. DAS28-CRP did not correlate with the total joint set or the different joint subsets. Conclusion The present study of patients with RA shows that the US examination of both hands only for assessing disease activity is highly correlated for with the 46-joint evaluation at all time points, both regarding GS and Doppler sum scores. Using hands as a reduced joint set US assessment of inflammation could be an option to increase the feasibility of US in routine clinical practice. Disclosure of Interests Dolores Ramos-Bello: None declared, Hilde Berner Hammer Grant/research support from: AbbVie, Pfizer and Roche, Paid instructor for: AbbVie, Pfizer, UCB, Novartis, Roche, Speakers bureau: AbbVie, Pfizer, UCB, Novartis, Roche, Mette BjOrndal Axelsen: None declared, Mikkel Ǿstergaard Grant/research support from: Abbvie, Celgene, Centocor, Merck, Novartis, Consultant for: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Sin Ngai Ng: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis, Susanne Juhl Pedersen: None declared, Lene Terslev Speakers bureau: Speakers fee from : Roche, Novartis, Pfizer, MSD, BMS, Celgene

Background Psoriatic arthritis (PsA) is a chronic inflammatory disorder associated with skin and joint manifestations, several extra-articular symptoms, various comorbidities, and disability[1,2]. The emergence of tumour necrosis factor inhibitor (TNFi) therapy has dramatically changed the course of disease. Additional TNFi therapies (certolizumab pegol and golimumab) have been marketed, and recently ustekinumab has become available for PsA. Objectives To assess the use of biological agents (bDMARDs) in PsA from 2006-2017, using data from the Nordic Rheumatology registers. Methods Based on data from the registers DANBIO, ICEBIO, NOR-DMARD, ROB-FIN, and SRQ, PsA patients initiating bDMARDs or biosimilars, as a first or subsequent biological therapy were identified. Adalimumab, etanercept and infliximab were grouped as 1st generation therapies; certolizumab pegol, golimumab were grouped as 2nd generation therapies and biosimilar treatments were grouped. Treatments with ustekinumab were also identified. Pearson correlation tests were calculated and p>0.05 were considered significant. R2≈1 showed a strong correlation between the baseline characteristics. Results A total of 18,089 treatment initiations were identified (DANBIO 4,361, ICEBIO 449, NOR-DMARD 1,948, ROB-FIN 1,069, SRQ 10,262). 53.68% of the patients were female. Overall, 6,198 patients initiated 1st generation therapies, 1,447 2nd generation therapies, 1,353 biosimilars and 52 ustekinumab, as their first course of bDMARDs. Initiations of second or subsequent bDMARDs were 4,560, 1,630, 2,176 and 376 patients, respectively. The total of first course bDMARD initiators increased significantly from 2006-2017 (p Conclusion Across the Nordic countries the prescription pattern for biological therapies for PsA has changed significantly over time. The decreasing levels of both CRP scores and SJC suggest that PsA patients who initiate bDMARD treatment have changed towards a less active inflammatory phenotype from 2006-2017. Collaboration across registers will allow for robust assessment of the uptake of newer biological therapies. Overall the number of prescribed therapies increased during the observational period, indicating a previously unmet need for biological therapies in the Nordic population. References [1] Ballegaard C, Kristensen L. E, et al. Impact of comorbidities on tumour necrosis factor inhibitor therapy in psoriatic arthritis: a population-based cohort study. Arthritis. 2018;70(4):592-599. [2] Kristensen L. E, Jorgensen T. S, et al, Societal costs and patients’ experience of health inequities before and after diagnosis of psoriatic arthritis: a Danish cohort study. Ann Rheum Dis. 2017;(76):1495-1501. Acknowledgement This study was partly funded by a grant from NordForsk and FOREUM Disclosure of Interests Rebekka L. Hansen: None declared, Tanja Schjodt Jorgensen Consultant for: Abbvie, Roche, Novartis, UCB, Biogen, Eli Lilly., Speakers bureau: Abbvie, Roche, Novartis, UCB, Biogen, Eli Lilly., Lene Dreyer Consultant for: MSD, UCB and Janssen Pharmaceuticals, Speakers bureau: MSD, UCB and Janssen Pharmaceuticals, Speakers bureau: UCB, MSD, Eli Lilly and Janssen Pharmaceuticals., Bjorn Gudbjornsson: None declared, Johan Askling Grant/research support from: Karolinska Institutet (JA) has or has had research agreements with the following pharmaceutical companies, mainly in the context of the ATRIS national safety monitoring programme for rheumatology biologicals: Abbvie, BMS, MSD, Eli Lilly, Pfizer, Roche, Samsung Bioepis, and UCB., Consultant for: Karolinska Institutet has received remuneration for JA participating in ad boards arranged by Lilly, Novartis, and Pfizer., Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis, Bente Glintborg Grant/research support from: Biogen, Pfizer, AbbVie, Daniela Di Giuseppe: None declared, Lennart T.H. Jacobsson Consultant for: LJ has received lecture and consulting fees from Pfizer, Abbvie, Novartis, Eli-Lily and Janssen, Tore K. Kvien Grant/research support from: AbbVie, BMS, MSD, Pfizer, Roche and UCB., Consultant for: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Hospira, Merck-Serono, MSD, Novartis, Oktal, Orion Pharma, Pfizer, Roche, Sandoz, Sanofi, Mylan and UCB, Speakers bureau: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Hospira, Merck-Serono, MSD, Novartis, Oktal, Orion Pharma, Pfizer, Roche, Sandoz, Sanofi and UCB, Dan Nordstrom Grant/research support from: MSD, Pfizer, Consultant for: AbbVie, BMS, MSD, Novartis, Roche, Pfizer, UCB, Speakers bureau: Novartis, UCB, Kalle Aaltonen: None declared, Sella Aarrestad Provan Consultant for: Novartis, Speakers bureau: Lilly, Eirik kristianslund: None declared, Johan K Wallman Consultant for: Consultant for AbbVie, Celgene, Eli Lilly, Novartis, and UCB Pharma., Thorvardur Jon Love Consultant for: Received reimbursment from Celgene for speaking about guidelines for the treatment of psoriatic arthritis, Lars Erik Kristensen Grant/research support from: UCB, Biogen, Janssen Pharmaceuticals, and Novartis, Consultant for: Consultant for AbbVie, Amgen, Biogen, BMS, Celgene, Eli Lilly, Janssen Pharmaceuticals, MSD, Novartis, Pfizer, Roche, Sanofi, and UCB Pharma., Speakers bureau: Pfizer, AbbVie, Amgen, UCB, BMS, Biogen, MSD, Novartis, Eli Lilly and Company, and Janssen Pharmaceuticals

Background Patients with RA have shorter life expectancy than the background population. Severe disease, as reflected in high disease activity, comorbid conditions and functional disability have historically been associated with increased mortality (1-2). Mortality after the introduction of biological therapies has not been investigated in detail, and little is known about the predictive value of sociodemographic and lifestyle factors. Objectives To investigate the predictive value of a panel of potential predictors of death in a cohort of patients with RA followed for up to 12 years during the era of biological treatments. Methods Outpatients with RA were recruited consecutively between July 2006 and July 2007 and followed in routine care with prospective registrations in the DANBIO registry until death or August 30th 2018, whichever occurred first. Baseline variables considered to be potential predictors were: disease activity, disease duration, IgM-rheumatoid factor (IgM-RF), radiographic status (erosive disease yes/no) and medical therapy as well as patient-reported marital status, educational level, comorbid conditions, smoking, exercise, body mass index (BMI) and health assessment questionnaire (HAQ). Vital status and date of death were extracted from the Danish National Register. A cox proportional hazards model was used to estimate the hazard ratio for death for each of the potential predictors. Results 3693 patients were recruited at baseline, 75% women, 77% IgM-rheumatoid factor positive, 65% with erosive disease, median (IQR) age 62 years (52-71), disease duration 7 years (3-15), DAS28 3.0 (2.2-3.9), HAQ 0.63 (0.25-1.25). 20% received a biological disease modifying anti-rheumatic drug (DMARD), 71% received a synthetic DMARD and 9% received no DMARD. The median (IQR) duration of follow-up was 11 years (9-11); 1041 patients (28%) died during follow-up. 640 patients were excluded from the regression model due to missing baseline data; these individuals were slightly (median of 3 years) older than those who entered, but with similar disease duration and disease activity. All baseline variables were statistically significant predictors in univariable analyses. Table shows hazard ratio estimates in the multivariable model, which included 3053 patients; 762 (25%) deaths. IgM-RF positivity, higher HAQ score, glucocorticoid therapy, smoking (current and former) and two or more comorbid conditions were predictors of death. Low BMI was a borderline significant predictor for death. Female sex, weekly exercise and cohabiting decreased the risk of death. Conclusion In a large cohort of RA patients followed for a decade in the era of biological treatments, we identified strong clinical (high HAQ, comorbidity), treatment related (glucocorticoid last month), sociodemographic and lifestyle related (male sex, living alone, smoking, physical inactivity, low BMI) risk factors for death. In the effort to prevent a poor long term outcome in patients with RA, this study provides new insight into potentially modifiable baseline variables. References [1] Mok, CC, et al. Life expectancy, standardized mortality ratios, and causes of death in six rheumatic diseases in Hong Kong, China. Arthritis Rheum2011; 63: 1182-1189. [2] Sokka, T, et al. Mortality in rheumatoid arthritis: 2008 update. Clin exp Rheumatol. 2008Sep-Oct; 26 (5 suppl 51) S: 35-61. Acknowledgement We thank the Danish Rheumatism Association for supporting the study. Disclosure of Interests Louise Linde: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis

Background Tumour necrosis factor inhibitors (TNFi) are efficacious in patients with axial spondyloarthritis (axSpA), but some patients switch to a different TNFi because of adverse effects (AE) or lack of effect (LOE). The EuroSpA Collaboration has previously demonstrated a 1-year retention rate of 79% and 6 months LUNDEX adjusted BASDAI Objectives Firstly, to investigate retention and response rates at 6, 12 and 24 months in patients with axSpA initiating the 2nd and 3rd TNFi in clinical practice across Europe. Secondly, to investigate whether the outcomes were associated with the reason for withdrawal (AE or LOE) from the previous treatment. Methods Prospectively collected data on axSpA patients in routine care from 12 European registries were pooled. Kaplan-Meier estimation was used to investigate TNFi retention rates. LUNDEX adjusted2 response rates were calculated for BASDAI Results A total of 7953 patients initiating their 2nd TNFi and 2782 patients initiating 3rd TNFi were included. Baseline characteristics are shown in the Table. The overall retention rates for both 2nd and 3rd TNFi at 12 months were 72% (Figure). Corresponding retention rates for the individual registries ranged from 52-90% and 54-89%, respectively. In both patients who stopped 1st TNFi due to AE or LOE, 12-month retention rate for the 2nd TNFi treatment was 68%. In patients who stopped the 2nd TNFi due to AE or LOE, 12-month retention rates for the 3rd TNFi treatment were 68% and 69%, respectively. For the 2nd and 3rd TNFi, 6 months LUNDEX adjusted BASDAI Conclusion Data from 12 European countries demonstrated decreasing response rates with increasing number of previous TNFi, although with only minor difference between 2nd and 3rd. Patients who had withdrawn from the previous TNFi due to LOE had retention rates and remission rates similar to those who had withdrawn due to AE. References [1] Brahe, et al. ACR2018 [2] Arthritis Rheum, 2006, 54(2), p:600-6. Acknowledgement Novartis Pharma AG and IQVIA for supporting the EuroSpA collaboration Disclosure of Interests Lykke Ornbjerg Grant/research support from: Unrestricted grant: Novartis, Cecilie Heegaard Brahe Grant/research support from: Unrestricted grant: Novartis, Anne Gitte Loft: None declared, Johan Askling Grant/research support from: Karolinska Institutet (JA) has or has had research agreements with the following pharmaceutical companies, mainly in the context of the ATRIS national safety monitoring programme for rheumatology biologicals: Abbvie, BMS, MSD, Eli Lilly, Pfizer, Roche, Samsung Bioepis, and UCB., Consultant for: Karolinska Institutet has received remuneration for JA participating in ad boards arranged by Lilly, Novartis, and Pfizer., Adrian Ciurea Consultant for: AbbVie, Celgene, Janssen-Cilag, MSD, Eli Lilly, Novartis, Pfizer, UCB, Speakers bureau: Abbvie, Celgene, Janssen-Cilag, MSD, Eli Lilly, Novartis, Pfizer, UCB, Heřman Mann Consultant for: Pfizer, Eli Lilly, Sanofi, Speakers bureau: AbbVie, Roche, Pfizer, MSD, Eli Lilly, Sanofi, Servet Akar Grant/research support from: MSD, Abbvie, Roche, UCB, Novartis, Pfizer, Amgen, Consultant for: MSD, Abbvie, Roche, UCB, Novartis, Pfizer, Amgen, Speakers bureau: Pfizer, Eirik kristianslund: None declared, Dan Nordstrom Grant/research support from: MSD, Pfizer, Consultant for: AbbVie, BMS, MSD, Novartis, Roche, Pfizer, UCB, Speakers bureau: Novartis, UCB, Maria Jose Santos: None declared, Catalin Codreanu: None declared, Manuel Pombo-Suarez: None declared, Ziga Rotar: None declared, Bjorn Gudbjornsson: None declared, Daniela Di Giuseppe: None declared, Michael Nissen Consultant for: AbbVie, Lilly, Novartis, and Pfizer, Karel Pavelka: None declared, Soner Senel: None declared, Joe Sexton: None declared, Kari Eklund: None declared, Anabela Barcelos: None declared, Ruxandra Ionescu: None declared, Carlos Sanchez-Piedra: None declared, Matija Tomsic: None declared, Arni Jon Geirsson: None declared, Irene van der Horst-Bruinsma Grant/research support from: MSD, Pfizer, AbbVie, Consultant for: Abbvie, UCB, MSD, Novartis, Speakers bureau: BMS, AbbVie, Pfizer, MSD, Gary Macfarlane Grant/research support from: Have received research grants (not current) from Abbvie and Pfizer. Have received research grants (not current) from the British Society for Rheumatology, who received the funds from Abbive, Pfizer and UCB. Have received research grant (current) from the British Society for Rheumatology, who received the funds from Celgene., Florenzo Iannone Consultant for: F Iannone has received consultancy fees and/or speaker honoraria from Pfizer, AbbVie, MSD, BMS, Novartis, Lilly, UCB outside this work, Speakers bureau: F Iannone has received consultancy fees and/or speaker honoraria from Pfizer, AbbVie, MSD, BMS, Novartis, Lilly, UCB outside this work, Brigitte Michelsen: None declared, Lise Hyldstrup: None declared, Niels Steen Krogh: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis, Mikkel Ǿstergaard Grant/research support from: Abbvie, Celgene, Centocor, Merck, Novartis, Consultant for: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB

Background Vitamin D is often low in Rheumatoid Arthritis(RA), and immunomodulatory properties of vitamin D might be associated with disease-course in RA.(1) Objectives To evaluate association between baseline vitamin D metabolites and one-year remission, in newly diagnosed, treatment-naive RA patients, aggressively treated during follow-up. Methods The CIMESTRA-cohort comprises 160 newly diagnosed RA patients, treated aiming at remission with methotrexate and intraarticular steroid, further randomized 1:1 to ciclosporine or placebo-ciclosporine.(2) A total of 158 patients had vitamin D metabolites measured at time of diagnosis. Dietary vitamin D supplementation was recommended in accordance with the national guidelines. Serum vitamin Dtotal (sum of 25OHD2 and 25OHD3) and 1,25(OH)2D at time of diagnoses were measured by LC-MS/MS or RIA. Dtotal were dichotomized at 50 nmol/l, and 1,25(OH)2D categorized in tertiles. Primary outcome was remission (DAS28-CRP ≤ 2.6) after one year. Associations were calculated using logistic regression, presented as Odds Ratios with 95% Confidence Intervals (95%CIs). Adjustment of analyses included sex, age, symptom duration prior to diagnosis, DAS28-CRP and season of diagnosis. Results In univariate analyses, neither Dtotal nor 1,25(OH)2D at time of diagnosis predicted remission at year one. In adjusted analysis, Dtotal Conclusion Low Dtotal at time of diagnosis is associated to increased odds for achieving remission at year one in early, treatment naive RA patients, treated aggressively during follow-up. References [1] Jeffery LE, et al. Vitamin D in rheumatoid arthritis-towards clinical application. NatRevRheumatol. 2015. [2] Hetland ML, et al. Combination treatment with methotrexate, cyclosporine, and intraarticular betamethasone compared with methotrexate and intraarticular betamethasone in early active rheumatoid arthritis: an investigator-initiated, multicenter, randomized, double-blind, parallel-group, placebo-controlled study. Arthritis Rheum. 2006;54:1401-9. Acknowledgement Soren Moller, biostatistician at OPEN, Odense, for statistical support Disclosure of Interests Mette Herly Grant/research support from: Pfizer Denmark, unrestricted grant, used for salary. The Danish Rheumatism Association, patient association, 6 months salary as part of PHD study, Speakers bureau: The Danish Rheumatism Association, patient association, speakers Fee 500 Euro, Kristian Stengaard-Pedersen: None declared, Peter Vestergaard Speakers bureau: Amgen, Eli Lilly, Novartis, MSD, Servier, Robin Christensen Grant/research support from: AbbVie Inc, and the Oak Foundation, Speakers bureau: Roche, Mikkel Ostergaard Grant/research support from: Abbvie, Celgene, Centocor, Merck, Novartis, Consultant for: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Peter Junker: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis, Kim Horslev-Petersen Grant/research support from: AbbVie during the conduct of the study, Torkell Ellingsen: None declared

Background: Patients with rheumatoid arthritis (RA), axial spondyloarthritis (axSpA) and psoriatic arthritis (PsA) treated with biological drugs (bDMARDs) have increased risk of hospitalized infection (i.e. infection causing admission to hospital) compared to the general population. Since patients with RA, axSpA and PsA have different age distributions, and age is an important predictor for infection, we found it of interest to quantify the excess burden of hospitalized infection in patients with inflammatory arthritis treated with bDMARDs compared to the general population and to investigate whether risk depended on age and diagnosis. Objectives: To compare the risk of hospitalized infection in bio-naive patients with inflammatory arthritis, who started treatment with a bDMARD with that of the general population, and to explore how this risk was influenced by age and diagnosis. Methods: Matched cohort study based on data from The Danish Rheumatology Register (DANBIO) linked with The Danish National Patient Register and The Danish National Prescription Register. Patients with a diagnosis of RA, PsA or axSpA in DANBIO initiating first bDMARD January 2006-December 2016 were included. For each patient, 10 controls from the general population, matched by age, sex, postal code and date were obtained. Infection risk in patients and matched controls were compared in analyses stratified by age and diagnosis, with Cox proportional hazards models accounting for matching. Follow-up time was 12 months irrespective of whether treatment was continued or changed during follow-up. Clinicaltrials.gov: NCT03496831. Results: In total, 11,372 patients and 113,715 controls were included. Overall, hospitalized infection was observed during follow-up in 4.6% of patients and 1.3% of controls; hazard ratio 3.7 (95% confidence interval (CI): 3.4-4.1). The absolute risk was highest in RA patients, followed by PsA, axSpA and controls (unadjusted comparison). When stratified by age, the absolute risk increased with age, but was largely similar across diagnoses (Figure). In the stratum ≥60 years, RA patients appeared to have higher risk than axSpA patients, but the subgroup of axSpA patients ≥60 years was small. Conclusion: The risk of hospitalized infection during 12 months of follow-up was approximately four times higher in bio-naive patients with inflammatory arthritis who started treatment with a biological drug (bDMARD) compared to matched controls from the general population. When stratified by age, the absolute risk was largely similar across the diagnoses RA, axSpA and PsA. Thus, attention to preventive strategies such as vaccination seems prudent in these patients, especially those ≥60 years of age. Disclosure of Interests: Simon Krabbe: None declared, Kathrine L. Gron: None declared, Bente Glintborg Grant/research support from: Biogen, Pfizer, AbbVie, Frank Mehnert: None declared, Dorte E. Jarbol: None declared, Mikkel Ǿstergaard Grant/research support from: Abbvie, Celgene, Centocor, Merck, Novartis, Consultant for: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis

Background There is a lack of real-life data on secukinumab exposure, treatment outcomes and retention rates in axial spondyloarthritis (axSpA) patients. Objectives Primary objective: To assess the proportion of axSpA patients in BASDAI low disease activity ( Methods Data from axSpA patients treated with secukinumab in routine care from 12 countries in the European Spondyloarthritis Research Collaboration (EuroSpA) were pooled. Time from treatment initiation to data cut was >= 6 months. Group comparisons were performed with independent t-test, Mann-Whitney U-test, ANOVA, Kruskal-Wallis and Chi-square test, as appropriate. Kaplan-Meier analyses with log rank test were performed for comparison of secukinumab drug survival. Results A total of 1556 axSpA patients were included. Overall 6-month BASDAI Drug retention was higher for bDMARD naive compared with non-naive patients (figure 1a). Baseline characteristics and disease activity (data not shown) as well as drug retention differed in-between the European registries (figure 1b). Conclusion This study of >1500 patients in 12 European countries provides real-world data on the effectiveness of secukinumab in patients with axSpA, adding evidence to existing RCTs. A majority of the patients was previous bDMARD users and had long disease duration. BASDAI Acknowledgement Novartis Pharma AG and IQVIA for supporting the EuroSpA collaboration Disclosure of Interests Brigitte Michelsen Grant/research support from: Unrestricted grant: Novartis, Consultant for: Novartis, UCB, Cecilie Heegaard Brahe Grant/research support from: Unrestricted grant: Novartis, Johan Askling Grant/research support from: Karolinska Institutet (JA) has or has had research agreements with the following pharmaceutical companies, mainly in the context of the ATRIS national safety monitoring programme for rheumatology biologicals: Abbvie, BMS, MSD, Eli Lilly, Pfizer, Roche, Samsung Bioepis, and UCB., Consultant for: Karolinska Institutet has received remuneration for JA participating in ad boards arranged by Lilly, Novartis, and Pfizer., Catalin Codreanu: None declared, Adrian Ciurea Consultant for: AbbVie, Celgene, Janssen-Cilag, MSD, Eli Lilly, Novartis, Pfizer, UCB, Speakers bureau: Abbvie, Celgene, Janssen-Cilag, MSD, Eli Lilly, Novartis, Pfizer, UCB, Anne Gitte Loft: None declared, Heřman Mann Consultant for: Pfizer, Eli Lilly, Sanofi, Speakers bureau: AbbVie, Roche, Pfizer, MSD, Eli Lilly, Sanofi, Manuel Pombo-Suarez: None declared, Fatos Onen: None declared, Joe Sexton: None declared, Ziga Rotar: None declared, Maria Jose Santos: None declared, Kari Eklund: None declared, Bjorn Gudbjornsson: None declared, Florenzo Iannone Consultant for: F Iannone has received consultancy fees and/or speaker honoraria from Pfizer, AbbVie, MSD, BMS, Novartis, Lilly, UCB outside this work, Speakers bureau: F Iannone has received consultancy fees and/or speaker honoraria from Pfizer, AbbVie, MSD, BMS, Novartis, Lilly, UCB outside this work, Daniela Di Giuseppe: None declared, Ruxandra Ionescu: None declared, Michael Nissen Consultant for: AbbVie, Lilly, Novartis, and Pfizer, Karel Pavelka: None declared, Carlos Sanchez-Piedra: None declared, Servet Akar Grant/research support from: MSD, Abbvie, Roche, UCB, Novartis, Pfizer, Amgen, Consultant for: MSD, Abbvie, Roche, UCB, Novartis, Pfizer, Amgen, Speakers bureau: Pfizer, Eirik kristianslund: None declared, Matija Tomsic: None declared, Helena Santos: None declared, Nina Trokovic: None declared, Arni Jon Geirsson: None declared, Ennio Giulio Favalli: None declared, Irene van der Horst-Bruinsma Grant/research support from: MSD, Pfizer, AbbVie, Consultant for: Abbvie, UCB, MSD, Novartis, Speakers bureau: BMS, AbbVie, Pfizer, MSD, Gary Macfarlane Grant/research support from: Have received research grants (not current) from Abbvie and Pfizer. Have received research grants (not current) from the British Society for Rheumatology, who received the funds from Abbive, Pfizer and UCB. Have received research grant (current) from the British Society for Rheumatology, who received the funds from Celgene., Lise Hyldstrup: None declared, Niels Steen Krogh: None declared, Mikkel Ǿstergaard Grant/research support from: Abbvie, Celgene, Centocor, Merck, Novartis, Consultant for: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis

Background: Co-inhibitory receptors are important for the regulation of inflammation in autoimmune diseases. Among these, T-cell Immunoglobulin and mucin domain-3 (Tim-3) has recently gained attention, as it is expressed on exhausted T cells co-expressing PD-1 (1). Objectives: To investigate Tim-3’s role in rheumatoid arthritis (RA). Methods: Early RA (eRA) patients were randomized to conventional methotrexate (MTX) treatment + placebo or MTX + adalimumab (ADA) (2). Plasma were analysed by ELISA at baseline (n=98) and after 3 and 12 months of treatment. Clinical follow up including 28-joint Disease Activity Score with CRP (DAS28CRP) and Total Sharp Score (TSS) were available. Intrasubject differences in sTim-3 between baseline and 3 months were assessed by parametric paired t tests and compared with plasma from HV (n=44) by parametric unpaired t tests. Spearman correlation and Mann-Whitney test were used to investigate relations between sTim-3 and clinical follow up. From chronic RA (cRA) patients (n=17) plasma and synovial fluid were analysed by ELISA and peripheral blood mononuclear cells (PBMC) and synovial fluid mononuclear cells (SFMC) (n=8) were analysed by flow cytometry. Intrasubject differences were assessed by paired parametric t tests, and comparison with PBMC from HV (n=6) by unpaired parametric t test. Parametric data are reported as mean differences (MD) [95%CI]. P values Results: Among memory prone T cells (CD3+CD4+CD45RO+) in SFMC, the percentage of Tim-3+ cells were increased compared with similar gated PBMC from patients (MD 17.4%, [10.7;24.1], p Conclusion: Tim-3 expression is upregulated in memory prone T cells in RA joints and the majority co-express PD-1. Levels of sTim-3 are increased in SF. In eRA, baseline sTim-3 plasma levels are elevated and correlate with DAS28CRP. Decrease of sTim-3 during treatment associates with future radiographic progression. We suggest, that Tim-3 expression and sTim-3 plasma and SF levels reflect ongoing immune response, thus immune regulation in RA. These data indicate that maintenance of sTim-3 plasma levels during treatment is favourable, consistent with Tim-3 being a co-inhibitory receptor. Reference [1] Ana C. et al. Immunity 2016;44:989-1004, 2 Horslev-Petersen K, et al. Ann Rheum Dis 2014;73:654-661. Disclosure of Interests: Caecilie Skejo: None declared, Morten Aagaard Nielsen: None declared, Malene Hvid: None declared, Aida Solhoj Hansen: None declared, Kristian Stengaard-Pedersen: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis, Kim Horslev-Petersen: None declared, Peter Junker: None declared, Mikkel Ǿstergaard Grant/research support from: Abbvie, Celgene, Centocor, Merck, Novartis, Consultant for: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Stinne Ravn Greisen: None declared, Mette Deleuran: None declared, Bent Deleuran: None declared

Background The efficacy of Tumour Necrosis Factor inhibitor (TNFi) in patients with psoriatic arthritis (PsA) has been investigated in randomized controlled trials (RCTs) with strict inclusion and exclusion criteria. Patients treated in routine care are more heterogeneous and only ≈20-30% of patients receiving TNFi in routine care would have been eligible to be enrolled in the RCTs1. This emphasizes the need for real-world observational data as a valuable supplement to RCTs. Studying large patient groups from several European countries would increase the external validity of the results. Objectives To investigate Tumour Necrosis Factor inhibitor (TNFi) retention rates at 12 months (primary objective), 6 and 24 months, and remission rates at the same time-points in biologic-naive patients with PsA from the EuroSpA Collaboration. Methods Prospectively collected data on PsA patients from 12 European registries were uploaded through the secure Virtual Private Network pipelines to the EuroSpA server, and pooled. Baseline characteristics were investigated with non-parametric descriptive statistics. TNFi retention rates (Kaplan-Meier statistics), and 28-joint count Disease activity Score (DAS28) Results Overall, 14,261 patients with PsA initiated a 1st TNFi. Baseline characteristics of the pooled population are shown in the Table. The median 12-month retention rate (95%CI) was 77% (76-78%), ranging from 68-90% across registries (Figure). Overall, DAS28/DAPSA28 remission rates at 6 months were 56%/27% (LUNDEX-adjusted: 45%/22%). In patients initiating a 1stTNFi after 2009 with registered fulfillment of CASPAR criteria (n=1,980) or registered ≥1 swollen joint at baseline (n=5,803), the retention rates and remission rates were similar to those found overall (Table). Conclusion Approximately half of >14,000 patients with PsA who initiated 1st TNFi treatment in routine care were in DAS28-remission after 6 months, and three out of four were still on the drug after 1 year. References [1] Clin Exp Rheumatol, 2018, 36(6):1068-1073 [2] arthritis Rheum, 2006, 54(2): 600-6 Acknowledgement Novartis Pharma aG and IQVIA for supporting the EuroSpA collaboration. Disclosure of interests Cecilie Heegaard Brahe Grant/research support from: Unrestricted grant: Novartis, Lykke Ornbjerg Grant/research support from: Unrestricted grant: Novartis, Lennart T.H. Jacobsson Consultant for: LJ has received lecture and consulting fees from Pfizer, abbvie, Novartis, Eli-Lily and Janssen, Michael Nissen Consultant for: abbVie, Lilly, Novartis, and Pfizer, Eirik kristianslund: None declared, Heřman Mann Consultant for: Pfizer, Eli Lilly, Sanofi, Speakers bureau: abbVie, Roche, Pfizer, MSD, Eli Lilly, Sanofi, Maria Jose Santos: None declared, Manuel Pombo-Suarez: None declared, Dan Nordstrom Grant/research support from: MSD, Pfizer, Consultant for: abbVie, BMS, MSD, Novartis, Roche, Pfizer, UCB, Speakers bureau: Novartis, UCB, Ziga Rotar: None declared, Bjorn Gudbjornsson: None declared, Fatos onen: None declared, Catalin Codreanu: None declared, Ulf Lindstrom: None declared, Burkhard Moeller Consultant for: Swissmedic Human Medicines Expert Committee Member (regulatory agency), Joe Sexton: None declared, Karel Pavelka: None declared, anabela Barcelos: None declared, Carlos Sanchez-Piedra: None declared, Kari Eklund: None declared, Matija Tomsic: None declared, Thorvardur Jon Love Consultant for: Received reimbursment from Celgene for speaking about guidelines for the treatment of psoriatic arthritis, Gercek Can: None declared, Ruxandra Ionescu: None declared, anne Gitte Loft: None declared, Marleen van de Sande Grant/research support from: van Janssen, Novartis, Eli Lily, Consultant for: Novartis and abbvie, Irene van der Horst-Bruinsma Grant/research support from: MSD, Pfizer, abbVie, Consultant for: abbvie, UCB, MSD, Novartis, Speakers bureau: BMS, abbVie, Pfizer, MSD, Gary Macfarlane Grant/research support from: Have received research grants (not current) from abbvie and Pfizer. Have received research grants (not current) from the British Society for Rheumatology, who received the funds from abbive, Pfizer and UCB. Have received research grant (current) from the British Society for Rheumatology, who received the funds from Celgene., Florenzo Iannone Consultant for: F Iannone has received consultancy fees and/or speaker honoraria from Pfizer, abbVie, MSD, BMS, Novartis, Lilly, UCB outside this work, Speakers bureau: F Iannone has received consultancy fees and/or speaker honoraria from Pfizer, abbVie, MSD, BMS, Novartis, Lilly, UCB outside this work, Lise Hyldstrup: None declared, Niels Steen Krogh: None declared, Mikkel Ǿstergaard Grant/research support from: abbvie, Celgene, Centocor, Merck, Novartis, Consultant for: abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Speakers bureau: abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Merete L. Hetland Grant/research support from: BMS, MSD, abbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis

Background: The optimal sequencing of biologic Disease Modifying Anti-Rheumatic Drugs (bDMARDs) in Rheumatoid Arthritis (RA) is unknown. Evidence regarding the effectiveness of a 2nd non-TNFi bDMARD, as well as of TNFi, in patients whose 1st bDMARD has been a non-TNFi is limited. Objectives: To characterize patients switching for medical reasons after failure of a non-TNFi used as 1st bDMARD, and to assess the effectiveness of rituximab (RTX), abatacept (ABA) or tocilizumab (TCZ) vs. a TNFi. Methods: Patients from 5 national registers (Sweden, Norway, Denmark, Iceland and Finland) with RA who started treatment with a non-TNFi as a 1st bDMARD after 2010 and switched to a 2nd bDMARD within 3 months after the discontinuation of the 1st (with the exception of RTX for which a 6-month window was used), were identified. Clinical effectiveness was assessed by DAS28 change at 6 months. Results: 611 patients were included in the analyses. 80% were female, the majority were positive for RF (76%) and anti-CCP (69%). The mean (±SD) age, DAS28 and HAQ at baseline was 58 (13), 4.5 (1.4) and 1.3 (0.7), respectively, while the median (IQR) disease duration was 5.0 (2.2-12.0) years. Baseline characteristics of patients and the clinical response for each switching strategy are shown in table 1. Moderate responses were observed for most switching strategies. 63% of patients were still on treatment with their 2nd bDMARD at 6 months after switch. Conclusion: The six-month drug retention for a 2nd bDMARD in patients with RA switching due to failure of a non-TNFi bDMARD as 1st ever bDMARD was lower than two thirds (63%). More detailed analyses are exploring potential subgroups of patients for whom specific switching strategies are more effective. Acknowledgement: The study was partly funded by a study grant from NordForsk and Foreum. Disclosure of Interests: Katerina Chatzidionysiou: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis, Thomas Frisell: None declared, Daniela Di Giuseppe: None declared, Karin Hellgren: None declared, Bente Glintborg Grant/research support from: Biogen, Pfizer, AbbVie, Dan Nordstrom Grant/research support from: MSD, Pfizer, Consultant for: AbbVie, BMS, MSD, Novartis, Roche, Pfizer, UCB, Speakers bureau: Novartis, UCB, Kalle Aaltonen: None declared, Nina Trokovic: None declared, Eirik kristianslund: None declared, Tore K. Kvien Grant/research support from: AbbVie, BMS, MSD, Pfizer, Roche and UCB., Consultant for: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Hospira, Merck-Serono, MSD, Novartis, Oktal, Orion Pharma, Pfizer, Roche, Sandoz, Sanofi, Mylan and UCB, Speakers bureau: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Hospira, Merck-Serono, MSD, Novartis, Oktal, Orion Pharma, Pfizer, Roche, Sandoz, Sanofi and UCB, Sella Aarrestad Provan Consultant for: Novartis, Speakers bureau: Lilly, Bjorn Gudbjornsson: None declared, Gerdur Grondal : None declared, Lene Dreyer Consultant for: MSD, UCB and Janssen Pharmaceuticals, Speakers bureau: MSD, UCB and Janssen Pharmaceuticals, Speakers bureau: UCB, MSD, Eli Lilly and Janssen Pharmaceuticals., Lars Erik Kristensen Grant/research support from: UCB, Biogen, Janssen Pharmaceuticals, and Novartis, Consultant for: Consultant for AbbVie, Amgen, Biogen, BMS, Celgene, Eli Lilly, Janssen Pharmaceuticals, MSD, Novartis, Pfizer, Roche, Sanofi, and UCB Pharma., Speakers bureau: Pfizer, AbbVie, Amgen, UCB, BMS, Biogen, MSD, Novartis, Eli Lilly and Company, and Janssen Pharmaceuticals, Tanja Schjodt Jorgensen Consultant for: Abbvie, Roche, Novartis, UCB, Biogen, Eli Lilly., Speakers bureau: Abbvie, Roche, Novartis, UCB, Biogen, Eli Lilly., Lennart T.H. Jacobsson Consultant for: LJ has received lecture and consulting fees from Pfizer, Abbvie, Novartis, Eli-Lily and Janssen, Johan Askling Grant/research support from: Karolinska Institutet (JA) has or has had research agreements with the following pharmaceutical companies, mainly in the context of the ATRIS national safety monitoring programme for rheumatology biologicals: Abbvie, BMS, MSD, Eli Lilly, Pfizer, Roche, Samsung Bioepis, and UCB., Consultant for: Karolinska Institutet has received remuneration for JA participating in ad boards arranged by Lilly, Novartis, and Pfizer.

Background Most infections in patients with rheumatoid arthritis (RA) are treated in primary care with a prescription of antibiotics. Only a small fraction requires hospitalization. Existing studies of infection risk in patients with RA, who receive non-tumor-necrosis-factor-inhibitor biologic (non-TNFi) therapy, however, have focused primarily on hospitalized infections.(1) Objectives In Danish RA patients treated in routine care with the three non-TNFi abatacept, rituximab and tocilizumab 1) to compare adjusted incidence rates (IR) of infections overall, and 2) to estimate the relative risk (RR) of infections across the drugs during the first year of non-TNFi treatment. Methods We conducted an observational cohort study including all RA patients in DANBIO who started a non-TNFi treatment between January 2010 and December 2017. Clinical characteristics at baseline were described. We defined infections as either a prescription of antibiotics or a hospitalization due to infection. Baseline comorbidities, antibiotic prescriptions and hospitalized infections were identified through linkage to national registries. We calculated IRs of infections per 100 person-years (age and gender adjusted) and rate ratios (as estimates of RRs, adjusted for additional covariates) during the first year of treatment (Poisson regression). Results We identified 3,696 treatment series of non-TNFi (abatacept 1,115/rituximab 1,017/tocilizumab 1,564). Patients receiving rituximab tended to be older, had longer disease duration and more previous malignancies. During the first year of treatment, 1,747 infections were identified. Age and gender adjusted IRs per 100 person years were (abatacept/rituximab/tocilizumab): 76.1(69.3; 83.6)/87.3(79.3; 96.1)/77.4(71.4; 83.9). Adjusted RRs (Table) were 0.88(0.76; 1.02) for abatacept and 0.87(0.75; 1.00) for tocilizumab compared to rituximab. For abatacept vs. tocilizumab it was 1.02 (0.89; 1.16). Conclusion In patients with RA receiving treatment with abatacept, rituximab or tocilizumab in routine care, rituximab had the highest risk of infection during first year of treatment. However, this finding should be interpreted with caution due to differences in baseline characteristics across drugs and potential residual confounding. References [1] Gron KL, Arkema EV, Glintborg B, Mehnert F, et al. Risk of serious infections in patients with rheumatoid arthritis treated in routine care with abatacept, rituximab and tocilizumab in Denmark and Sweden. Annals of the rheumatic diseases. 2019. Acknowledgement Thanks to all departments that contributed data Disclosure of Interests Kathrine Gron Grant/research support from: BMS, Bente Glintborg Grant/research support from: Biogen, Pfizer, AbbVie, Frank Mehnert: None declared, Mikkel Ǿstergaard Grant/research support from: Abbvie, Celgene, Centocor, Merck, Novartis, Consultant for: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Lene Dreyer Consultant for: MSD, UCB and Janssen Pharmaceuticals, Speakers bureau: MSD, UCB and Janssen Pharmaceuticals, Speakers bureau: UCB, MSD, Eli Lilly and Janssen Pharmaceuticals., Mette Norgaard: None declared, Niels Steen Krogh: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis

Background Discordance between baseline patient’s and evaluator’s global assessment of disease activity is common.1 However, the impact of such discordance on retention and remission rates of TNF inhibitor (TNFi) therapy in axial spondyloarthritis (axSpA) patients remains unexplored. Objectives To assess the impact of baseline discordance, defined as “patient’s minus evaluator’s global assessment of disease activity” (ΔPEG), on retention and remission rates of first TNFi in female and male axSpA patients across Europe. Methods AxSpA patients from 10 European registries participating in the European Spondyloarthritis Research Network Collaboration (EuroSpA) were included. Retention rates after 6/12/24 months’ treatment with first TNFi were assessed with Kaplan-Meier analyses, with comparison between baseline ΔPEG quartiles with log rank test, stratified by gender. Proportions of patients in BASDAI remission (≤2) and ASDAS inactive disease ( Results A total of 9013 axSpA patients were included. Mean(SD) age for women(n=3639)/men(n=5374) were 42.7(12.0)/41.7(12.0) years, disease duration 5.1(7.4)/6.9(8.7) years, median(25-75 percentiles) baseline ΔPEG 20(3-42)/15(0-37) mm. TNFi retention rates and proportions of patients achieving BASDAI≤2 and ASDAS Conclusion In patients receiving their first TNFi, high baseline patient’s compared with evaluator’s global assessment is negatively associated with retention rates as well as proportions of patients achieving BASDAI remission and ASDAS inactive disease after 6, 12 as well as 24 months follow-up, both in female and male axSpA patients. References [1] Lindstrom, et al., J Rheumatol2015;42:1781-5. Acknowledgement Novartis Pharma AG and IQVIA for supporting the EuroSpA collaboration Disclosure of Interests Brigitte Michelsen Grant/research support from: Unrestricted grant: Novartis, Consultant for: Novartis, UCB, Lykke Ornbjerg Grant/research support from: Unrestricted grant: Novartis, Anne Gitte Loft: None declared, Joseph Sexton: None declared, Adrian Ciurea Consultant for: AbbVie, Celgene, Janssen-Cilag, MSD, Eli Lilly, Novartis, Pfizer, UCB, Speakers bureau: Abbvie, Celgene, Janssen-Cilag, MSD, Eli Lilly, Novartis, Pfizer, UCB, Heřman Mann Consultant for: Pfizer, Eli Lilly, Sanofi, Speakers bureau: AbbVie, Roche, Pfizer, MSD, Eli Lilly, Sanofi, Kari Eklund: None declared, Ayten Yazici: None declared, Maria Jose Santos: None declared, Johan Askling Grant/research support from: Karolinska Institutet (JA) has or has had research agreements with the following pharmaceutical companies, mainly in the context of the ATRIS national safety monitoring programme for rheumatology biologicals: Abbvie, BMS, MSD, Eli Lilly, Pfizer, Roche, Samsung Bioepis, and UCB., Consultant for: Karolinska Institutet has received remuneration for JA participating in ad boards arranged by Lilly, Novartis, and Pfizer., Ziga Rotar: None declared, Bjorn Gudbjornsson: None declared, Manuel Pombo-Suarez: None declared, Catalin Codreanu: None declared, Irene van der Horst-Bruinsma Grant/research support from: MSD, Pfizer, AbbVie, Consultant for: Abbvie, UCB, MSD, Novartis, Speakers bureau: BMS, AbbVie, Pfizer, MSD, Eirik kristianslund: None declared, Michael Nissen Consultant for: AbbVie, Lilly, Novartis, and Pfizer, Karel Pavelka: None declared, Nina Trokovic: None declared, Nevsun Inanc: None declared, Elsa Vieira-Sousa Grant/research support from: MSD, Novartis, Daniela Di Giuseppe: None declared, Matija Tomsic: None declared, Arni Jon Geirsson: None declared, Ruxandra Ionescu: None declared, Marleen van de Sande Grant/research support from: Research support from Janssen, Novartis, Eli Lily, Consultant for: Received consultation fees from Abbvie and Novartis, Florenzo Iannone Consultant for: F Iannone has received consultancy fees and/or speaker honoraria from Pfizer, AbbVie, MSD, BMS, Novartis, Lilly, UCB outside this work, Speakers bureau: F Iannone has received consultancy fees and/or speaker honoraria from Pfizer, AbbVie, MSD, BMS, Novartis, Lilly, UCB outside this work, Carlos Sanchez-Piedra: None declared, Gareth T. Jones Grant/research support from: Have received research grants (not current) from Abbvie and Pfizer. Have received research grants (not current) from the British Society for Rheumatology, who received the funds from Abbive, Pfizer and UCB. Have received research grant (current) from the British Society for Rheumatology, who received the funds from Celgene., Lise Hyldstrup: None declared, Niels Steen Krogh: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis, Mikkel Ǿstergaard Grant/research support from: Abbvie, Celgene, Centocor, Merck, Novartis, Consultant for: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB

Background The first infliximab biosimilar (CT-P13) was introduced in Europe in 2014, followed by a rapid, but differential, uptake across the Nordic countries [1]. Pre and post-marketing randomized controlled trials have shown similar efficacy and safety of originator infliximab (INF) versus CT-P13, but a number of observational studies have indicated potential differences in long-term treatment retention. However, no large observational study has hitherto directly compared the treatment retention of INF with CT-P13 in bio-naive patients with spondyloarthritis (SpA) starting infliximab during the same calendar-time period. Objectives To compare one- and two-year treatment retention of INF versus CT-P13 in SpA, when used as a first line biologic, and to explore baseline characteristics in the two cohorts. Methods Observational cohort study. Bio-naive patients with ankylosing spondylitis (AS), non-radiographic axial SpA (nrax-SpA) or undifferentiated SpA (uSpA), starting INF or CT-P13 as their first ever TNFi during the time-period Jan 2014 through Jun 2017 were identified in biological registers in the five Nordic countries. SpA comorbidities were identified through linkage to national registers. Treatment retention of INF versus CT-P13 was assessed through survival probability curves and one- and two-year retention rates. Results In total 1319 bio-naive patients with SpA started infliximab during the time-period, 24% started INF and 76% CT-P13. Baseline characteristics of patients in the two treatment groups were comparable (Table 1). The survival probability curves were identical for INF compared to CT-P13 (Figure 1), and the proportion of patients remaining on treatment after one and two years were similar: one year INF 62% (95%CI 57-68%), CT-P13 63% (95%CI 60-66%); two years: INF 44% (95%CI: 38-50%) and CT-P13 46% (95%CI: 42-51%). Further confounder-adjusted analyses, are planned and will be presented at the conference. Conclusion We found remarkably similar treatment retentions for the infliximab originator and biosimilar when used as the first line biologic in 1319 patients with SpA. The baseline characteristics of the patients starting the originator and the biosimilar suggest that the cohorts are comparable, and the results thus supports the equivalence of the treatments. Reference [1] Glintborg, et al. Biological treatment in ankylosing spondylitis in the Nordic countries during 2010-2016: a collaboration between five biological registries. Scand J Rheumatol. 2018;47:465-74. Acknowledgement This study received funding from NordForsk and from FOREUM. Disclosure of Interests Ulf Lindstrom: None declared, Bente Glintborg Grant/research support from: Biogen, Pfizer, AbbVie, Daniela Di Giuseppe: None declared, Johan Askling Grant/research support from: Karolinska Institutet (JA) has or has had research agreements with the following pharmaceutical companies, mainly in the context of the ATRIS national safety monitoring programme for rheumatology biologicals: Abbvie, BMS, MSD, Eli Lilly, Pfizer, Roche, Samsung Bioepis, and UCB., Consultant for: Karolinska Institutet has received remuneration for JA participating in ad boards arranged by Lilly, Novartis, and Pfizer., Dan Nordstrom Grant/research support from: MSD, Pfizer, Consultant for: AbbVie, BMS, MSD, Novartis, Roche, Pfizer, UCB, Speakers bureau: Novartis, UCB, Sella Aarrestad Provan Consultant for: Novartis, Speakers bureau: Lilly, Bjorn Gudbjornsson: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis, Kalle Aaltonen: None declared, Niels Steen Krogh: None declared, Arni Jon Geirsson: None declared, Lennart T.H. Jacobsson Consultant for: LJ has received lecture and consulting fees from Pfizer, Abbvie, Novartis, Eli-Lily and Janssen

Background Progression of structural joint damage occurs in 20-30 % of patients with rheumatoid arthritis (RA) in clinical remission1. Magnetic resonance imaging (MRI)-detected synovitis and in particular osteitis/bone marrow edema (BME) are known predictors of structural progression in both active RA and in remission, but the predictive value of adding MRI tenosynovitis assessment as potential predictor in patients in clinical remission has not been investigated. Objectives To investigate the predictive value of baseline MRI inflammatory and damage parameters on 2 year MRI and X-ray damage progression in an RA cohort in clinical remission, following MRI and conventional treat-to-target (T2T) strategies. Methods 200 RA patients in clinical remission (DAS28-CRP The following potentially predictive baseline variables: MRI BME, synovitis, tenosynovitis, MRI and X-ray erosion and joint space narrowing (JSN) score, CRP, DAS28, smoking status, gender, age and patient group were tested in univariate logistic regression analyses with 2-year progression in MRI combined damage score, Total Sharp Score (TSS), and MRI and X-ray JSN and erosion scores as dependent variables. Variables with p Results Based on univariate analyses MRI BME, synovitis, tenosynovitis, x-ray erosion and JSN, gender and age were included in subsequent multivariable analyses. Independent MRI predictors of structural progression were BME (MRI progression) and tenosynovitis (MRI and X-ray progression), see table. MRI combined damage score: sum score of MRI erosion and JSN scores. Conclusion This trial is the first to report that MRI tenosynovitis independently predicts both X-ray and MRI damage progression in RA patients in clinical remission. Further studies are needed to confirm MRI-determined tenosynovitis as predictor of progressive joint destruction in RA clinical remission. References [1] Lillegraven, et al. Ann Rheum Dis 2012 [2] Moller-Bisgaard et al. JAMA, accepted Dec 2018 Acknowledgement AbbVie for financial study support Disclosure of Interests Signe Moller-Bisgaard Grant/research support from: Grants and non financial support from AbbVie during the conduct of the study, Speakers bureau: BMS, Kim Horslev-Petersen Grant/research support from: AbbVie during the conduct of the study, Bo Ejbjerg: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis, Lykke Ornbjerg Grant/research support from: Unrestricted grant: Novartis, Daniel Glinatsi: None declared, Jakob Mollenbach Moller: None declared, Mikael Boesen Grant/research support from: Image Analysis Group, Eli Lilly, UCB, AbbVie, Esaote, Kristian Stengaard-Pedersen: None declared, Ole Madsen Grant/research support from: Sobi, AbbVie, Merck Sharp and Dohme, Pfizer, Eli Lilly, Celgene, Novartis, UCB, Sanofi Aventis, Roche, Amgen and BMS, Bente Jensen: None declared, Jan Villadsen: None declared, Ellen Margrethe Hauge Grant/research support from: Have received grants from Roche and Novartis, outside the submitted work., Speakers bureau: Have received personal fees from MSD, Pfizer, UCB and Sobi, Philip Bennett Grant/research support from: Eli Lilly, Merck Sharp and Dohme, Novartis, Oliver Hendricks Grant/research support from: AbbVie, Novartis, Karsten Asmussen: None declared, Marcin Kowalski: None declared, Hanne Merete Lindegaard: None declared, Henning Bliddal Grant/research support from: AbbVie. Oak Foundation, Niels Steen Krogh: None declared, Torkell Ellingsen: None declared, Agnete Nielsen: None declared, Lone Balding: None declared, Anne Grethe Jurik: None declared, Henrik Thomsen: None declared, Mikkel Ǿstergaard Grant/research support from: Abbvie, Celgene, Centocor, Merck, Novartis, Consultant for: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB

Background Methotrexate remains the anchoring drug for the treatment of rheumatoid arthritis (RA). Patients with RA often have comorbidities e.g. diabetes or pulmonary disease. Although methotrexate has been used for decades, little is known about the impact of various comorbidities on treatment outcomes. Objectives To describe the prevalence of comorbidities in csDMARD naive RA patients initiating treatment with methotrexate in routine care and to explore the impact of common comorbidities on methotrexate treatment outcomes (achieving remission and adherence to treatment). Methods Observational cohort study based on the Danish nationwide quality registry, DANBIO. Adult RA patients who started treatment with methotrexate (oral or injection) as first csDMARD year 2010-2017 and who had been followed since onset of disease with regular controls were included. Concomitant treatment with other DMARDs were allowed. Treatment outcomes after ≈ 6 months of treatment were identified in DANBIO. Data were censored by April 2018. Seven different comorbidities (Figure) prior to start of methotrexate were identified in the national patient registry (NPR) through linkage by social security numbers. Impact of each comorbidity was explored as 1) overall methotrexate treatment retention rate and 2) DAS28 remission rate (after 6 months’ treatment). Analyses were by Cox- and logistic-regression analyses (adjusted for gender and age). The comorbidities were included one by one in the models. Finally, similar analyses were performed summed for all the seven comorbidities as any comorbidity yes/no. Results 5828 patients were included (66% female, median age 61 (IQR 51-70) years), whereof 906 (15.5%) had ≥1 of the predefined comorbidities (63% female, median age 68 (60-74) years). Only 70 patients (1.4%) had ≥2 comorbidities. Patients with comorbidities had increased withdrawal rate of methotrexate with hazard ratios ranging from 1.10-2.06 (Figure). Similarly, patients with comorbidities had poorer remission rate with odds ratios ranging from 0.38-0.74 except for previous cancer. Conclusion In this nationwide cohort of >5000 RA patients treated with methotrexate in routine care, approximately 15% of patients had comorbidities at treatment start. Patients with comorbidities had higher rate of withdrawal and poorer remission rates. This warrants specific attention when treating these patient groups in routine care. Acknowledgement Thank you for the Danish departments of Rheumatology for reporting to DANBIO Disclosure of Interests Bente Glintborg Grant/research support from: Biogen, Pfizer, AbbVie, Niels Steen Krogh: None declared, Frank Mehnert: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis

Background The marketing approval of the etanercept biosimilar SB4 was based on phase III studies on patients with rheumatoid arthritis, but extended to all etanercept indications. Currently, no randomized controlled trials have compared etanercept originator (ETN) with SB4 in patients with spondyloarthritis (SpA). However, the uptake of etanercept biosimilars in the treatment of SpA has been exponential in the Nordic countries, with marked differences across the countries [1]. Objectives To compare the one-year treatment retention in bio-naive patients with SpA treated with ETN versus SB4. Furthermore, to explore baseline characteristics in the two patient groups. Methods Observational cohort study. Patients with SpA (ankylosing spondylitis (AS), non-radiographic axial SpA (nrax-SpA) or uSpA)), starting etanercept as their first ever TNFi Jan 2014 through Jun 2017 were identified in biologics registers in the five Nordic countries. Baseline characteristics were retrieved from each biological register and comorbidity data through linkage to national registers. The country-specific data were then pooled for further analysis. Comparisons of treatment retention between ETN and SB4 were assessed through survival probability curves and one-year retention rates. Results In total, 1015 patients were included, whereof 49% started ETN and 51% SB4. Baseline characteristics were similar in the two patient groups (Table?1). One-year survival probability curves were similar for ETN compared to SB4 (Figure 1), and the proportions of patients remaining on drug after one year were comparable: ETN 66% (95%CI: 61-70%) and SB4 73% (95%CI: 68-78%). Further confounder-adjusted analyses are planned and will be presented at the conference. Conclusion In this observational study of 1015 patients with SpA from five Nordic countries, biologics-naive patients starting treatment with originator versus biosimilar etanercept had similar baseline characteristics and similar one-year treatment retention rates, suggesting similar effectiveness and tolerability of the two drugs. Reference [1] Glintborg, et al. Biological treatment in ankylosing spondylitis in the Nordic countries during 2010-2016: a collaboration between five biological registries. Scand J Rheumatol. 2018;47:465-74. Acknowledgement This study received funding from NordForsk and from FOREUM. Disclosure of Interests Bente Glintborg Grant/research support from: Biogen, Pfizer, AbbVie, Ulf Lindstrom: None declared, Daniela Di Giuseppe: None declared, Johan Askling Grant/research support from: Karolinska Institutet (JA) has or has had research agreements with the following pharmaceutical companies, mainly in the context of the ATRIS national safety monitoring programme for rheumatology biologicals: Abbvie, BMS, MSD, Eli Lilly, Pfizer, Roche, Samsung Bioepis, and UCB., Consultant for: Karolinska Institutet has received remuneration for JA participating in ad boards arranged by Lilly, Novartis, and Pfizer., Dan Nordstrom Grant/research support from: MSD, Pfizer, Consultant for: AbbVie, BMS, MSD, Novartis, Roche, Pfizer, UCB, Speakers bureau: Novartis, UCB, Sella Aarrestad Provan Consultant for: Novartis, Speakers bureau: Lilly, Bjorn Gudbjornsson: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis, Kalle Aaltonen: None declared, Arni Jon Geirsson: None declared, Niels Steen Krogh: None declared, Lennart T.H. Jacobsson Consultant for: LJ has received lecture and consulting fees from Pfizer, Abbvie, Novartis, Eli-Lily and Janssen

Background Nationwide Danish guidelines regarding RA patients (pts) initiating bDMARDs are issued approximately annually. For bio-naive pts on concomitant methotrexate (MTX) the recommended drugs (year, recommended compliance) were: certolizumab pegol(CTZ)(2013-2014, 80%)/abatacept(ABA)(2014-2015, 80%)/biosimilar infliximab(CT-P13)(2015-2016, 50%). We hypothesized that the guidelines could be perceived as a surrogate randomization tool where calendar-time rather than patient-specific factors defined choice of bDMARD. Objectives To assess compliance to guidelines (justifying the assumption of surrogate randomization) and compare effectiveness of CTZ/ABA/CT-P13 in Danish RA patients treated according to guidelines. Methods Observational cohort study analyzed like a randomized clinical trial (RCT, intention-to-treat). RA patients were identified in DANBIO. Compliance in each calendar period was defined as number of pts adherent to guideline/numbers of all bio-naive pts initiating bDMARD+MTX. Outcomes were DAS28-remission-rates (at 6 and 12-months) and one-year retention rates, compared across treatments (confounder-adjusted multivariable logistic and Cox regression analyses). Results Compliance to guidelines was 70%/65%/59%, and 776 patients were included (CTZ/ABA/CT-P13: 336/215/225). Baseline characteristics were similar across drugs. DAS28 remission-rates after 6 and 12 months were: 37%/34%/44% and 37%/33%/36%, respectively. Adjusted odd ratios for achieving DAS28 remission were at 6 months: 0.96(95% CI: 0.6;1.5) for ABA and 1.38(0.9;2.1) for CT-P13; 12 months: 0.74(0.5;1.2) and 0.96(0.6;1.5), CTZ reference drug(figure). The adjusted hazard ratios for withdrawal were 1.16(95% CI: 0.84;1.60) for ABA and 0.83 for CT-P13(0.59;1.17)(table). Variables are median (IQR) unless otherwise mentioned. *age, gender, DAS28, HAQ, smoking, CCI Abbreviations: CCI: Charlson Comorbidity Index: CI: confidence intervals, DAS28: Disease Activity Score of 28 joints, HAQ: Health assessment questionnaire Conclusion Compliance to guidelines was high. Direct comparison showed that remission and retention rates were highest for CT-P13, intermediate for certolizumab and lowest for abatacept. Results should, however, be interpreted with caution due to wide CIs and risk of residual confounding. Acknowledgement Thanks to Laura Kocher from Karolinska Institutet, Stockholm, Sweden for help with the figure Disclosure of Interests Kathrine Gron Grant/research support from: BMS, Bente Glintborg Grant/research support from: Biogen, Pfizer, AbbVie, Mette Norgaard: None declared, Frank Mehnert: None declared, Mikkel Ostergaard Grant/research support from: Abbvie, Celgene, Centocor, Merck, Novartis, Consultant for: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Lene Dreyer Consultant for: MSD, UCB and Janssen Pharmaceuticals, Speakers bureau: MSD, UCB and Janssen Pharmaceuticals, Speakers bureau: UCB, MSD, Eli Lilly and Janssen Pharmaceuticals., Niels Steen Krogh: None declared, Jakob B. Bjorner Employee of: Optum, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis

Background Large observational studies become more common in rheumatoid arthritis (RA). Disease registers [1] allow to analyse the effectiveness and safety of RA treatments in real-world populations, but observational studies suffer from missing data. To minimise bias, it has been shown that imputing missing data is superior to the use of complete case analysis [2]. Although some imputation methods have been studied in clinical trials of rheumatic diseases [3] and in small registers [4], the various imputation techniques have never been systematically compared in large registers. Objectives To compare the effects of available imputation methods on the estimated values and on RA remission rate for missing disease activity measures in large registers. Methods We used 1000 patients with complete data for disease activity (Disease Activity Score (DAS28) and Clinical Disease Activity Index (CDAI)) at baseline (treatment initiation), 6, 12, and 24 months after initiation of abatacept or a tumor-necrosis factor inhibitor (TNFi) from an existing register collaboration (PANABA). Simulation procedure: Values were deleted randomly and imputed with three types of imputation methods: (1) methods imputing forward in time, such as Last Observation Carried Forward (LOCF) or Linear Forward Extrapolation (LFE); (2) methods considering data both forward and backward in time, such as Nearest Available Observation (NAO), Linear Extrapolation (LE) or Polynomial Extrapolation (PE); and (3) methods using computer-intensive multi-individual imputations, such as Linear Mixed Effects cubic regression (LME3) and Multiple Imputation by Chained Equation (MICE). We conducted a simulation study by performing this procedure 1000 time and computing the mean difference between the true and the imputed values, and between the true remission rate (CDAI and DAS28) and the imputed ones. Results Results are summarised in Fig. 1. At baseline, all methods underestimated the true values by at least 20%. Despite this, LME3 and MICE were able to provide estimates of baseline remission rates with less than 3% of error. For follow-up data, missingness at 6, 12, or 24 months, NAO, LE and PE led to relative bias of the mean values ≤15%, and almost unbiased remission rate. LOCF and LFE respectively over and under-estimated the mean imputed values up to 20%, leading respectively to a non-negligible under and over-estimation of the remission rate. Although LME3 and MICE had low bias in estimating the mean values, they narrowed the distribution of the imputed values and thus strongly underestimated remission rate Conclusion When imputing disease activity in rheumatoid arthritis register data, researchers should prefer Linear Mixed Effects cubic regression (LME3) for baseline and nearest available observation (NAO) for follow-up data. References [1] Finckh A, Courvoisier D. Joint Bone Spine2018;85:271–4. doi:10.1016/j.jbspin.2017.12.005 [2] van der Heijden GJMG, T. Donders AR, Stijnen T, et al. Journal of Clinical Epidemiology2006;59:1102–9. doi:10.1016/j.jclinepi.2006.01.015 [3] van der Heijde D, Fleischmann R, Wollenhaupt J, et al. Ann Rheum Dis2014;73:233–7. doi:10.1136/annrheumdis-2013-203697 [4] Descalzo MA, Garcia VV, Gonzalez-Alvaro I, et al. Rheumatology (Oxford)2013;52:331–6. doi:10.1093/rheumatology/kes245 Disclosure of Interests Denis Mongin: None declared, Kim Lauper Grant/research support from: reports an unrestricted research grant from AbbVie and non-financial support from Pfizer, outside the submitted work, Carl Turesson: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis, Eirik kristianslund: None declared, Tore K. Kvien Grant/research support from: AbbVie, BMS, MSD, Pfizer, Roche and UCB., Consultant for: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Hospira, Merck-Serono, MSD, Novartis, Oktal, Orion Pharma, Pfizer, Roche, Sandoz, Sanofi, Mylan and UCB, Speakers bureau: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Hospira, Merck-Serono, MSD, Novartis, Oktal, Orion Pharma, Pfizer, Roche, Sandoz, Sanofi and UCB, Maria Jose Santos: None declared, Karel Pavelka: None declared, Florenzo Iannone Consultant for: F Iannone has received consultancy fees and/or speaker honoraria from Pfizer, AbbVie, MSD, BMS, Novartis, Lilly, UCB outside this work, Speakers bureau: F Iannone has received consultancy fees and/or speaker honoraria from Pfizer, AbbVie, MSD, BMS, Novartis, Lilly, UCB outside this work, Axel Finckh Grant/research support from: Bristol-Myers Squibb, Pfizer Inc, Consultant for: AbbVie, A2Bio, Bristol-Myers Squibb, MSD, Roche, Pfizer Inc, and UCB, Delphine Courvoisier Grant/research support from: has received an unrestricted grant from MSD for this study, Consultant for: has received consulting fees from BMS, Pfizer, AB2 Bio and Janssen., Paid instructor for: Janssen

Background Whole body MRI (WBMRI) is a new promising tool for assessing synovitis in the whole body in one session, but is less validated. Ultrasound (US) is another sensitive and well-validated imaging technique that can assess the whole body in one session. Objectives To evaluate the agreement between US, WBMRI and clinical assessment of joint inflammation in rheumatoid arthritis (RA) patients on joint and patient level. Methods US, WBMRI and clinical assessment for tender joints (TJ) and swollen joints (SwJ) were performed in 19 RA patients (90% Women, median age 55 (26-73), diseases duration 5.5 years (1-42), SwJ(28) 5 (1-13), TJ(28) 7 (2-24) and DAS28-CRP 4.66 (3.48 -6.66))) fulfilling ACR 1987 criteria for RA. The 28 conventional joints, bilateral ankles and MTP 1-5 were assessed by WBMRI and US. Joint inflammation by US was graded 0-3 on both B-mode and colour Doppler (CD), and subsequently converted to +/- by defining US synovitis as B mode >2 or CD >1, and scored for individual joint. For WBMRI, joint inflammation was defined in two ways; 1) as presence of synovitis and/or osteitis, 2) as the presence of synovitis only. The total inflammatory burden was established as sum scores for the 28 conventional joints for US (US28) and for 26 joints (WBMRI26) for WMBRI - same 28 joints except elbows (due to poor image quality). The max score of a joint in US and WBMRI including osteitis was 2, while WMBRI excluding osteitis was 1. The agreement between the clinical joint assessment, US and WBMRI for joint inflammation was calculated with Cohen’s kappa (κ). The correlations between US28, WBMRI26 and DAS28-CRP were calculated by Spearman correlation coefficient (rho). Results When considering joint inflammation by WBMRI as synovitis and/or osteitis, US28 for synovitis and WBMRI26 sum scores showed good correlation rho= 0.72 (p=0.003) (Fig. 1), whereas US28 and WBMRI26 did not correlate with DAS28 CRP (rho=-0.26, p=0.28; rho=0.20, p=0.47 respectively). Moderate-good agreement was found between US and WBMRI in wrists and MCP 1, 2 and 5(κ= 0.42–0.62) but poor in other joints (κ By comparing WBMRI synovitis (excluding osteitis) with US synovitis, US28 and WBMRI26 sum scores showed weakened correlation rho= 0.46 (p=0.049) (Fig. 2), and without correlation between WBMRI26 and DAS28 CRP (rho=-0.07, p=0.78). At joint level, moderate-good agreement was found between US and WBMRI in wrists, MCP 2 and 5, and PIP 5(κ= 0.41–0.62) but poor in other joints (κ Agreement between US and clinical joint tenderness was poor (all κ Conclusion WBMRI and US sum scores of joint inflammation showed good correlation in RA patients for the overall inflammatory burden. The agreement at joint level was variable. Disclosure of Interests: Sin Ngai Ng: None declared, Mette Bjorndal Axelsen: None declared, Mikkel Ǿstergaard Grant/research support from: Abbvie, Celgene, Centocor, Merck, Novartis, Consultant for: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, and UCB, Iris Eshed: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen, Pfizer, Consultant for: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck, Samsung Bioepis, Jakob Mollenbach Moller: None declared, Susanne Juhl Pedersen: None declared, Lene Terslev Speakers bureau: Speakers fee from : Roche, Novartis, Pfizer, MSD, BMS, Celgene

Background Although the etiology of rheumatoid arthritis (RA) remains unclear, there are evidences suggesting a role of sex steroid hormones in determining the onset and progression of the disease. Objectives The aim of this study was to evaluate whether 47 single nucleotide polymorphisms (SNPs) in steroid hormone-related genes are associated with the risk of RA and anti-TNF drug response. Methods We conducted a case-control study in 3 European populations including 2936 RA patients and 2197 healthy controls. Of those a total of 1985 RA patients were treated with anti-TNF blockers. The association of potentially interesting markers with RA risk or drug response in the discovery population was validated through meta-analysis with data from DREAM and DANBIO registries. Results were corrected for multiple testing (Meff method; p=0.0011). The value of steroid hormone-related variants for prediction of anti-TNF drug response was also assessed using stepwise logistic regression analyses. The area under the curve (AUC) of a receiver operating characteristic (ROC) curve analysis and a −2 log likelihood ratio (LR) test were used to assess whether the genetic model fitted significantly better the data compared to the reference model. A randomization test (50.000 iterations) was run to confirm the consistency of the results. Results Although none of the selected variants played a relevant role in modulating RA risk, the meta-analysis of the linear regression data with those from the DREAM and DANBIO registries showed a significant correlation of the CYP3A4 rs11773597 and CYP2C9 rs1799853 variants with changes in DAS28 after the administration of anti-TNF drugs (p=0.00074, and p=0.006). An overall haplotype analysis also showed that the ESR2 GGG haplotype significantly associated with a reduced chance of having poor response to anti-TNF drugs (p=0.0009). Finally, a ROC curve analysis confirmed that a model built with 8 steroid hormone-related variants significantly improved the ability to predict drug response compared with the reference model including demographic and clinical variables (AUC=0.633 vs. 0.556; P LRtest =1.52·10–6). Conclusions These data suggest that steroid hormone-related genes play a role in determining the response to anti-TNF drugs. Disclosure of Interest L. Canet: None declared, J. Sanchez-Maldonado: None declared, A. Rodriguez-Ramos: None declared, C. Lupianez: None declared, H. Canhao: None declared, M. Martinez-Bueno: None declared, A. Escudero: None declared, J. Segura-Catena: None declared, S. Sorensen: None declared, M. Hetland: None declared, M. Soto-Pino: None declared, M. Ferrer: None declared, A. Garcia: None declared, B. Glintborg: None declared, I. Filipescu: None declared, E. Perez-Pampin: None declared, A. Gonzalez-Utrilla: None declared, M. Lopez-Nevot: None declared, P. Conesa-Zamora: None declared, A. den Broeder: None declared, S. da Vita: None declared, S. Hove Jacobsen: None declared, E. Collantes: None declared, L. Quartuccio: None declared, J. Fonseca: None declared, M. Coenen: None declared, V. Andersen Consultant for: VA has received compensation for consultancy and for being a member of an advisory board from MSD (Merck) and Janssen, R. Caliz-Caliz: None declared, J. Sainz: None declared

Background Targeting MRI remission in rheumatoid arthritis (RA) patients in clinical remission may improve clinical outcome and halt joint damage progression. Objectives To determine whether a treat-to-target (T2T) strategy based on structured MRI assessments targeting absence of osteitis/bone marrow oedema (BME) would lead to improved clinical and radiographic outcomes, compared with a conventional T2T strategy in RA patients in clinical remission. Methods The IMAGINE-RA study was a 2 year investigator-initiated, randomised, open-label multicentre study. Two hundred RA patients in clinical remission (defined as: DAS28-CRP Results Primary and secondary clinical and radiographic outcomes at 24 months are presented in the table 1. 76 patients in the MRI T2T arm and 95 patients in conventional T2T arm completed the study. Of them 64 patients (85%) in the MRI T2T arm and 83 patients (88%) in the conventional T2T arm reached the primary clinical endpoint (chi-square=0.324, p=0.569) and 49 patients (66%) in the MRI T2T arm and 58 (62%) in the conventional T2T arm reached the primary radiographic endpoint (chi-square=0.265, p=0.606). ACR/EULAR remission rates, swollen joint count, patient VAS global and HAQ favoured the MRI T2T arm (p Conclusions Targeting absence of MRI BME in addition to a conventional T2T strategy in RA patients in clinical remission had no effect on the probability of achieving DAS28-CRP remission or halt radiographic progression. However, more patients achieved ACR/EULAR remission and improvements in physical function when MRI was used for treatment guidance. Clinicaltrials.gov Identifier: NCT01656278 Disclosure of Interest None declared

Background In Denmark, patients (pts) treated with originator etanercept (ETA) 50 mg SC conducted a mandatory non-medical switch to biosimilar SB4 in April 2016 (switchers). Pts treated with 25 mg ETA or 50 mg powder-solution were not mandated to switch (non-switchers). Some switchers resumed ETA during follow-up (back-switchers). Objectives To investigate the frequency of back-switching after the non-medical switch from ETA to SB4, and in back-switchers to study, 1) baseline characteristics at the time of initial switch (ETA->SB4), 2) reasons for SB4 withdrawal, 3) changes in disease activity during treatment with SB4 and after back-switching. Methods Patient data were retrieved from the DANBIO registry (censored August 2017). For back-switchers, disease activity at the start of SB4 (=baseline) and at the time of back-switching to ETA were compared, and changes in disease activity between the two time points were calculated (=delta values), stratified by indication (RA/PsA/AxSpA). Baseline characteristics of back-switchers were compared to the rest of the switch population (Chi-sq, Mann-Whitney U-test). Abbreviations are shown in table 1. Results 1641 pts switched from ETA to SB4. Of these, 299 (18%) withdrew SB4 therapy during 1 year follow-up and either switched back to ETA (n=120, 7%), started another bDMARD (n=104), died (n=9), were lost to follow-up (n=1) or did not re-start bDMARDs (n=65). Among the 120 back-switchers, SB4 was withdrawn due to LOE (52%), AE (39%), or other/unknown reasons (9%). The reasons for withdrawal of SB4 in back-switchers are listed in table 1. No major safety events occurred. The median time on SB4 before back-switching was 120 (IQR 73–193) days, and the time between stop of SB4 and re-start of ETA was 11–1 days. Baseline characteristics of back-switchers vs the rest of the switch population were similar (all p>0.05). Among back-switchers who stopped SB4 due to LOE, PGA increased during SB4 treatment, whereas CRP and SJC were largely unchanged (table 1). At the date of censoring, 104/120 back-switchers (87%) were still treated with originator ETA (median treatment duration 236 (155–302) days). Conclusions In a nationwide cohort of 1621 arthritis patients that were switched from ETA to SB4, 7% switched back to ETA. Back-switchers had no distinct clinical or disease characteristics upon start of SB4. AEs prior to back-switching were largely unspecific. In pts who withdrew SB4 due to LOE, PGA had increased. Reasons for back-switching appeared to be predominantly subjective rather than objective (nocebo effect). Originator drug was still available (25 mg or 50 mg powder-solution), which may have encouraged back-switching. References [1] Glintborg, et al. Arthritis Rheum2017;69(suppl 10). [2] Glintborg, et al. Abstract, EULAR2018. Acknowledgements Partly sponsored by Biogen Disclosure of Interest B. Glintborg Grant/research support from: Abbvie, Biogen, Pfizer, I. Sorensen: None declared, E. Omerovic: None declared, F. Mehnert: None declared, N. Manilo: None declared, K. Danebod: None declared, D. Jensen: None declared, H. Nordin: None declared, A. G. Loft Grant/research support from: AbbVie, MSD, Novartis, Pfizer, Roche, UCB, O. Hendricks Grant/research support from: Abbvie, Roche, Novartis, S. Chrysidis: None declared, B. Andersen: None declared, J. Raun: None declared, H. Lindegaard: None declared, J. Espesen: None declared, S. Jakobsen: None declared, I. M. Hansen Grant/research support from: Roche, E. Dalsgaard: None declared, D. Pedersen: None declared, S. Kristensen: None declared, A. Linauskas: None declared, L. Andersen: None declared, J. Grydehoj: None declared, N. Krogh: None declared, M. Hetland Grant/research support from: Abbvie, Biogen, BMS, CellTrion, MSD, Novartis, Orion, Pfizer, Samsung, UCB

Background In Denmark, rheumatoid arthritis(RA), psoriatic arthritis(PsA) and axial spondyloarthritis(AxSpA) patients (pts) treated with originator etanercept (ETA) 50 mg SC conducted a mandatory non-medical switch to biosimilar Etanercept (SB4) in April 2016 (switchers). Pts treated with 25 mg ETA or 50 mg powder solution were not mandated to switch (non-switchers). Objectives To characterise switchers and non-switchers, and to compare 1 year treatment retention in switchers with non-switchers and a historic cohort of ETA treated pts. Methods Pt data were retrieved from the DANBIO registry and national registries. We applied Chi-square/Mann-Whitney for comparisons and Kaplan-Meier/Cox regression analyses (crude, adjusted for gender/age/MTX/remission/comorbidities/ETA-start-year) for drug retention. The historic cohort encompassed pts treated with ETA by Jan 1st 2015. Results Of 2,061 ETA treated pts by April 2016, 79% switched to SB4 (933RA/351PsA/337AxSpA), whereas 21% (286RA/56PsA/98AxSpA) continued ETA. In RA, compared to switchers, non-switchers more often received 25 mg ETA, had higher disease activity and HAQ (table 1). Similar patterns were seen for PsA and AxSpA. Median(IQR) follow-up was 383(314–414)days. In all 3 cohorts, withdrawals were mainly due to lack of effect. Retention rate was lowest in non-switchers (figure 1). 1 year adjusted rates were 83% (95% CI 79–87) in switchers, 77%(72–82 in non-switchers and 90%(88–92 in historic cohort. Pts not in remission had poorer retention than pts in remission both in switchers (hazard ratio 1.7 (1.3–2.2) and non-switchers (2.4 (1.7–3.6)). Numbers are medians (IQR) unless otherwise stated. * DAS28 Conclusions Of >2000 ETA treated pts, ≈80% switched to SB4. Non-switchers had higher disease activity and more often received 25 mg ETA. Switchers had poorer retention rate than a historic ETA-cohort, but better than non-switchers. Withdrawal was most common in pts not in remission. These real-world data indicate that a switching-to-biosimilar option facilitated clinical decision making in standard care, leading to withdrawal from ineffective therapy in both switchers and non-switchers. Acknowledgements Partly sponsered by Biogen Disclosure of Interest B. Glintborg Grant/research support from: Abbvie, Biogen, Pfizer, I. Sorensen: None declared, E. Omerovic: None declared, F. Mehnert: None declared, N. Manilo: None declared, K. Danebod: None declared, D. Jensen: None declared, H. Nordin: None declared, A. G. Loft Grant/research support from: AbbVie, MSD, Novartis, Pfizer, Roche, UCB, O. Hendricks Grant/research support from:: Abbvie, Roche, Novartis, S. Chrysidis: None declared, B. Andersen: None declared, J. Raun: None declared, H. Lindegaard: None declared, J. Espesen: None declared, S. Jakobsen: None declared, I. M. Hansen Grant/research support from: Roche, E. Dalsgaard: None declared, D. Pedersen: None declared, S. Kristensen: None declared, A. Linauskas: None declared, L. Andersen: None declared, J. Grydehoj: None declared, N. Krogh: None declared, M. Hetland Grant/research support from: Abbvie, Biogen, BMS, CellTrion, MSD, Novartis, Orion, Pfizer, Samsung, UCB

Background Few RCTs have investigated long-term (>10 years (yrs)) outcomes of goal-directed synovitis suppression in early rheumatoid arthritis (RA). The CIMESTRA trial was a 2-year double-blinded Danish multicenter study on aggressive treatment with csDMARDS (methotrexate (MTX) versus MTX and cyclosporine) in combination with intra-articular glucocorticoids (1+2). Disease control after 2 yrs was excellent with $≈ $50% in remission and halted radiographic progression in both groups. We present 11 yr follow-up data. Objectives The aims were to 1) investigate the clinical and radiographic status and 2) identify baseline predictors of functional status and erosive progression. Methods Of 160 patients (pts) included, 130 pts also had MRI of the wrist performed at baseline. 17 pts had died since baseline. All living pts were contacted and 120 signed informed consent to participate in a 11 yrs9 follow-up visit assessing e.g. treatment, disease activity (DAS28, CRP, 4 variables), physical function (HAQ), X-ray of hands and feet. Baseline MRI was scored by OMERACT rheumatoid arthritis MRI scoring (RAMRIS) system, X-rays by Sharp-van der Heijde total Sharp Score (TSS). Multivariable linear regression analyses of a panel of baseline variables (see foot note in table) with backward selection were performed with HAQ at 11 yrs (HAQ 11 ) and radiographic progression since baseline (ΔTSS 0–11 ) as dependent variables. Results 120 of 160 pts (75%) completed the 11 yrs visit. 96 pts with available baseline MRI and X-rays of both time points were included in the prediction models. Withdrawal analysis comparing the 160 pts with the 40 and 64 pts who were not included showed similar baseline characteristics except for higher DAS28 and HAQ score for withdrawers. Follow-up was after 11.6 yrs (10.7–12.2) (median (IQR)). Pts were 63 yrs (55–72) and 70% females. 20% received biologics (+/- csDMARD), 53% csDMARD alone, 27% were in drug free remission. DAS28 was 2.0 (1.5–2.6); pain score: 1 cm (0.3–3); pt. global: 1.1 cm (0.2–2.9); swollen joint count (28SJC): 0 (0–0); tender joint count (28TJC): 0 (0–1). 76% of pts were in DAS28 remission; HAQ-score was 0.25 (0–0.75); ΔTSS 0–11 (median (IQR)):4 (0–13); ΔTSS 0–11 (mean±SD): 10.9±16.9). The annual progression rate since baseline was median (IQR):0.4 (0–1.1); mean±SD:0.96±1.52. Multivariable linear regression analyses are shown in Table. Conclusions 11 years after diagnosis 75% were in DAS28 remission. HAQ-score was low, and mean radiographic progression was References Arthritis Rheum 2006; 54: 1401–9. Ann Rheum Dis 2008; 67: 815–22. Disclosure of Interest M. L. Hetland Grant/research support from: AbbVie, BMS, MSD, Pfizer, Orion, Novartis, Biogen, Eli Lilly, K. Stengaard-Petersen: None declared, P. Junker: None declared, H. Lindegaard: None declared, T. Ellingsen: None declared, J. Podenphant: None declared, H. Skjodt: None declared, A. Vestergaard: None declared, B. Ejbjerg: None declared, S. Jacobsen: None declared, N. S. Krogh: None declared, M. Ostergaard Grant/research support from: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Centocor, GSK, Hospira, Janssen, Merck, Mundipharma, Novartis, Novo, Orion, Pfizer, Regeneron, Schering-Plough, Roche, Takeda, UCB, K. Horslev-Petersen: None declared

Background None of the currently accepted remission criteria in rheumatoid arthritis (RA) incorporate inflammation on imaging. Signs of inflammation on ultrasound (US) and magnetic resonance imaging are frequently seen in RA patients in clinical remission.(1–3) It is not known whether patients in longstanding clinical and radiographic remission obtained through a DAS28 driven treat to target (T2T) strategy by conventional synthetic disease modifying anti-rheumatic drugs (csDMARD) or by biologic (bDMARD) therapy differ with respect to US detected synovitis. Objectives In RA patients in longstanding clinical and radiographic remission, achieved by a DAS28-driven T2T strategy, to investigate if US signs of inflammation differs between RA patients, treated with csDMARD or bDMARD (+/- csDMARD). Methods Eighty-seven patients with RA in longstanding clinical (continuous DAS28 Results Clinical characteristics and US findings are shown in the table. All 87 patients fulfilled DAS28 remission criteria at entry and CDAI remission was fulfilled in 76% and 79% in the csDMARD and bDMARD group, respectively. Complete absence of any signs of US inflammation (GSS=0 and CDA=0) was seen in 0% and 14% in the csDMARD and bDMARD groups, respectively (p=0.01), while minimal US inflammation (GSS≤1 and CDA=0) was seen in 33% and 40% (NS). CDA in at least one joint was seen in the majority of patients in both groups, 58% and 57% respectively. Conclusions The majority of RA patients, in this cohort of patients in longstanding clinical and radiographic remission obtained through a DAS28 driven T2T strategy, had signs of inflammation as assessed by US, irrespective of receiving biologic treatment or not. For patients in clinical remission, the consequences of sustained US inflammation still have to be investigated. References Brown AK et al.: Arthritis Rheum 2006;54(12):3761–73. Saleem B et al.: Arthritis Rheum 2009;60(7):1915–22. Gandjbakhch F et al.: J Rheumatol 2011;38(9):2039–44. Disclosure of Interest None declared

Background The multi-biomarker disease activity (MBDA) test uses a validated algorithm with 12 serum protein biomarkers to assess disease activity in patients with RA. The MBDA score has previously been found to be a predictor of risk for radiographic progression (RP). Objectives To evaluate data from six cohorts to collectively establish the relationship between the MBDA score and risk for RP. Methods Clinical, MBDA score and radiographic data were analyzed for 6 cohorts with N>100: Leiden, SWEFOT Year 1, SWEFOT Year 2, OPERA Year 1, and AMPLE Year 1 (abatacept and adalimumab arms) (see Figure). Analyses used published results when available or patient-level data when not (i.e., for Leiden; and for OPERA CRP analyses). Frequency of RP over one year was determined by category of MBDA score (low, moderate [30–44], high on a scale of 1–100) at the start of the year for four cohorts and by category of MBDA score at the end of the year for AMPLE cohorts (as published). RP was defined using the threshold for change in total modified Sharp score (ΔmTSS) specific to each study (2 to >5 TSS units). Positive and negative predictive values (PPV and NPV) were determined for each study by comparing patients with high MBDA score (>44), DAS28-(ESR/CRP) (>5.1 or >4.09) or CRP (>3 mg/dL) vs. those in a not-high category. Relative risk (RR) for RP was determined for each study, and in a meta-analysis of the non-overlapping patient groups with MBDA scores available at the start of the year (Leiden, SWEFOT Year 1 and OPERA Year 1). Results of multivariate analyses and analyses that combined MBDA score with other risk factors for RP were summarized. Results The 6 study cohorts included patients receiving csDMARDs alone or with adalimumab, infliximab or abatacept. Overall rates of RP were 10–26%. In each study, RP was most frequent among patients with a high vs. not-high MBDA score (>44 vs. ≤44). For high MBDA scores, NPVs were 93–97% and PPVs were 18–32%, with RR values of 3.6–9.5 (P=0.002 to 5) or high DAS28-CRP, with PPV as high as 57%. Conclusions High MBDA scores were associated with increased risk for RP in 6 study cohorts, including patients treated with csDMARDs, TNFi and abatacept. Based on high NPVs (≥93%), the MBDA score used alone had clinical value for identifying patients with little or no risk of RP. Combining the MBDA score with clinical measures yielded PPVs approaching 60%, suggesting that biomarkers can help stratify patients by their risk for RP. Disclosure of Interest J. Curtis Grant/research support from: Crescendo Bioscience Inc., Consultant for: Crescendo Bioscience Inc., C. Brahe: None declared, M. Ostergaard Grant/research support from: AbbVie, BMS, Boehringer-Ingelheim, Eli Lilly, Janssen, Merck, Pfizer, Roche, UCB, Celgene, Sanofi, Regeneron, Novartis, T Jensen, M. Hetland Grant/research support from: AbbVie, BMS, MSD, Pfizer, Crescendo Bioscience Inc., UCB, Eli Lilly, Speakers bureau: Orion, K. Hambardzumyan: None declared, S. Saevarsdottir: None declared, X. Wang Shareholder of: Myriad Genetics, Inc., Employee of: Crescendo Bioscience Inc., E. Sasso Shareholder of: Myriad Genetics, Inc., Employee of: Crescendo Bioscience Inc., T. Huizinga Consultant for: Merck, UCB, Bristol Myers Squibb, Biotest AG, Pfizer, GSK, Novartis, Roche, Sanofi-Aventis, Abbott, Crescendo Bioscience Inc., Nycomed, Boeringher, Takeda, Zydus, Epirus, Eli Lilly

Background Psoriatic arthritis (PsA) is a chronic inflammatory disorder associated with skin and joint manifestations, several extra-articular symptoms, various comorbidities, and disability. The emergence of tumour necrosis factor inhibitor (TNFi) therapy has dramatically changed the course of disease. Over the past decade new TNFi therapies have emerged (certolizumab pegol and golimumab), and recently ustekinumab and secukinumab have also become available for PsA. Objectives The objective of this study was to assess the relative use of biological agents (bDMARDs) in PsA from 2006 through 2014, using data from the Nordic Rheumatology registers. Methods Based on data from the observational registers DANBIO, ICEBIO, NOR-DMARD, ROB-FIN, and SRQ registers, PsA patients initiating treatment with bDMARDs as a first or subsequent biological therapy were identified. Adalimumab, etanercept and infliximab were grouped as “first generation TNFi therapies”; certolizumab pegol and golimumab were grouped as “second generation TNFi”. Treatments with ustekinumab during the study period were also identified. Descriptive statistics for prescription patterns of bDMARD therapy were calculated. Results A total of 11,458 treatment initiations were identified (DANBIO 3,068, ICEBIO 357, NOR-DMARD 1,113, ROB-FIN 708, SRQ 6,212). 54% of the patients were female. Overall, 5,695 patients initiated a first generation TNFi, 912 a second generation TNFi, and 16 ustekinumab, as their first course of biological treatment. The corresponding numbers for those initiating a second (or more) biological treatment were 3,606, 1,090 and 139 patients, respectively. The figure displays the annual number of treatment initiations stratified by treatment type. The total yearly number of first course biological treatment increased significantly throughout the period (p Conclusions Across the Nordic countries the prescription pattern for biological therapies for PsA has changed significantly over time. After 2012 initiation of the first generation TNFi is decreasing both as first and second course therapy, whereas second generation TNFi are increasing both as first and second course of biologic intervention. Collaboration across registers will allow for robust assessment of the uptake of newer biological therapies. Acknowledgements This study was partly funded by a grant from NordForsk and Janssen Pharmaceuticals. Disclosure of Interest T. S. Jorgensen Speakers bureau: Abbvie, Roche, Novartis, UCB, Biogen, L. Dreyer Speakers bureau: MSD, UCB and Janssen Pharmaceuticals, B. Guðbjornsson Speakers bureau: Actavis, Celgene, MSD, Pfizer, M. Hetland Speakers bureau: BMS, MSD, AbbVie, Roche, Eli Lilly, Pfizer, Orion, Novartis, B. Glintborg Speakers bureau: Abbvie, J. Askling Grant/research support from: AstraZeneca, UCB, Lilly, Pfizer, Roche, Merck,Samsung, Janssen, K. Chatzidionysiou Speakers bureau: AbbVie, Pfizer, Eli Lilly, UCB, Roche., D. Di Giuseppe: None declared, L. Jacobsson Consultant for: Abbvie, Celegen, MSD, Novartis and UCB, J. Wallman Consultant for: Novartis, Celgene, UCB, E. Kristianslund: None declared, I. Olsen: None declared, K. Fagerli: None declared, E. Lie Speakers bureau: AbbVie, Celgene, Hospira and Pfizer., D. Nordstrom Speakers bureau: AbbVie, BMS, Lilly, MSD, Novartis, Pfizer, Roche, UCB., K. Aaltonen: None declared, J. Joensuu Speakers bureau: Pfizer., T. J. Love: None declared, A. J. Geirsson: None declared, L. E. Kristensen Speakers bureau: Pfizer, AbbVie, Amgen, UCB, Celgene, BMS, MSD

Background In Denmark, biological drugs are provided free by the hospitals to the patients via a tax-based system. In 2015 a non-medical switch from originator infliximab to CT-P13 was conducted (1). According to national guidelines in April 2016, a non-medical switch from originator (ETA, Enbrel® 50 mg/week) to biosimilar etanercept (SB4, Benepali®) was dictated when SB4 was marketed, including patients with inflammatory rheumatic diseases treated in routine care. Objectives To investigate 3 months9 disease activity and 5 months9 treatment withdrawal in ETA-treated patients (pts) with rheumatoid arthritis (RA), psoriatic arthritis (PsA) and axial spondyloarthrits (SpA), who were switched to SB4 and monitored prospectively in the DANBIO registry. Methods Pts with RA/PsA/SpA followed in DANBIO since start of first bDMARD were included. Disease activity at 3 months before switch (pre-switch), at the switch and after 3 months (post-switch) and changes over time (Δpre-switch and Δpost-switch) were calculated. Disease flare was defined as ΔDAS28≥1.2 (RA/PsA) or ΔASDAS≥1.3 (SpA). Factors associated with withdrawal (gender/age/diagnosis/bDMARD-treatment-no/comedication methotrexate/baseline CRP/patient9s global score) were explored by multivariable Cox regression analysis. Results In total, 1548 switch pts were identified (891 RA, 335 PsA, 322 SpA). 60% were women, age (median (IQR) 56 (44–65) yrs)). Prior ETA treatment duration was 5.2 (3.2–8.0) yrs. ETA was the first biological treatment in 49%, and the second in 33% of pts. Concomitant MTX was given in 60% (RA)/49% (PsA)/15% (SpA). Median follow-up time was 154 (110–178) days. Disease activity remained largely unchanged 3 months prior to vs. after the switch (Table). The proportion of patients with disease flare pre-/post switch was 8%/13% (RA), 9%/13% (PsA), 5%/5% (SpA). Overall, 129 pts (9%) stopped SB4 treatment during 5 months9 follow-up (Table). Prior ETA treatment duration in these patients was 4.5 (2.7–7.1) years. Higher patient9s global score (HR 1.12/cm, 95% CI (1.05–1.21), p=0.002) and no concomitant methotrexate (HR 2.28 (1.48–3.52), p Conclusions In 1548 patients with inflammatory rheumatic diseases treated with ETA for >5 years, disease activity was largely unaffected in the majority of patients 3 months after non-medical switch to SB4 and comparable to the fluctuations observed in the 3 months prior to the switch. Several patients (≈9%) stopped treatment during 5 months follow-up. Higher patient9s global score and no use of methotrexate were associated with withdrawal. Longer follow-up will offer additional understanding of the potential efficacy and safety consequences of the non-medical switch. References Glintborg et al. Arthritis Rheumatol. 2016; 68 (suppl 10): Abstract no 951. Acknowledgements Data analysis was partly financially supported by Biogen. Disclosure of Interest B. Glintborg Grant/research support from: Abbvie, Biogen, I. Sorensen: None declared, A. G. Loft: None declared, J. Esbesen: None declared, H. Lindegaard: None declared, D. Jensen: None declared, K. Danebod: None declared, S. Dieperink: None declared, O. Hendricks: None declared, I. M. Hansen Grant/research support from: Roche, A. Linauskas: None declared, S. Kristensen: None declared, L. Andersen: None declared, M. Hossein: None declared, H. Nordin: None declared, B. Andersen: None declared, S. Chrysidis: None declared, J. Raun: None declared, N. Manilo: None declared, J. Grydehoj: None declared, E. Dalgaard: None declared, D. Pedersen: None declared, N. Krogh: None declared, M. Hetland Grant/research support from: Orion, BMS, AbbVie, Biogen, Pfizer, MSD, Eli Lilly

Background Rheumatoid factor (RF) and anti-citrulinated protein antibodies (ACPA) are used as diagnostic tools, but may also be used as prognostic factors or as predictors of response to therapy, as these biomarkers have been associated with better clinical responses to some bDMARDs. Objectives To examine whether seropositivity has a similar impact on drug discontinuation of different bDMARDs with a non-anti-TNF mode of action (non-aTNF bDMARDs). Methods This is a pooled analysis of 10 observational European RA registries (FR, CZ, DK, NO, PT, RO, ES, SE, CH, NL). Inclusion criteria were a diagnosis of RA, initiation of treatment with abatacept (ABA), rituximab (RTX) or tocilizumab (TCZ) and available information on RF and/or ACPA status. The exposure of interest was seropositivity, which was defined as positive if RF or ACPA was positive and negative if both were negative. The primary endpoint was overall drug discontinuation, defined as the period between treatment initiation and treatment discontinuation. Because national differences may constitute a potential confounder, we only included national registries with information for all 3 bDMARD and pooled data across registries only after excluding significant effect modification by country. Drug discontinuation was analyzed using a Cox proportional hazard model, including drug, seropositivity, and their interaction, adjusting for age, gender, disease duration, baseline DAS28, concomitant synthetic DMARD (sDMARDs), number of previous sDMARDs and bDMARDs, and stratifying by country and calendar year. Results We found no effect modification by country, allowing us to pool data from 12040 patients (Table). In crude analyses, seropositivity was associated with a lower drug discontinuation with all 3 bDMARD (p-value interaction 0.22), with a hazard ratio for seropositive vs. seronegative (HR) 0.89 (95% CI: 0.82–0.97). In adjusted analyses, seropositivity remained associated with a lower drug discontinuation, but the effect differed by drug (p interaction 0.01): ABA: HR for seropositive vs. seronegative: 0.76 (95% CI 0.66–0.88), RTX: 0.88, (95% CI: 0.70–1.10), and TCZ: 1.08, (95% CI: 0.89–1.31). Two-by-two drug to drug comparisons showed that the effect of seropositivity differed between ABA and TCZ (p=0.004), but not between ABA and RTX (p=0.29), or between TCZ and RTX (p=0.16). Other factors associated with discontinuation were higher baseline disease activity and more previous bDMARD. Conclusions Data from this pooled european registry analysis suggests that seropositivity is associated with lower drug discontinuation of non-aTNF bDMARDs. This effect differed between drugs and was significant for ABA, but not for TCZ or RTX. The impact of seropositivity on other measures of effectiveness still needs to be investigated. Disclosure of Interest A. Finckh Grant/research support from: BMS, Speakers bureau: Abbvie, Roche, Pfizer, UCB, D. Courvoisier: None declared, J.-E. Gottenberg: None declared, X. Mariette: None declared, J. Morel: None declared, S. A. Bergstra: None declared, V. Hernandez: None declared, C. Codreanu Grant/research support from: Abbvie, Pfizer, Roche, Consultant for: MSD, Pfizer, Roche, Paid instructor for: Abbvie, Bristol-Myers Squibb, Janssen, MSD, Pfizer, Roche and UCB, T. K. Kvien: None declared, M. J. Santos: None declared, K. Pavelka: None declared, M. Hetland Grant/research support from: AbbVie, BMS, MSD, Biogen, UCB, Pfizer, Eli Lilly, Roche, Speakers bureau: Orion, K. Chatzidionysiou Consultant for: AbbVie, Pfizer, Eli Lilly, UCB, Roche, J. Askling Grant/research support from: Abbvie, UCB, Lilly, Janssen, Samsung, Pfizer, MSD, Roche, C. Turesson Grant/research support from: Abbvie, Pfizer, Roche, Consultant for: MSD, Pfizer, Roche, Paid instructor for: Abbvie, Bristol-Myers Squibb, Janssen, MSD, Pfizer, Roche and UCB, C. Gabay: None declared, R. Van Vollenhoven: None declared

Background Studies in established rheumatoid arthritis (RA) have shown that radiographic progression is associated with increasing health assessment questionnaire (HAQ) score. However, most studies have failed to demonstrate this association at the early stage of the disease. In addition, little is known about how specific pathologies, e.g. joint inflammation, tenosynovitis and joint damage, contribute to different patient-reported outcomes (PROs). Objectives To examine the association between MRI wrist inflammation and damage with PROs in patients with early RA. Methods MRIs of the wrist and hand were obtained from 210 early RA patients participating in two investigator-initiated, randomized, controlled studies (CIMESTRA/OPERA), which aimed at achieving inflammatory control by use of conventional and/or biologic drugs combined with intra-articular injection of glucocorticoids. The image-sets were assessed according to the RA MRI scoring system (RAMRIS) for inflammation (synovitis, tenosynovitis, osteitis) and damage (bone erosions, joint space narrowing) at baseline (n=210), 1 (n=206) and 5 (n=113) years follow-up. Data from the two studies were pooled and assessed for associations between MRI features and HAQ, patient global visual analogue scales (VAS-PtGlobal) and VAS pain using Spearman correlation for status and change scores, univariate and multivariable linear regression analyses for change scores and generalized estimating equations for status and change scores. MRI features were further tested for trends against specific hand-related HAQ questions using the Jonckheere trend test. Results MRI inflammation, but not damage, showed statistically significant associations with HAQ, VAS-PtGlobal and VAS pain for status and change scores, independently of swollen joint count and level of C-reactive protein. Synovitis and tenosynovitis were the MRI features most consistently associated with PROs, particularly VAS-PtGlobal and VAS pain (Table 1). MRI synovitis and tenosynovitis mean scores increased with the level of difficulty to cut meat and open a milk carton (p Conclusions MRI-assessed inflammation, but not damage, in the early RA wrist is associated with patient-reported physical impairment, global disease activity and pain, and the amount of wrist inflammation influences physical hand function. Disclosure of Interest D. Glinatsi: None declared, J. Baker: None declared, M. Hetland Grant/research support from: BMS, AbbVie, Pfizer, UCB-Nordic, MSD, K. Horslev-Petersen Consultant for: AbbVie and UCB, B. Ejbjerg: None declared, K. Stengaard-Pedersen: None declared, P. Junker: None declared, T. Ellingsen: None declared, H. Lindegaard: None declared, I. Hansen: None declared, T. Lottenburger: None declared, J. Moller: None declared, L. Ornbjerg: None declared, A. Vestergaard: None declared, A. G. Jurik: None declared, H. Thomsen: None declared, T. Torfing: None declared, S. Bisgaard: None declared, M. Axelsen Grant/research support from: Abbvie, M. Ostergaard Grant/research support from: Abbvie, BMS, Janssen and Merck, Consultant for: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Centocor, GSK, Hospira, Janssen, Merck, Mundipharma, Novartis, Novo, Orion, Pfizer, Regeneron, Schering-Plough, Roche, Takeda, UCB, and Wyeth

Background According to Danish national guidelines issued in 2015, pts (pts) with inflammatory rheumatic diseases in routine care treatment with originator infliximab (INX) must switch to the cheaper biosimilar infliximab (CT-P13). This switch was done for economic reasons (CT-P13 64% cheaper than INX). Since any treatment change potentially induces additional guidance of pts and use of hospital services, it is relevant to investigate whether the switch affected use of hospital resources. Objectives To study difference in rates of outpatient activities and services provided 6 months before vs after the switch to CT-P13 for pts treated at rheumatologic departments which provide infliximab treatment. Methods The switch population and switch dates were identified in the Danish quality registry, DANBIO (1). Vital status was validated in the Central Person Registry. The Danish National Patient Registry (NPR) provided information regarding outpatient contacts and services. The use of 16 types of services relevant to the rheumatologic specialty was identified and included outpatient visits, infliximab infusion, nurse counselling, phone consultation, and rheumatologic ultrasound. Number of days with these services was counted. Services performed on the switch date were analyzed separately. Thus, for each patient the following rates were calculated 6 months before and after the switch: 1) days with at least one outpatient service provided, and 2) number of services provided. In addition, the weekly rate of days with services was calculated. Only pts who were alive and could be followed in the NPR for 6 full months after the switch were included. Paired t-tests were used to compare rates before and after switch. A graphical interrupted time series analysis was conducted for weekly number of services provided. Results Among 802 pts identified, 769 had available NPR outpatient data from hospital departments of rheumatology. The 769 pts had 1484 outpatient treatment contacts at the included rheumatology departments with a total of 9243 days with services provided (including 693 on the switch date). The mean rate of days with services provided was 5.4 before the switch and 5.7 after switch (p=0.0003). The weekly rate of days with services showed no obvious differences before and after the switch but had a clear 8-week pattern (corresponding to the average infusion interval) (Figure). The total number of services provided was 19,752 (2,019 of these on the switch date). There were significant increases in the rates before vs after switch for 6 of the 16 service categories, although the mean rates were small: telephone consultations (mean rate 1.0 before vs. 1.2 after), patient guidance (0.5 vs. 0.4), intravenous medication (0.0 vs. 0.1), clinical controls (2.1 vs. 2.3) and clinical investigations (0.3 vs. 0.5), whereas the rate of infliximab treatment decreased (3.1 vs 3.0) (all p Conclusions This analysis showed that there were only small differences in the rates of days with outpatient services and rates of services 6 months before and after the switch from original to biosimilar infliximab. Thus, it is unlikely that the switch is associated with substantially higher cost of health care resources. References Glintborg et al. Arthritis Rheumatol. 2016; 68 (suppl 10). Disclosure of Interest B. Glintborg Grant/research support from: Abbvie, J. Sorensen Grant/research support from: Abbvie, M. Hetland Grant/research support from: Orion, BMS, AbbVie, Biogen, Pfizer, MSD

Background High quality data from prospective, real life patients with spondyloarthritis (SpA) is needed to strengthen patient-level research in non-experimental clinical settings. A research network collaboration of registries collecting data on patients with SpA, “EuroSpA” offers opportunities to enhance research capabilities in the real world setting. Objectives To assess patient numbers, data extent and completeness in European SpA registries and establish an international research collaboration and common data set to address key data gaps for SpA patients treated in routine clinical practice. Methods The “EuroSpA” research network collaboration was established between registries collecting data on SpA patients. A survey was conducted via email and follow-up interviews April-December 2016 to assess patient numbers, data availability and completeness in participating registries. Our survey tool was based on key variables identified through literature review and expert interviews. Results 14 European rheumatology registries submitted information on their data covering approximately 63479 SpA patients, including patients with psoriatic arthritis (PsA), ankylosing spondylitis (AS) and non-radiographic axial spondyloarthritis (nr-axSpA) (Table). Data coverage was comprehensive for comorbidities, demographic and treatment variables, but limited for imaging and in PsA for skin and nail manifestations (figure). Conclusions A European research collaboration network of SpA registries, “EuroSpA”, including $≈ $ 63500 SpA patients enables the collection of key patient variables and strengthens research through increased patient numbers and cross-country comparative research. While core disease activity measures for SpA patients are widely collected, an enhanced standardized core dataset could strengthen future collaboration. Acknowledgements The authors acknowledge Craig Richardson from Novartis Pharma AG, Carol Lines and Seline Eisenring from Quintiles IMS for support in survey data collection and editorial assistance, and Novartis Pharma AG, Basel, Switzerland for financial support of the EuroSpA initiative. Disclosure of Interest M. L. Hetland Grant/research support from: AbbVie, BMS, MSD, Pfizer, Orion, Novartis, Biogen, Eli Lilly, M. Ostergaard Grant/research support from: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Centocor, GSK, Hospira, Janssen, Merck, Mundipharma, Novartis, Novo, Orion, Pfizer, Regeneron, Schering-Plough, Roche, Takeda, UCB, J. Askling: None declared, C. Gabay Grant/research support from: Roche, Pfizer, AB2 Bio, Consultant for: Sanofi, AB2 Bio, AbbVie, Pfizer, BMS, MSD, Roche, Novartis, D. Nordstrom: None declared, O. FitzGerald Grant/research support from: Pfizer, Abbvie, BMS, Novartis, UCB, Janssen, Celgene and Lilly, M. Hernandez Miguel: None declared, M. Santos: None declared, Z. Rotar: None declared, H. Mann: None declared, F. Iannone Consultant for: AbbVie, BMS, Eli Lilly, Janssen, MSD, Novartis, Pfizer, Roche, UCB, M. J. Nissen: None declared, E. Hauge: None declared, J. Gomez-Reino: None declared, F. Diaz-Gonzalez: None declared, M. Tomsic: None declared, K. Pavelka: None declared, F. O9Shea: None declared, C. Sullivan: None declared, M. van de Sande: None declared, I. E. van der Horst-Bruinsma: None declared, G. J. Macfarlane Grant/research support from: Pfizer, AbbVie and UCB, G. T. Jones Grant/research support from: AbbVie, Pfizer, UCB, B. Gudbjornsson: None declared, T. K. Kvien Consultant for: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celltrion, Eli Lilly, Epirus, Janssen, Merck-Serono, MSD, Mundipharma, Novartis, Oktal, Orion Pharma, Hospira/Pfizer, Roche, Sandoz and UCB