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Background: We aimed to describe the uptake of newer biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs) in psoriatic arthritis (PsA) in the Nordic countries and to compare their retention and effectiveness.Methods: Patients with PsA starting a b/tsDMARD in 2012-2020 in five Nordic rheumatology registers were included. Uptake and patient characteristics were described, with comorbidities identified from linkages to national patient registries. One-year retention and 6-month effectiveness (proportions achieving low disease activity (LDA) on the Disease Activity Index for PSoriatic Arthritis based on 28-joint evaluation) for the newer b/tsDMARDs (abatacept/apremilast/ixekizumab/secukinumab/tofacitinib/ustekinumab) were compared with adalimumab through adjusted regression models stratified by treatment course (first, second/third, and fourth or more).Results: In total, 5659 treatment courses with adalimumab (56% biologic-naïve) and 4767 courses with a newer b/tsDMARD (21% biologic-naïve) were included. The uptake of newer b/tsDMARDs increased from 2014 and plateaued in 2018. Patient characteristics appeared similar across treatments at treatment start. Adalimumab was more often used as the first course and newer b/tsDMARDs more often in biologic-experienced patients. Used as a second/third b/tsDMARD, the retention rate and the proportion achieving LDA were significantly better for adalimumab (rate 65%, proportion 59%) compared with abatacept (45%, 37%), apremilast (43%, 35%), ixekizumab (LDA only, 40%) and ustekinumab (LDA only, 40%), but not significantly different from other b/tsDMARDs.Conclusion: Uptake of newer b/tsDMARDs occurred mainly in biologic-experienced patients. Regardless of mode of action, only a minority of patients starting a second or later b/tsDMARD course remained on drug and achieved LDA. Superior outcomes for adalimumab indicate that the positioning of newer b/tsDMARDs in the PsA treatment algorithm remains to be established. Background: We aimed to describe the uptake of newer biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs) in psoriatic arthritis (PsA) in the Nordic countries and to compare their retention and effectiveness. Methods: Patients with PsA starting a b/tsDMARD in 2012-2020 in five Nordic rheumatology registers were included. Uptake and patient characteristics were described, with comorbidities identified from linkages to national patient registries. One-year retention and 6-month effectiveness (proportions achieving low disease activity (LDA) on the Disease Activity Index for PSoriatic Arthritis based on 28-joint evaluation) for the newer b/tsDMARDs (abatacept/apremilast/ixekizumab/secukinumab/tofacitinib/ustekinumab) were compared with adalimumab through adjusted regression models stratified by treatment course (first, second/third, and fourth or more). Results: In total, 5659 treatment courses with adalimumab (56% biologic-naïve) and 4767 courses with a newer b/tsDMARD (21% biologic-naïve) were included. The uptake of newer b/tsDMARDs increased from 2014 and plateaued in 2018. Patient characteristics appeared similar across treatments at treatment start. Adalimumab was more often used as the first course and newer b/tsDMARDs more often in biologic-experienced patients. Used as a second/third b/tsDMARD, the retention rate and the proportion achieving LDA were significantly better for adalimumab (rate 65%, proportion 59%) compared with abatacept (45%, 37%), apremilast (43%, 35%), ixekizumab (LDA only, 40%) and ustekinumab (LDA only, 40%), but not significantly different from other b/tsDMARDs. Conclusion: Uptake of newer b/tsDMARDs occurred mainly in biologic-experienced patients. Regardless of mode of action, only a minority of patients starting a second or later b/tsDMARD course remained on drug and achieved LDA. Superior outcomes for adalimumab indicate that the positioning of newer b/tsDMARDs in the PsA treatment algorithm remains to be established.

BackgroundEvidence demonstrates sex differences in disease presentation, physical function, treatment response and drug retention in patients with psoriatic arthritis (PsA). Data from observational cohort studies indicate female sex is associated with reduced effectiveness of tumor necrosis factor inhibitors (TNFis)1,2. Although, conflicting results are also reported3,4. We sought to validate prior studies using data from a large multinational cohort based on real-life clinical practice.ObjectivesTo investigate sex differences in treatment response and drug retention rates in clinical practice among patients with PsA, treated with their first TNFi.MethodsData from biologic-naïve PsA patients initiating a TNFi in the EuroSpA registries were pooled. In the primary analysis, propensity-score weighting was applied to assess the causal effect of sex on low disease activity (LDA) according to DAS28-CRP at 6 months. A generalized linear regression model was used to estimate the causal risk difference (RD) and relative risk (RR) of sex on LDA. Possible covariates influencing the outcome were determined a priori and selected based on availability in the database (ResultsIn total, 7,679 PsA patients with available data on DAS28-CRP at 6 months were assessed for treatment response. Baseline characteristics are shown in the Table 1. In the adjusted analysis, the probability for females to have LDA was 17% (RR, 0.83; 95% confidence interval [CI], 0.81 to 0.85) lower compared to males and the difference in probability for having LDA was 13 percentage points (RD, 0.13; 95% CI, 0.11 to 0.15). The survival analysis included 18,599 PsA patients with available data on retention rates. The TNFi 6/12/24-month retention rates were significantly lower in females (81%/68%/56%) compared to males (89%/80%/69%), see Figure 1.Table 1.Baseline characteristics of all biologic-naïve PsA patients treated with their first TNFi and available DAS28-CRP at 6 month, data pooled across all countriesFemaleMaleMean (SD), median [IQR] or percentagesMean (SD), median [IQR] or percentagesAge (years)49.7 (12.5)47.8 (11.9)Disease duration (years)4.0 [1.0, 10.0]4.0 [1.0, 10.0]TNFi start year 1999-200929%29% 2010-201326%27% 2014-201625%24% 2017-202020%20%Concomittant csDMARD75%77%DAS28-CRP4.4 (1.2)4.2 (1.2)DAPSA2832 (16)29 (16)CRP (mg/L)7.0 [3.0, 17.0]8.0 [3.3, 19.0]SJC (0-28)3.0 [1.0, 6.0]3.0 [1.0, 6.0]TJC (0-28)6.0 [2.0, 10.0]4.0 [2.0, 9.0]VAS pain, mm61 (23)55 (23)VAS fatigue, mm62 (26)53 (27)Data are as observed, mean (SD), median [IQR] or percentage. TNFi, tumor necrosis factor inhibitor; csDMARD, Conventional synthetic disease-modifying antirheumatic drugs; DAS28-CRP, Disease Activity Score 28-joint count C reactive protein; DAPSA28, Disease Activity in PsA 28; CRP, C-reactive protein; SJC, swollen joint count; TJC, tender joint count.ConclusionTreatment efficacy and retention rates are lower among female patients with PsA initiating their first TNFi. Females presented with higher 28-tender joint count and higher scores on patient reported outcomes at baseline, reflecting differences in disease expression. Recognizing these sex differences is of relevance for customized patient care and may improve patient education.References[1]Højgaard, et al. Rheumatology (Oxford). 2018 Sep 1;57(9):1651-1660.[2]Vieira-Sousa, et al. J Rheumatol. 2020 May 1;47(5):690-700.[3]Kristensen, et al. Ann Rheum. Dis. 2008 Mar;67(3):364-9.[4]Iervolino, et al. J Rheumatol. 2012 Mar;39(3):568-73.AcknowledgementsNovartis Pharma AG and IQVIA for supporting the EuroSpA collaboration.Disclosure of InterestsPasoon Hellamand Grant/research support from: Novartis, Marleen G.H. van de Sande Speakers bureau: UCB, Consultant of: Abbvie, Eli Lily, Novartis, UCB, Grant/research support from: Novartis, Janssen, UCB and Eli Lilly, Lykke Midtbøll Ørnbjerg Grant/research support from: Novartis, Thomas Klausch: None declared, Nina Trokovic: None declared, Tuulikki Sokka-Isler Consultant of: Abbvie, Amgen, BMS, Celgene, DiaGraphIT, Medac, MSD, Novartis, Orionpharma, Pfizer, Roche, Sandoz, and UCB, Maria Jose Santos Speakers bureau: Abbvie, AstraZeneca, Lilly, Novartis and Pfizer, Elsa Vieira-Sousa Speakers bureau: MSD, Celgene, Novartis, Janssen, Abbvie and Pfizer, Consultant of: MSD, Celgene, Novartis, Janssen, Abbvie and Pfizer, Grant/research support from: MSD, Celgene, Novartis, Janssen, Abbvie and Pfizer, Anne Gitte Loft Speakers bureau: AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, and UCB, Consultant of: AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, and UCB, Grant/research support from: Novartis, Bente Glintborg Grant/research support from: Pfizer, Abbvie, BMS, Mikkel Østergaard Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi and UCB, Consultant of: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi and UCB, Grant/research support from: Abbvie, BMS, Merck, Celgene, Novartis, Ulf Lindström: None declared, Johan K Wallman Consultant of: AbbVie, Amgen, Celgene, Eli Lilly and Novartis, Brigitte Michelsen Grant/research support from: Novartis, Burkhard Moeller Speakers bureau: MSD, Synergy, Eli Lilly, Bristol-Myers-Squibb, Janssen-Cilag, AbbVie and Pfizer, Raphael Micheroli: None declared, Catalin Codreanu Speakers bureau: AbbVie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis and Pfizer, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis and Pfizer, Corina Mogosan Speakers bureau: AbbVie, Ewopharma, Lilly, Novartis and Pfizer, Consultant of: AbbVie, Ewopharma, Lilly, Novartis and Pfizer, Karin Laas Speakers bureau: Amgen, Janssen, Novartis and Abbvie, Ziga Rotar Speakers bureau: Abbvie, Novartis, MSD, Medis, Biogen, Eli Lilly, Pfizer, Sanofi, Lek and Janssen, Consultant of: Abbvie, Novartis, MSD, Medis, Biogen, Eli Lilly, Pfizer, Sanofi, Lek and Janssen, Karen Minde Fagerli: None declared, Matija Tomsic Speakers bureau: Abbvie, Amgen, Biogen, Eli Lilly, Janssen, Medis, MSD, Novartis, Pfizer, Sanofi, Sandoz-Lek, Consultant of: Abbvie, Amgen, Biogen, Eli Lilly, Janssen, Medis, MSD, Novartis, Pfizer, Sanofi, Sandoz-Lek, Isabel Castrejon Speakers bureau: Lilly, BMS, Janssen, MSD and Abbvie, Consultant of: Lilly, BMS, Janssen, MSD and Abbvie, Manuel Pombo-Suarez Consultant of: Abbvie, MSD and Roche, Björn Gudbjornsson Speakers bureau: Amgen and Novartis, Consultant of: Amgen and Novartis, Thorvardur Love: None declared, Karel Pavelka Speakers bureau: Pfizer, MSD, BMS, UCB, Amgen, Egis, Roche and AbbVie, Consultant of: Pfizer, MSD, BMS, UCB, Amgen, Egis, Roche and AbbVie, Jakub Zavada Speakers bureau: Abbvie, Elli-Lilly, Sandoz, Novartis, Egis and UCB, Consultant of: Abbvie, Elli-Lilly, Sandoz, Novartis, Egis and UCB, Gökçe Kenar: None declared, Handan Yarkan-Tuğsal: None declared, Merete Lund Hetland Grant/research support from: Abbvie, Biogen, BMS, Celltrion, Eli Lilly, Janssen Biologics B.V, Lundbeck Fonden, MSD, Medac, Pfizer, Roche, Samsung Biopies, Sandoz and Novartis, Irene van der Horst-Bruinsma Speakers bureau: BMS, AbbVie, Pfizer and MSD, Consultant of: Abbvie, UCB, MSD, Novartis and Lilly, Grant/research support from: MSD, Pfizer, AbbVie and UCB

© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. http://creativecommons.org/licenses/by-nc/4.0/This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/., Background: Comedication with conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) during treatment with tumour necrosis factor inhibitors (TNFi) is extensively used in psoriatic arthritis (PsA), although the additive benefit remains unclear. We aimed to compare treatment outcomes in patients with PsA treated with TNFi and csDMARD comedication versus TNFi monotherapy. Methods: Patients with PsA from 13 European countries who initiated a first TNFi in 2006-2017 were included. Country-specific comparisons of 1 year TNFi retention were performed by csDMARD comedication status, together with HRs for TNFi discontinuation (comedication vs monotherapy), adjusted for age, sex, calendar year, disease duration and Disease Activity Score with 28 joints (DAS28). Adjusted ORs of clinical remission (based on DAS28) at 12 months were calculated. Between-country heterogeneity was assessed using random-effect meta-analyses, combined results were presented when heterogeneity was not significant. Secondary analyses stratified according to TNFi subtype (adalimumab/infliximab/etanercept) and restricted to methotrexate as comedication were performed. Results: In total, 15 332 patients were included (62% comedication, 38% monotherapy). TNFi retention varied across countries, with significant heterogeneity precluding a combined estimate. Comedication was associated with better remission rates, pooled OR 1.25 (1.12-1.41). Methotrexate comedication was associated with improved remission for adalimumab (OR 1.45 (1.23-1.72)) and infliximab (OR 1.55 (1.21-1.98)) and improved retention for infliximab. No effect of comedication was demonstrated for etanercept. Conclusion: This large observational study suggests that, as used in clinical practice, csDMARD and TNFi comedication are associated with improved remission rates, and specifically, comedication with methotrexate increases remission rates for both adalimumab and infliximab.

ObjectivesTo compare the 1-year, 2-year and 5-year incidences of acute coronary syndrome (ACS) in patients with rheumatoid arthritis (RA) starting any of the biologic disease-modifying antirheumatic drugs (bDMARDs) currently available in clinical practice and to anchor these results with a general population comparator.MethodsObservational cohort study, with patients from Denmark, Finland, Norway and Sweden starting a bDMARD during 2008–2017. Time to first ACS was identified through register linkages. We calculated the 1-year, 2-year and 5-year incidence rates (IR) (on drug and ever since treatment start) and used Cox regression (HRs) to compare ACS incidences across treatments taking ACS risk factors into account. Analyses were further performed separately in subgroups defined by age, number of previous bDMARDs and history of cardiovascular disease. We also compared ACS incidences to an individually matched general population cohort.Results24 083 patients (75% women, mean age 56 years) contributing 40 850 treatment courses were included. During the maximum (5 years) follow-up (141 257 person-years (pyrs)), 780 ACS events occurred (crude IR 5.5 per 1000 pyrs). Overall, the incidence of ACS in RA was 80% higher than that in the general population. For all bDMARDs and follow-up definitions, HRs were close to 1 (etanercept as reference) with the exception of the 5-year risk window, where signals for abatacept, infliximab and rituximab were noted.ConclusionThe rate of ACS among patients with RA initiating bDMARDs remains elevated compared with the general population. As used in routine care, the short-term, intermediate-term and longer-term risks of ACS vary little across individual bDMARDs.

BackgroundEvidence reveals sex differences in physiology, disease presentation and response to treatment in axial spondyloarthritis (axSpA). Pooled data from four randomized controlled trials demonstrated reduced treatment efficacy of a tumor necrosis factor inhibitor (TNFi) in females compared to males with ankylosing spondylitis1. However, real-life evidence confirming these data in large cohorts is scarce. We sought to validate prior studies using data from a large multinational cohort based on real-life clinical practice.ObjectivesTo investigate sex differences in treatment response and drug retention rates in clinical practice among patients with axSpA, treated with their first TNFi.MethodsData from biologic-naïve axSpA patients initiating a TNFi in the EuroSpA registries were pooled. In the primary analysis, propensity-score weighting was applied to assess the causal effect of sex on clinically important improvement (CII) according to ASDAS-CRP at 6 months. A generalized linear regression model was used to estimate the causal risk difference (RD) and relative risk (RR) of sex on CII. Possible covariates influencing the outcome were determined a priori and selected based on availability in the database (ResultsIn total, 6,451 axSpA patients with available data on ASDAS-CRP at baseline and 6 months were assessed for treatment response. Baseline characteristics are shown in the Table 1. In the adjusted analysis, the probability for females to have CII was 15% (RR, 0.85; 95% confidence interval [CI], 0.82 to 0.89) lower compared to males and the difference in probability for having CII was 9.4 percentage points (RD, 0.094; 95% CI, 0.069 to 0.12). The survival analysis included 28,608 axSpA patients with available data on retention rates. The TNFi 6/12/24-month retention rates were significantly lower in females (81%/69%/58%) compared to males (89%/81%/72%), see Figure 1.Table 1.FemaleMaleMean (SD), Median [IQR] or percentagesMean (SD), Median [IQR] or percentagesAge (years)42.0 (12.1)41.4 (12.3)Fulfilment of mNYC66%80%Disease duration (years)2.0 [1.0, 7.0]3.0 [1.0, 9.0]TNFi start year Start 1999-20097.2%9.8% Start 2010-201326%27% Start 2014-201637%36% Start 2017-202030%27%BASDAI, mm59 (20)54 (21)BASFI, mm48 (25)46 (24)ASDAS, units3.5 (0.9)3.5 (1.0)CRP (mg/L)6.7 [2.5, 16.0]11.9 [4.0, 25.0]SJC (0-28)0 [0, 0]0 [0, 0]TJC (0-28)0 [0, 2]0 [0, 1]VAS pain, mm63 (22)59 (24)VAS fatigue, mm65 (25)59 (26)mNYC, modified New York criteria; TNFi, tumor necrosis factor inhibitor; BASDAI, Bath Ankylosing Spondylitis Disease Activity Indexf; BASFI, Bath Ankylosing Spondylitis Functional Index; ASDAS, Ankylosing Spondylitis Disease Activity Score; CRP, C-reactive protein; SJC, swollen joint count; TJC, tender joint count; VAS, visual analogue scale.ConclusionTreatment efficacy and retention rates are lower among female patients with axSpA initiating their first TNFi. Females presented with lower C-reactive protein levels and higher scores on patient reported outcomes at baseline, reflecting differences in disease expression. Recognizing these sex differences is of relevance for customized patient care and may improve patient education.References[1]van der Horst-Bruinsma et al. Ann Rheum Dis. 2013 Jul;72(7):1221-4.AcknowledgementsNovartis Pharma AG and IQVIA for supporting the EuroSpA collaboration.Disclosure of InterestsPasoon Hellamand Grant/research support from: Novartis, Marleen G.H. van de Sande Speakers bureau: UCB, Consultant of: Abbvie, Eli Lily, Novartis and UCB, Grant/research support from: Novartis, Janssen, UCB and Eli Lilly, Lykke Midtbøll Ørnbjerg Grant/research support from: Novartis, Thomas Klausch: None declared, Michael Nurmohamed Speakers bureau: Abbvie, Janssen and Celgene, Consultant of: Abbvie, Grant/research support from: Abbvie, Amgen, Pfizer, Galapagos, BMS, Ronald van Vollenhoven Consultant of: AbbVie, AstraZeneca, Biogen, BMS, Galapagos, Janssen, Miltenyi, Pfizer, UCB and speaker fees from Abbvie, Galapagos, GSK, Janssen, Pfizer, R-Pharma and UCB, Grant/research support from: BMS, GSK and UCB, Dan Nordström Consultant of: Abbvie, BMS, Lilly, MSD, Novartis, Pfizer, Roche and UCB, Anna-Mari Hokkanen Grant/research support from: MSD, Maria Jose Santos Speakers bureau: Abbvie, AstraZeneca, Lilly, Novartis and Pfizer, Elsa Vieira-Sousa Speakers bureau: MSD, Celgene, Novartis, Janssen, Abbvie and Pfizer, Consultant of: MSD, Celgene, Novartis, Janssen, Abbvie and Pfizer, Grant/research support from: MSD, Celgene, Novartis, Janssen, Abbvie and Pfizer, Anne Gitte Loft Consultant of: AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche and UCB, Grant/research support from: Novartis, Bente Glintborg Grant/research support from: Pfizer, Abbvie and BMS, Mikkel Østergaard Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi and UCB, Consultant of: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi and UCB, Grant/research support from: Abbvie, BMS, Merck, Celgene and Novartis, Ulf Lindström: None declared, Johan K Wallman Consultant of: AbbVie, Amgen, Celgene, Eli Lilly and Novartis, Brigitte Michelsen Grant/research support from: Novartis, Adrian Ciurea Speakers bureau: AbbVie and Novartis, Michael J. Nissen Speakers bureau: AbbVie, Eli Lilly, Janssens, Novartis and Pfizer, Consultant of: AbbVie, Eli Lilly, Janssens, Novartis and Pfizer, Catalin Codreanu Speakers bureau: AbbVie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis and Pfizer, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis and Pfizer, Corina Mogosan Speakers bureau: AbbVie, Ewopharma, Lilly, Novartis and Pfizer, Consultant of: AbbVie, Ewopharma, Lilly, Novartis and Pfizer, Gary Macfarlane Grant/research support from: GSK, Gareth T. Jones Grant/research support from: AbbVie, Pfizer, UCB, Amgen and GSK, Karin Laas Speakers bureau: Amgen, Janssen, Novartis and Abbvie, Ziga Rotar Speakers bureau: Abbvie, Novartis, MSD, Medis, Biogen, Eli Lilly, Pfizer, Sanofi, Lek and Janssen, Consultant of: Abbvie, Novartis, MSD, Medis, Biogen, Eli Lilly, Pfizer, Sanofi, Lek and Janssen, Matija Tomsic Speakers bureau: Abbvie, Amgen, Biogen, Eli Lilly, Janssen, Medis, MSD, Novartis, Pfizer, Sanofi and Sandoz-Lek, Consultant of: Abbvie, Amgen, Biogen, Eli Lilly, Janssen, Medis, MSD, Novartis, Pfizer, Sanofi and Sandoz-Lek, Isabel Castrejon Speakers bureau: Eli Lilly, BMS, Janssen, MSD and Abbvie, Consultant of: Eli Lilly, BMS, Janssen, MSD and Abbvie, Manuel Pombo-Suarez Consultant of: Abbvie, MSD and Roche, Björn Gudbjornsson Speakers bureau: Amgen and Novartis, Consultant of: Amgen and Novartis, Arni Jon Geirsson: None declared, Eirik kristianslund: None declared, Jiří Vencovský Speakers bureau: Abbvie, Argenx, Boehringer-Ingelheim, Eli-Lilly, Gilead, MSD, Novartis, Octapharma, Pfizer, Roche, Sanofi and UCB, Consultant of: Abbvie, Argenx, Boehringer-Ingelheim, Eli-Lilly, Gilead, MSD, Novartis, Octapharma, Pfizer, Roche, Sanofi and UCB, Lucie Nekvindova: None declared, Semih Gulle: None declared, Berrin Zengin: None declared, Merete Lund Hetland Grant/research support from: Abbvie, Biogen, BMS, Celltrion, Eli Lilly, Janssen Biologics B.V, Lundbeck Fonden, MSD, Medac, Pfizer, Roche, Samsung Biopies, Sandoz and Novartis, Irene van der Horst-Bruinsma Speakers bureau: BMS, AbbVie, Pfizer and MSD, Consultant of: Abbvie, UCB, MSD, Novartis and Lilly, Grant/research support from: MSD, Pfizer, AbbVie and UCB.

BackgroundIn axial spondyloarthritis (axSpA), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) is a key patient-reported outcome. However, one or more of its components may be missing when recorded in clinical practice.ObjectivesTo determine whether an individual patient’s BASDAI at a given timepoint can be reliably calculated with different single imputation techniques and to explore the impact of the number of missing components and/or differences between missingness of individual components.MethodsReal-life data from axSpA patients receiving tumour necrosis factor inhibitors (TNFi) from 13 countries in the European Spondyloarthritis (EuroSpA) Research Collaboration Network were utilized [1]. We studied missingness in BASDAI components based on simulations in a complete dataset, where we applied and expanded the approach of Ramiro et al. [2]. After introducing one or more missing components completely at random, BASDAI was calculated from the available components and with three different single imputation techniques: possible middle value (i.e. 50) of the component and mean and median of the available components. Differences between the observed (original) and calculated scores were assessed and correct classification of patients as having BASDAIResultsA total of 19,894 axSpA patients with at least one complete BASDAI registration at any timepoint were included. 59,126 complete BASDAI registrations were utilized for the analyses with a mean BASDAI of 38.5 (standard deviation 25.9). Calculating BASDAI from the available components and imputing with mean or median showed similar levels of agreement (Table 1). When allowing one missing component, >90% had a difference of ≤6.9 mm between the original and calculated scores and >95% were correctly classified as BASDAI90% (Figure 1, upper panels). As expected, it was observed that regardless of the BASDAI component set to missing and the imputation technique used, correct classification of patients as BASDAITable 1.Level of agreement between the original and calculated BASDAI and correct classification for BASDAILevel of agreement with Dif≤6.9 mm* (%)Correct classification for BASDAI1 missing componentAvailable93.996.9Value 5073.996.3Mean94.296.8Median93.196.82 missing componentsAvailable83.794.8Value 5040.792.8Mean83.594.8Median82.894.73 missing componentsAvailable71.992.6Value 5028.187.3Mean72.292.6Median69.792.2* The levels of agreement with a difference (Dif) of ≤6.9 mm between the original and calculated scores were based on the half of the smallest detectable change. Agreement of >90% was considered as acceptable. ** Correct classification of >95% was considered as acceptable.Figure 1.Level of agreement between the original and calculated BASDAI and correct classification for BASDAIConclusionBASDAI calculation with available components gave similar results to single imputation of missing components with mean or median. Only when missing one of BASDAI components 5 or 6, single imputation techniques can reliably calculate individual BASDAI scores. However, missing any single component value results in misclassification of patients with original BASDAI scores close to 40.References[1]Ørnbjerg et al. (2019). Ann Rheum Dis, 78(11), 1536-1544.[2]Ramiro et al. (2014). Rheumatology, 53(2), 374-376.AcknowledgementsNovartis Pharma AG and IQVIA for supporting the EuroSpA collaboration.Disclosure of InterestsStylianos Georgiadis Grant/research support from: Novartis, Myriam Riek Grant/research support from: Novartis, Christos Polysopoulos Grant/research support from: Novartis, Almut Scherer Grant/research support from: Novartis, Daniela Di Giuseppe: None declared, Gareth T. Jones Speakers bureau: Janssen, Grant/research support from: AbbVie, Pfizer, UCB, Amgen, GSK, Merete Lund Hetland Grant/research support from: Abbvie, Biogen, BMS, Celltrion, Eli Lilly, Janssen Biologics B.V, Lundbeck Fonden, MSD, Medac, Pfizer, Roche, Samsung Biopies, Sandoz, Novartis, Mikkel Østergaard Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi, UCB, Consultant of: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi, UCB, Grant/research support from: Abbvie, BMS, Merck, Celgene, Novartis, Simon Horskjær Rasmussen Grant/research support from: Novartis, Johan K Wallman Consultant of: AbbVie, Amgen, Celgene, Eli Lilly, Novartis, Bente Glintborg Grant/research support from: Pfizer, Abbvie, BMS, Anne Gitte Loft Speakers bureau: AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, UCB, Consultant of: AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, UCB, Karel Pavelka Speakers bureau: Pfizer, MSD, BMS, UCB, Amgen, Egis, Roche, AbbVie, Consultant of: Pfizer, MSD, BMS, UCB, Amgen, Egis, Roche, AbbVie, Jakub Zavada Speakers bureau: Abbvie, Elli-Lilly, Sandoz, Novartis, Egis, UCB, Consultant of: Abbvie, Elli-Lilly, Sandoz, Novartis, Egis, UCB, Merih Birlik: None declared, Ayten Yazici Grant/research support from: Roche, Brigitte Michelsen Grant/research support from: Novartis, Eirik kristianslund: None declared, Adrian Ciurea Speakers bureau: AbbVie, Eli Lilly, Merck Sharp & Dohme, Novartis, Pfizer, Consultant of: AbbVie, Eli Lilly, Merck Sharp & Dohme, Novartis, Pfizer, Michael J. Nissen Speakers bureau: AbbVie, Eli Lilly, Janssens, Novartis, Pfizer, Consultant of: AbbVie, Eli Lilly, Janssens, Novartis, Pfizer, Ana Maria Rodrigues Speakers bureau: Abbvie, Amgen, Consultant of: Abbvie, Amgen, Grant/research support from: Novartis, Pfizer, Amgen, Maria Jose Santos Speakers bureau: Abbvie, AstraZeneca, Lilly, Novartis, Pfizer, Gary Macfarlane Grant/research support from: GSK, Anna-Mari Hokkanen Grant/research support from: MSD, Heikki Relas Speakers bureau: Abbvie, Celgene, Pfizer, UCB, Viatris, Consultant of: Abbvie, Celgene, Pfizer, UCB, Viatris, Catalin Codreanu Speakers bureau: AbbVie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis, Pfizer, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis, Pfizer, Corina Mogosan: None declared, Ziga Rotar Speakers bureau: Abbvie, Novartis, MSD, Medis, Biogen, Eli Lilly, Pfizer, Sanofi, Lek, Janssen, Consultant of: Abbvie, Novartis, MSD, Medis, Biogen, Eli Lilly, Pfizer, Sanofi, Lek, Janssen, Matija Tomsic Speakers bureau: Abbvie, Amgen, Biogen, Eli Lilly, Janssen, Medis, MSD, Novartis, Pfizer, Sanofi, Sandoz-Lek, Consultant of: Abbvie, Amgen, Biogen, Eli Lilly, Janssen, Medis, MSD, Novartis, Pfizer, Sanofi, Sandoz-Lek, Björn Gudbjornsson Speakers bureau: Amgen, Novartis, Consultant of: Amgen, Novartis, Arni Jon Geirsson: None declared, Pasoon Hellamand Grant/research support from: Novartis, Marleen G.H. van de Sande Speakers bureau: Eli Lilly, Novartis, UCB, Janssen, Abbvie, Consultant of: Eli Lilly, Novartis, UCB, Janssen, Abbvie, Grant/research support from: Eli Lilly, Novartis, UCB, Janssen, Abbvie, Isabel Castrejon: None declared, Manuel Pombo-Suarez Consultant of: Abbvie, MSD, Roche, Bruno Frediani: None declared, Florenzo Iannone Speakers bureau: Abbvie, Amgen, AstraZeneca, BMS, Galapagos, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, UCB, Consultant of: Abbvie, Amgen, AstraZeneca, BMS, Galapagos, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, UCB, Lykke Midtbøll Ørnbjerg Grant/research support from: Novartis

ObjectivesJoint swelling and tenderness are considered a proxy for inflammation in patients with rheumatoid arthritis (RA). With ultrasound-detected inflammation as reference, our objectives were to explore on patient and joint level the associations between ultrasound synovitis and joint swelling, tenderness and patient-reported joint pain (PRJP).Methods209 patients with established RA were examined six times during 12 months with assessment of 32 joints in upper/lower extremities for joint swelling/tenderness and Grey scale (GS)/power Doppler (PD) synovitis. PRJP was assessed on a manikin. Correlations between different sum scores were at each examination calculated using Spearman’s rho (r), agreement at joint level was examined by Cohen’s kappa and logistic regression models were used to explore the associations between joint assessment and GS/PD scores.ResultsAt patient level, swollen joints were strongly correlated with GS/PD sum scores (r=0.64–0.88), while tender joints were primarily associated with PRJP (r=0.54–0.68). At joint level, GS/PD pathology had higher agreement with swelling (kappa 0.54–0.57) than tenderness (kappa 0.20–0.21) or PRJP (0.23–0.25). Higher percentages of joints were swollen according to increasing GS/PD scores, independently of joint tenderness. However, joints being tender, but not swollen, were not associated with GS/PD scores. Receiver operating curves showed swollen but not tender joints to be associated with GS/PD scores.ConclusionsSwollen joints were strongly associated with ultrasound detected synovitis at both patient and joint level, while this association was not found for tender joints. These results may question if tender joints reflect ongoing inflammation in established RA.

BackgroundSeveral autoimmune inflammatory diseases, including rheumatoid arthritis (RA), are associated with increased risk of malignant lymphomas. There is also a longstanding concern of lymphoma development with tumour necrosis factor inhibitor (TNFi) treatment, but most studies in RA to date do not indicate an additionally increased risk. Corresponding studies in psoriatic arthritis (PsA), both with respect to the underlying risks, and risks in relation to treatment with TNFi, are limited. Data on myeloid malignancies in PsA are scarce.ObjectivesTo estimate the risk of haematological malignancy overall and by lymphoid and myeloid types in TNFi treated versus (vs.) biologics-naïve patients with PsA across the five Nordic countries. Additionally, we investigated the underlying risk of haematological malignancies in PsA as compared to the general population.MethodsWe identified patients with PsA starting a first ever TNFi from the clinical rheumatology registers (CRR) in Sweden (SE), Denmark (DK), Norway (NO), Finland (FI), and Iceland (ICE) from 2006 through 2019 (n=10 621). We identified biologics-naïve patients with PsA from a) the CRR (n=18 705, all countries) and b) the national patient registers (NPR, n=27 286, SE and DK only). To estimate the underlying risk of haematological malignancy in PsA, we randomly sampled general population comparators in SE and DK matched on year of birth, sex, and calendar year at start of follow-up, to the patients with PsA.Through linkage to the mandatory national cancer registers in all five countries, we collected information on haematological malignancy overall, and categorised into lymphoid or myeloid types. By applying a modified Poisson regression, we estimated pooled incidence rate ratio (IRR) with 95% confidence intervals (CI) for TNFi treated vs. biologics-naïve PsA and for PsA vs. the general population, adjusted for age (18-55, 56-65, 66-70, >70 years), sex, calendar period (2006-2010, 2011-2019) and country, and using robust standard errors.ResultsWe observed 40 events of haematological malignancies (during 59 827 person-years) among TNFi treated PsA, resulting in a crude incidence rate (IR) of 67 per 100 000 person-years. The corresponding IR was 91 (63 events) for biologics-naïve PsA from the CRR, and 118 (172 events) for biologics-naïve PsA from NPR. This resulted in a pooled IRR of 0.97 (0.69 to 1.37) for TNFi-treated vs. biologics-naïve PsA patients from the CRR, and 0.84 (0.64 to 1.10) vs. biologics-naïve PsA patients from the NPR. The pooled IRR of haematological malignancies in PsA overall vs. the general population was 1.35 (1.17 to 1.55). Throughout, the estimates were largely similar for lymphoid and myeloid malignancies (Figure 1). The crude IR of haematological malignancies were substantially akin across different TNFi agents.Figure 1.Pooled incidence rate ratios (IRRs) (95% CI) of haematological malignancy overall and by lymphoid and myeloid types, in first ever TNFi treated versus biologics-naïve patients with PsA, and versus general population comparators. Legend: Lymphoid malignancies include international classification of diseases (ICD) 10 codes C81-86, C88, C90-91. Myeloid malignancies include ICD10 codes C92-95, D45-D46, D47.1, D47.3-5. Incidence rate ratios adjusted for age (18-55, 56-65, 66-70, >70 years), sex, calendar period (2006-2010, 2011-2019) and country, and using robust standard errors.ConclusionIn this large five-country cohort study, we did not observe any increased risk of haematological malignancies overall, nor for lymphoid and myeloid types, in patients with PsA treated with TNFi. By contrast, there were signals of a moderately increased underlying risk of haematological malignancies, both of lymphoid and myeloid types, in patients with PsA overall as compared to the general population. The findings are of importance from a patient information perspective.AcknowledgementsWe would like to acknowledge the NordForsk and FOREUM, and especially the patient representatives of the NordForsk collaboration for their valuable contribution to this study.Disclosure of InterestsRené Cordtz: None declared, Johan Askling Consultant of: Abbvie, Astra-Zeneca, BMS, Eli Lilly, MSD, Pfizer, Roche, Samsung Bioepis, Sanofi, and UCB, Grant/research support from: Abbvie, Astra-Zeneca, BMS, Eli Lilly, MSD, Pfizer, Roche, Samsung Bioepis, Sanofi, and UCB, Bénédicte Delcoigne: None declared, Karin Ekström Smedby: None declared, Eva Baecklund: None declared, Christine Ballegaard: None declared, Pia Isomäki Speakers bureau: AbbVie, Eli Lilly and Pfizer, Consultant of: AbbVie, Eli Lilly, Pfizer, Roche and ViforPharma, Grant/research support from: Pfizer, Kalle Aaltonen: None declared, Björn Gudbjornsson Speakers bureau: Novartis, not related to this work, Consultant of: Novartis, not related to this work, Thorvardur Love Speakers bureau: Celgene, Sella Aa. Provan: None declared, Brigitte Michelsen Grant/research support from: Novartis, not related to this work, Joe Sexton: None declared, Lene Dreyer Speakers bureau: Eli Lilly, Galderma and Janssen, Grant/research support from: BMS not related to this work, Karin Hellgren: None declared

BackgroundRecent years of progress in conventional and biologic disease-modifying anti-rheumatic drugs development and improved treatment strategies (treat to target) have yield in improved outcome in psoriatic arthritis (PsA) patients. [1,2]. Still, despite modern treatment and clinical monitoring methods, we might miss dimensions of disease burden outside our main focus including quality of life (QoL), which are of high importance from patients’ perspective.ObjectivesMain objective of this study was to explore how clinical aspects of disease activity and QoL measures will change in PsA patients in an ordinary outpatient clinic in Norway, followed for 5 years, in the biological treatment era.MethodsPsA patients fulfilling the CASPAR criteria visiting an outpatient clinic in Norway between January 2013 and February 2020 were consecutively included in the study. Data collection included variables for demographics, treatment, laboratory assessment of ESR and CRP, joint counts, disease activity score in psoriatic arthritis (DAPSA), global assessments – patient’s (PGA) and investigator’s (IGA), reported joint and global pain, patient reported outcomes (PROMs) regarding different aspects of quality of life (QoL), (MHAQ, RAID, QoL15D and reported fatigue level). Patients were analyzed at baseline and after 5-year follow-up period. Statistics included paired sample t test and McNemar test.ResultsAmong 140 PsA patients included at baseline, 114 (81.4%) were re-examined after 5 years. Mean age at baseline was 52 years (95%CI 50.3-53.7) and percentage of women was 50.7%. Proportion of patients treated with biologics increased from 32.9% to 39.5%, but the difference wasn’t statistically significant. During the 5 year follow up period most clinical disease activity measures decreased and QoL was maintained (Table 1).Table 1.Demographic data, clinical activity measures and patient reported outcomes regarding quality of life in PsA patients followed for 5 years. Values are mean (95CI) or number (%).Baseline (140)5-years follow up (114)pAge (years)52.0 (50.3, 53.7)56.3 (54.4, 58.3)Women71 (50.7%)56 (49.1%)Exercise >1h week62 (44.3%)59 (51.8%)0.28BMI (kg/m2)28.4 (27.5, 29.2)28.2 (27.3, 29.1)0.89Current smoker24 (17.1%)17 (14.9%)0.90Current bDMARD treatment46 (32.9%)45 (39.5%)0.65DAPSA18.6 (16.2, 21.0)12.8 (10.8, 14.8)TJC684.1 (3.2, 5.0)1.8 (1.3, 2.4)SJC660.7 (0.5, 0.9)0.3 (0.2, 0.4)ESR15.9 (13.9, 18.0)10.7 (7.8, 13.5)CRP4.9 (3.5, 6.3)5.3 (2.5, 8.2)0.41IGA (VAS 0-100)4.1 (3.2, 5.0)1.8 (1.3, 2.4)PGA (VAS 0-100)36.6 (32.5, 40.8)29.3 (25.0, 33.6)0.12Global pain (VAS 0-100)35.1 (31.2, 39.0)28.9 (24.4, 33.5)0.42Joint pain (VAS 0-100)33.8 (29.9, 37.8)27.5 (23.2, 31.9)0.31MHAQ (0-3)0.4 (0.4, 0.5)0.3 (0.3, 0.4)0.72RAID (0-10)3.5 (3.1, 3.9)3.2 (2.9, 3.6)0.41QoL15D (15-75)24.2 (23.1, 25.2)22.7 (21.6, 23.9)0.85Fatigue (VAS 0-100)47.8 (41.5, 54.2)39.1 (32.8, 45.4)0.16ConclusionIn our cohort of PsA patients after 5 years follow up disease activity was reduced and QoL maintained. Our data adds to the evidence that the burden of disease in PsA patients has decreased in the biologic treatment era however is still significant. Further improvement in pharmacological and non-pharmacological treatments in PsA patients is still needed.References[1]Coates LC, Moverley AR, McParland L, et al. Effect of tight control of inflammation in early psoriatic arthritis (TICOPA): a UK multicentre, open-label, randomised controlled trial. Lancet. 2015;386(10012):2489-2498. doi:10.1016/S0140-6736(15)00347-5[2]Coates LC, Helliwell PS. Treating to target in psoriatic arthritis: how to implement in clinical practice. Ann Rheum Dis. 2016;75(4):640-643. doi:10.1136/annrheumdis-2015-208617AcknowledgementsNurses and doctors from Division of Rheumatology at Sørlandet Hospital in Kristiansand, Norway contributed to data collection.Disclosure of InterestsNone declared

Background:Rheumatoid Arthritis (RA) is associated with increased cardiovascular co-morbidity including acute coronary syndrome (ACS), partly due to effects of systemic inflammation. Disease-modifying anti-rheumatic drugs (DMARDs) may reduce RA disease activity, but act through several pathways and may themselves have an impact on cardiovascular risks. Whether the risks of ACS associated with biologic (b) and targeted synthetic (ts) DMARDs differ is still unknown.Objectives:To assess and compare incidences of ACS during treatment of RA with etanercept (ETA), adalimumab (ADA), infliximab (INF), certolizumab pegol (CTZ), golimumab (GOL), rituximab (RIT), abatacept (ABA), tocilizumab (TCZ), baricitinib (BAR) or tofacitinib (TOF).Methods:We defined and pooled treatment cohorts of patients starting any of the above treatments between 2008 and 2017 from clinical rheumatology registers in Denmark (DK), Finland (FI), Norway (NO), and Sweden (SE). One patient could contribute several treatment episodes. Age, sex, co-medication (methotrexate, prednisolone), number of previous b/tsDMARDs, CRP, comorbidities (cardiovascular (including ACS (defined as ICD-10: I20.0, I21.0-4, I21.9) and cerebrovascular disease, thromboembolic events, diabetes, hospitalized infection, cancer, kidney failure, COPD) and associated drugs were extracted and used as adjustment in Cox regression analyses comparing the incidence of ACS between treatments. We used several follow-up lengths (1, 2, and up to 5 years) and two different risk windows (ACS on drug [ending follow-up on treatment discontinuation] and ACS ever since treatment start [disregarding any treatment discontinuation]). We also stratified by age and number of previous b/tsDMARDs.Results:We included 40850 treatment courses in 24083 patients (DK 7271, FI 3732, NO 1540, and SE 11540; around 75% women). ETA was the most common treatment (27%) whereas BAR and TOF comprised We found 780 incident ACS events during 141 326 person-years (pyrs) in the 5-year follow-up time and “ACS ever since treatment start” risk window, resulting in a crude incidence rate of 5.5 events per 1000 pyrs. No event was recorded for BAR nor TOF, which also had the shortest follow-up. Adjusted hazard ratios (HR) increased slightly with longer follow-up times, but the two risk windows provided similar HRs. For the 5-year follow-up, RIT was associated with an increased risk of ACS compared to ETA (Table), while no association was observed for shorter follow-up times. Stratifying on age did not modify the associations. Separate analyses by number of previous b/tsDMARDs suggested that ABA (HR=1.8, 95% CI 1.0-3.3), INF (HR=2.2, 95% CI 1.0-4.6) and RIT (HR=1.9, 95% CI 1.1-3.4) were associated with increased risks of ACS compared to ETA in the subgroup of patients with two or more previous bDMARDs (Figure), whereas no differences were found among patients starting either drug as 1st/2nd bDMARD.Table 1.Comparisons of risks for ACS during a 5-year follow-up since start of bDMARD treatment.DrugN eventspyrsCrude incidence rate/ 1000 pyrsHR (95% CI)1ETA175359174.9ref.ADA115240934.81.0 (0.8-1.3)CTZ54141583.80.9 (0.6-1.2)GOL4090064.41.1 (0.8-1.5)INF106178036.01.2 (0.9-1.5)ABA70107956.51.1 (0.8-1.4)RIT158166229.51.3 (1.0-1.6)TCZ62128664.80.9 (0.5-1.2)BAR036TOF030Pyrs: person-years; HR: hazards ratio1 adjustment: see text.Conclusion:In this cohort including ≥ 24,000 patients followed for up to 5 years, the ACS incidence rate was 5.5/1000 pyrs, with RIT showing an increased risk compared to ETA. In clinical practice, the choice of bDMARD does not seem to influence ACS risk in the short term. In the longer term, differences in ACS risk between bDMARDs may reflect channeling to these, or truly differential effects in subpopulations of patients.Acknowledgements:Partly funded by Nordforsk and ForeumDisclosure of Interests:Bénédicte Delcoigne: None declared, Lotta Ljung: None declared, Sella Aa. Provan Speakers bureau: Novartis, Consultant of: Novartis, Grant/research support from: Boehringer- Ingelheim, Bente Glintborg Grant/research support from: Pfizer, BMS, AbbVie, Kathrine Lederballe Gron Grant/research support from: BMS, Merete L. Hetland Consultant of: Abbvie, Biogen, BMS, Celltrion, Eli Lilly, Janssen Biologics B.V, Lundbeck Fonden, MSD, Pfizer, Roche, Samsung Biopies, Sandoz, Novartis, Grant/research support from: Abbvie, Biogen, BMS, Celltrion, Eli Lilly, Janssen Biologics B.V, Lundbeck Fonden, MSD, Pfizer, Roche, Samsung Biopies, Sandoz, Novartis, Niels Steen Krogh: None declared, Nina Trokovic: None declared, Heikki Relas Speakers bureau: Abbvie, Celgene, Pfizer, Grant/research support from: Abbvie, Celgene, Pfizer, Carl Turesson Speakers bureau: Abbvie, Bristol-Myers Squibb, Medac, Pfizer, Roche, Consultant of: Roche, Brigitte Michelsen Consultant of: Novartis (paid to employer), Grant/research support from: Novartis (paid to employer), Johan Askling Consultant of: Abbvie, Astra-Zeneca, BMS, Eli Lilly, MSD, Pfizer, Roche, Samsung Bioepis, Sanofi, and UCB. These entities have entered into agreements with Karolinska Institutet with JA as principal investigator, mainly in the context of safety monitoring of biologics via the ARTIS national safety monitoring system.

Background:Knowledge of changes over time in baseline characteristics and tumor necrosis factor inhibitor (TNFi) response in bio-naïve axial spondyloarthritis (axSpA) patients treated in routine care is limited.Objectives:To investigate secular trends in baseline characteristics and retention, remission and response rates in axSpA patients initiating a first TNFi.Methods:Prospectively collected data on bio-naïve axSpA patients starting TNFi in routine care from 15 European countries were pooled. According to year of TNFi initiation, three groups were defined a priori based on bDMARD availability: Group A (1999–2008), Group B (2009–2014) and Group C (2015–2018). Retention rates (Kaplan-Meier), crude and LUNDEX adjusted1 remission (Ankylosing Spondylitis Disease Activity Score (ASDAS) Results:In total, 27189 axSpA patients were included (5945, 11255 and 9989 in groups A, B and C).At baseline, patients in group A were older, had longer disease duration and a larger proportion of male and HLA-B27 positive patients compared to B and C, whereas disease activity was similar across groups.Retention rates at 6, 12 and 24 months were highest in group A (88%/81%/71%) but differed little between B (84%/74%/64%) and C (85%/76%/67%).In all groups, median ASDAS and BASDAI had decreased markedly at 6 months (Table 1). The ASDAS values at 12 and 24 months and BASDAI at 24 months were higher in group A compared with groups B and C. Similarly, crude remission and response rates were lowest in group A. After adjustments for drug retention (LUNDEX), remission and response rates showed less pronounced between-group differences regarding ASDAS measures and no relevant differences regarding BASDAI measures.Conclusion:Nowadays, axSpA patients initiating TNFi are younger with shorter disease duration and more frequently female and HLA-B27 negative than previously, while baseline disease activity is unchanged. Drug retention rates have decreased, whereas crude remission and response rates have increased. This may indicate expanded indication but also a stable disease activity threshold for TNFi initiation over time, an increased focus on targeting disease remission and more available treatment options.References:[1]Arthritis Rheum 2006; 54: 600-6.Table 1.Secular trends in baseline characteristics, treatment retention, remission and response rates in European axSpA patients initiating a 1st TNFiBaseline characteristicsGroup A(1999–2008)Group B(2009–2014)Group C(2015–2018)Age, years, median (IQR)57 (49–66)51 (42–60)46 (37–56)Male, %666057HLA-B27, %877772Years since diagnosis, median (IQR)5 (1–12)2 (0–8)2 (0–7)Smokers, %232425ASDAS, median (IQR)3.5 (2.8–4.1)3.4 (2.8–4.1)3.5 (2.8–4.1)BASDAI, median, (IQR)57 (42–71)59 (43–72)57 (41–71)TNFi drug, % (Adalimumab /Etanercept / Infliximab /Certolizumab / Golimumab)22 / 35 / 43 / 0 / 037 / 21 / 20 / 4 / 1827 / 28 / 24 / 8 / 13Follow up6 months12 months24 monthsGr AGr BGr CGr AGr BGr CGr AGr BGr CRetention rates, %, (95% CI)88 (88–89)84 (83–85)85 (84–86)81 (80–82)74 (74–75)76 (75–76)71 (70–72)64 (63–65)67 (66–68)ASDAS, median, (IQR)1.8 (1.2–2.8)1.9 (1.2–2.8)1.8 (1.2–2.6)1.9 (1.3–2.6)1.7 (1.2–2.5)1.6 (1.1–2.4)1.9 (1.4–2.6)1.7 (1.1–2.4)1.5 (1.1–2.2)ASDAS inactive disease, %, c/L28 / 2528 / 2430 / 2624 / 1932 / 2434 / 2623 / 1634 / 2039 / 23ASDAS CII, %, c/L57 / 5159 / 5063 / 5461 / 5063 / 4767 / 5159 / 4168 / 4074 / 45ASDAS MI, %, c/L31 / 2732 / 2737 / 3232 / 2637 / 2741 / 3130 / 2042 / 2546 / 28BASDAI, median, (IQR)23 (10–40)26 (11–48)24 (10–44)21 (10–38)23 (10–42)20 (8–39)22 (9–40)20 (8–39)16 (6–35)BASDAI remission, %, c/L44 / 4040 / 3443 / 3645 / 3645 / 3450 / 3844 / 3048 / 2956 / 34BASDAI 50 response, %, c/L53 / 4750 / 4253 / 4557 / 4656 / 4258 / 4457 / 3960 / 3563 / 38Gr, Group; c/L, crude/LUNDEX adjusted.Acknowledgements:Novartis Pharma AG and IQVIA for supporting the EuroSpA Research Collaboration Network.Disclosure of Interests:Lykke Midtbøll Ørnbjerg Grant/research support from: Novartis, Sara Nysom Christiansen Speakers bureau: BMS and GE, Grant/research support from: Novartis, Simon Horskjær Rasmussen: None declared, Anne Gitte Loft Speakers bureau: AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, UCB, Consultant of: AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, UCB, Grant/research support from: Novartis, Ulf Lindström: None declared, Jakub Zavada: None declared, Florenzo Iannone: None declared, Fatos Onen: None declared, Michael J. Nissen Speakers bureau: Novartis, Eli Lilly, Celgene, and Pfizer, Consultant of: Novartis, Eli Lilly, Celgene, and Pfizer, Brigitte Michelsen Consultant of: Novartis, Grant/research support from: Novartis, Maria Jose Santos Speakers bureau: AbbVie, Novartis, Pfizer, Gary Macfarlane Grant/research support from: GlaxoSmithKline, Dan Nordström Consultant of: Abbvie, BMS, MSD, Novartis, Pfizer, Roche, UCB, Manuel Pombo-Suarez: None declared, Catalin Codreanu Speakers bureau: AbbVie, Amgen, Egis, Novartis, Pfizer, UCB, Grant/research support from: AbbVie, Amgen, Egis, Novartis, Pfizer, UCB, Matija Tomsic Speakers bureau: Abbvie, Amgen, Biogen, Medis, MSD, Novartis, Pfizer, Consultant of: Abbvie, Amgen, Biogen, Medis, MSD, Novartis, Pfizer, Irene van der Horst-Bruinsma Speakers bureau: Abbvie, BMS, MSD, Novartis, Pfizer, Lilly, UCB, Björn Gudbjornsson Speakers bureau: Amgen and Novartis, Johan Askling: None declared, Bente Glintborg Grant/research support from: Pfizer, Biogen, AbbVie, Karel Pavelka Speakers bureau: AbbVie, Roche, MSD, UCB, Pfizer, Novartis, Egis, Gilead, Eli Lilly, Consultant of: AbbVie, Roche, MSD, UCB, Pfizer, Novartis, Egis, Gilead, Eli Lilly, Elisa Gremese: None declared, Nurullah Akkoc: None declared, Adrian Ciurea Speakers bureau: Abbvie, Eli-Lilly, MSD, Novartis, Pfizer, Eirik kristianslund: None declared, Anabela Barcelos: None declared, Gareth T. Jones Grant/research support from: Pfizer, AbbVie, UCB, Celgene, Amgen, GSK, Anna-Mari Hokkanen Grant/research support from: MSD, Carlos Sánchez-Piedra: None declared, Ruxandra Ionescu Speakers bureau: Abbvie, Amgen, Boehringer-Ingelheim Eli-Lilly,Novartis, Pfizer, Sandoz, UCB, Ziga Rotar Speakers bureau: Abbvie, Amgen, Biogen, Medis, MSD, Novartis, Pfizer, Consultant of: Abbvie, Amgen, Biogen, Medis, MSD, Novartis, Pfizer, Marleen G.H. van de Sande: None declared, Arni Jon Geirsson: None declared, Mikkel Østergaard Speakers bureau: 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, Consultant of: 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, Merete L. Hetland Speakers bureau: Abbvie, Biogen, BMS, Celltrion, Eli Lilly, Janssen Biologics B.V, Lundbeck Fonden, MSD, Pfizer, Roche, Samsung Biopies, Sandoz, Novartis.

Background:Interstitial lung disease (ILD) is an established extra-articular manifestation of rheumatoid arthritis (RA). Few studies have investigated the prevalence of ILD in patients with psoriatic arthritis (PsA). Methotrexate (MTX) is frequently used in the treatment of both RA and PsA and has been suggested to be a risk factor for the development of ILD. It is of interest to understand the interaction between disease and treatment in the development of ILD.Objectives:To compare the incidence of ILD between patient with PsA and RA treated with biologic disease modifying antirheumatic drugs (bDMARDS), with or without MTX as a co-medication.Methods:Cohorts of patients with RA and PsA starting bDMARD were identified in Nordic registers (Danish nationwide clinical register for patients with RA (DANBIO), Register on antirheumatic and biological therapy in Finland (ROB-FIN), Icelandic nationwide database of biologic therapy (ICEBIO), Norwegian Antirheumatic Drug Register (NOR-DMARD), and the Swedish Rheumatology Quality Register (SRQ)). Linkages to the National Patient Registers and to the Cause of Death Registers were performed in each country to identify cases of ILD. Each individual patient could contribute several treatment courses. ILD was identified as hospital or death certificate ICD10 codes of ILD (J84.1, J84.8, J84.9, J70.2, J70.3, J70.4, J99.0, J99.1, J99.8) given during the follow-up period which was defined as the treatment course duration, plus a 30-day wash-out period added to the end of treatment course period. MTX co-medication was specified as use of MTX at the start of bDMARD. Incidence rates (IR) for any ILD were calculated per 1000 person years at risk (PYR) for each country. The five cohorts were pooled and incidence rate ratios (IRR) for PsA vs. RA were calculated. Hazard ratios (HR) for any ILD in PsA vs. RA were estimated in Cox regression models adjusted for age, gender and repeated observations, and stratified for the use of MTX co-medication.Results:Overall 47 987 individual patients representing 89 239 bDMARD treatment courses and contributing 201 279 PYR were included in the study (Table 1). Methotrexate was reported as comedication in 29 916 (33.5 %) of the treatment courses (PsA vs. RA, 30.4 % vs 34.5 %). 970 cases of ILD were identified during the follow-up period. The risk of ILD was consistently lower in patients with PsA compared to patients with RA in all countries. In models stratified for co-medication the HR for ILD in PsA vs. RA was 0.34 (0.21-0.57) in patients treated with MTX and 0.26 (0.18-0.36) in patients not treated with MTX.Table 1.Interstitial lung disease in PsA vs. RA in five Nordic biologic registersDENMARKFINLANDICELANDNORWAYSWEDENRAPsARAPsARAPsARAPsARAPsANumber of individuals78293386494610916754701590999205966393Number of treatment courses17 07266408634184512808592379142738 27910 824Age baseline (SD)57.3 (13.1)49.0 (12.6)53.8 (13.4)48.8 (11.4)53.9 (14.2)50.1 (13.3)53.8 (13.7)48.7 (12.0)57.1 (13.7)50.6 (12.8)Female n (%)12 963 (76)3929 (59)6571 (76)933 (51)969 (76)551 (65)1815 (77)818 (57)29 635 (77)6162 (57)Number of PYR4023513986217984910451727994556265312033427412ILD-events within PYR2182213287232668028IR pr 1000 PYR5.41.66.11.61.50.77.02.35.71.0IRR PsA vs RA crude0.29 (0.18-0.45)0.27 (0.11-0.55)0.46 (0.05-2.42)0.32(0.11-0.78)0.18 (0.12-0.26)HR PsA vs RA0.31 (0.17-0.56)0.46 (0.22-0.96)0.62 (0.12-3.14)0.19 (0.06-0.54)0.25 (0.17-0.37)PYR: Patient years at risk, IR: Incidence rates, IRR: Incidence rate ratios, HR: Hazard RatiosConclusion:In these preliminary analyses, the incidence of ILD is lower in bDMARD treated PsA vs. RA patients, irrespective of co-medication with MTX. This indicates that the clinician should consider the rheumatological diagnosis when assessing the risk for future ILD in patients treated with bDMARDs and MTX.Acknowledgements:Partly funded by NordForsk and FOREUMDisclosure of Interests:Sella Aarrestad Provan Consultant of: Novartis, Grant/research support from: Boehringer-Ingelheim, Brigitte Michelsen: None declared, Lotta Ljung: None declared, Thorarinn Jonmundsson: None declared, Björn Gudbjornsson Speakers bureau: Amgen and Novartis, Daniela Di Giuseppe: None declared, Merete Lund Hetland Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck and Samsung Bioepis, Consultant of: Eli Lilly, Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen and Pfizer, Guðrún Björk Reynisdóttir: None declared, Bente Glintborg: None declared, Eirik kristianslund: None declared, Heikki Relas: None declared, Kalle Aaltonen: None declared, Dan Nordström Speakers bureau: Abbvie, BMS, Celgene, Eli Lilly, MSD, Novartis, Pfizer, Roche and UCB., Consultant of: Abbvie, BMS, Celgene, Eli Lilly, MSD, Novartis, Pfizer, Roche and UCB., Tore K. Kvien Speakers bureau: Amgen, Celltrion, Egis, Evapharma, Ewopharma, Hikma, Oktal, Sandoz, Sanofi., Consultant of: AbbVie, Amgren, Biogen, Celltrion, Eli Lilly, Gilead, Mylan, Novartis, Pfizer, Roche, Sandoz, Sanofi., Johan Askling Grant/research support from: Abbvie, BMS, Eli Lilly, Merck, Pfizer, Roche, Samsung Bioepis, and Sanofi

Background:In clinical practice, some patients with axial spondyloarthritis (axSpA) fail several consecutive biological treatments (bDMARDs). How this group of ”refractory” patients should best be defined, how common they are, and what their characteristics are, is poorly understood.Objectives:To explore the point prevalence of bDMARD refractory disease in axSpA over time, according to different definitions, and to describe the characteristics of refractory vs. not-refractory patients upon start of their first bDMARD.Methods:Observational prospective cohort study. Patients with axSpA (ankylosing spondylitis/non-radiographic axial SpA) starting a first bDMARD 2009-2018 were identified in biologic registries in Denmark, Sweden, Finland, Norway and Iceland. Clinical characteristics and treatments were retrieved, and data were pooled for analysis.Refractory disease was defined based on the number of different bDMARD treatments started in individual patients: mild (≥3 bDMARDs), moderate (≥4), and strict (5 or more). Restart of same bDMARD with another bDMARD in between counted as separate courses whereas switch from originator to corresponding biosimilar was ignored.Proportions of patients fulfilling each definition of refractory disease at 2 and 5 years after the start of 1st bDMARD were calculated.Point-prevalence per calendar-year was calculated as the number of patients with refractory disease at the end of each year, divided by the total number of patients ever having starting a first bDMARD before that time-point, and who were still alive and resident in the country.Results:The point prevalence of refractory axSpA increased with calendar-time (Figure). Among 12,037 included axSpA patients (64% male), the point-prevalence of bDMARD refractory disease in 2018 was 16%/7%/3% according to mild/moderate/strict definitions (Table).Table 1.Biologic refractory axSpA according to three definitionsA.Baseline characteristics upon start 1st bDMARDRefractory definitionOverall cohortMILDMODERATESTRICTN120371969832351Age, years42 (13)41 (12)41 (12)41 (12)Male, %64%57%54%56%Disease duration, years7 (10)6 (9)6 (8)5 (8)BASDAI, 0-10053 (28)60 (29)63 (27)66 (35)ASDAS3.3 (1.1)3.5 (1.2)3.6 (1.0)3.7 (1.1)CRP, mg/L16 (23)18 (26)21 (28)23 (32)Patient global, VAS, 0-10059 (25)65 (22)66 (22)67 (23)Patient Pain, VAS, 0-10057 (24)62 (22)63 (22)63 (22)Fatigue, VAS, 0-10059 (27)66 (26)66 (26)68 (25)B.Proportions of patients having refractory disease 2 and 5 years after start of their first bDMARD2 years, %5%1%0%5 years, %13%4%1%Numbers are means (SD) unless otherwise statedUpon start of their 1st bDMARD, patients later fulfilling the definitions for refractory axSpA were more frequently women, had shorter disease duration, higher C-reactive protein and higher patient reported outcomes.Overall, 5%/1%/0% had mild/moderate/strict refractory disease 2 years after start of first bDMARD, after 5 years it was 13%/4%/1% (Table).Conclusion:In this large Nordic observational cohort of axSpA patients treated in routine care, we could demonstrate that a substantial proportion of all patients had used multiple bDMARDs. In 2018, one in six patients had received ≥3 bDMARDs, indicating a bDMARD refractory disease. Multiple switching was more frequent during later years, probably due to more bDMARDs becoming available. The characteristics of refractory axSpA, including sex and disease activity, will have to be further explored, as will the impact of refractory disease on long-term outcomes.Acknowledgements:the DANBIO, SRQ, ICEBIO, ROB-FIN and NOR-DMARD registries.Partly sponsored by Nordforsk and Foreum.Disclosure of Interests:Daniela Di Giuseppe: None declared, Ulf Lindström: None declared, Kalle Aaltonen: None declared, Heikki Relas Speakers bureau: Abbvie, Celgene, MSD, Roche, Sella Aarrestad Provan: None declared, Björn Gudbjornsson Speakers bureau: Amgen and Novartis, Merete L. Hetland Grant/research support from: AbbVie, Biogen, BMS, Celtrion, Eli Lilly Denmark A/S, Janssen Biologics B.V, Lundbeck Fonden, MSD, Pfizer, Roche, Samsung Biopis, Sandoz. MLH chairs the steering committee of the Danish Rheumatology Quality Registry (DANBIO), which receives public funding from the hospital owners and funding from pharmaceutical companies. MLH co-chairs the EuroSpA research collaboration, which generates real-world evidence of treatment of psoriatic arthritis and axial spondyloarthritis based on secondary use of quality data and is partly funded by Novartis., Johan Askling: None declared, Tanja Schjødt Jørgensen: None declared, Lene Dreyer Speakers bureau: Eli-Lilly and Galderma, Grant/research support from: BMS, Dan Nordström: None declared, Brigitte Michelsen: None declared, Arni Jon Geirsson: None declared, Lennart T.H. Jacobsson: None declared, Bente Glintborg Grant/research support from: Abbvie, BMS, Pfizer, Lundbeck foundation

ObjectiveTo investigate the predictive value of baseline depression/anxiety on the likelihood of achieving joint remission in rheumatoid arthritis (RA) and psoriatic arthritis (PsA) as well as the associations between baseline depression/anxiety and the components of the remission criteria at follow-up.MethodsWe included 1326 patients with RA and 728 patients with PsA from the prospective observational NOR-DMARD study starting first-time tumour necrosis factor inhibitors or methotrexate. The predictive value of depression/anxiety on remission was explored in prespecified logistic regression models and the associations between baseline depression/anxiety and the components of the remission criteria in prespecified multiple linear regression models.ResultsBaseline depression/anxiety according to EuroQoL-5D-3L, Short Form-36 (SF-36) Mental Health subscale ≤56 and SF-36 Mental Component Summary ≤38 negatively predicted 28-joint Disease Activity Score ConclusionDepression and anxiety may reduce likelihood of joint remission based on composite scores in RA and PsA and should be taken into account in individual patients when making a shared decision on a treatment target.

Background:Axial spondylarthritis (axSpA) patients treated with a tumour necrosis factor inhibitor (TNFi) may receive a concomitant conventional synthetic disease-modifying anti-rheumatic drug (csDMARD), although the value of combination therapy remains unclear.Objectives:Describe the proportion and phenotype of patients with axSpA initiating their first TNFi as monotherapy compared to TNFi+csDMARD combination therapy, and to compare the 1-year TNFi retention between the two groups.Methods:Data from 13 European registries was collected. Two exposure treatment groups were defined: TNFi monotherapy at baseline (=TNFi start date) and TNFi+csDMARD combination therapy. TNFi retention rates were assessed with Kaplan-Meier curves for each country and combined. Hazard ratios (HR, 95% CI) for discontinuing the TNFi were obtained with Cox models: (i) crude; adjusted for (ii) country, and (iii) country, sex, age, calendar year, disease duration and BASDAI. Participating countries were dichotomized into two strata, depending on their 1-year retention rate being above (stratum A) or below (stratum B) the average retention rate across all countries.Results:22,196 axSpA patients were included with 34% on TNFi+csDMARD combination therapy. Baseline characteristics are presented in table 1. Overall, the crude TNFi retention rate was marginally longer in the combination therapy group (80% (79-81%)) compared to the monotherapy group (78% (77-79%)) and was primarily driven by differences in stratum B (fig. 1). TNFi retention rates varied significantly across countries (range:-11.0% to +11.3%), with a clear distinction between the 2 strata. The HRs for discontinuation over 1-year (reference=TNFi monotherapy) in the 3 models were: (i) 0.88 (0.82-0.93), (ii) 0.87 (0.82-0.92), (iii) 0.88 (0.82-0.93).Table 1Baseline characteristicsAll patients(n=22196)Country stratum ACountry stratum BTNFi mono(n=4940)csDMARD + TNFi(n=2547)TNFi mono(n=9693)csDMARD + TNFi(n=5016)Age (years), mean (SD)42.6 (12.5)43.4 (12.0)42.8 (12.2)41.6 (12.7)43.7 (12.7)Females, %41.137.738.242.044.2Disease duration (yrs), mean (SD)5.7 (8.0)6.2 (7.7)6.7 (7.4)4.9 (8.2)6.1 (8.2)Enthesitis, %50.316.733.957.859.7SJC-28, median (IQR)0 (0-1)0 (0-0)0 (0-2)0 (0-0)0 (0-2)VAS pain (0-100), mean (SD)60.9 (24.5)63.3 (26.5)67.8 (23.3)60.2 (23.4)57.2 (24.3)CRP (mg/L), median (IQR)8 (3-20)7.8 (2-20)18 (6.7-32.6)6.0 (2.7-15)8.0 (3-22)BASDAI (0-10), mean (SD)5.7 (2.1)5.7 (2.2)6.2 (2.1)5.6 (2.0)5.4 (2.2)BASFI (0-10), mean (SD)4.4 (2.5)4.4 (2.6)4.9 (2.5)4.3 (2.4)4.2 (2.9)ASDAS, mean (SD)3.5 (1.1)3.7 (1.0)4.0 (1.0)3.3 (1.0)3.3 (1.1)On Infliximab, %25.721222436Baseline csDMARD use, %-Methotrexate045063-Sulfasalazine068033-Leflunomide0801Conclusion:Considerable differences were observed across countries in the use of combination therapy and TNFi retention in axSpA patients. The overall 1-year TNFi retention was higher with csDMARD co-therapy compared to TNFi monotherapy. TNFi monotherapy had a 12-13% higher risk of treatment discontinuation.Acknowledgments:Novartis Pharma AG and IQVIAMN and BD participated equallyDisclosure of Interests:Michael Nissen Grant/research support from: Abbvie, Consultant of: Novartis, Lilly, Abbvie, Celgene and Pfizer, Speakers bureau: Novartis, Lilly, Abbvie, Celgene and Pfizer, Bénédicte Delcoigne: None declared, Daniela Di Giuseppe: None declared, Lennart T.H. Jacobsson Consultant of: AbbVie, Eli Lilly, Janssen, Novartis and Pfizer, Karen Fagerli: None declared, Anne Gitte Loft Grant/research support from: Novartis, Consultant of: AbbVie, MSD, Novartis, Pfizer and UCB, Speakers bureau: AbbVie, MSD, Novartis, Pfizer and UCB, Adrian Ciurea Consultant of: Consulting and/or speaking fees from AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly, Merck Sharp & Dohme, Novartis and Pfizer., Dan Nordström Consultant of: Abbvie, Celgene, Lilly, Novartis, Pfizer, Roche and UCB., Speakers bureau: Abbvie, Celgene, Lilly, Novartis, Pfizer, Roche and UCB., Ziga Rotar Consultant of: Speaker and consulting fees from Abbvie, Amgen, Biogen, Eli Lilly, Medis, MSD, Novartis, Pfizer, Roche, Sanofi., Speakers bureau: Speaker and consulting fees from Abbvie, Amgen, Biogen, Eli Lilly, Medis, MSD, Novartis, Pfizer, Roche, Sanofi., Florenzo Iannone Consultant of: Speaker and consulting fees from AbbVie, Eli Lilly, Novartis, Pfizer, Roche, Sanofi, UCB, MSD, Speakers bureau: Speaker and consulting fees from AbbVie, Eli Lilly, Novartis, Pfizer, Roche, Sanofi, UCB, MSD, Maria Jose Santos Speakers bureau: Novartis and Pfizer, Manuel Pombo-Suarez Consultant of: Janssen, Lilly, MSD and Sanofi., Speakers bureau: Janssen, Lilly, MSD and Sanofi., Björn Gudbjornsson Speakers bureau: Novartis and Amgen, Heřman Mann: None declared, Nurullah Akkoc: None declared, Catalin Codreanu Consultant of: Speaker and consulting fees from AbbVie, Accord Healthcare, Alfasigma, Egis, Eli Lilly, Ewopharma, Genesis, Mylan, Novartis, Pfizer, Roche, Sandoz, UCB, Speakers bureau: Speaker and consulting fees from AbbVie, Accord Healthcare, Alfasigma, Egis, Eli Lilly, Ewopharma, Genesis, Mylan, Novartis, Pfizer, Roche, Sandoz, UCB, Irene van der Horst-Bruinsma Grant/research support from: AbbVie, Novartis, Eli Lilly, Bristol-Myers Squibb, MSD, Pfizer, UCB Pharma, Consultant of: AbbVie, Novartis, Eli Lilly, Bristol-Myers Squibb, MSD, Pfizer, UCB Pharma, Brigitte Michelsen: None declared, Gary Macfarlane: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen and Pfizer, Consultant of: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck and Samsung Bioepis, Matija Tomsic: None declared, Burkhard Moeller: None declared, Pedro Ávila-Ribeiro Grant/research support from: Novartis, Carlos Sánchez-Piedra: None declared, Heikki Relas Grant/research support from: Abbvie., Consultant of: Abbvie, Celgene, and Pfizer., Speakers bureau: Abbvie, Celgene, and Pfizer., Arni Jon Geirsson: None declared, Lucie Nekvindova: None declared, Gozde Yildirim Cetin Speakers bureau: AbbVie, Novartis, Pfizer, Roche, UCB, MSD, Ruxandra Ionescu Consultant of: Consulting fees from Abbvie, Eli-Lilly, Novartis, Pfizer, Roche, Sandoz, Speakers bureau: Consulting and speaker fees from Abbvie, Eli-Lilly, Novartis, Pfizer, Roche, Sandoz, Niels Steen Krogh: None declared, Johan Askling Grant/research support from: JA acts or has acted as PI for agreements between Karolinska Institutet and the following entities, mainly in the context of the ARTIS national safety monitoring programme of immunomodulators in rheumatology: Abbvie, BMS, Eli Lilly, Merck, MSD, Pfizer, Roche, Samsung Bioepis, Sanofi, and UCB Pharma, Bente Glintborg Grant/research support from: Grants from Pfizer, Biogen and Abbvie, Ulf Lindström: None declared

Background:Tumor necrosis factor inhibitors (TNFi) have been available for more than a decade for treatment of spondyloarthrtitis (SpA). Secukinumab (SEC) represents a new mode of action, but few studies have compared outcomes in patients(pts) treated with SEC vs TNFi – and the optimal treatment strategy in routine care remains to be established. Comparative studies between SEC and adalimumab (ADA) are ongoing.Objectives:To describe baseline characteristics and compare 1-yr treatment retention of SEC vs TNFi (ADA/certolizumab pegol(CLZ)/etanercept(ETN)/golimumab(GOL)/infliximab(IFX)) in SpA-pts from 5 Nordic countries.Methods:Observational, prospective cohort study. Pts with SpA (ankylosing spondylitis/non-radiographic axial SpA/undifferentiated SpA) starting SEC or any TNFi during 2015-2018 were identified in clinical rheumatology registries of the Nordic countries. Baseline characteristics were retrieved. Country-specific data were pooled. 1-yr treatment retention of SEC vs TNFi was assessed through crude survival probability curves, retention rates and adjusted Cox regression analyses (ADA reference). Analyses were stratified by line of bDMARD and TNFi type.Results:In total, 10692 treatment courses (834 SEC, 9858 TNFi) in 7952 patients were included. SEC was rarely used as 1stbDMARD (Table 1), whereas it was the drug most frequently used as 3rd+ line (Table 2). Baseline characteristics were numerically similar for SEC vs TNFi (Table 1).Table 1.Patient characteristics at treatment start1stline2ndline3rd+ lineSECTNFiSECTNFiSECTNFiN70518615626056082067Male, %535544534546Age, yrs45 (14)41 (14)45 (12)44 (13)47 (12)46 (13)BASDAI, mm45 (28)53 (22)52 (22)52 (24)63 (22)58 (24)Concomitant csDMARD, %182723232726Means (SD) unless otherwise statedTable 2.Table 2. 1-yr treatment retention (Kaplan Meier, Cox Regression)DrugRetentions rates, 1 yr % (95% CI)Adjusted* HR (95% CI) for discontinuation1stlineADA76 (73-79)1CLZ68 (63-72)1.4 (1.1-1.8)ETN74 (71-76)1.1 (0.9-1.3)GOL80 (77-84)0.8 (0.6-1.0)IFX65 (62-67)1.5 (1.3-1.8)SEC76 (62-85)0.9 (0.5-1.6)2ndlineADA72 (68-75)1CLZ58 (51-64)1.5 (1.2-1.9)ETN65 (61-68)1.2 (1.0-1.5)GOL73 (67-77)0.9 (0.7-1.2)IFX67 (63-71)1.2 (0.9-1.5)SEC67 (58-74)1.1 (0.8-1.5)3rd+ lineADA73 (68-77)1CLZ52 (46-57)2.0 (1.6-2.6)ETN65 (61-70)1.3 (1.0-1.6)GOL65 (60-70)1.3 (1.0-1.7)IFX61 (56-66)1.5 (1.2-1.9)SEC61 (57-65)1.4 (1.1-1.8)* by sex, baseline age, BASDAI, concomitant csDMARD (y/n/missing). Pts with missing baseline BASDAI (41-60%) excluded1-yr treatment retention varied between the TNFi (Figure,Table 2), with SEC showing retention rates comparable to ADA when used as 1stor 2ndline therapy. However, SEC retention was poorer than ADA when used as 3rd+ therapy, but comparable to retention of other TNFi.In adjusted Cox regression analyses, confidence intervals were wide and included 1 for SEC vs ADA (1st, 2ndline), whereas there was slightly poorer retention of SEC versus ADA when used as 3rd+ bDMARD (Table 2).Conclusion:These observational data in >10.000 biological treatment courses in SpA, showed that SEC was mainly used in bDMARD experienced pts. Baseline characteristics were similar in pts treated with SEC vs TNFi. The 1-yr retention for SEC was similar to that of the TNFi when used as 1stor 2ndline, but poorer than ADA regarding 3rd+ courses. Further analyses are planned to explore confounding by indication and channeling towards treatment.Acknowledgments:Glintborg/Lindström shared 1st author, Kristensten/Jacobsson shared last.Partly funded by NordForsk and FOREUMDisclosure of Interests:Bente Glintborg Grant/research support from: Grants from Pfizer, Biogen and Abbvie, Ulf Lindström: None declared, Daniela Di Giuseppe: None declared, Sella Aarrestad Provan Consultant of: Novartis, Björn Gudbjornsson Speakers bureau: Novartis and Amgen, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen and Pfizer, Consultant of: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck and Samsung Bioepis, Brigitte Michelsen Grant/research support from: Research support from Novartis, Consultant of: Consulting fees Novartis, Johan K Wallman Consultant of: AbbVie, Celgene, Eli Lilly, Novartis and UCB Pharma, Kalle Aaltonen: None declared, Anna-Mari Hokkanen Grant/research support from: MSD, Tanja Schjødt Jørgensen Speakers bureau: Abbvie, Pfizer, Roche, Novartis, UCB, Biogen, and Eli Lilly, Rebekka L. Hansen: None declared, Arni Jon Geirsson: None declared, Kathrine L. Grøn Grant/research support from: BMS, Niels Steen Krogh: None declared, Johan Askling Grant/research support from: JA acts or has acted as PI for agreements between Karolinska Institutet and the following entities, mainly in the context of the ARTIS national safety monitoring programme of immunomodulators in rheumatology: Abbvie, BMS, Eli Lilly, Merck, MSD, Pfizer, Roche, Samsung Bioepis, Sanofi, and UCB Pharma, Lars Erik Kristensen Consultant of: UCB Pharma (Advisory Board), Sannofi (Advisory Board), Abbvie (Advisory Board), Biogen (Advisory Board), Speakers bureau: AbbVie, Amgen, Biogen, Bristol-Myers Squibb,Celgene, Eli Lilly, Gilead, Forward Pharma, Janssen Pharmaceuticals, MSD, Novartis, Pfizer, and UCB Pharma, Lennart T.H. Jacobsson Consultant of: AbbVie, Eli Lilly, Janssen, Novartis and Pfizer

Background:To determine the real-life 6- and 12-month secukinumab effectiveness in Europe overall, as well as stratified by prior biologic disease-modifying anti-rheumatic drug (bDMARD)/targeted synthetic (ts)DMARD use.Objectives:Real-life data from axSpA patients treated with secukinumab from 13 countries in the European Spondyloarthritis (EuroSpA) Research Collaboration Network were pooled. We calculated proportions of patients achieving Bath Ankylosing Spondylitis Disease Activity Score (BASDAI) Methods:A total of 1860 axSpA patients were included (Table 1). Overall 6/12-month secukinumab retention rates were 82%/72% and higher in bionaïve patients (Table 2, Figure). Significant differences in retention rates in-between the registries were found. Inactive disease/low-disease-activity (LDA) were achieved more often in bionaïve patients (Table 2).Table 1All patients (n=1860)b/tsDMARD naïve (n=414)1 prior b/tsDMARD (n=448)≥2 prior b/tsDMARDs (n=998)Age (years), mean (SD)47 (12)45 (12)47 (12)48 (12)Men, %57%68%58%49%Years since diagnosis, mean (SD)10 (9)8 (9)10 (9)11 (9)Current smokers, %25 %27%25%23%Patient’s global (0-100), median (IQR)70 (50-81)80 (60-90)64 (50-80)70 (50-82)Physician’s global (0-100), median (IQR)45 (25-63)64 (43-78)45 (22-60)40 (20-58)C reactive protein (mg/L), median (IQR)8 (3-25)15 (5-31)7 (3-25)6 (2-22)Erythrocyte sedimentation rate (mm/h), median (IQR)22 (9-44)30 (14-44)24 (8-45)18 (8-42)Pain (0-100), median (IQR)70 (50-81)80 (65-90)65 (49-80)70 (50-80)BASDAI, median (IQR)6.2 (4.6-7.6)6.8 (5.2-8.0)5.9 (4.2-7.2)6.1 (4.4-7.6)BASFI, median (IQR)5.5 (3.2-7.3)6.1 (3.2-7.6)4.8 (2.8-6.8)5.5 (3.3-7.2)ASDAS, median (IQR)3.6 (2.9-4.3)4.2 (3.5-4.8)3.5 (2.7-4.2)3.5 (2.8-4.2)Table 2MonthsAll patients (n=1860)b/tsDMARD naïve (n=414)1 prior b/tsDMARD (n=448)≥2 prior b/tsDMARDs (n=998)p-value*Secukinumab retention rate, % (95%CI)682% (80-84%)90% (87-93%)83% (79-86%)78% (76-81%)0.0011272% (69-74%)84% (81-88%)73% (69-78%)66% (63-69%)BASDAI Crude626373518 LUNDEX adjusted21342813 Crude1225412918 LUNDEX adjusted16311811BASDAI Crude651716040 LUNDEX adjusted40654730 Crude1251765639 LUNDEX adjusted32573623ASDAS Crude69131360.001 LUNDEX adjusted712115 Crude1211181570.002 LUNDEX adjusted713940.002ASDAS Crude6243226200.002 LUNDEX adjusted19292115 Crude1227442721 LUNDEX adjusted17331712*Comparisons between b/tsDMARD naïve, 1 prior and ≥2 prior b/tsDMARD users were performed with Kaplan-Meier with log-rank test or Chi-Square test, as appropriateConclusion:In this real-life study of 1860 patients with axSpA in 13 European countries secukinumab retention was high and significantly higher for bionaïve patients. Overall, a higher proportion of bionaïve than previous b/tsDMARD users achieved inactive disease/LDA.FigureAcknowledgments:Novartis and IQVIA for supporting the EuroSpA RCNDisclosure of Interests:Brigitte Michelsen Grant/research support from: Research support from Novartis, Consultant of: Consulting fees Novartis, Ulf Lindström: None declared, Catalin Codreanu Consultant of: Speaker and consulting fees from AbbVie, Accord Healthcare, Alfasigma, Egis, Eli Lilly, Ewopharma, Genesis, Mylan, Novartis, Pfizer, Roche, Sandoz, UCB, Speakers bureau: Speaker and consulting fees from AbbVie, Accord Healthcare, Alfasigma, Egis, Eli Lilly, Ewopharma, Genesis, Mylan, Novartis, Pfizer, Roche, Sandoz, UCB, Adrian Ciurea Consultant of: Consulting and/or speaking fees from AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly, Merck Sharp & Dohme, Novartis and Pfizer., Jakub Zavada Speakers bureau: Abbvie, UCB, Sanofi, Elli-Lilly, Novartis, Zentiva, Accord, Anne Gitte Loft Grant/research support from: Novartis, Consultant of: AbbVie, MSD, Novartis, Pfizer and UCB, Speakers bureau: AbbVie, MSD, Novartis, Pfizer and UCB, Manuel Pombo-Suarez Consultant of: Janssen, Lilly, MSD and Sanofi., Speakers bureau: Janssen, Lilly, MSD and Sanofi., Fatos Onen: None declared, Tore K. Kvien Grant/research support from: Received grants from Abbvie, Hospira/Pfizer, MSD and Roche (not relevant for this abstract)., Consultant of: Have received personal fees from Abbvie, Biogen, BMS, Celltrion, Eli Lily, Hospira/Pfizer, MSD, Novartis, Orion Pharma, Roche, Sandoz, UCB, Sanofi and Mylan (not relevant for this abstract)., Paid instructor for: Have received personal fees from Abbvie, Biogen, BMS, Celltrion, Eli Lily, Hospira/Pfizer, MSD, Novartis, Orion Pharma, Roche, Sandoz, UCB, Sanofi and Mylan (not relevant for this abstract)., Speakers bureau: Have received personal fees from Abbvie, Biogen, BMS, Celltrion, Eli Lily, Hospira/Pfizer, MSD, Novartis, Orion Pharma, Roche, Sandoz, UCB, Sanofi and Mylan (not relevant for this abstract)., Ziga Rotar Consultant of: Speaker and consulting fees from Abbvie, Amgen, Biogen, Eli Lilly, Medis, MSD, Novartis, Pfizer, Roche, Sanofi., Speakers bureau: Speaker and consulting fees from Abbvie, Amgen, Biogen, Eli Lilly, Medis, MSD, Novartis, Pfizer, Roche, Sanofi., Maria Jose Santos Speakers bureau: Novartis and Pfizer, Florenzo Iannone Consultant of: Speaker and consulting fees from AbbVie, Eli Lilly, Novartis, Pfizer, Roche, Sanofi, UCB, MSD, Speakers bureau: Speaker and consulting fees from AbbVie, Eli Lilly, Novartis, Pfizer, Roche, Sanofi, UCB, MSD, Anna-Mari Hokkanen: None declared, Björn Gudbjornsson Speakers bureau: Novartis and Amgen, Johan Askling Grant/research support from: JA acts or has acted as PI for agreements between Karolinska Institutet and the following entities, mainly in the context of the ARTIS national safety monitoring programme of immunomodulators in rheumatology: Abbvie, BMS, Eli Lilly, Merck, MSD, Pfizer, Roche, Samsung Bioepis, Sanofi, and UCB Pharma, Ruxandra Ionescu Consultant of: Consulting fees from Abbvie, Eli-Lilly, Novartis, Pfizer, Roche, Sandoz, Speakers bureau: Consulting and speaker fees from Abbvie, Eli-Lilly, Novartis, Pfizer, Roche, Sandoz, Michael Nissen Grant/research support from: Abbvie, Consultant of: Novartis, Lilly, Abbvie, Celgene and Pfizer, Speakers bureau: Novartis, Lilly, Abbvie, Celgene and Pfizer, Karel Pavelka Consultant of: Abbvie, MSD, BMS, Egis, Roche, UCB, Medac, Pfizer, Biogen, Speakers bureau: Abbvie, MSD, BMS, Egis, Roche, UCB, Medac, Pfizer, Biogen, Carlos Sánchez-Piedra: None declared, Servet Akar: None declared, Joe Sexton: None declared, Matija Tomsic: None declared, Helena Santos Speakers bureau: AbbVie, Eli-Lilly, Janssen, Pfizer, Novartis, Marco Sebastiani: None declared, Jenny Osterlund: None declared, Arni Jon Geirsson: None declared, Gareth T. Jones Grant/research support from: Pfizer, AbbVie, UCB, Celgene and GSK., Irene van der Horst-Bruinsma Grant/research support from: AbbVie, Novartis, Eli Lilly, Bristol-Myers Squibb, MSD, Pfizer, UCB Pharma, Consultant of: AbbVie, Novartis, Eli Lilly, Bristol-Myers Squibb, MSD, Pfizer, UCB Pharma, Stylianos Georgiadis Grant/research support from: Novartis, Cecilie Heegaard Brahe Grant/research support from: Novartis, Lykke Midtbøll Ørnbjerg Grant/research support from: Novartis, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen and Pfizer, Consultant of: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck and Samsung Bioepis, Mikkel Ǿstergaard Grant/research support from: AbbVie, Bristol-Myers Squibb, Celgene, Merck, and Novartis, Consultant of: AbbVie, Bristol-Myers Squibb, Boehringer Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo Nordisk, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi, and UCB, Speakers bureau: AbbVie, Bristol-Myers Squibb, Boehringer Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo Nordisk, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi, and UCB

Background:Knowledge of changes over time in baseline characteristics and tumor necrosis factor inhibitor (TNFi) response in bionaïve psoriatic arthritis (PsA) patients treated in routine care is limited.Objectives:To investigate secular trends in baseline characteristics and retention, remission and response rates in PsA patients initiating a first TNFi.Methods:Prospectively collected data on bionaïve PsA patients starting TNFi in routine care from 15 European countries were pooled. According to year of TNFi initiation, three groups were defined a priori based on bDMARD availability: Group A (1999–2008), Group B (2009–2014) and Group C (2015–2018).Retention rates (Kaplan-Meier), crude and LUNDEX adjusted1 remission (Disease Activity Score (DAS28) Results:A total of 17453 PsA patients were included (4069, 7551 and 5833 in groups A, B and C).Patients in group A were older and had longer disease duration compared to B and C. Retention rates at 6, 12 and 24 months were highest in group A (88%/77%/64%) but differed little between B (83%/69%/55%) and C (84%/70%/56%).Baseline disease activity was higher in group A than in B and C (DAS28: 4.6/4.3/4.0, DAPSA28: 29.9/25.7/24.0, CDAI: 21.8/20.0/18.6), and this persisted at 6 and 12 months. Crude and LUNDEX adjusted remission rates at 6 and 12 months tended to be lowest in group A, although crude/LUNDEX adjusted ACR50 response rates at all time points were highest in group A. At 24 months, disease activity and remission rates were similar in the three groups (Table).Table 1.Secular trends in baseline characteristics, treatment retention, remission and response rates in European PsA patients initiating a 1st TNFiBaseline characteristicsGroup A(1999–2008)Group B(2009–2014)Group C(2015–2018)Age, median (IQR)62 (54–72)58 (49–67)54 (45–62)Male, %514847Years since diagnosis, median (IQR)5 (2–10)3 (1–9)3 (1–8)Smokers, %161717DAS28, median (IQR)4.6 (3.7–5.3)4.3 (3.4–5.1)4.0 (3.2–4.8)DAPSA28, median (IQR)29.9 (19.3–41.8)25.7 (17.2–38.1)24.0 (16.1–35.5)CDAI, median (IQR)21.8 (14.0–31.1)20.0 (13.0–29.0)18.6 (12.7–26.1)TNFi drug, % (Adalimumab / Etanercept / Infliximab / Certolizumab / Golimumab)27 / 43 / 30 / 0 / 036 / 31 / 14 / 5 / 1421 / 40 / 21 / 8 / 10Follow up6 months12 months24 monthsGr AGr BGr CGr AGr BGr CGr AGr BGr CRetention rates, % (95% CI)88 (87–89)83 (82–84)84 (83–85)79 (78–80)72 (71–73)72 (71–73)68 (67–69)60 (59–61)60 (59–62)DAS28, median (IQR)2.7 (1.9–3.6)2.4 (1.7–3.4)2.3 (1.7–3.2)2.5 (1.8–3.4)2.2 (1.6–3.1)2.1 (1.6–2.9)2.1 (1.6–3.1)2.0 (1.6–2.9)1.9 (1.5–2.6)DAPSA28, median (IQR)10.6 (4.8–20.0)9.5 (3.9–18.3)8.7 (3.6–15.9)9.1 (4.1–17.8)7.7 (3.1–15.4)7.6 (2.9–14.4)6.7 (2.7–13.7)6.6 (2.7–13.5)5.9 (2.4–11.8)CDAI, median (IQR)7.8 (3.0–15.2)8.0 (3.0–15.0)6.4 (2.6–12.2)6.4 (2.5–13.0)6.2 (2.5–12.1)5.8 (2.2–11.4)5.0 (2.0–11.0)5.5 (2.0–11.2)5.0 (2.0–9.0)DAS28 remission, %, c/L47 / 4255 / 4661 / 5153 / 4362 / 4566 / 4864 / 4268 / 3775 / 41DAPSA28 remission, %, c/L22 / 1926 / 2228 / 2325 / 2031 / 2232 / 2336 / 2334 / 1938 / 21CDAI remission, %, c/L23 / 2123 / 1926 / 2227 / 2127 / 2029 / 2134 / 2231 / 1735 / 19ACR50 response, %, c/L26 / 2322 / 1824 / 2027 / 2223 / 1721 / 1523 / 1518 / 1014 / 8Gr, Group; c/L, crude/LUNDEX.Conclusion:Over the past 20 years, patient age, disease duration and disease activity level at the start of the first TNFi in PsA patients have decreased. Furthermore, TNFi retention rates have decreased while remission rates have increased, especially remission rates within the first year of treatment. These findings may reflect a greater awareness of early diagnosis in PsA patients, a lowered threshold for initiating TNFi and the possibility for earlier switching in patients with inadequate treatment response.References:[1]Arthritis Rheum 2006; 54: 600-6.Acknowledgements:Novartis Pharma AG and IQVIA for supporting the EuroSpA Research Collaboration Network.Disclosure of Interests:Sara Nysom Christiansen Speakers bureau: BMS and GE, Grant/research support from: Novartis, Lykke Midtbøll Ørnbjerg Grant/research support from: Novartis, Simon Horskjær Rasmussen: None declared, Anne Gitte Loft Speakers bureau: AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, UCB, Consultant of: AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, UCB, Grant/research support from: Novartis, Johan K Wallman Consultant of: Celgene, Eli Lilly, Novartis, Florenzo Iannone Speakers bureau: Abbvie, MSD, Novartis, Pfizer and BMS, Brigitte Michelsen Consultant of: Novartis, Grant/research support from: Novartis, Michael J. Nissen Speakers bureau: Novartis, Eli Lilly, Celgene, and Pfizer, Consultant of: Novartis, Eli Lilly, Celgene, and Pfizer, Jakub Zavada: None declared, Maria Jose Santos Speakers bureau: AbbVie, Novartis, Pfizer, Manuel Pombo-Suarez: None declared, Kari Eklund: None declared, Matija Tomsic Speakers bureau: Abbvie, Amgen, Biogen, Medis, MSD, Novartis, Pfizer, Consultant of: Abbvie, Amgen, Biogen, Medis, MSD, Novartis, Pfizer, Björn Gudbjornsson Speakers bureau: Amgen and Novartis, İsmail Sari: None declared, Catalin Codreanu Speakers bureau: AbbVie, Amgen, Egis, Novartis, Pfizer, UCB, Grant/research support from: AbbVie, Amgen, Egis, Novartis, Pfizer, UCB, Daniela Di Giuseppe: None declared, Bente Glintborg Grant/research support from: Pfizer, Biogen, AbbVie, Marco Sebastiani: None declared, Karen Minde Fagerli: None declared, Burkhard Moeller: None declared, Karel Pavelka Speakers bureau: AbbVie, Roche, MSD, UCB, Pfizer, Novartis, Egis, Gilead, Eli Lilly, Consultant of: AbbVie, Roche, MSD, UCB, Pfizer, Novartis, Egis, Gilead, Eli Lilly, Anabela Barcelos: None declared, Carlos Sánchez-Piedra: None declared, Heikki Relas: None declared, Ziga Rotar Speakers bureau: Abbvie, Amgen, Biogen, Medis, MSD, Novartis, Pfizer, Consultant of: Abbvie, Amgen, Biogen, Medis, MSD, Novartis, Pfizer, Thorvardur Love: None declared, Servet Akar: None declared, Ruxandra Ionescu Speakers bureau: Abbvie, Amgen, Boehringer-Ingelheim Eli-Lilly,Novartis, Pfizer, Sandoz, UCB, Gary Macfarlane Grant/research support from: GlaxoSmithKline, Marleen G.H. van de Sande: None declared, Merete L. Hetland Speakers bureau: Abbvie, Biogen, BMS, Celltrion, Eli Lilly, Janssen Biologics B.V, Lundbeck Fonden, MSD, Pfizer, Roche, Samsung Biopies, Sandoz, Novartis., Mikkel Østergaard Speakers bureau: 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, Consultant of: 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:Women with rheumatoid arthritis (RA) are at increased risks of adverse pregnancy outcomes, especially preterm birth (PTB) and small for gestational age (SGA). However, the link between RA disease activity, type and timing of anti-rheumatic treatment, and the risk of these outcomes remains unclear.Objectives:To explore the associations between maternal RA and PTB/SGA in relation to disease activity and use of anti-rheumatic treatment before and during pregnancy.Methods:By linking national medical birth registers to prospective clinical rheumatology registers (CRRs) in Sweden (SRQ) and Denmark (DANBIO), we identified 1739 RA-pregnancies and 17390 control-pregnancies (matched 1:10 on maternal age, birth year, and parity) with delivery 2006-2018. From CRRs and prescribed drug registers, we collected information on RA disease activity (DAS28, CRP and HAQ-score) and anti-rheumatic drugs (biologics, conventional synthetic (cs)DMARDs and oral steroids) nine months before and during pregnancy. Using logistic regression, we estimated adjusted odds ratios (ORs) with 95% confidence intervals (CI) for PTB and SGA in RA-pregnancies vs. control-pregnancies overall, and stratified by disease activity and type of anti-rheumatic treatment before and during pregnancy. Apart from the matching variables we adjusted for body mass index, smoking, educational level and country.Results:Overall, RA-pregnancies were associated with increased ORs of PTB (1.92, 95% CI 1.56-2.35) and SGA (1.93, 95% CI 1.45-2.57). High maternal disease activity during pregnancy strengthened the associations with both PTB and SGA, whereas the ORs approached 1 for low disease activity (control-pregnancies constituting the reference), Table 1. Among RA-pregnancies with available information on DAS28-CRP (n=686, 39%), OR was 2.69 (95% CI 1.37-5.26) for PTB, and 3.39 (95% CI 1.43-8.06) for SGA, comparing DAS28-CRP >=3.2 vs.Table 1.Adjusted odds ratios (ORs)1 for PTB and SGA in RA-pregnancies in relation to disease activity and functional status during pregnancy vs. control pregnanciesPreterm birthSmall for gestational age1Pregnancies, nEvents,n (%)Adjusted OR(95% CI)Pregnancies, nEvents,n (%)Adjusted OR(95% CI)Control-pregnancies217312794 (5)1 (REF)17184418 (2)1(REF)All RA pregnancies21734144 (8)1.92 (1.56-2.35)172275 (4)1.93 (1.45-2.57)DAS28-CRP3,445926 (6)1.05 (0.64-1.72)45613 (3)0.96 (0.49-1.91)3.2-5.118217 (9)2.40 (1.40-4.11)18113 (7)3.13 (1.64-5.97)>5.1435 (12)2.77 (0.86-8.87)434 (9)4.59 (1.59-13.2)No information105096 (9)2.18 (1.71-2.78)104245 (4)2.06 (1.46-2.90)HAQ-score333819 (6)1.31 (0.79-2.16)3358 (2)0.93 (0.41-2.12)0.5-0.916615 (9)2.37 (1.34-4.19)1655 (3)1.50 (0.60-3.74)≥119619 (10)1.85 (1.06-3.24)19518 (9)3.70 (2.05-6.67)No information103491 (9)2.06 (1.60-2.64)102744 (4)1.98 (1.39-2.82)CRP, mg/L345521 (5)0.91 (0.55-1.51)45214 (3)1.09 (0.57-2.07)10-2919122 (11)2.58 (1.52-4.38)19012 (6)2.68 (1.38-5.22)≥30579 (16)4.59 (2.28-9.22)575 (9)4.12 (1.68-10.1)No information103192 (9)2.10 (1.64-2.70)102344 (4)2.05 (1.44-2.90)1Missingness on small for gestational age in 12 RA-pregnancies and 128 control-pregnancies 2Only among live births, i.e. stillbirths excluded. 3Maximum value any time during pregnancy 4Defined as DAS28-CRP without patient’s global health VASConclusion:During pregnancy, disease activity rather than treatment, appears to be the most important risk factor for PTB and SGA in RA. The findings highlight the importance of monitoring RA during pregnancy, especially in women receiving extensive anti-rheumatic treatment or with residual disease activity.Acknowledgements:The Nordic clinical rheumatology registers for allowing us to use their clinical data. We also would like to acknowledge the NordForsk and FOREUM, especially the patient representatives of the NordForsk collaboration.Disclosure of Interests:Karin Hellgren Consultant of: UCB, Anne Emilie Secher: None declared, Bente Glintborg Grant/research support from: Pfizer, Biogen and BMS, Ane Lilleoere Rom: None declared, Björn Gudbjornsson Speakers bureau: Amgen and Novartis, Brigitte Michelsen Consultant of: Novartis, Grant/research support from: Novartis, Fredrik Granath: None declared, Merete Lund Hetland Speakers bureau: Biogen, Celltrion, Janssen Biologics B.V, MSD, Pfizer, Samsung Biopis, Consultant of: Biogen, Celltrion, Janssen Biologics B.V, MSD, Pfizer, Samsung Biopis, Grant/research support from: AbbVie, Biogen, BMS, Eli Lilly Danmark A/S, Lundbeck Fonden, Pfizer, Roche, Sandoz, Novartis

Objective To investigate the association between clinical and ultrasonographic (US) evidence of inflammation in psoriatic arthritis (PsA), as well as to compare clinical and US remission criteria. Methods In this cross-sectional study 141 PsA outpatients were included. Minimal disease activity (MDA), 28-joint Disease Activity Score (DAS28), Disease Activity Index for PSoriatic Arthritis (DAPSA) and modified versions of Composite Psoriatic Disease Activity Index (CPDAI) and Psoriatic ArthritiS Disease Activity Score (PASDAS) were assessed. Remission criteria were explored. US evaluation was performed on 34 joints, in addition to joints being tender/swollen by 66/68 joint count, 30 tendons, 10 entheses and additionally entheses found to be tender by clinical examination of 19 other entheses. Power Doppler (PD) and grey scale global scores on joints, entheses and tendons were assessed. US remission was defined as no PD activity in joints, entheses and tendons. Results DAPSA and DAS28, but not CPDAI and PASDAS, were associated with PD activity. MDA was fulfilled in 22.7% and the clinical remission criteria in 5.7%–9.9% of the patients. US remission was found in 49.6% of the patients. The prevalence of PD activity at joints, entheses and tendons was similar for patients fulfilling versus not fulfilling MDA/clinical remission criteria. MDA (OR 2.3, p=0.048), DAPSA ≤3.3 (OR 4.2, p=0.025) and Boolean9s (OR=7.8, p=0.033) definitions of remission were found to predict US remission. Conclusions We found major discrepancies between US and clinical findings. DAPSA and DAS28 reflected US findings better than CPDAI and PASDAS. MDA, DAPSA and Boolean9s remission criteria predicted US remission.

Background:A head-to-head trial (EXCEED) has indicated similar effectiveness of secukinumab (SEC) and the tumor necrosis factor inhibitor (TNFi) adalimumab (ADA) in psoriatic arthritis (PsA). In the clinical setting, treatment retention serves as a combined measure of overall effectiveness and tolerability.Objectives:To explore baseline patient characteristics, and compare treatment retention rates for SEC and each of etanercept (ETN), infliximab (IFX), golimumab (GOL), certolizimab (CZP) and ADA in PsA.Methods:Patients starting SEC or any TNFi in 2015-2018, in the 5 Nordic countries, were identified in clinical rheumatology registers. Data were pooled for analysis and stratified by 1st, 2ndand ≥3rdline of treatment. One year treatment retention was compared by crude Kaplan-Meier curves and a proportional hazard model for risk of discontinuation, censored at 1 year and adjusted for sex, age, country and baseline CRP, patient global and use of csDMARD, with ADA as reference.Results:In total, 6062 patients with PsA were included, contributing 8172 treatment starts (table 1). SEC was mainly used as 2ndor ≥3rdline treatment. The survival curves and 1-year treatment retention rates, stratified by line of treatment, were similar for SEC compared to the TNFis, with some differences between the different TNFi (fig 1, table 2). Adjusted hazard ratios (HR) also indicated similar risk of SEC withdrawal compared to ADA (table 2).Table 1.Patient characteristics at treatment start1stline2ndline≥3rdlineSECN=164TNFiN=3808SECN=273TNFiN=1767SECN=767TNFiN=1393Females48%47%44%42%36%39%Age, years52 (13)49 (13)50 (12)50 (13)52 (12)51 (12)Disease duration, years12 (10)10 (10)13 (10)13 (10)16 (10)16 (10)Swollen joint count 283 (4)2 (3)2 (3)2 (3)3 (4)2 (3)CRP, mg/L10 (18)10 (17)7 (11)9 (17)13 (22)11 (20)Patient global score57 (24)58 (24)60 (25)59 (26)68 (23)65 (24)Concomitant therapycsDMARD30%60%41%57%49%53% Methotrexate24%49%31%48%40%44% Sulphasalazine2%9%5%5%4%6%Numbers are mean (SD) unless noted otherwiseTable 2.One year treatment retention and hazard of discontinuation for SEC and TNFiLine of treatmentDrugN1 year treatment retention % (95% CI)Adjusted HR (95% CI) for discontinuation1stlineADA56973 (69-76)RefCZP27366 (60-72)1.2 (0.9-1.6)ETN174773 (71-75)0.9 (0.7-1.1)GOL21267 (60-73)1.2 (0.9-1.7)IFX100762 (59-65)1.4 (1.1-1.7)SEC16472 (63-78)1.0 (0.7-1.4)2ndlineADA41569 (63-73)RefCZP17651 (43-58)1.6 (1.2-2.2)ETN70163 (59-66)1.2 (0.9-1.5)GOL15169 (61-76)0.9 (0.6-1.2)IFX32465 (59-70)1.0 (0.8-1.4)SEC27369 (62-74)0.9 (0.7-1.2)≥3rdlineADA34667 (62-72)RefCZP22149 (42-56)1.5 (1.2-2.0)ETN37262 (57-67)1.1 (0.9-1.5)GOL20656 (49-63)1.3 (1.0-1.8)IFX24857 (50-63)1.3 (1.0-1.8)SEC76763 (59-67)1.0 (0.8-1.3)Conclusion:In this large study of bDMARD treatment of PsA in clinical practice, SEC was most often used as 2ndor ≥3rdline treatment, and the treatment retention of SEC was comparable with that of TNFi. Further analyses, taking into account other comorbidities, channeling and effectiveness will be presented.Acknowledgments:UL and BG are shared first, and LJ and LEK shared last authors.Partly funded by Nordforsk and FOREUM.Disclosure of Interests:Ulf Lindström: None declared, Bente Glintborg Grant/research support from: Grants from Pfizer, Biogen and Abbvie, Daniela Di Giuseppe: None declared, Tanja Schjødt Jørgensen Speakers bureau: Abbvie, Pfizer, Roche, Novartis, UCB, Biogen, and Eli Lilly, Björn Gudbjornsson Speakers bureau: Novartis and Amgen, Kathrine L. Grøn Grant/research support from: BMS, Sella Aarrestad Provan Consultant of: Novartis, Brigitte Michelsen: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen and Pfizer, Consultant of: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck and Samsung Bioepis, Johan K Wallman Consultant of: AbbVie, Celgene, Eli Lilly, Novartis and UCB Pharma, Dan Nordström Consultant of: Abbvie, Celgene, Lilly, Novartis, Pfizer, Roche and UCB., Speakers bureau: Abbvie, Celgene, Lilly, Novartis, Pfizer, Roche and UCB., Nina Trokovic: None declared, Thorvardur Love: None declared, Niels Steen Krogh: None declared, Johan Askling Grant/research support from: JA acts or has acted as PI for agreements between Karolinska Institutet and the following entities, mainly in the context of the ARTIS national safety monitoring programme of immunomodulators in rheumatology: Abbvie, BMS, Eli Lilly, Merck, MSD, Pfizer, Roche, Samsung Bioepis, Sanofi, and UCB Pharma, Lennart T.H. Jacobsson Consultant of: AbbVie, Eli Lilly, Janssen, Novartis and Pfizer, Lars Erik Kristensen Consultant of: UCB Pharma (Advisory Board), Sannofi (Advisory Board), Abbvie (Advisory Board), Biogen (Advisory Board), Speakers bureau: AbbVie, Amgen, Biogen, Bristol-Myers Squibb,Celgene, Eli Lilly, Gilead, Forward Pharma, Janssen Pharmaceuticals, MSD, Novartis, Pfizer, and UCB Pharma

Background:Pain catastrophizing (the tendency to describe a pain experience in more exaggerated terms than the average person, to ruminate on it more, or to feel more helpless about it), has been associated with reduced likelihood of achieving remission in rheumatoid arthritis patients (1). Cultural and societal differences between countries may have an impact on outcome such as patients’ perceptions of disease.Objectives:To compare patient pain catastrophizing, patient perception of disease, objective measures of disease and treatment in psoriatic arthritis (PsA) patients between a Norwegian and a Finnish outpatient clinic. Further, to explore for associations with pain catastrophizing.Methods:All PsA patients followed at the outpatient clinics are routinely monitored using a structured medical support system (GoTreatIT® Rheuma). Data collection, done in 2018-19 is listed in the table.Patients reported their pain catastrophizing answering the two questions, “When I feel pain it is terrible and I feel it is never going to get any better. When I feel pain, I can’t stand it anymore.” Each question is scored 0-6 and mean value of both is calculated. Pain catastrophizing was defined if mean score ≥4.Categorical variables were presented as numbers (%) and continuous variables as mean (SD) and associates explored using univariate and multivariate analysis.Results:A total of 302 Finnish and 363 Norwegian PsA patients were examined. Pain catastrophizing was reported significantly less commonly among the Finnish as compared to the Norwegian PsA clinic patients, both expressed as mean (SD) values (1.48 (1.42) vs 2.05 (1.42), pFinland (n=302)Norway (n=363)PAge, years54.0 (13.3)54.7 (12.5)0.49Females153 (50.7%)181 (49.9%)0.84BMI. Kg/m228.8 (5.6)28.1(5.1)0.06Current smoking44 (14.6%)51 (14.1%)0.86Education, years13.6 (3.5)12.7 (3.8)0.001Disease duration, years4.7 (4.3)9.9 (8.9)CRP, mg/L4.3 (6.8)4.0 (8.8)0.69MDglobal assessment, VAS 0-100 mm6.84 (1.29)5.71 (8.50)0.1928 swollen joint count0.48 (1.35)0.31 (1.16)0.1428 tender joint count1.01 (2.83)1.37 (2.80)0.14DAPSA9.66 (8.95)11.33 (9.60)0.06Pain, VAS 0-100 mm30.73 (25.92)35.55 (25.76)0.023Fatigue, VAS 0-100 mm29.96 (29.24)42.56 (31.94)MHAQ, 0-30.39 (0.44)0.43 (0.41)0.24Body surface area for psoriasis2.45 (8.15)2.66 (6.15)0.17Current b-tsDMARDs121 (40.1%)139 (38.3%)0.64In univariate analyses female gender, higher BMI, less years of education, Dr. global, tender joint count, DAPSA, pain, fatigue, MHAQ and psoriasis body surface area were found to be associated with more pain catastrophizing.In multivariate analysis (mandatory adjusting for age, gender, BMI, years of education and disease duration) fewer years of education, higher scores for pain, fatigue and MHAQ and being patient at the Norwegian center were independently associated with more pain catastrophizing.Conclusion:Our data indicate that cultural differences across countries may have a significant impact on outcomes that reflecting patients’ perceptions of disease. This may have an implication when merging heterogeneous databases across countries.References:[1]Hammer HB et al. Arthritis Care Res 2018;70:703-12.Disclosure of Interests: :Glenn Haugeberg: None declared, Inger Johanne Widding Hansen: None declared, Hilde Berner Hammer: None declared, Arthur Kavanaugh Grant/research support from: Abbott, Amgen, AstraZeneca, BMS, Celgene Corporation, Centocor-Janssen, Pfizer, Roche, UCB – grant/research support, Brigitte Michelsen: None declared, Kirsi Paalanen: None declared, Tuulikki Sokka-Isler: None declared

Background:In psoriatic arthritis (PsA) both skin and musculoskeletal involvement can contribute to reduce health related quality of life (HRQoL) (1). Although itch is considered an important symptom in psoriasis, less is known about its extent and potential impact on HRQoL in PsA.Objectives:The aim of the study was to assess the prevalence of itchy, sore, painful or stinging skin in PsA patients and also to explore the impact of these symptoms on overall HRQoL and skin related HRQoL.Methods:PsA patients were consecutively recruited from a rheumatology outpatient clinic. Data collection included variables listed in the table. Patients also answered the question: “Over the last week, how itchy, sore, painful or stinging has your skin been? With answer alternatives: Not at all (score 0), a little (score 1), a lot (score 2) and very much (score 3)”. For analysis the variable was dichotomized; ‘Not at all’ and ‘a little’ were scored as ‘not itching’, and ‘a lot’ and ‘very much’ were scored as ‘itching’. HRQoL was assessed using the 15D questionnaire and skin HRQoL using the Dermatology Life Quality Index (DLQI). Categorical variables are presented as numbers and (%) and continuous variables as mean with (SD). An association with 15D and DLQI was explored using univariate and multivariate linear regression analysis.Results:Among 125 PsA patients (63 men and 63 women), means age was 52.2 years, BMI 28.3 kg/m2, disease duration 8.9 years; 15.2% were smokers. The number and percentage (%) of PsA patients reporting their skin to be itchy, sore, painful or stinging was as follows: Not at all 25 (20.0%), a little 71 (56.8%), a lot 23 (18.4%) and very much 6 patients (4.8%). The table shows data for all PsA patients and for patients defined to have no itching or having itching skin.Total (n=125)No itching (n=96)Itching (n=29)PAge (SD), years52.2 (10.1)52.3 (10.1)51.6 (10.2)0.73Women, n (%)62 (49.6%)49 (51.0%)13 (44.8%)0.56BMI (SD), kg/m228.3 (4.3)28.0 (4.0)29.4 (4.9)0.12Smoking, n (%)19 (15.2%)14 (14.6%)5 (17.2%)0.73Dis.dur. (SD), years8.9 (6.7)9.1 (6.7)8.0 (6.9)0.42CRP (SD), mg /L4.8 (8.5)4.4 (8.5)6.1 (8.5)0.37TJC68 (SD)9.70 (11.07)9.21 (10.32)11.39 (13.41)0.36SJC66 (SD)0.57 (0.99)0.56 (1.00)0.61 (0.96)0.84MASES (SD)2.9 (3.1)2.5 (2.9)4.0 (3.7)0.02IGA (SD), (VAS 0-100)14.0 (11.7)12.9 (10.2)17.8 (15.4)0.12PGA (SD), (VAS 0-100)35.3 (24.2)30.5 (22.6)50.9 (22.8)Pain (SD), (VAS 0-100)33.4 (23.4)28.6 (21.3)49.1 (23.6)Fatigue (SD), (VAS 0-100)45.1 (32.0)40.3 (31.7)61.0 (28.1)MHAQ (SD), (0-3)0.40 (0.35)0.35 (0.32)0.58 (0.39)PASI (SD), (0-72)2.4 (3.5)1.9 (3.2)4.1 (4.1)0.01DLQI (SD), (0-30)3.5 (3.6)2.2 (2.3)7.9 (3.9)15D (SD), (0-1)0.84 (0.09)0.86 (0.09)0.80 (0.08)bDMARDs, n (%)43 (34.7%)33 (34.7%)10 (34.5%)0.98csDMARDs, n (%)73 (58.4%)61 (63.5%)12 (41.4)0.03Dis.dur.: disease durationIn univariate analysis itching was found to be associated with impaired HRQoL assessed by 15D but not in adjusted analysis. In a regression model adjusting for age, gender, BMI and including variables with pConclusion:Skin itching was frequently reported in our PsA patients (20-25%) and was also found to be associated with impaired HRQoL, in particular for skin HRQoL (DLQI). The association was independent of the extent of skin involvement (PASI). More needs to be understood about subjective skin symptoms such as itch in order to improve HRQoL in PsA.References:[1]Kavanaugh A, et al. Ann Rheum Dis 2019;9:1215-9Disclosure of Interests:Glenn Haugeberg: None declared, Arthur Kavanaugh Grant/research support from: Abbott, Amgen, AstraZeneca, BMS, Celgene Corporation, Centocor-Janssen, Pfizer, Roche, UCB – grant/research support, Brigitte Michelsen Grant/research support from: Research support from Novartis, Consultant of: Consulting fees Novartis

Background:Previous studies have suggested similar effectiveness, but longer treatment retention, for tumor necrosis factor inhibitors (TNFi), when used in combination with a conventional synthetic disease modifying anti-rheumatic drug (csDMARD) in psoriatic arthritis (PsA).Objectives:To describe patients with PsA initiating a first TNFi as monotherapy compared to combination therapy, and to explore 1-year treatment retention of TNFi in the two groups.Methods:Patients with PsA starting a first TNFi (2006-2017) were identified in biologics registers of 13 European countries, and data were pooled for analysis. Co-medication with csDMARD was determined at TNFi start.Because of large inter-country variation in TNFi retention, countries were split into two strata, depending on each country’s 1-year retention rate for TNFi being above (stratum A) or below (stratum B) the average 1-year retention rate.TNFi treatment retention was compared through Kaplan-Meier curves; the proportion remaining on the TNFi at one year; and hazard ratios (HR) during the first year: (i) crude; adjusted for (ii) country-strata, and (iii) country-strata, sex, age, calendar year, DAS28 and disease duration. In model (iii) only registers contributing >1000 patients or Results:A total of 14778 patients with PsA starting a first TNFi were included. Baseline disease activity was similar within stratum B, but higher for the combination treatment group in stratum A (table 1).Table 1.Baseline characteristicsCountry strataStratum AStratum BTNFimonotherapyN=2120TNFi/csDMARDcombinationN=2128TNFimonotherapyN=3369TNFi/csDMARDcombinationN=7161Females52%51%53%51%Age, years49.7 (12.2)48.7 (11.8)48.8 (13.0)48.9 (12.2)Disease duration, yrs6.4 (7.0)6.8 (6.8)5.9 (7.5)5.9 (7.1)Tender joints 285.5 (6.3)8.0 (6.3)5.6 (6.0)5.6 (5.7)Swollen joints 282.8 (4.3)5.6 (5.0)3.0 (3.8)3.3 (3.8)VAS pain54 (29)62 (24)59 (23)56 (24)DAPSA-2824.6 (18.6)36.2 (17.6)27.3 (15.6)27.2 (15.2)DAS28 (CRP)3.5 (1.4)4.7 (1.3)4.0 (1.2)4.0 (1.1)Concomitant csDMARDMethotrexate-76%-79%Sulfasalazine-15%-15%Other csDMARD-49%-25%Numbers are means (sd) unless otherwise stated.The Kaplan-Meier curves for the treatment groups were similar within each stratum (fig 1), as were the proportions remaining on TNFi after one year, stratum A: monotherapy 86% (95%CI: 85-88) vs. combination 86% (84-87), stratum B: 71% (69-72) vs. 73% (72-74). The HRs for TNFi discontinuation (ref=TNFi monotherapy) were: (i) 1.06 (0.98-1.13), (ii) 0.94 (0.87-1.01), (iii) 0.89 (0.83-0.96), including 13078 patients (9 countries) for model (iii).Conclusion:In this exploratory study no benefit in TNFi retention was observed for csDMARD combination therapy in crude analyses, while in adjusted analyses an 11% lower risk of TNFi discontinuation was found. These preliminary results offer limited support for use of combination therapy in PsA. Further analyses will explore to what extent the results are affected by inter-country heterogeneity and differences between TNFi.Acknowledgments:UL and DDG contributed equally.Novartis Pharma AG and IQVIA support the EuroSpA collaboration.Disclosure of Interests:Ulf Lindström: None declared, Daniela Di Giuseppe: None declared, Bénédicte Delcoigne: None declared, Bente Glintborg Grant/research support from: Grants from Pfizer, Biogen and Abbvie, Burkhard Moeller: None declared, Manuel Pombo-Suarez Consultant of: Janssen, Lilly, MSD and Sanofi., Speakers bureau: Janssen, Lilly, MSD and Sanofi., Carlos Sánchez-Piedra: None declared, Kari Eklund Consultant of: Celgene, Lilly, Speakers bureau: Pfizer, Roche, Heikki Relas Grant/research support from: Abbvie., Consultant of: Abbvie, Celgene, and Pfizer., Speakers bureau: Abbvie, Celgene, and Pfizer., Björn Gudbjornsson Speakers bureau: Novartis and Amgen, Thorvardur Love: None declared, Gareth T. Jones Grant/research support from: Pfizer, AbbVie, UCB, Celgene and GSK., Adrian Ciurea Consultant of: Consulting and/or speaking fees from AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly, Merck Sharp & Dohme, Novartis and Pfizer., Catalin Codreanu Consultant of: Speaker and consulting fees from AbbVie, Accord Healthcare, Alfasigma, Egis, Eli Lilly, Ewopharma, Genesis, Mylan, Novartis, Pfizer, Roche, Sandoz, UCB, Speakers bureau: Speaker and consulting fees from AbbVie, Accord Healthcare, Alfasigma, Egis, Eli Lilly, Ewopharma, Genesis, Mylan, Novartis, Pfizer, Roche, Sandoz, UCB, Ruxandra Ionescu Consultant of: Consulting fees from Abbvie, Eli-Lilly, Novartis, Pfizer, Roche, Sandoz, Speakers bureau: Consulting and speaker fees from Abbvie, Eli-Lilly, Novartis, Pfizer, Roche, Sandoz, Lucie Nekvindova: None declared, Jakub Zavada Speakers bureau: Abbvie, UCB, Sanofi, Elli-Lilly, Novartis, Zentiva, Accord, Nuh Atas: None declared, Servet Yolbaş: None declared, Karen Fagerli: None declared, Brigitte Michelsen Grant/research support from: Research support from Novartis, Consultant of: Consulting fees Novartis, Ziga Rotar Consultant of: Speaker and consulting fees from Abbvie, Amgen, Biogen, Eli Lilly, Medis, MSD, Novartis, Pfizer, Roche, Sanofi., Speakers bureau: Speaker and consulting fees from Abbvie, Amgen, Biogen, Eli Lilly, Medis, MSD, Novartis, Pfizer, Roche, Sanofi., Matija Tomsic: None declared, Florenzo Iannone Consultant of: Speaker and consulting fees from AbbVie, Eli Lilly, Novartis, Pfizer, Roche, Sanofi, UCB, MSD, Speakers bureau: Speaker and consulting fees from AbbVie, Eli Lilly, Novartis, Pfizer, Roche, Sanofi, UCB, MSD, Maria Jose Santos Speakers bureau: Novartis and Pfizer, Pedro Ávila-Ribeiro Grant/research support from: Novartis, Lykke Midtbøll Ørnbjerg Grant/research support from: Novartis, Mikkel Ǿstergaard Grant/research support from: AbbVie, Bristol-Myers Squibb, Celgene, Merck, and Novartis, Consultant of: AbbVie, Bristol-Myers Squibb, Boehringer Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo Nordisk, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi, and UCB, Speakers bureau: AbbVie, Bristol-Myers Squibb, Boehringer Ingelheim, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo Nordisk, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi, and UCB, Lennart T.H. Jacobsson Consultant of: AbbVie, Eli Lilly, Janssen, Novartis and Pfizer, Johan Askling Grant/research support from: JA acts or has acted as PI for agreements between Karolinska Institutet and the following entities, mainly in the context of the ARTIS national safety monitoring programme of immunomodulators in rheumatology: Abbvie, BMS, Eli Lilly, Merck, MSD, Pfizer, Roche, Samsung Bioepis, Sanofi, and UCB Pharma, Michael Nissen Grant/research support from: Abbvie, Consultant of: Novartis, Lilly, Abbvie, Celgene and Pfizer, Speakers bureau: Novartis, Lilly, Abbvie, Celgene and Pfizer