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Background:Incidence of rheumatoid arthritis (RA) in Norway has not been evaluated in a nationwide setting.Objectives:To estimate the incidence of RA and real-life penetration of disease-modifying antirheumatic drug (DMARD) use in Norway.Methods:The Norwegian Cardio-Rheuma register comprises pseudonymized data from nationwide registries including the total Norwegian population ≥18 years during 2008-2017. Demographic and socioeconomic data were retrieved from the National Population Register and Statistics Norway. Data on public or private somatic specialized care episodes were collected from the Norwegian Patient register (NPR) (ICD-10 codes for diagnoses and medical procedure codes for biologic DMARD infusions). Dispensed DMARD prescriptions were captured from the Norwegian Prescription Database. RA cases were defined as persons with NPR records of all of the following: 1) 1st episode with ICD-10 code M05/M06 as main or contributory diagnosis (index date), 2) 2nd episode with code M05/M06 within 2-year period following index date, 3) M05/M06 recorded in an internal medicine or rheumatology department during the 2-year period. Years 2008-2010 served as a look-back period to identify prevalent RA cases. To estimate person-years (pyrs) at risk, we calculated number of persons aged ≥ 18 living in Norway on the 1st of January of each year 2011-2015 and multiplied it by one year (prevalent RA cases excluded). Standardized estimates were calculated with 5-year age groups using Norwegian adult population 1st of January 2015 as the standard.Results:Between 2011 and 2015, 9,493 persons fulfilled the RA definition (62.4% seropositive based on ICD-10 codes). Incidence rate was 49/100,000 pyrs (32 in men and 65 in women). A sensitivity analysis excluding cases who had dispensed DMARDs >12 months before index date yielded 8,125 RA cases (incidence 42/100,000 pyrs). Whereas absolute number of incident cases was highest among those aged 60-69 in both sexes, incidence was highest among those aged 70-79 (Figure 1). Both crude and age- and sex-standardized incidences were lower among persons with higher education level (crude/standardized incidence per 100,000 pyrs for those below upper secondary education 60/57; upper secondary or post-secondary non-tertiary education 53/52; higher education 36/39). Of incident cases, 94% received any DMARD treatment or glucocorticoids, 78% methotrexate, and 17% biologic DMARDs within 2 years after index date (Table 1).Conclusion:Contemporary register-based estimate of RA incidence in Norway is comparable to other Nordic countries.1,2 In line with treatment recommendations, methotrexate is the most commonly used DMARD in the initial treatment strategy in Norway. One in six patients used a biologic DMARD within 2 years from 1st recorded RA diagnosis.References:[1]Eriksson JK, Neovius M, Ernestam S et al. Incidence of rheumatoid arthritis in Sweden: a nationwide population-based assessment of incidence, its determinants, and treatment penetration. Arthritis Care Res 2013;65:870-878.[2]Puolakka K, Kautiainen H, Pohjolainen T et al. Rheumatoid arthritis remains a threat to work productivity: a nationwide register-based incidence study from Finland. Scand J Rheumatol 2010;39:436-438.Figure 1.Table 1.Characteristics and treatment penetration of incident RA patients 2011-2015AllExcluding cases with DMARDs >12 months before index dateN94938125Women, n (%)6339 (66.8)5379 (66.2)Age at index date, median (IQR)60.5 (48.5 - 70.5)60.8 (48.8 - 70.9)RF positive, n (%)5927 (62.4)5193 (63.9)Use of DMARDs after index date, n (%)12 months24 months12 months24 months Any conventional DMARD7797 (82.1)8023 (84.5)6682 (82.2)6855 (84.4) Methotrexate7133 (75.1)7402 (78.0)6228 (76.7)6436 (79.2) Sulfasalazine902 (9.5)1218 (12.8)745 (9.2)1034 (12.7) Any biologic DMARD1102 (11.6)1642 (17.3)754 (9.3)1219 (15.0) TNF-inhibitors1006 (10.6)1513 (15.9)690 (8.5)1130 (13.9) Oral glucocorticoids6524 (68.7)6974 (73.5)5858 (72.1)6199 (76.3) Any DMARD or glucocorticoids8789 (92.6)8957 (94.4)7498 (92.3)7639 (94.0)Acknowledgements:This work has been supported by a research grant from FOREUM Foundation for Research in Rheumatology.Disclosure of Interests:Anne Kerola Speakers bureau: Boehringer-Ingelheim, Consultant of: Pfizer, Gilead, Boehringer-Ingelheim, Joseph Sexton: None declared, Grunde Wibetoe: None declared, Silvia Rollefstad: None declared, Cynthia S. Crowson: None declared, Espen Haavardsholm: None declared, Tore K. Kvien Speakers bureau: Amgen, Celltrion, Egis, Evapharma, Ewopharma, Hikma, Oktal, Sandoz, Sanofimgen, Celltrion, Egis, Evapharma, Ewopharma, Hikma, Oktal, Sandoz, Sanofi, Consultant of: AbbVie, Amgen, Biogen, Celltrion, Eli Lilly, Gilead, Mylan, Novartis, Pfizer, Sandoz, Sanofi, Grant/research support from: research funding to Diakonhjemmet Hospital from AbbVie, Amgen, BMS, MSD, Pfizer and UCB, Anne Grete Semb Speakers bureau: AbbVie, Bayer, Lilly, Novartis, and Sanofi, Consultant of: Sanofi, Grant/research support from: collaborative research support from Lilly, outside the submitted work.

Background:Industry, regulators, and the rheumatology community have recognized the need for observational studies to monitor the safety of new antirheumatic agents. Registries provide a unique opportunity to understand the safety of newer therapies, but pharmacovigilance studies require large number of patients to evaluate rare drug-related adverse-events (AEs). Because JAK-inhibitors (JAKi) have only recently been approved for the treatment of rheumatoid arthritis, it makes sense to combine data from several registries in order to obtain a sufficiently large sample size to promote earlier detection of adverse events.Objectives:The purpose of this analysis was to evaluate how AEs are assessed in the various registries in preparation for a collaborative pharmacovigilance analysis, and present preliminary results.Methods:The “JAK-pot” collaboration includes 19 RA registries. The principal investigators of the participating registries were sent a structured questionnaire on AE assessment and 18 (94%) provided complete responses on the AE assessment procedures of their registries. We present simple descriptive statistics of the AE assessment procedures employed by the participating registries.Results:The 19 registries represent 7186 patients initiating a JAKi (Table 1), who are on average 57 years old, with a mean disease duration 11 years, seropositive (83%), female (82%) and with moderate disease activity at treatment initiation.Table 1.Country, registryN° of patients on JAKi includedAustria, BIOREG87Belgium, TARDIS2113Canada, RHUMADATA363Czech Republic, ATTRA197Denmark, DANBIO506Finland, ROB-FIN229Germany, RABBIT620Italy, GISEA244Israel, I-RECORD96Netherlands, METEOR4Norway, NOR-DMARD97Portugal, REUMA.PT44Romania, RRBR252Russia, ARBITER428Slovenia, biorx.si141Spain, BIOBADASER139Switzerland, SCQM738Turkey, TURKBIO404UK, BSRBR484After ineffectiveness, AEs was the second most common reason for JAKi discontinuation (25.5%), with large differences between registries (Figure 1).Of the participating registries, 2 registries do not collect AEs, while 16 (89%) assess incident AEs, by means of a pre-specified extraction form (3 registries), by free text (5 registries), by a combination of both (6 registries) and/or the use of linkage to external electronic records (3registries). AEs are coded using a predefined coding system by 11 registries (MeDRA (8), other (3)), but nearly all are recording the severity of the AE (15, 94%), AE related-death (15, 94%), or AE-related hospitalisation (15, 94%). AEs of special interest, such as serious infections (15, 94%), thromboembolic events (15, 94%), or shingles (9, 56%), are recorded by most registries. Incident AEs are linked by the treating physician to specific therapies in 11 registries (69%), while the other 5 registries extrapolate potential causal associations based on therapy start and stop dates. A pre-specified adjudication process for AEs is made only by 5 registries (31%).Conclusion:Substantial heterogeneity exists among registries regarding AE assessment within the JAK-pot collaboration. These differences must be taken into account when analysing the safety of JAKi across different countries in collaborative studies. For comparative analyses, stratified analyses by country are required to account for differential AE assessment and varying degrees of potential under-reporting.Disclosure of Interests:Kim Lauper: None declared, Denis Mongin: None declared, Sytske Anne Bergstra: None declared, Denis Choquette: None declared, Catalin Codreanu: None declared, Diederik De Cock: None declared, Lene Dreyer: None declared, Ori Elkayam: None declared, Kimme Hyrich: None declared, Florenzo Iannone: None declared, Nevsun Inanc: None declared, Eirik kristianslund: None declared, Tore K. Kvien: None declared, Burkhard Leeb: None declared, Galina Lukina: None declared, Dan Nordström: None declared, Karel Pavelka: None declared, Manuel Pombo-Suarez: None declared, Ziga Rotar: None declared, Maria Jose Santos: None declared, Anja Strangfeld: None declared, Delphine Courvoisier: None declared, Axel Finckh Speakers bureau: Eli-Lilly, Pfizer, Consultant of: Eli-Lilly, Pfizer, Grant/research support from: BMS, Pfizer.

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: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:Remission is the preferred treatment target in rheumatoid arthritis (RA), and many patients require biologic DMARDs to reach this state. It is debated whether tapering of tumor necrosis factor inhibitor (TNFi) treatment to discontinuation should be considered in RA patients who sustain remission on treatment (1).Objectives:The primary study objective was to assess the effect of tapering and withdrawal of TNFi on the risk of flares in RA patients in clinical remission.Methods:In the non-inferiority ARCTIC REWIND trial, RA patients in remission for at least 12 months on stable TNFi therapy were randomly assigned to continued stable TNFi or tapering (half-dose TNFi for 4 months, thereafter withdrawal of TNFi), with visits every four months. csDMARD co-medication was kept stable in both arms. Patients had to be in DAS remission at inclusion with 0/44 swollen joints. The primary endpoint was the proportion of patients with disease flare during the 12-month study period (defined as DAS>1.6, change in DAS>0.6 and 2 or more swollen joints, or the physician and patient agreed that a clinically significant flare had occurred). Full-dose TNFi was reinstated in case of flares in the tapering arm. The non-inferiority margin was 20%, with a predefined superiority test if non-inferiority was not shown. The inferiority null-hypothesis was tested in the per-protocol population by mixed effect logistic regression. Radiographs were scored by van der Heijde modified Sharp score (0 and 12 months, average of two readers, progression: ≥1 unit change). ClinicaltrialsNCT01881308.Results:We randomised 99 patients, 92 received the allocated treatment strategy, 84 were included in the per-protocol population. Baseline characteristics, clinical and ultrasound disease activity were balanced (Table). csDMARD co-medication was used by 93% in the stable and 88% in the tapering arm. In the primary analysis, 5% of patients in the stable TNFi arm experienced a flare during 12 months, compared to 63% in the tapering TNFi arm. The risk difference (95% CI) was 58% (42% to 74%, Fig 1), with stable treatment being deemed superior to tapering. 90% in the stable and 81% in the tapering arm did not show progression of radiographic joint damage, difference (95% CI) -9% (-24%, 6%). At 12 months, DAS scores, DAS remission and function were similar between groups (Fig 2). The numbers of adverse events (AE)/serious AE in the stable and tapering arm were 57/2 and 50/3, respectively, with 26 and 15 infections.Conclusion:In a randomised clinical trial assessing patients in prolonged and deep RA remission, we observed a large increase in the flare rate in patients who tapered and discontinued TNFi. Patients responded well to reinstated treatment and remission rates in the two study arms were comparable at 12 months.References:[1]Smolen et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2019 update. ARD 2020Table 1.Baseline values – n (%), mean (SD), or median (IQR)Stable, n=45Tapering, n=47Age, yrs57 (11)58 (13)Female30 (67%)25 (53%)ACPA+35 (78%)36 (77%)Symptom duration, yrs10 (7)12 (7)DAS0.9 (0.4)0.8 (0.3)CRP mg/L1 (1 – 2)1 (1 – 3)No ulttrasound power Doppler signal in any of 32 joints42 (96%)44 (94%)Disclosure of Interests:Siri Lillegraven: None declared, Nina Paulshus Sundlisæter: None declared, Anna-Birgitte Aga: None declared, Joe Sexton: None declared, Inge Olsen: None declared, Åse Lexberg: None declared, Tor Magne Madland: None declared, Hallvard Fremstad: None declared, Christian A. Høili Consultant of: Novartis, Gunnstein Bakland Consultant of: Novartis, UCB, Cristina Spada: None declared, Hilde Haukeland Consultant of: Novartis, Inger M. Hansen: None declared, Ellen Moholt: None declared, Till Uhlig Consultant of: Lilly, Pfizer, Speakers bureau: Grünenthal, Novartis, Daniel Solomon Grant/research support from: Funding from Abbvie and Amgen unrelated to this work, Désirée van der Heijde Consultant of: AbbVie, Amgen, Astellas, AstraZeneca, BMS, Boehringer Ingelheim, Celgene, Cyxone, Daiichi, Eisai, Eli-Lilly, Galapagos, Gilead Sciences, Inc., Glaxo-Smith-Kline, Janssen, Merck, Novartis, Pfizer, Regeneron, Roche, Sanofi, Takeda, UCB Pharma; Director of Imaging Rheumatology BV, 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)., Espen A Haavardsholm Grant/research support from: AbbVie, UCB Pharma, Pfizer Inc, MSD Norway, Roche Norway, Consultant of: Pfizer, AbbVie, Janssen-Cilag, Gilead, UCB Pharma, Celgene, Lilly, Paid instructor for: UCB Pharma, Speakers bureau: Pfizer, AbbVie, UCB Pharma, Celgene, Lilly, Roche, MSD

Background:In many countries, JAK-inhibitors (JAKi) have only recently been approved as treatment for patients with rheumatoid arthritis (RA).Objectives:To evaluate the effectiveness of JAKi compared to bDMARDs in RA patients in the real-world population in an international collaboration of registers (the “JAK-pot” collaboration).Methods:Patients initiating either JAKi, TNFi, IL-6i or abatacept (ABA) during a time period when JAKi were available in each country (19 registers, Table) were included. We compared the effectiveness of JAKi and bDMARDs in terms of retention using crude and adjusted survival analysis. Missing covariates were imputed using multiple imputation.Results:Among 25521 included patients, 6063 initiated a JAKi, 13879 a TNFi, 2348 ABA, and 3231 an IL-6i. Patients were on average 55 years old, with a mean disease duration 10 years, mostly seropositive (67%), female (77%) and with moderate disease activity at treatment initiation. The main reason of stopping treatment was ineffectiveness (49%), followed by adverse events (21%). Patients on JAKi were treated more often as monotherapy, had higher CRP and disease activity at baseline and had experienced more previous ts/bDMARDs. Crude median retention was 1.4 (95% CI 1.2-1.5) years for JAKi, 1.6 (1.6-1.7) for TNFi, 1.5 (1.3-1.7) for IL6i and 1.1 (1.0-1.3) for ABA. After adjustment, the hazard ratio (HR) for discontinuation tended to be lower for JAKi (HR 0.86 (0.65-1.13)) compared to TNFi, but comparable for ABA (1.02 (0.94-1.10)) and IL6i (0.99 (0.88-1.10)) (Figure 1). HRs differed notably between countries (Figure 2).Table 1.RegistersCountry, registerNJAKi, n (%)Austria, BIOREG*Belgium, TARDIS62882113 (33.6)Canada, RHUMADATA528114 (21.6)Czech Republic, ATTRA374253 (67.6)Denmark, DANBIO4721506 (10.7)Finland, ROB-FIN807234 (29.0)Germany, RABBIT*Italy, GISEA757250 (33.0)Israel, I-RECORD40094 (23.5)Netherlands, METEOR16424 (0.2)Norway, NOR-DMARD50799 (19.5)Portugal, REUMA.PT79744 (5.5)Romania, RRBR593328 (55.3)Russia, ARBITER526483 (91.8)Slovenia, BIORX.SI583146 (25.0)Spain, BIOBADASER781139 (17.8)Switzerland, SCQM2956796 (26.9)Turkey, TURKBIO2150397 (18.5)UK, BSRBR111163 (5.7)*Registers planning to participate in future studies but not included yetConclusion:The adjusted overall drug retention of JAKi tended to be higher than for TNFi, with large variation between countries. Other measures of effectiveness, such as the evaluation of CDAI remission and low disease activity are planned to shape a more comprehensive picture of JAKi effectiveness in the real world.Disclosure of Interests:Kim Lauper: None declared, Denis Mongin: None declared, Sytske Anne Bergstra: None declared, Denis Choquette Grant/research support from: Rhumadata is supported by grants from Pfizer, Amgen, Abbvie, Gylead, BMS, Novartis, Sandoz, eli Lilly,, Consultant of: Pfizer, Amgen, Abbvie, Gylead, BMS, Novartis, Sandoz, eli Lilly,, Speakers bureau: Pfizer, Amgen, Abbvie, Gylead, BMS, Novartis, Sandoz, eli Lilly,, 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, Diederik De Cock: None declared, Lene Dreyer: None declared, Ori Elkayam Speakers bureau: AbbVie, BMS, Pfizer, Roche, Sanofi-Aventis, Novartis, Jansen, Kimme Hyrich Grant/research support from: Pfizer, UCB, BMS, Speakers bureau: Abbvie, 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, Nevsun Inanc: None declared, Eirik kristianslund: 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)., Burkhard Leeb Grant/research support from: chairman of BioReg, Consultant of: AbbVie, Pfizer, Roche, Lilly, Grünenthal, Gebro,, Paid instructor for: Lilly, Biogen, Speakers bureau: Biogen, Lilly, Pfizer, Grünenthal, Astropharma,, Galina Lukina Speakers bureau: Novartis, Pfizer, UCB, Abbvie, Biocad, MSD, Roche, Dan Nordström Consultant of: Abbvie, Celgene, Lilly, Novartis, Pfizer, Roche and UCB., Speakers bureau: Abbvie, Celgene, Lilly, Novartis, Pfizer, Roche and UCB., Karel Pavelka Consultant of: Abbvie, MSD, BMS, Egis, Roche, UCB, Medac, Pfizer, Biogen, Speakers bureau: Abbvie, MSD, BMS, Egis, Roche, UCB, Medac, Pfizer, Biogen, Manuel Pombo-Suarez Consultant of: Janssen, Lilly, MSD and Sanofi., Speakers bureau: Janssen, Lilly, MSD and Sanofi., 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, Anja Strangfeld Speakers bureau: AbbVie, BMS, Pfizer, Roche, Sanofi-Aventis, Delphine Courvoisier: None declared, Axel Finckh Grant/research support from: Pfizer: Unrestricted research grant, Eli-Lilly: Unrestricted research grant, Consultant of: Sanofi, AB2BIO, Abbvie, Pfizer, MSD, Speakers bureau: Sanofi, Pfizer, Roche, Thermo Fisher Scientific

Background:Pain is a hallmark symptom of hand osteoarthritis (OA). A subset of people with hand OA display centrally driven pain characteristics. Pain is driven by person-related factors, but how comorbidities are related to the hand OA pain experience is undetermined. Changes in pain pathophysiology and pain levels by for instants low-grade inflammation, might explain the link.Objectives:The purpose of this study was to determine whether the burden of comorbidities or the individual comorbidities were associated with pain and pain sensitization in persons with hand OA.Methods:These cross-sectional analyses included 282 participants with hand OA from the Nor-Hand study. Comorbidities were assessed by an index (subscales: Disease, Limitation and Treatment, (0-45 scale)) by Sangha et al. The participants completed pain questionnaires; Numeric Rating Scale (NRS) hand pain (0-10) and all joints (0-10), Australian/Canadian (AUSCAN) hand pain subscale (0-20 scale), Western Ontario & McMaster Universities Arthritis Index (WOMAC) pain subscale (0-20) and homunculus (painful joint sites last six weeks, (0-18)). Pressure pain threshold (PPT, handheld algometer, kg/cm2) at tibialis anterior and trapezius and Temporal summation (TS) at the distal radioulnar joint tapped with weighted probe (x10), assessed central pain sensitization. TS-delta was calculated of the first and peak measure of the fifth or tenth tap. Linear regression was used to examine all relations, while adjusted for age, sex, body mass index and education.Results:The participants (89% women, median (IQR) age: 61 (57-66)) showed broad range in pain severity. Most frequent comorbidities were back pain (n=170, 60%), hypertension (n= 85, 30%), stomach ulcer/abdominal disease (n=62, 22%) and depression (n=46, 16%). 281 (99.3%) participants reported >1 comorbidity other than OA. Mean (SD) comorbidity index value was 7.73 (4.25). Higher values were statistically significantly associated with greater pain severity by each pain questionnaire, lower PPT trapezium (borderline significant for PPT tibialis anterior), and greater TS (Table). Similar results were found for subscales. Depression, back pain and hypertension associated with most measures of pain. (Table). Included in the same model, results remained similar (not shown). No statistically significant association between individual comorbidities and pain sensitization (Table).Table.B (95% confidence interval per one SD of the comorbidity index/subscale) are reportedNRS hand painNRS painall jointsAUSCANhand painWOMAC knee/hip painPainful jointsPPT TrapeziumPPT Tibialis AnteriorTSComorbidity Index0.76 (0.12, 0.24)0.76 (0.12, 0.24)1.61 (0.15, 0.37)2.76 (0.26, 0.50)2.76 (0.42, 0.88)-0.38 (-0.15, -0.04)-0.25 (-0.13, 0.01)0.25 (0.02, 0.11)Disease0.69 (0.24, 0.52)0.56 (0.16, 0.46)0.89 (0.22, 0.75)1.34 (0.45, 1.02)2.19 (0.66, 1.76)-0.34 (-0.32, -0.06)-0.24 (-0.29, 0.04)0.23 (0.02, 0.23)Treatment0.56 (0.18, 0.48)0.58 (0.18 0.49)0.80 (0.19, 0.76)1.29 (0.46, 1.06)1.79 (0.47, 1.65)-0.31 (-0.32, -0.44)-0.19 (-0.28, 0.07)0.22 (0.01, 0.24)Limitations0.69 (0.32, 0.70)0.86 (0.44, 0.81)1.16 (0.51, 1.20)1.58 (0.78, 1,53)3.30 (1.72, 3.13)-0.41 (-0.47, -0.13)-0.26 (-0.41, 0.02)0.26 (0.04, 0.33)Depression0.96 (0.29, 1.63)0.66 (-0.04, 1.36)1.74 (0.46, 3.02)0.99 (-0.38, 2.35)3.43 (0.78, 6.09)-0.36 (-1.00, 0.29)-0.44 (-1.25, 0.37)0.02 (-0.50, 0.53)Back pain0.89 (0.38, 1.40)1.10 (0.57, 1.63)1.04 (0.08, 2.00)2.90 (1.87,3.93)2.64 (0.65, 4.64)0.08 (-0.41, 0.56)0.23 (-0.38, 0.84)0.22 (-0.17, 0.61)Hypertension0.64 (0.05, 1.22)0.45 (-0.17, 1.06)1.00 (-0.12, 2.11)1.32 (0.13, 2.52)2.74 (0.44, 5.05)-0.32 (-0.88, 0.23)-0.28 (-0.97, 0.40)0.17 (-0.28, 0.62)Conclusion:Higher burden of comorbidities was associated with greater pain intensity and central pain sensitization. Hypertension, back pain and depression were associated with most pain measures. The lack of relation between individual comorbidities and pain sensitization suggest the burden of comorbidity is more important.Disclosure of Interests:Elisabeth Mulrooney: None declared, Tuhina Neogi: None declared, Hanne Solveig Dagfinrud: None declared, Hilde Berner Hammer Speakers bureau: Speaker fee from Novartis, Lilly and AbbVie, Pernille Steen Pettersen: None declared, Torfinn Lødøen Gaarden: None declared, Knut Engedal: None declared, Tore K. Kvien Speakers bureau: Amgen, Celltrion, Egis, Evapharma, Ewopharma, Hikma, Oktal, Sandoz, Sanofi, Consultant of: AbbVie, Amgen, Biogen, Celltrion, Eli Lilly, Gilead, Mylan, Novartis, Pfizer, Sandoz, Sanofi, Grant/research support from: AbbVie, Amgen, BMS, MSD, Pfizer, UCB (to the institution)., Karin Magnusson: None declared, Ida K. Haugen Speakers bureau: Novartis, Grant/research support from: Pfizer

Background:Immunogenicity is related to loss of efficacy and safety to TNFα inhibitors and is frequently observed early in the treatment course. The highest rate of anti-drug antibody (ADAb) formation has been reported for infliximab (IFX). 1 Knowledge about risk factors for immunogenicity might contribute to better handling of this problem in clinical practice.Objectives:To identify risk factors for ADAb formation during the early phase of IFX treatment.Methods:411 patients with immune-mediated inflammatory diseases (84 rheumatoid arthritis (RA), 119 spondyloarthritis (SpA), 45 psoriatic arthritis, 83 ulcerative colitis, 58 Crohn’s disease and 22 psoriasis) initiating IFX treatment were included in the 38-week NOR-DRUM A trial and randomised 1:1 to therapeutic drug monitoring or standard IFX therapy.2 The primary endpoint was clinical remission at week 30. Serum (s) IFX levels and ADAb were measured at each infusion by in-house assays; time-resolved fluorometric assay for sIFX and inhibition assay for ADAb.2 In this sub-study, possible risk factors for ADAb formation including demographic variables, diagnosis, comedication, disease activity, IFX dose, sIFX and drug holidays, were assessed using logistic regression. Variables with a p-value Results:410 of 411 patients had at least one measurement of sIFX and were included in the present analyses. 76% of patients were biologic-naive and 45% (18% of RA patients) used IFX as monotherapy. Patients received a mean IFX dose of 3.2-5.9 mg/kg (RA 3.2 mg/kg). ADAb were detected in 78 (19%) patients. The Table 1 shows variables with a significant association to ADAb development. Analyses revealed an increased risk of ADAb development in patients with RA (Odds ratio (OR) 2.1, 95% confidence interval (CI) 1.1-3.9), while SpA had a lower risk (OR 0.5, CI 0.2-0.9) compared to the other diagnoses. These findings were consistent in both univariate- and multivariate analyses (Table 1). Figure 1 shows the cumulative hazard for ADAb development according to diagnosis. Other risk factors for ADAb (Table 1) were smoking (OR 1.8, CI 1.0-3.3) and drug holidays of more than 12 weeks (OR 4.7, CI 1.2-18.3). Additionally, the risk of ADAb increased with higher disease activity (OR 1.5, CI 1.0-2.3) and lower sIFX levels (0.7, 0.6-0.8). Patients co-treated with methotrexate (OR 0.4, CI 0.2-0.9) or thiopurines (OR 0.3, CI 0.1-0.8), or having one or more IFX dose increments (OR 0.4, CI 0.3-0.8), had a reduced risk of immunogenicity.Table 1.Risk factors for ADAb. Results from logistic regression analysesUnivariate analysesMultivariate analyses (Adjusted for diagnosis, disease activity, age and gender)ORCIORCIRA2.2**[1.3,3.8]2.1*[1.1,3.9]SpA0.4**[0.2,0.8]0.5*[0.2,0.9]Methotrexate1.1[0.7,1.9]0.4*[0.2,0.9]Thiopurine0.3*[0.1,0.9]0.3*[0.1,0.8]Current or former smoking2.2**[1.3,3.8]1.8*[1.0,3.3]Mean sIFX0.7***[0.6,0.8]0.7***[0.6,0.8]>12 weeks between infusions4.5*[1.3,16.0]4.7*[1.2,18.3]IFX dose increment0.5*[0.3,0.9]0.4**[0.3,0.8]Mean DAS28 (RA and PsA)1.5*[1.0,2.1]1.5*[1.0,2.3]Mean ESR1.1***[1.0,1.1]1.1***[1.0,1.1]Mean CRP1.1**[1.0,1.1]1.1**[1.0,1.1]* pOnly variables with a p-value Conclusion:This study identified smoking, drug holidays, high disease activity, IFX monotherapy and low sIFX levels as risk factors for ADAb development. Of particular interest, we found that RA patients had significantly increased risk of ADAb compared to the other immune-mediated inflammatory diseases. Whether this novel finding reflects different underlying disease mechanisms or the fact that RA patients receive a lower IFX dose, is not known and needs to be further explored.References:[1]Thomas SS et al. BioDrugs 2015;29(4):241-58 2 Syversen SW et al. Trials 2020 6;21(1):13Disclosure of Interests:Marthe Kirksæther Brun: None declared, Guro Løvik Goll Speakers bureau: Pfizer, AbbVie, Boehringer Ingelheim, Roche, Orion pharma, Sandoz and Novartis, Kristin Kaasen Jørgensen Speakers bureau: Celltrion, AOP Orphan Pharmaceuticals and Norgine, Joe Sexton: None declared, Johanna Elin Gehin Speakers bureau: Roche, Øystein Sandanger: None declared, Inge Olsen: None declared, Rolf Anton Klaasen: None declared, David J Warren: None declared, Cato Mørk Speakers bureau: Novartis Norge AS, LEO Pharma AS, ACO Hud Norge AS, Cellgene AS, Abbvie, Galderma Nordic and UCB, Tore K. Kvien Speakers bureau: TAmgen, Celltrion, Egis, Evapharma, Ewopharma, Hikma, Oktal, Sandoz and Sanofi, Consultant of: AbbVie, Amgen, Biogen, Celltrion, Eli Lilly, Gilead, Mylan, Novartis, Pfizer, Sandoz and Sanofi, Grant/research support from: Research funding to Diakonhjemmet Hospital from AbbVie, Amgen, BMS, MSD, Pfizer and UCB, Jørgen Jahnsen: None declared, Nils Bolstad Speakers bureau: Roche Pharmaceuticals and Novartis, Consultant of: Janssen, Espen A Haavardsholm Speakers bureau: Pfizer, AbbVie, Celgene, Novartis, Janssen, Gilead, Eli-Lilly and UCB, Silje Watterdal Syversen Speakers bureau: Thermo Fisher.

Background:Juvenile idiopathic arthritis (JIA) can cause considerable pain and disability in childhood and adulthood. Studies exploring the efficacy of medications in adult JIA patients are limited, although tumor necrosis factor inhibitors (TNFi) have been increasingly used in this patient group.Objectives:To explore the efficacy of TNFi ± comedication on disease activity in adult JIA patients, compared to a weighted rheumatoid arthritis (RA) cohort.Methods:Data from NOR-DMARD, a longitudinal observational study including patients > 18 years starting or switching DMARD treatment, was used [1]. Patients with a clinical JIA diagnosis, or patients with other inflammatory joint diseases diagnosed before 16 years were identified from the study population. RA patients were included for comparative purposes.Disease activity measurements and remission rates among patients starting treatment with TNFi ± comedication were collected at baseline, 3 and 6 months. Changes in disease activity and absolute remission rates after 3 and 6 months were calculated. Remission rates and change in disease activity from baseline were compared between JIA patients and a weighted RA cohort with weights based on age and gender, using linear and logistic regression for continuous and categorical variables, respectively.Results:281 JIA patients (68.9% female, mean (SD) age 32.1 (11.1) years, mean (SD) diagnosis duration 23.5 (12.2) years) and 1374 RA patients (71.6% female, mean (SD) age 52.7 (14.5) years, mean (SD) diagnosis duration 9.5 (10.0) years) were included in the analyses. Age, gender distribution and disease duration differed significantly between cohorts.Both groups had a significant improvement across all disease activity measures after 3 months (Table 1), which was maintained after 6 months across all measures except MHAQ. The RA group had a significantly greater 3- and 6-month improvement in SJC28. Both groups had an overall 6-month increase in absolute remission rates. The JIA group had a significantly higher 3-month DAS28 remission rate (Figure 1). This difference was not significant after 6 months, as remission rates from 3 to 6 months in the JIA group declined across all measures.Table 1.BaselineChange to 3 monthsChange to 6 monthsJIA*RA*Diff.§JIA*RA*Diff.§JIA*RA*Diff.§ESR, mm/h18.7 (18.9)25.5 (22.0)1.3 (-2.3 to 4.9)-7.4 (15.8)-7.6 (16.6)-0.3 (-4.4 to 3.8)-7.4 (16.8)-8.5 (18.2)0.0 (-5.7 to 5.7)SJC282.5 (3.6)5.5 (5.4)1.6 (1.3 to 2.0)-1.4 (3.4)-3.1 (4.7)-1.0 (-1.7 to -0.3)-1.6 (3.2)-3.5 (5.1)-1.0 (-1.9 to -0.1)TJC 284.0 (5.6)6.6 (6.4)1.3 (0.4 to 2.3)-1.8 (3.9)-3.1 (5.9)-0.6 (-1.4 to 0.2)-1.8 (3.9)-3.9 (6.2)-1.0 (-2.0 to 0.1)DAS283.6 (1.4)4.5 (1.6)0.3 (0.1 to 0.6)-1.2 (1.3)-1.2 (1.4)-0.0 (-0.3 to 0.3)-1.2 (1.3)-1.5 (1.4)-0.2 (-0.6 to 0.2)SDAI16.8 (10.6)23.1 (14.3)2.4 (0.3 to 4.5)-7.7 (9.9)-10.9 (12.7)-2.0 (-4.2 to 0.2)-7.9 (8.6)-13.2 (13.6)-2.8 (-5.8 to 0.2)PGA51.4 (26.3)49.9 (25.5)-4.0 (-8.5 to 0.5)-20.6 (26.7)-17.0 (26.7)2.7 (-2.2 to 7.6)-21.6 (25.3)-19.1 (28.7)3.4 (-3.0 to 9.8)MHAQ0.6 (0.5)0.7 (0.5)0.0 (-0.1 to 0.1)-0.24 (0.42)-0.22 (0.42)0.0(-0.1 to 0.1)-0.23 (0.40)-0.25 (0.45)0.0 (-0.1 to 0.1)*Mean (SD)§ Weighted group difference, RA coefficient (95 % confidence interval)Figure 1.Mean 3- and 6-month remission rates with error bars (SE)Conclusion:TNFi was equally effective in reducing disease activity in the JIA and RA cohort after 3 and 6 months, and in inducing remission after 6 months. Absolute remission rates in the JIA group declined from 3 to 6 months across all measures, and studies with longer duration are needed to explore the long-term efficacy of TNFi in the patient groups.References:[1]Kvien, T.K., et al., A Norwegian DMARD register: prescriptions of DMARDs and biological agents to patients with inflammatory rheumatic diseases. Clin Exp Rheumatol, 2005. 23(5 Suppl 39): p. S188-94.Disclosure of Interests:Imane Bardan: None declared, Karen Minde Fagerli: None declared, Joe Sexton: None declared, Gunnstein Bakland Speakers bureau: Abbvie, Consultant of: UCB, Pfizer, Novartis, Pawel Mielnik: None declared, Liz Marina Paucar Loli: None declared, Tore K. Kvien Speakers bureau: Fees for speaking: Amgen, Celltrion, Egis, Evapharma, Ewopharma, Hikma, Oktal, Sandoz, Sanofi, Consultant of: Fees for consulting: AbbVie, Amgen, Biogen, Celltrion, Eli Lilly, Gliead, Mylan, Novartis, Pfizer, Sandoz, Sanofi, Grant/research support from: Received research funding to Diakonhjemmet Hospital from Abbvie, Amgen, BMS, MSD, Pfizer and UCB, Eirik kristianslund: None declared, Anna-Birgitte Aga Grant/research support from: Dr. Aga reports personal fees from Abbvie, Eli Lilly, Novartis and Pfizer, outside the submitted work

Background:Juvenile idiopathic arthritis (JIA) can cause considerable pain and disability in childhood and adulthood. The number of studies exploring the efficacy of medications in adult JIA patients is limited. Methotrexate (MTX) is a commonly used medication for this patient group.Objectives:To explore the effects of MTX monotherapy (mono) on disease activity in adult patients diagnosed with JIA, compared to a weighted rheumatoid arthritis (RA) cohort.Methods:Data from NOR-DMARD, a longitudinal observational study enrolling patients > 18 years starting or switching DMARD treatment for inflammatory joint disease, was used [1]. Patients starting MTX mono treatment, and with a clinical diagnosis of JIA or other inflammatory arthropathies diagnosed before the age of 16 years, were identified from the study population. RA patients starting the same treatment regimen were included for comparative purposes.Disease activity measurements and remission rates were collected at baseline, 3 and 6 months. Changes in disease activity and absolute remission rates after 3 and 6 months were calculated. Remission rates and change in disease activity from baseline were compared between JIA patients and a weighted RA cohort with weights based on age and gender, using linear and logistic regression for continuous and categorical variables, respectively.Results:2201 patients were included in the analyses, 101 JIA patients (80.2% female, mean (SD) age 35.6 (13.0) years, mean (SD) diagnosis duration 24.8 (12.9) years), and 2100 RA patients (69.4% female, mean (SD) age 56.6 (13.6) years, mean (SD) diagnosis duration 4.1 (8.1) years) were included in the analyses. Age, gender distribution and disease duration differed significantly between cohorts.Both the JIA and RA group improved significantly across all disease activity measures from baseline to 3 and 6 months (Table 1). Both groups had a progressive increase in remission rates from baseline to 6 months (Table 1, Figure 1). The RA group had a significantly greater improvement in ESR after 3 months, SJC28 after 6 months and TJC28, DAS28, SDAI and MHAQ after 3 and 6 months. There were no significant group differences in remission rates.Table 1.BaselineChange to 3 monthsChange to 6 monthsJIA*RA*Diff.§JIA*RA*Diff.§JIA*RA*Diff.§ESR, mm/h20.4 (18.2)28.7 (22.2)3.7 (-0.6 to 8.1)-3.1 (15.8)-9.6 (18.7)-5.7 (-10.1 to -1.4)-3.0 (17.5)-11.3 (19.8)-5.4 (-10.8 to 0.03)SJC283.9 (4.8)6.9 (5.7)2.0 (0.9 to 3.2)-1.8 (3.3)-3.5 (5.5)-0.9 (-1.9 to 0.02)-1.8 (3.3)-4.2 (5.6)-1.5 (-2.6 to -0.5)TJC 284.5 (4.9)8.0 (7.1)3.1 (1.9 to 4.2)-0.8 (4.2)-3.5 (7.4)-1.9 (-3.1 to -0.7)-1.4 (3.8)-4.0 (6.8)-2.3 (-3.4 to -1.1)DAS284.0 (1.3)4.9 (1.3)0.6 (0.2 to 0.9)-0.6 (1.2)-1.2 (1.5)-0.5 (-0.9 to -0.2)-0.7 (1.2)-1.4 (1.5)-0.6 (-1.0 to -0.2)SDAI18.3 (11.3)26.0 (13.6)5.6 (2.7 to 8.4)-6.0 (9.7)-11.0 (14.0)-3.1 (-5.9 to -0.2)-6.3 (8.2)-12.8 (14.2)-5.1 (-7.8 to -2.2)PGA51.0 (24.6)48.3 (24.3)-4.5 (-10.0 to 1.1)-13.2 (25.3)-14.7 (26.5)-1.0 (-7.4 to 5.3)-11.3 (23.8)-14.3 (26.7)-4.6 (-11.9 to 2.7)MHAQ0.5 (0.5)0.7 (0.5)0.1 (-0.05 to 0.2)-0.2 (0.3)-0.2 (0.5)-0.1 (-0.2 to -0.0)-0.1 (0.3)-0.2 (0.5)-0.16 (-0.3 to -0.1)*Mean (SD)§ Weighted group difference, RA coefficient (95 % confidence interval)Figure 1.Mean 3- and 6-month remission rates with error bars (SE)Conclusion:Adult JIA patients had significant improvement across all the presented disease activity measures 3 and 6 months after treatment initiation with MTX mono. The magnitude of improvement was smaller than in the RA group, but JIA patients obtained remission at similar rates as RA patients.References:[1]Kvien, T.K., et al., A Norwegian DMARD register: prescriptions of DMARDs and biological agents to patients with inflammatory rheumatic diseases. Clin Exp Rheumatol, 2005. 23(5 Suppl 39): p. S188-94.Disclosure of Interests:Imane Bardan: None declared, Karen Minde Fagerli: None declared, Joe Sexton: None declared, Gunnstein Bakland Speakers bureau: Abbvie, Consultant of: UCB, Pfizer, Novartis, Pawel Mielnik: None declared, Liz Marina Paucar Loli: None declared, Tore K. Kvien Speakers bureau: Amgen, Celltrion, Egis, Evapharma, Ewopharma, Hikma, Oktal, Sandoz and Sanofi, Consultant of: AbbVie, Amgen, Biogen, Celltrion, Eli Lilly, Gilead, Mylan, Novartis, Pfizer, Sandoz and Sanofi, Grant/research support from: AbbVie, Amgen, BMS, MSD, Pfizer and UCB, Eirik kristianslund: None declared, Anna-Birgitte Aga Grant/research support from: Dr. Aga reports personal fees from Abbvie, Eli Lilly, Novartis and Pfizer, outside the submitted work

Background:In gout patients the extent of monosodium urate (MSU) crystal depositions can be quantitated by use of ultrasound. Gout may be associated with atherosclerotic disease which might be related to low-grade inflammation. Calprotectin is a major granulocyte protein reflecting the level of systemic inflammation.Objectives:To explore whether the extent of MSU crystal depositions is associated with low grade systemic inflammation as assessed by calprotectin/C-reactive protein (CRP) and with carotid pathologies in asymptomatic gout patients.Methods:The baseline data from NOR-GOUT, a prospective study of patients with crystal-proven gout with increased serum urate levels (>360 μmol/L), were used. All patients were assessed by ultrasound (GE Logiq E9 machine) to assess MSU depositions (OMERACT definitions; double contour (DC), tophi and aggregates) with bilateral assessment of wrist, MCP2, knee, ankle, MTP1 and insertions of triceps, quadriceps, proximal/distal patellar and Achilles tendons, all scored semi-quantitatively 0-3. Bilateral B-mode ultrasound assessments of the carotid arteries examined carotid intima-media thickness (cIMT; increased thickness >0.9mm). Atherosclerotic plaques were identified as protrusions of ≥1.5 mm or ≥ 2 times the adjacent IMT. Sum scores of each of the ultrasound elementary lesions for MSU depositions were calculated and the associations with calprotectin (plasma assessed by ELISA (Calpro), normal levels Results:A total of 202 gout patients without flare were included (95.5% men, mean (SD) age of 56.5 (13.8) years, 7.9 (7.7) years since first flare). The mean (SD) sum sore of DC was 4.4 (3.5), tophi 6.6 (6.6), aggregates 9.3 (5.6), calprotectin 801 (525) µg/L, CRP 7 (14) mg/L and serum urate (SUA) 499 (77) μmol/L. Carotid examinations were performed in 122 (60.4%) of the patients. Significant correlations were found between the MSU depositions and the inflammatory markers as well as cIMT. The 27% patients with increased calprotectin had the highest levels of each of the three elementary lesions (p=0.001) (Figure), and the 39% with elevated CRP levels had the highest levels of tophi and aggregates (pConclusion:In asymptomatic gout patients, higher load of MSU crystal depositions was associated with increased levels of inflammatory markers, cIMT and presence of atherosclerotic plaques in the carotid arteries. This may indicate that crystal depositions cause subclinical inflammation with subsequent systemic implications, but future longitudinal studies are needed to confirm such causal relationships.Sum scoredouble contourSum scoretophiSum score aggregatesCalprotectin0.26**0.32**0.28**CRP0.20*0.25**0.18*Right IMTNSNS0.18*Left IMTNSNS0.21*Sum bilateral IMTNSNS0.22*Spearman’s correlations. NS; Not significant, *pDisclosure of Interests:Hilde Berner Hammer Speakers bureau: AbbVie, Lilly and Novartis, Silvia Rollefstad: None declared, Gro Jensen: None declared, Lars Karoliussen: None declared, Lene Terslev Speakers bureau: Speakers fee from AbbVie, Janssen, Roche, Novartis, Pfizer, MSD, BMS and GE, Espen A Haavardsholm: None declared, Tore K. Kvien Speakers bureau: Tore K Kvien has received fees for speaking and/or consulting and/or research funding to Diakonhjemmet Hospital from AbbVie, Biogen, BMS, Celltrion, Egis, Evapharma, Ewopharma, Eli Lilly, Gilead, Hikma, MSD, Mylan, Novartis, Oktal, Pfizer, Sandoz, Sanofi and UCB., Anne Grete Semb: None declared, Till Uhlig: None declared

Background:Incidence estimates of PsA in Norway have varied from 6.9/100,000 person-years (pyrs) in Northern Norway to 41.3/100,000 pyrs in Central Norway, and point prevalence estimates have ranged from 1.3 to 6.9 per 1,000 adult inhabitants1,2, while nationwide epidemiologic data on PsA in Norway have been lacking.Objectives:To estimate prevalence, incidence and use of disease-modifying antirheumatic drugs (DMARDs) among PsA patients in Norway.Methods:The Norwegian Cardio-Rheuma register includes pseudonymized data from the total Norwegian population ≥18 years of age during 2008-2017, identified from the National Population register. Demographic and socioeconomic data were retrieved from Statistics Norway. Data on public or private somatic specialized care episodes were collected from the Norwegian Patient register (NPR) [ICD-10 codes for diagnoses and medical procedure codes for biologic DMARD infusions]. Information on dispensed DMARD prescriptions was captured from the Norwegian Prescription Database. Based on NPR data, PsA cases were defined as persons fulfilling three criteria: 1) 1st episode with ICD-10 code M07.0-M07.3 or L40.5 as main or contributory diagnosis (index date), 2) 2nd episode with code M07.0-M07.3 or L40.5 within 2-year period following index date, 3) an episode in internal medicine or rheumatology clinic with recorded M07.0-M07.3 or L40.5 within 2 years from index date. Years 2008-2010 served as a look-back period to identify prevalent PsA cases. To estimate pyrs at risk, we calculated number of individuals aged ≥ 18 years living in Norway on the 1st of January of each year 2011-2015 multiplied by one year (prevalent PsA cases excluded). Age- and sex-standardized incidence rates were calculated with 5-year age groups using the Norwegian adult population on January 1st 2015 as the standard.Results:During the look-back period 2008-2010, 7,697 cases fulfilled the PsA definition. In total, 6,183 incident PsA cases were identified during 2011-2015 (incidence 32/100,000 pyrs, 28 among men and 35 among women). Based on a sensitivity analysis comprising 5,065 PsA cases with no dispensed DMARD prescriptions ≥12 months before index date, incidence was slightly lower (26/100,000 pyrs). Patient characteristics and DMARD use are shown in Table 1. The incidence was highest among those aged 50-59 years in both sexes (Figure 1). PsA incidence was lower among those with higher education level (crude/age- and sex-standardized incidence per 100,000 pyrs for those below upper secondary education 34/38, upper secondary or post-secondary non-tertiary education 36/36, higher education 26/25). Point prevalence of PsA was 3.3/1,000 adult inhabitants on January 1st 2016.Table 1.Characteristics and treatment penetration of incident PsA patients 2011-2015AllExcluding cases with DMARDs >1 yr prior to index dateN61835065Women, n (%)3442 (55.7)2783 (54.9)Age at index date, median (IQR)50.5 (40.7 - 59.8)49.9 (40.2 - 59.3)Use of DMARDs after index date, n (%)12 months24 months12 months24 months Any conventional DMARD3706 (59.9)4048 (65.4)2894 (57.1)3184 (62.9) Methotrexate3313 (53.6)3650 (59.0)2638 (52.1)2933 (57.9) Sulfasalazine440 (7.1)586 (9.5)330 (6.5)457 (9.0) Any biologic DMARD842 (13.6)1197 (19.4)485 (9.6)771 (15.2) TNF-inhibitors810 (13.1)1154 (18.7)477 (9.4)758 (15.0) Oral glucocorticoids1773 (28.7)2240 (36.2)1449 (28.6)1807 (35.7) Any DMARD or glucocorticoids4365 (70.6)4742 (76.7)3384 (66.8)3725 (73.5)Conclusion:Our estimate of PsA incidence and prevalence are in the mid-range compared to studies from smaller regions in Norway. Methotrexate was initiated for more than half of PsA cases within one year from index date, whereas 19% had used biologic DMARDs within two years.References:[1]Hoff M, Gulati A, Romundstad P et al. Prevalence and incidence rates of psoriatic arthritis in central Norway: data from the Nord-Trondelag health study. Ann Rheum Dis 2015;74:60-64.[2]Nossent J & Gran J. Epidemiological and clinical characteristics of psoriatic arthritis in northern Norway. Scand J Rheumatol 2009; 8:251-5.Acknowledgements:This work has been supported by a research grant from FOREUM Foundation for Research in Rheumatology.Disclosure of Interests:Anne Kerola Speakers bureau: Boehringer-Ingelheim, Consultant of: Pfizer, Gilead and Boehringer-Ingelheim, Joseph Sexton: None declared, Silvia Rollefstad: None declared, Grunde Wibetoe: None declared, Cynthia S. Crowson: None declared, Espen Haavardsholm: None declared, Tore K. Kvien Speakers bureau: Amgen, Celltrion, Egis, Evapharma, Ewopharma, Hikma, Oktal, Sandoz, Sanofi, Consultant of: AbbVie, Amgen, Biogen, Celltrion, Eli Lilly, Gilead, Mylan, Novartis, Pfizer, Sandoz, Sanofi, Grant/research support from: research funding to Diakonhjemmet Hospital from AbbVie, Amgen, BMS, MSD, Pfizer and UCB, Anne Grete Semb Speakers bureau: AbbVie, Bayer, Lilly, Novartis, Sanofi, Consultant of: Sanofi, Grant/research support from: Collaborative research support from Lilly, outside the submitted work.

Background:Dual-energy computed tomography (DECT) detects urate depositions, and is included in the ACR/EULAR classification criteria for gout. There is lack of longitudinal studies in large patient populations for changes in urate deposition measured by DECT during urate lowering therapy (ULT).Objectives:To explore by DECT the longitudinal changes urate depositions during a treat-to-target approach in gout with ULT.Methods:In a prospective observational study, patients with crystal-proven gout were included if they presented after a recent gout flare and with increased serum urate levels (>360 μmol/L/>6 mg/dl). In a treat-to-target approach they received ULT with escalating drug doses with monthly follow-up during the first year until the treatment target was met with serum urate A DECT scanner (General Electric Discovery CT750 HD) acquired data from bilateral forefeet and ankles at 80 KW and 140 KV, processed with a software with a 2-material decomposition algorithm which colour codes urate. Follow-up DECT was performed after one and two years.Images were scored with a semiquantitative method (Bayat et al. 2015) by one experienced radiologist in known order and blinded to serum urate and clinical data. Each scan assessed four regions: the first metatarsophalangeal (MTP1) joint, the other joints of the toes, the ankles and midfeet, and all visible tendons in the feet and ankles. Each region was then scored according to the maximum amount of urate deposition observed on visual inspection (0=no deposits, 1=dots, 2=single deposit, 3=more than one deposit). A total DECT sum score was derived by adding all values from the four regions, with a maximum score of 12.Results:DECT was at baseline measured in 187 of 211 patients. 95.2% were males, mean (SD) age was 56.7 (13.7) years, disease duration 8.1 (7.9) years), and 17% had clinical tophi.The total DECT scores and all subscores decreased from baseline to 2 years (pThe mean (SD) serum urate level (μmol/L) decreased from 501 (80) at baseline to 311 (48) at 12 months and 322 (67) at 24 months. Reaching the treatment target Conclusion:During a treat-to-target approach urate deposition visualised by DECT were clearly reduced in ankles and feet after 1 year with further reduction after 2 years.Table 1.Baseline (n=187) Mean (SD)1 year (n=157) Mean (SD)2 years (n=166) Mean (SD)MTP1 (0-3)1.4 (2.0)1.0 (1.7)0.6 (1.3)Toes (0-3)1.0 (1.8)0.6 (1.4)0.3 (1.0)Ankle/Midfoot (0-3)1.2 (2.1)0.7 (1.60.3 (1.0)Tendons (0-3)1.0 (1.7)0.5 (1.2)0.3 (0.8)Sum score (0-12)4.6 (6.4)2.8 (4.7)1.5 (3.2)Disclosure of Interests:Till Uhlig Speakers bureau: Grünenthal, Novartis, Consultant of: Grünenthal, Novartis, Tron Eskild: None declared, Lars Fridtjof Karoliussen: None declared, Tore K. Kvien Consultant of: AbbVie, MSD, UCB, Hospira/Pfizer, Eli-Lilly, Roche, Hikma, Orion, Sanofi, Celltrion, Sandoz, Biogen, Amgen, Egis, Ewopharma, Mylan, Grant/research support from: BMS, AbbVie, MSD, UCB, Hospira/Pfizer, Eli-Lilly, Espen A Haavardsholm Consultant of: Pfizer, UCB, Eli Lilly, Celgene, Janssen-Cilag, AbbVie and Gilead, Nicola Dalbeth Speakers bureau: Menarini, AstraZeneca, Takeda, S. Nicolaou, Consultant of: AstraZeneca, Fonterra, Takeda, Pfizer, Cymabay, Crealta, Grant/research support from: AstraZeneca, Siemens Healthcare, Hilde Berner Hammer Consultant of: AbbVie, Lilly and Novartis

Background:Sustained remission is the goal of rheumatoid arthritis (RA) care, and more patients reach and maintain this state on conventional synthetic disease modifying anti-rheumatic drugs (csDMARDs) with treat-to-target strategies. The knowledge about whether csDMARDs can be tapered in RA remission is limited.Objectives:The primary objective of the study was to assess the effect of tapering of csDMARDs on the risk of flares in RA patients in sustained clinical remission.Methods:In the open, phase 4, non-inferiority ARCTIC REWIND trial, RA patients in clinical remission for ≥ 12 months on stable csDMARD therapy were randomised to continued stable csDMARD or half dose csDMARD. Patients had to be in DAS remission at inclusion with no swollen joints (of 44). The primary endpoint was the proportion of patients with a disease flare during 12 months (defined as a combination of DAS >1.6, change in DAS >0.6 and ≥2 swollen joints, or the physician and patient agreed that a clinically significant flare had occurred). Patients attended visits every 4 months, with extra visits in case of flares. The non-inferiority margin was 20%, with a predefined superiority test if non-inferiority was not shown. Mixed effect logistic regression was used to test the inferiority null-hypothesis in the per-protocol population. Radiographs at 0 and 12 months were scored by van der Heijde Sharp score (average score of two readers, progression: ≥1 unit change/year). Clinicaltrials.govNCT01881308.Results:We enrolled 160 patients, 155 received the allocated treatment strategy. Baseline characteristics were overall well balanced (Table). 78% of patients in the stable csDMARD arm and 84% in the half-dose csDMARD arm used methotrexate monotherapy. In the primary analysis, we observed flares in 6% of patients on stable csDMARD, compared to 25% in the half-dose csDMARD arm, giving a risk difference (95% CI) of 18.3% (7.2% to 29.3%, Fig 1). Non-inferiority could not be claimed, with the results showing superiority of the stable arm over the half-dose arm (Fig 1). Similar results were found in methotrexate monotherapy users. In the stable arm, 2/5 (40%) escalated DMARD medication following the flares, compared to 18/19 (95%) in the tapering arm. No progression of radiographic joint damage was observed in 79.5% of patients on stable DMARDs and 62.7% of those tapering, difference (95% CI) -17.7% (-33.0%, -2.3%, Fig 2E). At 12 months, 92% of patients in the stable and 85% of patients in the tapered arm were in DAS remission (Fig 2C). The frequency of adverse events was 75 in the stable arm and 53 in the tapered arm, with serious adverse events in 2 (2.6%) of patients in the stable and 4 (5.1%, including two serious infections) patients in the tapered arm.Conclusion:In RA patients in sustained remission on csDMARDs, continued csDMARD therapy with stable dosage led to significantly fewer disease activity flares and less frequent radiographic joint damage progression than tapered csDMARD treatment.Table.Baseline values; mean (SD), n (%) or median (IQR)Stable, n=78Tapering, n=78Age, yrs55 (12)56 (12)Female50 (64%)54 (69%)ACPA+57 (73%)63 (81%)Symptom dur., yrs3.7 (1.8)3.4 (1.4)DAS0.8 (0.4)0.8 (0.3)CRP mg/L2 (1, 3)2.0 (1,3)MTX monotherapy61 (78%)65 (84%)Disclosure of Interests:Siri Lillegraven: None declared, Nina Paulshus Sundlisæter: None declared, Anna-Birgitte Aga: None declared, Joe Sexton: None declared, Inge Olsen: None declared, Hallvard Fremstad: None declared, Cristina Spada: None declared, Tor Magne Madland: None declared, Christian A. Høili Consultant of: Novartis, Gunnstein Bakland Consultant of: Novartis, UCB, Åse Lexberg: None declared, Inger Johanne Widding Hansen: None declared, Inger M. Hansen: None declared, Hilde Haukeland Consultant of: Novartis, Maud-Kristine A Ljosa: None declared, Ellen Moholt: None declared, Till Uhlig Consultant of: Lilly, Pfizer, Speakers bureau: Grünenthal, Novartis, Daniel Solomon Grant/research support from: Funding from Abbvie and Amgen unrelated to this work, Désirée van der Heijde Consultant of: AbbVie, Amgen, Astellas, AstraZeneca, BMS, Boehringer Ingelheim, Celgene, Cyxone, Daiichi, Eisai, Eli-Lilly, Galapagos, Gilead Sciences, Inc., Glaxo-Smith-Kline, Janssen, Merck, Novartis, Pfizer, Regeneron, Roche, Sanofi, Takeda, UCB Pharma; Director of Imaging Rheumatology BV, 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)., Espen A Haavardsholm Grant/research support from: AbbVie, UCB Pharma, Pfizer Inc, MSD Norway, Roche Norway, Consultant of: Pfizer, AbbVie, Janssen-Cilag, Gilead, UCB Pharma, Celgene, Lilly, Paid instructor for: UCB Pharma, Speakers bureau: Pfizer, AbbVie, UCB Pharma, Celgene, Lilly, Roche, MSD

Background:A lack or loss of response to TNFα inhibitors (TNFi) has been associated with low serum drug levels and formation of anti-drug antibodies (ADAb). Therapeutic drug monitoring (TDM), an individualised treatment strategy based on regular assessments of serum drug levels, has been suggested to optimise efficacy of TNFi. It is still unclear if TDM improves clinical outcomes, and the value of TDM has recently been included in the research agenda across different specialities. This first randomised controlled trial on the effectiveness of TDM in a range of immune mediated inflammatory diseases including rheumatic diseases, the NORwegian DRUg Monitoring trial part A (NOR-DRUM (A)) focus on the induction period of infliximab (INX) treatment.Objectives:To assess if TDM is superior to standard treatment in order to achieve remission in patients starting INX.Methods:In the investigator-initiated, randomised, open-label, multicentre NOR-DRUM (A) study, adult patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), spondyloarthritis (SpA), ulcerative colitis (UC), Crohn’s disease (CD) and psoriasis (Ps) starting INX therapy were randomly assigned to administration of INX according to a treatment strategy based on TDM (TDM arm) or to standard administration of INX without TDM (control arm). Study visits were conducted at each infusion. The primary endpoint was remission at week 30. In the TDM arm, the dose and interval were adjusted according to INX trough levels to reach the therapeutic range (Figure 1). If the patient developed significant levels of ADAb, INX was terminated. To guide the investigators, the TDM strategy was integrated in an interactive eCRF. The primary endpoint was analysed by mixed effect logistic regression in the full analyses set (FAS), adjusting for diagnoses. Infections and infusion reactions were specified as adverse events (AEs) of special interest.Clinical trial.gov:NCT03074656Results:We enrolled 411 patients at 21 study centres between January 2017 and December 2018. 398 patients (RA 80, PsA 42, SpA 117, UC 80, CD 57, Ps 22) received the allocated strategy and were included in the FAS population. Demographic and baseline characteristics were comparable in both arms. TDM was not found to be superior to standard treatment with regard to the primary outcome. Remission at week 30 was reached in 100 (53%) and 106 (54%) of the patients in the TDM and control arm, respectively (adjusted difference, 1.5%; 95% confidence interval (CI), -8.2 to 11.1, p=0.78) (Figure 2). Consistent results were shown for all the secondary endpoints (Figure 3) and in the sensitivity analyses. Twenty patients (10%) in the TDM arm and 30 patients (15%) in the control arm developed significant levels of ADAb. The number of adverse events (AE) was similar in both groups, however infusion reactions were less frequent (5 patients (2.5%) vs 16 patients (8.0%)) in the TDM arm (difference 5.5% (95% CI 1.1, 9.8%))Conclusion:NOR-DRUM (A) is the first randomised trial to address effectiveness of TDM in the induction period of TNFi treatment, and the first trial to address TDM in rheumatic diseases. In this study, TDM was not superior to standard treatment in order to achieve remission. Although improved safety is indicated by a reduction in infusion reactions, implementation of TDM as a general strategy in the induction period of INX is not supported by the NOR-DRUM (A) study.Disclosure of Interests:Silje Watterdal Syversen Speakers bureau: Roche, Thermo Fisher, Guro Løvik Goll Consultant of: Novartis, Pfizer, Speakers bureau: Abbvie, Biogen, Boehringer Ingelheim, Orion Pharma, Eli Lilly, Novartis, Pfizer, MSD, Roche, UCB, Kristin Kaasen Jørgensen Consultant of: AOP Orphan, Celltrion, Sandoz, Speakers bureau: Norgine, Tillots, Øystein Sandanger: None declared, Joe Sexton: None declared, Inge Olsen: None declared, Johanna Gehin Speakers bureau: Roche, Marthe Kirksæther Brun: None declared, David Warren: None declared, Cato Mørk Consultant of: Abbot, Novartis, Celagene, Almiral, Galderma, ACO, Almiral, ACO, Speakers bureau: Novartis, Abbott, Abbvie, Celegene, LEO, Almiral, Galderma, 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)., Jørgen Jahnsen Consultant of: AbbVie, Boerhinger Ingelheim, Celltrion, Ferring, Janssen, Meda, MSD, Norgine, Novartis, Orion Pharma, Pfizer, Pharmacosmos, Takeda, and Sandoz., Speakers bureau: AbbVie, Astro Pharma, Boerhinger Ingelheim, BMS, Celltrion, Ferring, Hikma, Janssen, Meda, MSD, Napp Pharma, Orion Pharma, Pfizer, Pharmacosmos, Roche, Takeda, Tillotts and Sandoz, Nils Bolstad Consultant of: Pfizer, Janssen, Speakers bureau: Orion Pharma, Napp Pharmaceuticals, Takeda, Roche, Novartis, Espen A Haavardsholm Grant/research support from: AbbVie, UCB Pharma, Pfizer Inc, MSD Norway, Roche Norway, Consultant of: Pfizer, AbbVie, Janssen-Cilag, Gilead, UCB Pharma, Celgene, Lilly, Paid instructor for: UCB Pharma, Speakers bureau: Pfizer, AbbVie, UCB Pharma, Celgene, Lilly, Roche, MSD

Background:International EULAR and ACR recommendations support lifestyle changes, diet and urate lowering therapy (ULT) in gout. Treat-to-target ULT is often not performed, resulting in insufficient treatment of gout. We studied how many patients achieved the recommended treatment target of Objectives:We studied how many patients achieved the recommended treatment target of Methods:211 patients with crystal proven gout were included into the prospective, observational NOR-Gout study if they recently had a gout flare as well as insufficiently treated serum urate SUA >360 µmol/l).The intervention consisted of individual verbal information on lifestyle, including factors related to physical activity, diet and the importance of drug adherence. ULT (mainly allopurinol) was initiated and escalated monthly according to EULAR recommendations. Patients were during the first year seen by physician and nurse every three months with additional visits after month 1 and month 2, with further visits monthly as necessary until the treatment target of SUA Baseline age was 53.6 (SD 12.2) years, disease duration 7.8 years (SD 7.6), BMI 28.8 (SD 4.5) kg/m2, 95.3% were males. Baseline SUA was 500 (77) µmol/l and 16.6% had subcutaneous tophi. Assessments included questions on frequency of alcohol use, and application of the self-efficacy scales for symptoms (SES, range 10-100) as well as the beliefs in medicines questionnaire (BMQ), which included a scale for general overuse of medicines (range 4-16).186/211 (88.2%) patients completed the visit for the primary SUA endpoint at 12 months.Results:SUA continuously declined over 12 months and the frequency of responders increased (table 1):Table 1Responders and SUA levels during the treat-to-target interventionMonthMonth 01236912%n RespondersSUA00/21121.3 43/20248.794/19369.3131/18986.7151/18781.9136/16685.5159/186SUA µmol/l (mean, SD)500 (78)413 (77)371 (64)341 (61)327 (59)316 (56)311 (49)At 12 months 87.6% (163/186) of patients used allopurinol and 13.4% (23/186) febuxostat with mean daily doses of 289 mg (range 100-900) and 59 (20-120) mg, respectively.Reaching the treatment target of SUA after 12 months was bivariately related to work status, alcohol use, and beliefs in general overuse of medicines. In multivariable analyses in the final model also adjusted for baseline SUA, several variables predicted reaching the SUA target of Conclusion:Most patients (85.5%) with recent gout flare und increased SUA reached the target SUA after 12 months. A good treatment result was predicted by increasing age,less frequent alcohol use, when patients believed they could cope with symptoms and when they did not believe that drugs are generally overused.Disclosure of Interests: :Till Uhlig Consultant of: Lilly, Pfizer, Speakers bureau: Grünenthal, Novartis, Lars Fridtjof Karoliussen: 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)., Espen A Haavardsholm Grant/research support from: AbbVie, UCB Pharma, Pfizer Inc, MSD Norway, Roche Norway, Consultant of: Pfizer, AbbVie, Janssen-Cilag, Gilead, UCB Pharma, Celgene, Lilly, Paid instructor for: UCB Pharma, Speakers bureau: Pfizer, AbbVie, UCB Pharma, Celgene, Lilly, Roche, MSD, Hilde Berner Hammer: None declared

Background:Ankylosing Spondylitis Disease Activity Score (ASDAS) is a composite index measuring disease activity in axial spondyloarthritis (axSpA). It includes questions from the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Patient Global Assessment (PGA), and inflammation biomarkers. However, ASDAS calculation is not always possible because PGA is sometimes not collected.Objectives:To develop an alternative ASDAS to be used in research settings when PGA is unavailable.Methods:Longitudinal data from 4 axSpA cohorts and 2 RCTs were combined. Observations were randomly split in a development (N=1026) and a validation cohort (N=1059). Substitutes of PGA by BASDAI total score, single or combined individual BASDAI questions, and a constant value, were considered. In the development cohort, conversion factors for each substitute were defined by Generalized Estimating Equations. Validation was performed in the validation cohort according to the OMERACT filter, taking into consideration: 1) Truth (agreement with original-ASDAS in the continuous score, by intraclass correlation coefficient -ICC- and in disease activity states, by weighted kappa) 2) Discrimination (standardized mean difference –SMD- of ASDAS scores between high/low disease activity states defined by external anchors e.g Patient Acceptable Symptom State –PASS-; agreement -kappa- in the % of patients reaching ASDAS improvement criteria according to alternative vs. original formulae) 3) Feasibility.Results:Taking all psychometric properties into account and comparing the different formulae (Table), alternative-ASDAS using BASDAI total as PGA replacement proved to be: 1) truthful (agreement with original-ASDAS: ICC=0.98, kappa=0.90); 2) discriminative: it could discriminate between high/low disease activity states (e.g. scores between PASS no/yes: SMD=1.37 versus original-ASDAS SMD=1.43) and was sensitive to change (agreement with original-ASDAS in major improvement/clinically important improvement criteria: kappa=0.93/0.88; 3) feasible (BASDAI total often available; conversion coefficient≈1).Table.Psychometric properties of alternative ASDAS formulaeConclusion:Alternative-ASDAS using BASDAI total score as PGA replacement is the most truthful, discriminative and feasible instrument. This index enables ASDAS calculation in existing cohorts without PGA.Disclosure of Interests:Augusta Ortolan: None declared, Sofia Ramiro: None declared, Floris A. van Gaalen: 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)., Robert B.M. Landewé Consultant of: AbbVie; AstraZeneca; Bristol-Myers Squibb; Eli Lilly & Co.; Galapagos NV; Novartis; Pfizer; UCB Pharma, Pedro M Machado Consultant of: PMM: Abbvie, Celgene, Janssen, Lilly, MSD, Novartis, Pfizer, Roche and UCB, Speakers bureau: PMM: Abbvie, BMS, Lilly, MSD, Novartis, Pfizer, Roche and UCB, Adeline Ruyssen-Witrand Grant/research support from: Abbvie, Pfizer, Consultant of: Abbvie, BMS, Lilly, Mylan, Novartis, Pfizer, Sandoz, Sanofi-Genzyme, Astrid van Tubergen Consultant of: Novartis, Caroline Bastiaenen: None declared, Désirée van der Heijde Consultant of: AbbVie, Amgen, Astellas, AstraZeneca, BMS, Boehringer Ingelheim, Celgene, Cyxone, Daiichi, Eisai, Eli-Lilly, Galapagos, Gilead Sciences, Inc., Glaxo-Smith-Kline, Janssen, Merck, Novartis, Pfizer, Regeneron, Roche, Sanofi, Takeda, UCB Pharma; Director of Imaging Rheumatology BV

Background:Disease activity is a risk factor for the development of cardiovascular disease (CVD) in patients with rheumatoid arthritis (RA). Remission is the preferred treatment target in RA, and may be achieved by treatment with both conventional synthetic DMARDS (csDMARDs) and biologic DMARDS (bDMARDs).Objectives:To compare the risk of CVD in patients reaching RA disease remission vs. non-remission by 6 months. Additionally; to compare the risk of CVD in RA patients reaching remission on bDMARDs vs. csDMARDsMethods:The NOR-DMARD is a multi-centre prospective observational study that was established in 2000. Until 2012, patients who started on any DMARD were included, while only patients starting bDMARDSs were included after 2012. Disease activity and markers of inflammation (Erythrocyte Sedimentation Rate (ESR) and C-reactive protein (CRP mg/L) were measured at regular intervals. In these analyses we used data from baseline, 3-month and 6-month visits in patients with clinical RA included in the study from 2009. Patients with prior CVD were excluded from the study. Remission was assessed according to several criteria, and should be attained by the 6-month visit.NOR-DMARD data were linked to the National Death Registry and National Patient Register. The latter records all diagnoses given at any hospital admission, inpatient and outpatient, from 2009. CVD was defined as a diagnosis of myocardial infarction, chronic heart failure, cerebrovascular disease or sudden CV death in ICD10. Using cox-regression models, we compared the time until the first recorded CVD diagnosis RA disease remission vs non-remission for the first 4 years after start of therapy. The models were adjusted for age and gender. Additionally, we explored interactions between bDMARD vs. csDMARD, remission and non-remission in age and gender adjusted models.Results:Data were available for 3251 patients, mean (SD) age, 53.6 (13.5) years, number (%) females 2483 (76.4). The total patient years at risk were 5784, during which there were 65 CVD events. The HR across remission criteria are presented in table 1. Patients in disease remission had a significantly lower HR for CVD compared to those not in remission. There was no statistically significant difference in HR for CVD between patients in remission who were treated with bDMARDs vs csDMARDs.Table 1.NOR-DMARDN=3251pbDMARDsN=2622pcsDMARDsN=629pHR (95% CI)HR(95% CI)HR(95% CI)DAS28-ESR remission vs non-remission0.40 (0.21,0.74)0.010.30 (0.14,0.65)0.0020.75 (0.26,2.22)0.61DAS28-CRP remission vs non-remission0.48 (0.28,0.83)0.010.42 (0.23,0.81)0.010.68 (0.2,1.90)0.46CRP 0.55 (0.30,1.03)0.060.67 (0.31,1.47)0.320.46 (0.16,1.36)0.16Boolean remission0.63 (0.34,1.84)0.330.49 (0.15,1.59)0.230.93 (0.21,4.10)0.92SDAI remission0.70 (0.37,1.34)0.280.61 (0.28,1.34)0.221.04 (0.33,3.30)0.95CDAI remission0.69 (0.37,1.29)0.250.61 (0.28,1.34)0.251.04 (0.33,3.30)0.98DAS28-ESR and DAS28-CRP remission: Figure 1Conclusion:Patients on bDMARDs who achieved DAS28, DAS28-CRP remission, or CRP less than 10 mg/L by the 6-month follow-up were less likely to experience a CVD, compared to patients not achieving remission. The HRs for CVD were higher for patients in remission on csDMARDS, compared to patients on bDMARDss, but the difference was not statistically significant and should be further explored.Disclosure of Interests:Inger Jorid Berg: None declared, Siri Lillegraven: None declared, Eirik kristianslund: 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)., Sella Aarrestad Provan Consultant of: Novartis

Background:Ultrasound detects depositions of monosodium urate (MSU) crystals in gout patients. The OMERACT ultrasound group has developed definitions for elementary lesions in gout including the double contour (DC) sign (depositions of crystals on the surface of cartilage) and tophus (larger hypo-echoic aggregation of crystals, usually well delineated). Calprotectin is a major granulocyte protein found to be sensitive to reflect the level of inflammation in several immunological diseases. There may be an association between low grade inflammation and co-morbidity (including cardio-vascular pathology) in gout patients.Objectives:To explore whether the extent of depositions (e.g. DC and tophi) was associated with inflammation in gout patients.Methods:The baseline data from NOR-GOUT, a prospective observational study of patients with crystal-proven gout with increased serum urate levels (>360 μmol/L), were presently used. All patients had an extensive ultrasound examination(GE E9 machine, grey scale 15MHz) to assess MSU depositions (DC and tophi) with bilateral assessment of radiocarpal joint, MCP 2, insertion of triceps and quadriceps, proximal and distal patellar and the Achilles tendon, cartilage of distal femur (maximal flexed knee), the talar cartilage of tibiotalar joint and MTP 1 joint. The degree of elementary lesions was semi-quantitatively scored 0-3 (0=none, 1=possible, 2=certain, 3=major deposits). Total sum scores of DC and tophi were calculated and the associations with calprotectin (plasma assessed by ELISA (Calpro), normal levels Results:A total of 111 patients who had calprotectin assessed were included in the study (92% men, mean (SD) age 54.5 (14.5) years, disease duration 7.1 (6.6) years) when initiating MSU lowering treatment. The mean (SD) sum sore DC and tophi was 9.1 (7.8), calprotectin 780 (500) µg/L, CRP 7 (15) mg/L, serum urate (SUA) 505 (87) μmol/L, creatinine 96 (18) μmol/l and eGFR 79 (20) ml/min/1.73m2. Table 1 shows significant correlations between sum sore DC/tophi and calprotectin, CRP, SUA, creatinine and eGFR. Increased calprotectin levels (≥910 µg/L) were found in 28% and increased CRP (≥ 4 mg/L) in 39%. Patients with increased vs normal levels of calprotectin had significantly higher levels of DC/tophi depositions (mean (SD) 13.0 (10.4) vs 7.4 (5.8), p=0.01), and similar was found for CRP (11.4 (9.5) vs 7.6 (6.2), p=0.033) (illustrated in table 2).Conclusion:In gout patients, higher load of MSU depositions was associated with increased inflammatory markers. This indicates that the amount of depositions is associated with higher inflammatory activity, which could have systemic implications.Sum score DC and tophiCalprotectinCRPSUACreatinineCalprotectin0.31*CRP0.29*0.65**SUA0.31**0.22*0.19Creatinine0.34**0.25*0.150.36**eGFR-0.38**-0.27*-0.21*-0.18-0.86***p≤0.05, **p≤0.001Disclosure of Interests: :Hilde Berner Hammer Consultant of: Has received fees as consultant from Roche, AbbVie and Novartis., Speakers bureau: Has received fees for speaking from AbbVie, BMS, Pfizer, UCB, Roche, MSD and Novartis, Gro Jensen: None declared, Lars Karoliussen: None declared, Lene Terslev Speakers bureau: LT declares speakers fees from Roche, MSD, BMS, Pfizer, AbbVie, Novartis, and Janssen., Espen Andre Haavardsholm Grant/research support from: Research funding from Pfizer, UCB, Roche, MSD and AbbVie, Consultant of: Pfizer, Speakers bureau: Pfizer, UCB, Roche, and AbbVie,, 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)., Till Uhlig Consultant of: Lilly, Pfizer, Speakers bureau: Grünenthal, Novartis

Background Joint inflammation plays a role in the pathogenesis of hand osteoarthritis (OA), and previous studies have presented an association between pain and synovitis detected by MRI and ultrasound. No previous hand OA studies have explored the validity of fluorescence optical imaging (FOI), a novel imaging technique demonstrating altered microcirculation in wrist and finger joints, as a sign of inflammation. Objectives The aims of the current study were to quantify the distribution of FOI-findings in different joint groups in hand OA patients and explore the association between FOI findings and self-reported pain and tender joints on clinical examination. Methods The NOR-HAND study is an observational hand OA study, in which 251 patients (88% female, median age 61 (interquartile range 56–66) years) underwent FOI of both hands, bilateral clinical examination for tender joints on palpation and movement, and self-reported their pain in individual joints during the last 24 hours and the last 6 weeks on the homunculus. The FOI-scan was performed after the administration of an intravenous fluorescence dye (indocyanine green, ICG) and 360 images (1/second) were produced in 6 min. Based on the inflow and washing out of the dye the pictures were divided into 3 phases. Ultimately, the prima vista mode (PVM) represented a composite picture of the first 240 images of the examination. For each phase, fluorescence enhancement in the joints was graded from 0–3 based on signal intensity (grade 1=diffuse red, grade 2=intense red and diffuse white 50% of the joint). To study the association between FOI findings and pain in the same joint we applied logistic regression analyses with generalised estimating equations adjusting for age and sex. Separate models were applied for each of the FOI phases and pain outcomes. Results The median (interquartile range) number of DIP/PIP joints with FOI enhancement within each patient ranged from 0 (0–0) in phase 1, 1411–16 in phase 2, 3 (0–8) in phase 3 and 97–11 in PVM. CMC-1 and MCP-joints showed no and uncommon enhancement on the examination, respectively, regardless of the phase, and the associations between FOI and pain were therefore analysed in the DIP and PIP joints only. FOI enhancement in the DIP and PIP joints was associated with pain in the same joint, consistent for all three pain outcomes. A dose-response relationship was found for phase 2, phase 3 and PVM, but not in phase 1 (table 1). Few joints showed enhancement in phase 1 and a clear dose-response relationship was found for pain during the last 24 hours only (data not shown). Conclusions In this first hand OA study, FOI enhancement was frequently found in the DIP and PIP joints, whereas the method seems insensitive to detect inflammation in the CMC-1 joints. FOI enhancement was related to self-reported pain and to tender joints on clinical examination, supporting the validity of the FOI examination in patients with hand OA. Disclosure of Interest None declared

Background Clinical disease activity in patients with psoriatic arthritis (PsA) may be assessed by DAPSA- a sum score of tender (of 68) and swollen (of 66) joints, CRP (mg/dl), patient’s global assessment of disease activity (PGA) and patient’s pain (0–10 VAS for both). Ultrasound (US) with grey scale (GS) and power Doppler (PD) is used to detect inflammation in joints as well as extra- articular structures. Discrepancies have previously been described between DAPSA and US.1 Objectives To explore the associations between DAPSA and US assessments of disease activity during follow-up of patients with PsA starting bDMARD treatment. Methods Patients with PsA were included when initiating bDMARDs, and examined at 0, 3, 6, 9 and 12 months including 66 swollen/68 tender joint counts (SJC/TJC), examinator’s global assessment VAS (EGA), patient reported outcome measures (PROMs; PGA, patient`s pain, RAID, MHAQ), laboratory measures (CRP, ESR, calprotectin) and US (46 joints, 8 flexor tendons, 14 entheses and 4 bursae with calculated GS and PD sum scores). DAPSA was calculated. PD sum score zero was defined as US remission. Generalised Estimating Equations (GEE) was used for longitudinal analysis. Results 47 patients (mean (SD) age 48.4 (12.8) years, disease duration 12.7 (10.9) years, 60% women) were included (68% biologic-naive). The figure depicts high correlation between DAPSA and subjective assessments at baseline, while PD sum score was more strongly associated with SJC (r=0.49, p Conclusions In our observational PsA cohort DAPSA was mostly influenced by TJC and patient`s pain and had no significant association with a comprehensive US examination. This finding indicates possible limitations of using DAPSA in T2T strategy in PsA. Reference [1] Michelsen B, et al. Ann Rheum Dis2016;75:2108–13. Disclosure of Interest None declared

Background A research network collaboration of 15 European registries sharing data on patients with spondyloarthitis (SpA), “EuroSpA”, has recently been created to strengthen research capabilities in the real world setting1. Here we present the first results from the collaboration. Objectives To investigate the feasibility of creating a common database for axial SpA (axSpA), including non-radiographic SpA and ankylosing spondylitis, within the EuroSpA collaboration and to conduct proof-of-concept analyses by investigation of baseline characteristics, disease activity at baseline and after 6 months, and crude 12 months’ Tumour Necrosis Factor inhibitor (TNFi) retention rate in patients with axSpA initiating TNFi. Methods A common data model was agreed upon by the EuroSpA Scientific Committee. Virtual meetings between the EuroSpA and registry data managers clarified data availability and structure. This was followed by upload of anonymized data through the secure Virtual Private Network pipelines to the EuroSpA server. Baseline characteristics and disease activity at baseline and after 6 months were investigated with non-parametric descriptive statistics. Kaplan-Meier estimation was used to investigate TNFi retention rates. Results By January 8th 2018, four of the 15 registries participating in EuroSpA had completed data upload to the EuroSpA database resulting in 6756 patients with AxSpA in a pooled dataset. Baseline characteristics of the participating registry populations at initiation of first TNFi are shown in Table I. Crude 12 months’ TNFi retention rate varied from 66%–85% for 1 st TNFi and 61%–78% for 2nd TNFi (see figure 1). For the pooled dataset crude 12 months’ TNFi retention rates were 73% and 66% for the 1 st and 2nd TNFi, respectively. Conclusions Preliminary analyses showed differences across European registries regarding baseline characteristics and crude retention rates in axSpA patients initiating TNFi. These initial, preliminary analyses demonstrate that the creation of a large European database of axSpA patients treated in routine care based on a common data model is feasible, offering important opportunities for future research. Reference [1] Ann Rheum Dis2017;(suppl. 2):65. Acknowledgements The authors acknowledge Novartis Pharmaceuticals AG for financial support and Natasha Pillai and Carol Lines from QuintilesIMS and Craig Richardson from Novartis Pharmaceuticals AG for their assistance in setting up the EuroSpA collaboration. Disclosure of Interest L. Ornbjerg: None declared, M. Ostergaard: None declared, F. Onen: None declared, G. Can: None declared, Z. Rotar: None declared, M. Tomsic Consultant for: AbbVie, Eli Lilly, Johnson and Johnson, Medis, MSD, Novartis, Pfizer and Roche, B. Gudbjornsson: None declared, A. Geirsson: None declared, M. Santos: None declared, A. Barcelos: None declared, D. Nordstrom Consultant for: AbbVie, Celgene, BMS, Lilly, MSD, Novartis, Pfizer, UCB, K. Aaltonen: None declared, M. J. Nissen: None declared, A. Ciurea: None declared, E. Kristianslund: None declared, T. Kvien Grant/research support from: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Epirus, Hospira, Merck-Serono, MSD, Mundipharma, Novartis, Orion Pharma, Hospira/Pfizer, Sandoz, UCB, C. Codreanu: None declared, E.-M. Hauge: None declared, L. Jacobsson: None declared, H. Mann: None declared, G. Jones: None declared, F. Iannone: None declared, M. V. Hernandez: None declared, I. van der Horst-Bruinsma: None declared, L. H. Hyldstrup: None declared, N. S. Krogh: None declared, M. Hetland Grant/research support from: AbbVie, Biogen, BMS, CellTrion, MSD, Orion, Pfizer, Samsung, UCB

Biosimilars represent a new opportunity for lowering the cost of treatment with biological disease-modifying antirheumatic drugs (bDMARDs). Studies have demonstrated large inequities in the access to bDMARDs across countries and this inequity is related to economic parameters such as gross domestic product. Thus, reduced costs of bDMARDs should potentially lead to better treatment for more patients, especially in countries with low economy. The regulatory agencies in Europe and in US have set up strict guidelines for approval of biosimilars which include extensive pre-clinical examinations (structure and functional characteristics) but less clinical data than for an originator product. The clinical part of this comparability exercise focuses on efficacy, safety, pharmacokinetics as well as immunogenicity. Three biosimilars to adalimumab have also been approved but the patent of the reference product has not yet expired (expected to occur October 2018). (expected to occur October 2018). It is a growing acceptance about the use of these biosimilars, also in extrapolated indications when treatment are started or changed for medical reasons. Most rheumatologists will consider the biosimilars on the same level as originator products in these situations. However, replacing an originator product by a biosimilar is more controversial, but is important because of the large cost-savings. Switching evidence is available from four different types of studies which will be discussed: Extension of phase 3 RCTs Switching within RCTs Real life data (eg from DANBIO) Randomising patients on stable long–term treatment In the NOR-SWITCH trial totally funded by the Norwegian government 482 patients on stable treatment with the reference product infliximab across 6 indications (RA, SpA, PsA, UC, CD, PsO) were randomised to continued treatment with the reference product or switch to the biosimilar CT-P13; Jorgensen KK et al. Lancet 2017389:2304–2316). The primary endpoint was occurrence of disease worsening, defined by the disease-specific composite measures or clinically significant worsening leading to a major change in treatment. Overall, disease worsening occurred in 26.2% of patients who continued treatment with the originator infliximab and in 29.6% of patients who switched to CT-13. The adjusted treatment difference (95% CI) was −4.4% (−12.7–3.9) which was within the prespecified non-inferiority margin of −15%. The occurrence of adverse events, including infusion reactions, was similar across both groups. There were no differences between the two groups in secondary endpoints, including time to study drug discontinuation, remission rates, CRP levels, anti-drug antibody formation and drug trough levels. The extension study (not yet published) showed that switching from originator to biosimilar was not inferior to continued treatment with the biosimilar. In conclusion, the NOR-SWITCH study demonstrated that switching to CT-P13 was not inferior to continued treatment with originator infliximab, adding to the increasing real-world evidence that switching from originator to biosimilar bDMARD is safe and efficacious. Disclosure of Interest T. Kvien Consultant for: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Epirus, Hospira, Merck-Serono, MSD, Mundipharma, Novartis, Oktal, Orion Pharma, Hospira/Pfizer, Roche, Sandoz and UCB

Background Tocilizumab (TCZ) as monotherapy was more efficacious than the TNF inhibitor (TNFi) adalimumab as monotherapy for treatment of rheumatoid arthritis (RA) patients refractory to methotrexate (MTX) or in whom MTX was deemed inappropriate (ADACTA study).1 However, data are lacking regarding the comparative real life effectiveness of TCZ as monotherapy versus TNFi combined with conventional synthetic DMARDS (csDMARDs). Objectives To analyse treatment effectiveness by comparing drug retention rates and disease activity level in RA patients naive to biological DMARDs (bDMARDs) treated with TCZ as monotherapy (TCZ mono) or TNFi combined with csDMARDs (TNFi combo). Methods We included patients with RA across 10 European registries (TOCERRA collaboration) who were naive to bDMARDs and received treatment with either TCZ mono or TNFi combo from 2009 to 2016. Drug retention rate was analysed using a Kaplan–Meier model. The proportions of patients reaching CDAI low disease activity (LDA) and remission after one year were adjusted for attrition with the LUNDEX index.2 Results A total of 6315 patients were eligible, 253 on TCZ mono and 6062 on TNFi combo. Patients with TCZ mono were younger, smoked less, and used less glucocorticoids at baseline compared with TNFi combo patients (table 1). The crude median retention was 2.8 years (95% CI: 2.0–3.3) and 2.0 years (95% CI: 1.8–2.1) for TCZ mono and TNFi combo, respectively (p=0.21). At 1 year, the rates of LUNDEX corrected CDAI LDA (CDAI ≤10) and remission (CDAI ≤2.8) were similar between both groups (figure 1). The results were unchanged when considering the type of combination with csDMARDs and the dosage of MTX. Conclusions In routine care across 10 European countries, the retention and proportion of RA patients in LUNDEX corrected CDAI LDA and remission at 1 year were similar if treated with TCZ mono or TNFi combo. References [1] Gabay C, et al. Lancet2013;381:1541–50. doi:10.1016/S0140-6736(13)60250-0 [2] Kristensen LE, et al. Arthritis Rheum2006;54:600–6. doi:10.1002/art.21570 Disclosure of Interest K. Lauper: None declared, T. Kvien Grant/research support from: AbbVie, BMS, MSD, Pfizer, Roche and UCB, Consultant for: AbbVie, BMS, Celgene, Celltrion, Eli Lilly, Hospira, Merck-Serono, MSD, Orion Pharma, Pfizer, Roche, Sandoz and UCB, C. Codreanu: None declared, M. Hernandez: None declared, F. Ianonne: None declared, E. Kristianslund: None declared, G. Lukina Consultant for: BMS, Roche, MSD, AbbVie and Pfizer, D. Nordstrom Grant/research support from: AbbVie, BMS, MSD, Pfizer, Roche and UCB, Consultant for: AbbVie, BMS, MSD, Roche, UCB and Pfizer, K. Pavelka Grant/research support from: AbbVie, Roche, Medis, MSD and Pfizer, Consultant for: AbbVie, Roche, Amgen, MSD, BMS, UCB and Egis, Z. Rotar: None declared, M. Santos: None declared, S. Gale Employee of: Genentech, M. John Employee of: F. Hoffmann-La Roche, Y. Luder Employee of: F. Hoffmann-La Roche, D. Courvoisier: None declared, C. Gabay Grant/research support from: Roche, AbbVie, MSD and Pfizer, Consultant for: AbbVie, BMS, Roche, Pfizer, Celgene, MSD, Janssen Cilag, Amgen, UCB

Background: Norway9s government funded the NOR-SWITCH study to investigate switching from originator infliximab (INX) to biosimilar CT-P13 in Crohn’s disease (CD), ulcerative colitis (UC), spondyloarthritis (SpA), rheumatoid arthritis (RA), psoriatic arthritis (PsA) and chronic plaque psoriasis (Ps). Previously, the main analyses have been published1. Immunogenicity is associated with treatment failure and is of particular concern in switching2. Objectives: To evaluate the consistency and fine specificity of anti-drug antibody (ADAb) responses to INX and CT-P13, in arthritis and IBD patients, after switching from INX to CT-P13. Methods: The study included adult patients with CD, UC, SpA, RA, PsA or Ps1. Assays for drug serum levels and ADAb have been described1. ADAb positive sera were tested for cross-reactivity to 5 batches of INX and CT-P13. We quantified IgG4 ADAb, testing for functional inhibition. Infliximab peptides were used to compare epitope recognition of positive sera. Immunogenic infliximab-epitopes were identified by ELISA and sera compared across diseases. Results: We tested 15 controls, 15 arthritis, 21 IBD patients. No Ps patients had ADAbs in our study. All 23 anti-CT-P13 and 13 anti-INX sera cross-reacted with INX and CT-P13, respectively. ADAb concentrations to INX or CT-P13 correlated strongly (r values between 0.92 and 0.99, p Conclusions: ADAbs to INX also recognize CT-P13, with similar epitopes. We found no consistent difference in ADAb epitope specificity between diagnoses. However, two specific minor epitopes are only recognized by IBD patients which might reflect the importance of HLA background for ADAb. References 1. Jorgensen KK, Olsen IC, Goll GL, et al. Switching from originator infliximab to biosimilar CT-P13 compared to maintained treatment with originator infliximab (NOR-SWITCH): a 52-week randomised double-blind non-inferiority trial. Lancet, 2017Jun 10;389(10086):2304–2316. [Epub 2017 May11]. 2. Dorner T, Jay J. Biosimilars in rheumatology: current perspectives and lessons learnt. Nat Rev Rheumatol2015Dec;11(12):713–24. Disclosure of Interest: G. Goll Consultant for: AbbVie, Biogen, Eli Lilly, Novartis, Pfizer, MSD, Roche, UCB, Boehringer Ingelheim, Orion Pharma, N. Bolstad Consultant for: Pfizer, Orion Pharma, Napp Pharmaceuticals, I. Iria: None declared, R. Klaasen: None declared, K. Jorgensen Consultant for: Tillott, Celltrion, Intercept, I. Olsen Consultant for: Pfizer, A. Valido: None declared, M. Saavedra: None declared, J. Fonseca Consultant for: AbbVie, Ache, Amgen, Biogen, BMS, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, UCB, K. Lundin Grant/research support from: MSD, Consultant for: Takeda, Orion, AbbVie, Rfizer, MSD, D. Warren: None declared, E. Haavardsholm Consultant for: AbbVie, Pfizer, MSD, Roche, UCB, J. Jahnsen Consultant for: AbbVie, Takeda, Janssen, Celltrion, Napp, AstroPharma, Hikma, Orion, Pfizer, T. Kvien Consultant for: AbbVie, Biogen, Eli Lilly, Novartis, Pfizer, MSD, Roche, UCB, Boehringer Ingelheim, Orion Pharma, J. Goncalves Consultant for: AbbVie, Amgen, Biogen, MSD, Pfizer

Background Measurement of serum drug levels can help clinicians tailor treatment with TNF-inhibitors. An association between certolizumab pegol (CP) serum levels and response has previously been found in patients (pts) with rheumatoid arthritis.1 Data for pts with axial spondyloarthritis (axSpA) are lacking. Objectives To examine the association between serum CP levels and treatment response in pts with axSpA and to identify a therapeutic target level. Methods Patients with a clinical diagnosis of axSpA starting standard treatment with CP included in the NOR-DMARD study with biobank sample at 3 months follow-up, were included in the present analyses. Serum drug levels (non-trough) were analysed with an in-house immunofluorometric assay automated on the AutoDELFIA immunoassay platform. Associations between CP level and improvement in ASDAS-CRP and response (defined as ASDAS clinically important improvement (CII)) were assessed by multivariable linear and logistic regression (adjusting for age, sex and prior bDMARD (Y/N)), respectively. Results Median serum drug level at 3 month follow up was 35.0 mg/L (IQR 21.3–45.3) in 116 pts. Response data were available in 110/116 patients. Serum CP level ≥20 mg/L was associated with improvement in ASDAS at 3 months (β=0.55, (95% CI 0.12–1.98), p=0.01). Serum CP level ≥20 mg/L was associated with ASDAS CII at 3 months (OR 3.4 (95% CI 1.0–11.1, p=0.045)). Only 18.2% of pts with CP level Conclusions Serum CP level was associated with clinical response after 3 months of treatment in pts with axSpA. We suggest 20 mg/L as a lower target level for non-trough samples. No additional benefit of having a certolizumab level over 40 mg/L was observed. These results suggest that a therapeutic level of 20–40 mg/L can be implemented in clinical practice for non-trough serum samples in pts with axSpA. Reference [1] Jani M, et al. Ann Rheum Dis2017;76(1):208–13. Disclosure of Interest J. E. Gehin Consultant for: Roche, S. Syversen Consultant for: Roche, D. Warren: None declared, G. Goll Consultant for: Abbvie, Biogen, Boehringer Ingelheim, Orion Pharma, Eli Lilly, Novartis, Pfizer, MSD, Roche, UCB, J. Sexton: None declared, E. Strand Consultant for: Pfizer, T. Kvien Consultant for: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Epirus, Hospira, Merck-Serono, MSD, Mundipharma, Novartis, Oktal, Orion Pharma, Hospira/Pfizer, Roche, Sandoz, UCB, N. Bolstad Consultant for: Pfizer, Orion Pharma, Napp pharmaceuticals, Takeda, Roche, E. Lie: None declared

Background Low adherence to medication is a concern in gout where urate lowering therapy (ULT) is indicated to prevent disease severity and comorbidities. The beliefs patients have about medication may impact on the success of achieving these treatment goals. Objectives To study which factors were associated to beliefs about medicines in patients with a recent gout attack and a need for ULT. Methods Baseline data from a prospective observational study were used in patients with crystal-proven gout who presented after a recent gout flare with insufficiently treated serum urate (sUA) level (>360 μmol/L/>6 mg/dl). In these patients a treat-to-target approach was planned to meet the treatment target (sUA The Beliefs in Medicines Questionnaire (BMQ)(1 assesses patient beliefs about medicines on four subscales: necessity and concerns specific for the patient, and generally on overuse and harm. Respondents indicated their degree of agreement with each individual statement about medicines on a 5-point Likert scale, (1=strongly disagree to 5=strongly agree). Scores within the four subscales (necessity, concerns, overuse, harm) were summed (ranges 5–25 and 4–20). Calculation of the necessity-concerns differential gave the relative importance for the patient for taking medicines. Results 163 patients were included at baseline, 93.3% men, 90.5% caucasian, mean (SD) age 57.0 (14.1) years, disease duration 8.0 (7.7) years). Mean sUA level was 487 (SD 82) µmol/L at baseline, body mass index 28.9 (4.7) kg/m2, comorbidity score (SCQ) 3.6 (3.2), and physical function (HAQ) 0.35 (0.55). 18.8% (n=28) had tophi, and 30.1% (n=43) were using allopurinol. Scores for the BMQ subscales (SD) were for necessity 16.8 (4.3), concerns 13.7 (5.0), overuse 10.6 (2.7), and harm 9.5 (2.4). The specific necessity-concerns differential was 3.1 (5.7), with median 2.5. Patients expressing higher versus lower beliefs in importance of medication (necessity-concern higher than median) demonstrated in bivariate comparisons statistically significantly differences (table 1). The level of serum urate was not associated with any BMQ subscale. In logistic regression analyses, also adjusting for age and gender in the final model, high beliefs in the relative importance of medication were independently associated with not using allopurinol medication (OR 0.41, 95% CI 0.18–0.94), with higher BMI (OR=1.11 per unit, 95% CI 1.02–1.20), and better mental health (SF36 MCS) (OR 1.04 per unit, 95% CI 1.01–1.08). Conclusions Unexpectedly, using allopurinol medication was inversely associated with high beliefs, whereas higher BMI and better mental health were positively associated with high beliefs in the importance of medication in gout patients. These findings do not allow conclusions on causality, and beliefs in medicines in gout patients should also be studied longitudinally and in relationship to therapy response. Reference [1] Horne R, et al. Psychology & Health1999;14(1):1–24. Disclosure of Interest None declared

Background The mortality rate in patients with rheumatoid arthritis (RA) has been estimated to be 1.5–1.6 compared to the general public. Moreover, RA patients are still not benefitting fully from the declining mortality rate that the general population has enjoyed and cardiovascular disease (CVD) continues to be a major concern. Objectives To examine the all-cause and CVD mortality in 3 consecutive cohorts of patients with incident RA, compared to population controls Methods The Oslo RA register (ORAR) was established in 1994. The inclusion criteria were a diagnosis of RA according to the 1987 ACR criteria and residency in Oslo. The register was updated annually until 2009, and validated for completeness. 1 In January 2012, 3328 patients were registered in ORAR. We grouped patients into 3 successive incidence cohorts; 1996(1994–1998), 2001 (1999–2003) and 2006(2004–2008). For each patient we identified 5 historical population controls matched according to age at disease incidence, gender and postal code of residence. Patients and controls were linked to the Norwegian Cause of Death Registry. Counts were compared using chi 2 tests. The hazard ratio (HR) for survival was calculated using stratified cox-regression models adjusted for highest achieved level of education. Results 422, 477 and 459 patients in the 1996, 2001 and 2006 cohorts were matched to 2110, 2385 and 2295 controls respectively. 20, 15 and 10 years follow-up for 1996, 2001 and 2006 cohorts were available in 201, 292 and 311 patients respectively. Results are presented in the table 1. Conclusions RA patients with disease incidence in the period 1994–2003 had increased all-cause and CVD related mortality after 10–15 years of disease duration, compared to the population of Oslo. The increased mortality was not observed in the 2004–2008 cohort. Improved survival in recent years may be related to more effective therapies and earlier diagnosis, but further analyses are warranted. Reference [1] Kvien, Uhlig. J Rheumatol2004. Disclosure of Interest None declared

Background: Patient Acceptable Symptom State (PASS) is the highest acceptable level of symptoms which patients consider satisfactory. In the Rheumatoid Arthritis Impact Disease (RAID) questionnaire, seven domains of health of importance for RA patients are collected.1. It is possible that levels judged acceptable by patients vary according to the domain of health. Objectives: To explore the relationship between seven RA domains of health (collected in the RAID) and PASS, and to define their PASS cut-off values. Methods: This is a post-hoc analysis of the cross-sectional study for RAID validation. Each of 7 domains (table 1) was evaluated through a Numeric Rating Scale from 0 (best) to 10 (worst). PASS was calculated using the anchored method based on patients’ perspective. Disease activity was assessed based on the DAS28–3 values (joint counts and ESR). Comparison of patients in PASS or not was assessed through Mann-Whitney or Chi-square test, as adequate. Variables with p Results: 549 patients [78% female, mean age 56.7 years, mean disease duration 12.3 years, mean (SD) DAS 28–3 2.7(1.2)] were analysed. The majority of patients (60.7%) considered themselves to be in PASS. Disease activity (DAS 28–3 mean 2.3 vs 3.4, p The cut-off for PASS was ≤4.2 for the total RAID score but varied across the seven domains (table 1), with Pain (≤5) and Fatigue (≤5) having the highest acceptability cut-offs. Sleep Disturbance and Coping were the domains with lowest thresholds compatible with PASS (≤3). Conclusions: Pain and physical well-being appeared as major drivers of PASS. The cut-offs defining PASS were not the same for all RAID domains, indicating that being in PASS doesn’t mean the same acceptable severity for all domains of health. This observation suggests that individualised management, for each domain, should be considered. Reference 1) Gossec L, et al. Ann Rheum Dis2011;70:935–942. Acknowledgements: RAID Study Group: Balanescu A, Boumpas DT, Carmona L, de Wit M, Dijkmans BA, Dougados M, Englbrecht M, Gogus F, Heiberg T, Kirwan JR, Mola EM, Cerinic MM, Otsa K, Sokka T Disclosure of Interest: None declared

Background: Measurement of serum drug levels can help clinicians tailor treatment with TNF-inhibitors. An association between certolizumab pegol (CP) serum levels and treatment response in rheumatoid arthritis (RA) patients (pts) has previously been demonstrated in a prospective observational study (1). These results need to be confirmed in other studies, with particular focus on finding an optimal therapeutic serum level for CP. Objectives: To examine the association between serum CP drug levels and treatment response in RA pts and to identify a therapeutic target level. Methods: Patients with a clinical diagnosis of RA starting standard treatment with CP included in the NOR-DMARD registry with biobank sample at 3 months follow-up, were included in the present analyses. Serum drug levels (non-trough) were analysed with an in-house immunofluorometric assay automated on the AutoDELFIA immunoassay platform. We studied association between serum CP level and xDAS28 and EULAR good/moderate response at 3 months by multivariable linear and logistic regression analyses, respectively, adjusting for age, sex and prior bDMARD (Y/N). Results: In 91 included patients, median serum drug level at 3 months follow up was 34.7 mg/L (17.6–44.6). Response data were available in 81/91 patients. Serum CP level ≥20 mg/L was associated with greater improvement in DAS28 at 3 months (β=0.89 (95% CI 0.03–1.74), P=0.04. 44.4 % of pts with CP level Conclusions: Certolizumab serum levels ≥20 mg/L were associated with DAS28 improvement, but not significantly with EULAR response after 3 months treatment in RA pts. We suggest 20 mg/L as a lower target limit for non-trough CP samples in RA-patients. No additional benefit of having a certolizumab level over 40 mg/L was observed. Reference [1]Jani M, et al. AnnRheum Dis2017;76(1):208–13. Disclosure of Interest: J. E. Gehin Consultant for: Roche, S. Syversen Consultant for: Roche, D. Warren: None declared, G. Goll Consultant for: Abbvie, Biogen, Boehringer Ingelheim, Orion Pharma, Eli Lilly, Novartis, Pfizer, MSD, Roche, UCB, J. Sexton: None declared, E. Strand Consultant for: Pfizer, T. Kvien Consultant for: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Epirus, Hospira, Merck-Serono, MSD, Mundipharma, Novartis, Oktal, Orion Pharma, Hospira/Pfizer, Roche, Sandoz, UCB, N. Bolstad Consultant for: Pfizer, Orion Pharma, Napp pharmaceuticals, Takeda, Roche, E. Lie: None declared

Background Rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPA) are used as diagnostic tools, but may also be used as prognostic factors, as these biomarkers have been associated with better clinical responses to some biologic agents in rheumatoid arthritis (RA). Objectives To compare the impact of seropositivity on drug discontinuation and effectiveness for abatacept (ABA) and TNF inhibitors (TNFi) in patients (pts) with RA. Methods Pooled analysis of 13 observational RA registries from countries (FR, IT, CZ, DK, NO, PT, RO, ES, SE, CH, NL, JP, CA) where both ABA and TNFi were available concomitantly. Inclusion criteria were RA diagnosis, treatment with ABA or TNFi, and available RF or ACPA status. Main exposure was seropositivity: positive if RF or ACPA were positive, negative if both were negative, and missing if one was missing and the other was negative. Primary endpoint was drug discontinuation, analysed using Cox models, including treatment, seropositivity, and their interaction, adjusting for patient-, treatment-, and disease-characteristics, using strata terms for country and calendar year. We first tested for effect modification by country by additionally including an interaction term between treatment, seropositivity and country. Since we found no effect modification, we took out the interaction term. Effectiveness was analysed using DAS28 remission and low disease activity (LDA) at 1 year, corrected for attrition using Lundex1. Results Using data from 39 266 treatment-courses, in crude analyses, seronegativity was associated with higher drug discontinuation for pts on ABA but not on TNFi (p interaction The proportion of pts reaching DAS28 remission or LDA at 1 year was significantly higher for seropositive vs seronegative pts on ABA (difference in proportion: remission: 5.0%; LDA: 9.7%), but similar for seropositive vs seronegative pts on TNFi (difference in proportion: remission: −2.7%; LDA: −2.3%). Conclusions Data from this large pooled registry suggests that seropositivity in RA pts is associated with increased drug retention and effectiveness for ABA but not for TNFi. Reference [1] Kristensen, et al. AR(54):600–6. Acknowledgements Unrestricted research grant from BMS Disclosure of Interest D. Courvoisier Consultant for: BMS, D. Mongin: None declared, M. Hetland Consultant for: Abbvie, Biogen, BMS, CellTrion, MSD, Novartis, Orion, Pfizer, Samsung, UCB, K. Pavelka Grant/research support from: Ministry of Health, Czech Republic 023728, Consultant for: AbbVie, Roche, MSD, BMS, Amgen, Egis, Medac, UCB, Pfizer, Biogen, C. Turesson Grant/research support from: Abbvie, Bristol Myers-Squibb, Roche. Consultant for: MSD, Bristol Myers-Squibb, Roche, Paid instructor for: Abbvie, Bristol-Myers Squibb, Janssen, MSD, Pfizer, Roche, UCB, S. A. Bergstra: None declared, T. Kvien Grant/research support from: AbbVie, BMS, MSD, Pfizer, Roche, UCB, Consultant for: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Epirus, Hospira, Merck-Serono, MSD, Mundipharma, Novartis, Oktal, Orion Pharma, Hospira/Pfizer, Roche, Sandoz, UCB, M. J. Santos: None declared, V. Hernandez: None declared, F. Iannone Consultant for: BMS, J.-E. Gottenberg Consultant for: BMS, X. Mariette Consultant for: BMS, S. Kubo Speakers bureau: BMS, Pfizer, Takeda, Y. Tanaka Grant/research support from: Mitsubishi-Tanabe, Takeda, Bristol-Myers, Chugai, Astellas, Abbvie, Daiichi-Sankyo, Pfizer, Eisai, Ono, Consultant for: Daiichi-Sankyo, Astellas, Pfizer, Mitsubishi-Tanabe, BMS, Chugai, YL Biologics, Eli Lilly, Sanofi, Janssen, UCB, D. Choquette: None declared, R. Ionescu: None declared, A. Finckh Grant/research support from: BMS, Consultant for: BMS, AbbVie, AB2BIO, MSD, Pfizer, Roche, UCB

Cardiovascular risk age and vascular age estimations in predicting cardiovascular events in rheumatoid arthritis patients

Background: Workforce requirement studies should be conducted in order to ensure the right number of people with the right skills, in the right place at the right time to deliver organizational objectives. Objectives: As part of the EULAR project to develop points to consider for the conduction of workforce studies in rheumatology, we reviewed the literature on workforce prediction with the aim to develop a workforce prediction quality appraisal tool and apply it to existing studies in rheumatology. Methods: Two literature searches were performed in Ovid MEDLINE, EMBASE, CINAHL, Cochrane Library and the grey literature comprising: (1) an update of a previous systematic literature review (SLR) of workforce prediction studies in rheumatology[1] and (2) a hierarchical SLR of workforce prediction studies in other medical fields. We extracted data on type of model used, details on need, demand and supply factors considered in the model, and other relevant aspects such as regional heterogeneity or uncertainty analyses. Based on the results, key general as well as specific need/demand, and supply factors for workforce calculation in rheumatology were identified and each factor was assigned a quality level (low, moderate, high). The quality appraisal tool was applied to the existing workforce modeling studies in rheumatology. Results: Data was extracted from 14 original workforce prediction studies in rheumatology and 10 SLRs in other fields. Studies used a variety of prediction models based on a heterogeneous set of need and/or demand and/or supply factors. While only a few studies attempted to empirically validate the prediction quality of the model (n=3), the consensus was that an integrated model including all these factors is expected to have the highest validity. Based on the different factors considered in existing studies, our quality appraisal tool included the three groups of factors: general factors (e.g. type of the model, stakeholder involvement), need/demand factors (e.g. scope of diseases covered by rheumatologists, morbidity, demography) and supply factors (e.g. time dedicated to clinical work, entry to profession, demographic composition of workforce) (table 1). The majority of studies scored low or moderate on most of the factors. Conclusions: The existing evidence on workforce prediction in rheumatology and other fields is scarce, heterogeneous and of low or moderate quality. The workforce prediction quality appraisal tool will enable future evaluation of workforce prediction studies. This review informs the EULAR points to consider for the conduction of workforce requirement studies in rheumatology. Reference 1. Dejaco C, et al. Arthritis Care Res (Hoboken)2016. Disclosure of Interest: None declared

Background In randomised controlled trials, subcutaneous tocilizumab (TCZ sc) has been found non-inferior to intravenous TCZ (TCZ iv) for the treatment of rheumatoid arthritis (RA) patients. However, to our knowledge, there are no observational studies comparing these two different routes of administration in routine care. Objectives To compare the real-world effectiveness of TCZ sc and TCZ iv in RA patients. Methods We included RA patients treated with TCZ from 8 European registries. We compared drug retention using Kaplan-Meier and Cox models. The proportions of patients achieving CDAI remission and low disease activity (LDA) at 1 year were compared using LUNDEX correction with computation of confidence intervals by bootstrapping.1 Results 2896 patients were retrieved from the collaborative registries before January 2017, including 2469 TCZ iv and 427 TCZ sc. Baseline demographics were similar between both groups, but patients in the TCZ iv group had a more severe disease activity, with higher DAS28, CDAI, tender joint count (TJC), swollen joint count (SJC), ESR and physician global assessment values (table 1). Crude median retention was 2.14 years (95% CI 2.03–2.33) for TCZ iv and 1.00 year for TCZ sc (95% CI 0.83–1.10), p 3.8%); CDAI LDA: 37.3% in TCZ iv vs.33.7% in TCZ sc (difference: −3.6%; bootstrap 95% CI: −9.4%; 2.5%)). Likewise, DAS28 remission and LDA at 1 year (LUNDEX corrected) were comparable between TCZ sc and TCZ iv (difference in DAS28 remission: −2.7%; bootstrap 95% CI: −8.8%; 3.5%; difference in DAS28 LDA: −5.8%; bootstrap 95% CI: −11.9%; 0.4%). Conclusions Drug retention and clinical effectiveness, assessed by CDAI and DAS28 changes and responses, were similar in both groups of patients, treated with TCZ sc or TCZ iv. Reference [1] Kristensen LE, et al. Arthritis Rheum2006;54:600–6. doi:10.1002/art.21570 Disclosure of Interest K. Lauper: None declared, M. Santos: None declared, F. Ianonne: None declared, Z. Rotar: None declared, D. Nordstrom Grant/research support from: AbbVie, BMS, MSD, Pfizer, Roche and UCB, Consultant for: AbbVie, BMS, MSD, Roche, UCB and Pfizer, C. Codreanu: None declared, T. Kvien: None declared, E. Kristianslund: None declared, K. Pavelka Grant/research support from: AbbVie, Roche, Medis, MSD and Pfizer, Consultant for: AbbVie, Roche, Amgen, MSD, BMS, UCB and Egis, G. Lukina Consultant for: BMS, Roche, MSD, AbbVie and Pfizer, M. Hernandez: None declared, S. Gale Employee of: Genentech, K. Sarsour Employee of: Genentech, Y. Luder Employee of: F. Hoffmann-La Roche, D. Courvoisier: None declared, C. Gabay Grant/research support from: Roche, AbbVie, MSD and Pfizer, Consultant for: AbbVie, BMS, Roche, Pfizer, Celgene, MSD, Janssen Cilag, Amgen, UCB

Background Erosive hand osteoarthritis (OA) is a phenotype characterised by more inflammation and erosions of the subchondral bone. Fluorescence optical imaging (FOI) is a novel imaging technique demonstrating altered microcirculation in wrist and finger joints as a sign of inflammation. No previous hand OA study has explored the validity of FOI against radiography. Objectives The aim of the current study was to explore the association between radiographic findings and FOI enhancement in the distal (DIP) and proximal interphalangeal (PIP) joints. Methods The NOR-HAND study is an observational hand OA study, in which 251 patients (88% female, median age 61 (interquartile range 56–66) years, 35% erosive hand OA) underwent FOI and x-rays of both hands. The FOI-scan was performed after the administration of an intravenous fluorescence dye (indocyanine green, ICG) and 360 images (1/second) were produced in 6 min. Based on the inflow and washing out of the dye the pictures were divided into 3 phases. Finally, the prima vista mode (PVM) represented a composite picture of the first 240 images of the examination. For each phase, fluorescence enhancement in the joints was graded from 0–3 based on signal intensity. Radiographic severity of the joints was evaluated with the Verbruggen Veys (VV) anatomical phase scoring system, which is based on the assumption that OA in finger joints will progress through different phases. To study whether more advanced radiographic phases were associated with FOI enhancement in the same joint, we applied logistic regression analyses with generalised estimating equations adjusting for age, sex, BMI and absence/presence of erosive hand OA, defined at patient level as having at least one DIP and PIP joint(s) in the erosive or remodelled phase. Results FOI demonstrated no and uncommon enhancement of the metacarpophalangeal and thumb base joints, respectively, thus we analysed DIP and PIP joints only. FOI enhancement was most commonly seen in phase 2 and PVM, also in the non-affected joints (table 1). The frequency of enhancement was lower for phase 3 and in particular for phase 1. Joints in the erosive phase had statistically significantly higher odds of FOI enhancement in phase 1, 2 and PVM as compared to the non-affected joints (table 1). Having erosive hand OA in other DIP and PIP joints was also associated with FOI enhancement (p Conclusions Joints in the erosive phase have more frequent FOI enhancement than non-affected joints. Furthermore, FOI enhancement in non-erosive phases is more common in patients with erosive vs non-erosive hand OA, suggesting that erosive hand OA is a more inflammatory phenotype. FOI enhancement in phase 2, 3 and PVM was common in joints without radiographic pathology, whereas enhancement in phase 1 was uncommon in joints with severe pathology. Thus, there is a need to consider other FOI scoring methods for the assessment of FOI enhancement in hand OA. Disclosure of Interest None declared