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ObjectiveTo compare the effectiveness of tumor necrosis factor inhibitors (TNFi) ± comedication and methotrexate (MTX) monotherapy between patients with adult juvenile idiopathic arthritis (JIA) and patients with rheumatoid arthritis (RA).MethodsAdult patients with JIA and RA were identified from the Norwegian Antirheumatic Drug Register (NOR-DMARD) register. Disease activity measurements at baseline, 3, 6, and 12 months were compared between patients with JIA and RA starting (1) TNFi and (2) MTX monotherapy, using age- and gender-weighted analyses. We calculated differences between JIA and RA in mean changes in Disease Activity Score in 28 joints (DAS28), Clinical Disease Activity Index (CDAI), and Simplified Disease Activity Index (SDAI), among other disease activity measures. DAS28, CDAI, SDAI, and American College of Rheumatology (ACR)/European Alliance of Associations for Rheumatology (EULAR) remission rates at 3, 6, and 12 months, as well as 6- and 12-month Lund Efficacy Index (LUNDEX)-corrected rates, were calculated.ResultsWe identified 478 patients with JIA (TNFi/MTX monotherapy, n = 358/120) and 4637 patients with RA (TNFi/MTX monotherapy, n = 2292/2345). Patients with JIA had lower baseline disease activity compared to patients with RA across treatment groups. After baseline disease activity adjustment, there were no significant differences in disease activity change from baseline to 3, 6, and 12-months of follow-up between patients with JIA and RA for either treatment group. Twelve-month remission rates were similar between groups based on DAS28 (TNFi: JIA 55.2%, RA 49.5%; MTX monotherapy: JIA 45.3%, RA 41.2%) and ACR/EULAR remission criteria (TNFi: JIA 20.4%, RA 20%; MTX monotherapy: JIA 17%, RA 12.7%). Median drug survival (yrs) was similar for JIA and RA in both treatment groups (TNFi: JIA 1.2, RA 1.4; MTX monotherapy: JIA 1.3, RA 1.6).ConclusionTNFi and MTX monotherapy are effective in adult JIA, with similar effectiveness to that shown in RA.

Objectives: To estimate the incidence of serious infections (SIs) in patients with rheumatoid arthritis (RA) and psoriatic arthritis (PsA) treated with tumour necrosis factor inhibitor (TNFi), and compare risk of SIs between patients with RA and PsA. Methods: We included patients with RA and PsA from the NORwegian-Disease Modifying Anti-Rheumatic Drug registry starting TNFi treatment. Crude incidence rates (IRs) and IR ratio for SIs were calculated. The risk of SIs in patients with RA and PsA was compared using adjusted Cox-regression models. Results: A total of 3169 TNFi treatment courses (RA/PsA: 1778/1391) were identified in 2359 patients. Patients with RA were significantly older with more extensive use of co-medication. The crude IRs for SIs were 4.17 (95% CI 3.52 to 4.95) in patients with RA and 2.16 (95% CI 1.66 to 2.81) in patients with PsA. Compared with the patients with RA, patients with PsA had a lower risk of SIs (HR 0.59, 95% CI 0.41 to 0.85, p=0.004) in complete set analysis. The reduced risk in PsA versus RA remained significant after multiple adjustments and consistent across strata based on age, gender and disease status. Conclusions: Compared with patients with RA, the risk of SIs was significantly lower in patients with PsA during TNFi exposure. Methods We included patients with RA and PsA from the NORwegian-Disease Modifying Anti-Rheumatic Drug registry starting TNFi treatment. Crude incidence rates (IRs) and IR ratio for SIs were calculated. The risk of SIs in patients with RA and PsA was compared using adjusted Cox-regression models. Results A total of 3169 TNFi treatment courses (RA/ PsA: 1778/1391) were identified in 2359 patients. Patients with RA were significantly older with more extensive use of co-medication. The crude IRs for SIs were 4.17 (95% CI 3.52 to 4.95) in patients with RA and 2.16 (95% CI 1.66 to 2.81) in patients with PsA. Compared with the patients with RA, patients with PsA had a lower risk of SIs (HR 0.59, 95% CI 0.41 to 0.85, p=0.004) in complete set analysis. The reduced risk in PsA versus RA remained significant after multiple adjustments and consistent across strata based on age, gender and disease status. Conclusions Compared with patients with RA, the risk of SIs was significantly lower in patients with PsA during TNFi exposure.

The objective of this study was to compare the efficacy and safety of rituximab in older vs younger patients with rheumatoid arthritis. Data on 367 patients with rheumatoid arthritis treated with rituximab in the Norwegian Disease-Modifying Antirheumatic Drug (NOR-DMARD) register were analysed, comparing patients aged ≥ 65 years (n = 91) with patients aged

To assess the 2-year effect on disease activity and health-related quality of life (HRQoL) of implementing a clinical practice treat-to-target (T2T) strategy in patients with rheumatoid arthritis (RA).Patients in the Norwegian Very Early Arthritis Cohort 2.0 (NOR-VEAC 2.0), included 2010-2015, were treated according to T2T principles with visits at baseline, 3, 6, 9, 12 months, then every 6 months plus monthly visits until DAS28 2.6. These patients were compared to a pre-T2T cohort of patients included in the Norwegian Disease Modifying Anti-Rheumatic Drug (NOR-DMARD) register 2006-2009. Both groups had a clinical diagnosis of RA (≤1 year) and were DMARD naïve. Disease activity and HRQoL outcomes were analysed, and the primary outcome was SDAI remission (≤3.3) at 2years.The T2T cohort included 293 patients (mean (SD) age 54 (13) years, 66% females, disease duration median (25,75 perc) 98 (57,164) days) and the routine care cohort 392 patients (age 54 (13) years, 68% females, 4 (0,30) days since diagnosis). At 2years, the proportion of patients achieving SDAI remission was 46% in the T2T cohort compared to 31% in the routine care cohort. EQ-5D was similar at baseline, but differed significantly between groups at 2years (median (25,75 perc) 0.77 (0.69, 0.85) vs 0.73 (0.59, 0.80), p 0.001). Methotrexate monotherapy was the dominant DMARD regimen used to achieve SDAI remission in both cohorts.Higher remission rates and better HRQoL were achieved in patients following a T2T strategy in clinical practice compared to routine care.

IntroductionIn the multisystem inflammatory disorder systemic sclerosis (SSc), gastrointestinal tract (GIT) affliction is highly prevalent. There are no known disease modifying therapies and the negative impact is substantial. Aiming for a new therapeutic principle, and inspired by recent work showing associations between gut microbiota changes and GIT symptoms in SSc, we performed a pilot study on faecal microbiota transplantation (FMT) with the single-donor bacterial culture ‘Anaerobic Cultivated Human Intestinal Microbiome (ACHIM)’. Motivated by positive pilot study signals, we designed the ReSScue trial as a phase II multicentre, placebo-controlled, randomised 20-week trial to evaluate safety and efficacy on lower GIT symptoms of FMT by ACHIM in SSc.Methods and analysesWe aim to include 70 SSc participants with moderate to severe lower GIT symptoms, defined by the validated patient-reported University of California Los Angeles Scleroderma Clinical Trial Consortium GIT 2.0 2.0 questionnaire. The trial includes three parts. In part A1 (induction phase) lasting from week 0 to week 12, participants will be randomised 1:1 to repeat infusions of 30 mL ACHIM or placebo at week 0 and 2 by gastroduodenoscopy. In part A2, which is an 8-week subsequent maintenance phase, all study participants will receive 30 mL ACHIM at week 12 and followed until week 20 on continued blind. In part B, which will last until the last participant completes part A2, the participants will be followed through a maximum 16-week extended monitoring period, for longer-term data on safety and intervention effects. Primary endpoint is change from baseline to week 12 in UCLA GIT subscale scores of diarrhoea or bloating, depending on the worst symptom at baseline evaluated separately for each patient. Secondary endpoints are safety measures and changes in UCLA GIT scores (total, diarrhoea and bloating).Ethics and disseminationThis protocol was approved by the Northern Norwegian Committee for Medical Ethics. Study findings will be published.Trial registration numberNCT04300426; Pre-results.Protocol versionV.3.1.

This randomized trial compares the effects of half-dose conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) vs stable-dose csDMARDs on the risk of flares in patients with rheumatoid arthritis in sustained remission.Importance Sustained remission has become an achievable goal for patients with rheumatoid arthritis (RA) receiving conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), but how to best treat patients in clinical remission remains unclear. Objective To assess the effect of tapering of csDMARDs, compared with continuing csDMARDs without tapering, on the risk of flares in patients with RA in sustained remission. Design, Setting, and Participants ARCTIC REWIND was a multicenter, randomized, parallel, open-label noninferiority study conducted in 10 Norwegian hospital-based rheumatology practices. A total of 160 patients with RA in remission for 12 months who were receiving stable csDMARD therapy were enrolled between June 2013 and June 2018, and the final visit occurred in June 2019. Interventions Patients were randomly assigned to half-dose csDMARDs (n = 80) or stable-dose csDMARDs (n = 80). Main Outcomes and Measures The primary end point was the proportion of patients with a disease flare between baseline and the 12-month follow-up, defined as a combination of Disease Activity Score (DAS) greater than 1.6 (threshold for RA remission), an increase in DAS score of 0.6 units or more, and at least 2 swollen joints. A disease flare could also be recorded if both the patient and investigator agreed that a clinically significant flare had occurred. A risk difference of 20% was defined as the noninferiority margin. Results Of 160 enrolled patients (mean [SD] age, 55.1 [11.9] years; 66% female), 156 received the allocated therapy, of which 155 without any major protocol violations were included in the primary analysis population (77 receiving half-dose and 78 receiving stable-dose csDMARDs). Flare occurred in 19 patients (25%) in the half-dose csDMARD group compared with 5 (6%) in the stable-dose csDMARD group (risk difference, 18% [95% CI, 7%-29%]). Adverse events occurred in 34 patients (44%) in the half-dose group and 42 (54%) in the stable-dose group, none leading to study discontinuation. No deaths occurred. Conclusions and Relevance Among patients with RA in remission taking csDMARD therapy, treatment with half-dose vs stable-dose csDMARDs did not demonstrate noninferiority for the percentage of patients with disease flares over 12 months, and there were significantly fewer flares in the stable-dose group. These findings do not support treatment with half-dose therapy.Question In patients with rheumatoid arthritis in remission taking conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), is reducing the csDMARDs to half dose noninferior to stable csDMARD dosage for the outcome of rheumatoid arthritis flares? Findings In this randomized clinical trial that included 160 patients with rheumatoid arthritis in remission taking csDMARD therapy, treatment with half-dose vs stable-dose csDMARDs resulted in disease flares in 25% vs 6% over 12 months; this did not meet the noninferiority criterion of a 20% difference. There were significantly fewer patients with flares in the stable-dose group. Meaning These findings do not support the use of half-dose treatment in patients with rheumatoid arthritis in remission taking csDMARDs.

Objective To evaluate and compare benefits and harms of three biological treatments with different modes of action versus active conventional treatment in patients with early rheumatoid arthritis. Design Investigator initiated, randomised, open label, blinded assessor, multiarm, phase IV study. Setting Twenty nine rheumatology departments in Sweden, Denmark, Norway, Finland, the Netherlands, and Iceland between 2012 and 2018. Participants Patients aged 18 years and older with treatment naive rheumatoid arthritis, symptom duration less than 24 months, moderate to severe disease activity, and rheumatoid factor or anti-citrullinated protein antibody positivity, or increased C reactive protein. Interventions Randomised 1:1:1:1, stratified by country, sex, and anti-citrullinated protein antibody status. All participants started methotrexate combined with (a) active conventional treatment (either prednisolone tapered to 5 mg/day, or sulfasalazine combined with hydroxychloroquine and intra-articular corticosteroids), (b) certolizumab pegol, (c) abatacept, or (d) tocilizumab. Main outcome measures The primary outcome was adjusted clinical disease activity index remission (CDAI≤2.8) at 24 weeks with active conventional treatment as the reference. Key secondary outcomes and analyses included CDAI remission at 12 weeks and over time, other remission criteria, a non-inferiority analysis, and harms. Results 812 patients underwent randomisation. The mean age was 54.3 years (standard deviation 14.7) and 68.8% were women. Baseline disease activity score of 28 joints was 5.0 (standard deviation 1.1). Adjusted 24 week CDAI remission rates were 42.7% (95% confidence interval 36.1% to 49.3%) for active conventional treatment, 46.5% (39.9% to 53.1%) for certolizumab pegol, 52.0% (45.5% to 58.6%) for abatacept, and 42.1% (35.3% to 48.8%) for tocilizumab. Corresponding absolute differences were 3.9% (95% confidence interval −5.5% to 13.2%) for certolizumab pegol, 9.4% (0.1% to 18.7%) for abatacept, and −0.6% (−10.1% to 8.9%) for tocilizumab. Key secondary outcomes showed no major differences among the four treatments. Differences in CDAI remission rates for active conventional treatment versus certolizumab pegol and tocilizumab, but not abatacept, remained within the prespecified non-inferiority margin of 15% (per protocol population). The total number of serious adverse events was 13 (percentage of patients who experienced at least one event 5.6%) for active conventional treatment, 20 (8.4%) for certolizumab pegol, 10 (4.9%) for abatacept, and 10 (4.9%) for tocilizumab. Eleven patients treated with abatacept stopped treatment early compared with 20-23 patients in the other arms. Conclusions All four treatments achieved high remission rates. Higher CDAI remission rate was observed for abatacept versus active conventional treatment, but not for certolizumab pegol or tocilizumab versus active conventional treatment. Other remission rates were similar across treatments. Non-inferiority analysis indicated that active conventional treatment was non-inferior to certolizumab pegol and tocilizumab, but not to abatacept. The results highlight the efficacy and safety of active conventional treatment based on methotrexate combined with corticosteroids, with nominally better results for abatacept, in treatment naive early rheumatoid arthritis. Trial registration EudraCT2011-004720-35, NCT01491815 .

ObjectivesTo investigate if inflammation detected by MRI or ultrasound at rheumatoid arthritis (RA) onset is predictive of erosive progression or poor response to methotrexate monotherapy, and to investigate if subclinical inflammation in remission is predictive of future treatment escalation or erosive progression.MethodsIn a 2-year study, 218 patients with disease-modifying antirheumatic drug-naïve early RA were treated by a tight-control treat-to-target strategy corresponding to current recommendations. MRI and ultrasound were performed at regular intervals. Baseline imaging-based inflammation measures were analysed as predictors for early methotrexate failure and erosive progression using univariate and multivariate regression adjusted for clinical, laboratory and radiographic measures. In patients in remission after 1 year, imaging measures were analysed as predictors of treatment escalation and erosive progression during the second year. The added value of imaging in prediction models was assessed using receiver operating characteristic analyses.ResultsBaseline MRI inflammation was associated with MRI erosive progression and ultrasound with radiographic erosive progression. No imaging inflammation measure was associated with early methotrexate failure. Imaging inflammation was present in a majority of patients in clinical remission. Tenosynovitis was associated with treatment escalation, and synovitis and tenosynovitis with MRI/radiographic erosive progression during the second year. Imaging information did not improve prediction models for any of the outcomes.ConclusionsImaging-detected inflammation, both at diagnosis and in remission, is associated with elements of future disease development. However, the lack of a significant effect on prediction models indicates limited value of systematic MRI and ultrasound in management of early RA.

Objective To investigate the prevalence of overweight and obesity, as well as the association between body mass index (BMI) and disease activity in patients with axial spondyloarthritis (axSpA). Methods Norwegian axSpA patients from the European Map of Axial Spondyloarthritis (EMAS) survey were included in this analysis. Sociodemographic, anthropomorphic, and disease-related variables (HLA-B27, comorbidities, BASDAI, and self-reported spinal stiffness) were reported. Patients were categorized into under/normal weight (BMI 2), overweight (BMI ≥ 25 to 2), and obese (≥ 30 kg/m2). Results Of the 509 participants in the EMAS survey, 35% were categorized as under/normal weight, 39% overweight, and 26% obese. Compared to under/normal-weight patients, overweight patients had significantly higher degree of spinal stiffness (mean (SD) 7.91 ± 2.02 vs 7.48 (2.15) and number of comorbidities (2.45 ± 2.11, vs 1.94), both p p p = 0.006), and number of comorbidities (3.43 ± 2.43 vs 1.94. ± .38, p Conclusion Obesity was associated with higher reported BASDAI score, and being overweight or obese was associated with a higher degree of spinal stiffness and number of comorbidities compared to under/normal weight respondents. The results highlight the serious impact of obesity on health status, and obesity should therefore be considered as a modifiable risk factor for disease activity within the disease management of axSpA.

OP0018 (2020) A MULTICENTER RANDOMIZED STUDY IN EARLY RHEUMATOID ARTHRITIS TO COMPARE ACTIVE CONVENTIONAL THERAPY VERSUS THREE BIOLOGICAL TREATMENTS: 24 WEEK EFFICACY RESULTS OF THE NORD-STAR TRIAL M. L. Hetland1, E. A. Haavardsholm1, A. Rudin1, D. Nordström1, M. Nurmohamed1, B. Gudbjornsson1, J. Lampa1, K. Hørslev-Petersen1, T. Uhlig1, G. Gröndal1, M. Ǿstergaard1, M. Heiberg1, J. Twisk1, S. Krabbe1, K. Lend1, I. Olsen1, J. Lindqvist1, A. K. H. Ekwall1, K. L. Grøn1, M. C. Kapetanovic1, F. Faustini1, R. Tuompo1, T. Lorenzen1, G. Cagnotto1, E. Baecklund1, O. Hendricks1, D. Vedder1, T. Sokka-Isler1, T. Husmark1, M. K. A. Ljosa1, E. Brodin1, T. Ellingsen1, A. Soderbergh1, M. Rizk1, Å. Reckner1, P. Larsson1, L. Uhrenholt1, S. A. Just1, D. Stevens1, T. B. Laurberg1, G. Bakland1, R. Van Vollenhoven1 1Denmark, Finland, Iceland, Netherlands, Norway, Sweden Background: The optimal first-line treatment of patients (pts) with early rheumatoid arthritis (RA) is yet to be established. Objectives: The primary aim was to assess and compare the proportion of pts who achieved remission with active conventional therapy (ACT) and with three different biologic therapies after 24 wks. Secondary aims were to assess and compare other efficacy measures. Methods: The investigator-initiated NORD-STAR trial (NCT01491815) was conducted in the Nordic countries and Netherlands. In this multicenter, randomized, open-label, blinded-assessor study pts with treatment-naïve, early RA with DAS28>3.2, and positive RF or ACPA, or CRP >10mg/L were randomized 1:1:1:1. Methotrexate (25 mg/week after one month) was combined with: 1) (ACT): oral prednisolone (tapered quickly); or : sulphasalazine, hydroxychloroquine and mandatory intra-articular (IA) glucocorticoid (GC) injections in swollen joints

Copyright Nature Research. Source at https://doi.org/10.1038/s41598-018-26265-z. Tertiary lymphoid structures (TLS) develop in the kidneys of lupus-prone mice and systemic lupus erythematosus (SLE) patients with lupus nephritis (LN). Here we investigated the presence of mesenchymal stem cells (MSCs) in the development of TLS in murine LN, as well as the role of human MSCs as lymphoid tissue organizer (LTo) cells on the activation of CD4+ T cells from three groups of donors including Healthy, SLE and LN patients. Mesenchymal stem like cells were detected within the pelvic wall and TLS in kidneys of lupus-prone mice. An increase in LTβ, CXCL13, CCL19, VCAM1 and ICAM1 gene expressions were detected during the development of murine LN. Human MSCs stimulated with the pro-inflammatory cytokines TNF-α and IL-1β significantly increased the expression of CCL19, VCAM1, ICAM1, TNF-α, and IL-1β. Stimulated MSCs induced proliferation of CD4+ T cells, but an inhibitory effect was observed when in co-culture with non-stimulated MSCs. A contact dependent increase in Th2 and Th17 subsets were observed for T cells from the Healthy group after co-culture with stimulated MSCs. Our data suggest that tissue-specific or/and migratory MSCs could have pivotal roles as LTo cells in accelerating early inflammatory processes and initiating the formation of kidney specific TLS in chronic inflammatory conditions.

Renal DNase I is lost in advanced stages of lupus nephritis. Here, we determined if loss of renal DNase I reflects a concurrent loss of urinary DNase I, and whether absence of urinary DNase I predicts disease progression. Mouse and human DNase I protein and DNase I endonuclease activity levels were determined by western blot, gel, and radial activity assays at different stages of the murine and human forms of the disease. Cellular localization of DNase I was analyzed by immunohistochemistry, immunofluorescence, confocal microscopy, and immunoelectron microscopy. We further compared DNase I levels in human native and transplanted kidneys to determine if the disease depended on autologous renal genes, or whether the nephritic process proceeded also in transplanted kidneys. The data indicate that reduced renal DNase I expression level relates to serious progression of lupus nephritis in murine, human native, and transplanted kidneys. Notably, silencing of renal DNase I correlated with loss of DNase I endonuclease activity in the urine samples. Thus, urinary DNase I levels may therefore be used as a marker of lupus nephritis disease progression and reduce the need for renal biopsies.

Objective The European guidelines on cardiovascular disease (CVD) prevention advise use of relative risk and risk age algorithms for estimating CVD risk in patients with low estimated absolute risk. Patients with inflammatory joint diseases (IJD) are associated with increased risk of CVD. We aimed to estimate relative risk and risk age across IJD entities and evaluate the agreement between ‘cardiovascular risk age' and ‘vascular age models'. Methods Using cross-sectional data from a nationwide project on CVD risk assessment in IJD, risk age estimations were performed in patients with low/moderate absolute risk of fatal CVD. Risk age was calculated according to the cardiovascular risk age and vascular age model, and risk age estimations were compared using regression analysis and calculating percentage of risk age estimations differing ≥5years. Results Relative risk was increased in 53% and 20% had three times or higher risk compared to individuals with optimal CVD risk factor levels. Furthermore, 20–42% had a risk age ≥5years higher than their actual age, according to the specific risk age model. There were only minor differences between IJD entities regarding relative risk and risk age. Discrepancies ≥5years in estimated risk age were observed in 14–43% of patients. The largest observed difference in calculated risk age was 24years. Conclusion In patients with low estimated absolute risk, estimation of relative CVD risk and risk age may identify additional patients at need of intensive CVD preventive efforts. However, there is a substantial discrepancy between the risk age models.

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:The optimal first-line treatment of patients (pts) with early rheumatoid arthritis (RA) is yet to be established.Objectives:The primary aim was to assess and compare the proportion of pts who achieved remission with active conventional therapy (ACT) and with three different biologic therapies after 24 wks. Secondary aims were to assess and compare other efficacy measures.Methods:The investigator-initiated NORD-STAR trial (NCT01491815) was conducted in the Nordic countries and Netherlands. In this multicenter, randomized, open-label, blinded-assessor study pts with treatment-naïve, early RA with DAS28>3.2, and positive RF or ACPA, or CRP >10mg/L were randomized 1:1:1:1. Methotrexate (25 mg/week after one month) was combined with: 1) (ACT): oral prednisolone (tapered quickly);or: sulphasalazine, hydroxychloroquine and mandatory intra-articular (IA) glucocorticoid (GC) injections in swollen joints Results:812 pts were randomized. Age was 54.3±14.7 yrs (mean±SD), 31.2% were male, DAS28 5.0±1.1, 74.9% were RF and 81.9% ACPA positive. Fig 1 shows the adjusted CDAI remission rates over time with 95% CI. Table shows crude remission and response rates and absolute differences in adjusted remission and response rates (superiority analysis). Differences in remission and response rates with CZP and TCZ, but not with ABA, remained within the pre-defined non-inferiority margin versus ACT, Fig 2.Figure 1.CDAI remission over time (adj. estimates with 95% CI)Figure 2.Non-inferiority analysis of protocol population. Estimated differences in CDAI remission rates between Arm 1 (active conventional therapy) and Arms 2, 3, and 4 (biologic arms) as reference with 95% confidence intervals, adjusted for gender, ACPA status, country, age, body-mass index and baseline DAS28-CRP. ABA, abatacept; CZP, certolizumab-pegol; MTX, methotrexate; TCZ, tocilizumab.Conclusion:High remission rates were found across all four treatment arms at 24 wks. Higher CDAI remission rate was observed for ABA versus ACT (+9%) and for CZP (+4%), but not for TCZ (-1%). With the predefined 15% margin, ACT was non-inferior to CZP and TCZ, but not to ABA. This underscores the efficacy of active conventional therapy based on MTX combined with glucocorticoids and may guide future treatment strategies for early RA.Table.Primary and key secondary outcomes at 24 weeks (ITT)Active conventional therapy (ACT)Certolizumab+MTXAbatacept+MTXTocilizumab+MTXNo of pts (ITT)200203204188§Crude remission and response ratesCDAI remission42.0%47.8%52.5%41.0%ACR/EULAR Boolean remission34.0%38.4%37.3%31.4%DAS28 remission63.5%68.5%69.6%63.3%SDAI remission41.5%49.8%51.5%42.6%EULAR good response71.5%76.9%79.9%71.3%Difference (95% CI) in rates with Arm 1 as reference (adjusted)CDAI remissionRef4% (-5 to 13%)9% (0.1 to 19%)-1% (-10 to 9%)ACR/EULAR Boolean remissionRef4% (-6 to 13%)5% (-5 to 14%)-4% (-13 to 6%)DAS28 remissionRef3% (-6 to 11%)5% (-4 to 13%)-1% (-10 to 8%)SDAI remissionRef6% (-3 to 18%)9% (-0.3 to 18%)1% (-8 to 11%)EULAR good responseRef4% (-4 to 14%)8% (-2 to 18%)0.4% (-10 to 11%)§17 patients allocated to Tocilizumab did not receive it due to its unavailability and were excluded from ITT.Acknowledgments:Manufacturers provided CZP and ABA.Disclosure of Interests: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, 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, Anna Rudin Consultant of: Astra/Zeneca, Dan Nordström Consultant of: Abbvie, Celgene, Lilly, Novartis, Pfizer, Roche and UCB., Speakers bureau: Abbvie, Celgene, Lilly, Novartis, Pfizer, Roche and UCB., Michael Nurmohamed Grant/research support from: Not related to this research, Consultant of: Not related to this research, Speakers bureau: Not related to this research, Björn Gudbjornsson Speakers bureau: Novartis and Amgen, Jon Lampa Speakers bureau: Pfizer, Janssen, Novartis, Kim Hørslev-Petersen: None declared, Till Uhlig Consultant of: Lilly, Pfizer, Speakers bureau: Grünenthal, Novartis, Gerdur Gröndal: None declared, 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, Marte Heiberg: None declared, Jos Twisk: None declared, Simon Krabbe: None declared, Kristina Lend: None declared, Inge Olsen: None declared, Joakim Lindqvist: None declared, Anna-Karin H Ekwall Consultant of: AbbVie, Pfizer, Kathrine L. Grøn Grant/research support from: BMS, Meliha C Kapetanovic: None declared, Francesca Faustini: None declared, Riitta Tuompo: None declared, Tove Lorenzen: None declared, Giovanni Cagnotto: None declared, Eva Baecklund: None declared, Oliver Hendricks Grant/research support from: Pfizer, MSD, Daisy Vedder: None declared, Tuulikki Sokka-Isler: None declared, Tomas Husmark: None declared, Maud-Kristine A Ljosa: None declared, Eli Brodin: None declared, Torkell Ellingsen: None declared, Annika Soderbergh: None declared, Milad Rizk Speakers bureau: AbbVie, Åsa Reckner: None declared, Per Larsson: None declared, Line Uhrenholt Speakers bureau: Abbvie, Eli Lilly and Novartis (not related to the submitted work), Søren Andreas Just: None declared, David Stevens: None declared, Trine Bay Laurberg Consultant of: UCB Pharma (Advisory Board), Gunnstein Bakland Consultant of: Novartis, UCB, Ronald van Vollenhoven Grant/research support from: BMS, GSK, Lilly, UCB, Pfizer, Roche, Consultant of: AbbVie, AstraZeneca, Biogen, Biotest, Celgene, Gilead, Janssen, Pfizer, Servier, UCB, Speakers bureau: AbbVie, Pfizer, UCB

Background: Obesity increases the risk of developing chronic inflammatory diseases, including axial spondyloarthritis (axSpA)1,2. Information about how obesity correlates with disease activity in axSpA patients is limited. Objectives: The objective of this survey was to investigate the association between body mass index (BMI) and patient reported disease activity in Norwegian axSpA patients. Methods: The European Map of Axial Spondyloarthritis (EMAS), conducted from July 2017 to February 2018, was a cross-sectional on-line survey of 2,846 unselected patients with self-reported axSpA from 13 European countries (Austria, Belgium, France, Germany, Italy, Netherlands, Norway, Russia, Slovenia, Spain, Sweden, Switzerland, and the UK). Participants were recruited through an on-line panel and patient organizations. This analysis is based on data from the 509 Norwegian respondents. Sociodemographic variables (age, gender, BMI, comorbidity), and disease related variables (Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) (0-10), self-reported spinal stiffness (3-12) and General Health Questionnaire (0-12) (GHQ-12)) were reported. Results: Out of the 509 Norwegian participants with axSpA, 69.7% (N:355) were women. The mean age was 48±12 years, mean disease duration was 5.3±2.0 years, 82.3% were HLA-B27 positive, and 55.2% (N:281) were university educated. In total, 35% (N:180) of the participants were normal/underweight (BMI 25). The mean (sd) disease activity, as measured by BASDAI (0-10), was 5.3±2.0. Overweight/obese patients reported significantly higher disease activity (BASDAI 5.5±1.9) compared to normal weight patients (BASDAI 5.0± 2.1). Moreover, being overweight/obese was associated with a significantly higher degree of spinal stiffness, number of comorbidities and a numerically, but not significantly, higher GHQ-12 score. There was no significant differences in alcohol consumption, smoking, or prevalence of inflammatory bowel disease (Crohn’s disease or ulcerative colitis). Conclusion: Norwegian overweight/obese axSpA patients from the EMAS survey report significantly higher disease activity, spinal stiffness and number of comorbidities. The results highlight the serious impact of overweight and obesity on the health status of axSpA patients. Therefore, obesity should be considered as a preventable risk factor and within the disease management of axSpA. References [1] Maas, et al. Obesity Is Common in Axial Spondyloarthritis and Is Associated with Poor Clinical Outcome. The Journal of Rheumatology2016; 43 (2) 383-387. [2] Shan, et al. Impact of obesity on the efficacy of different biologic agents in inflammatory diseases: A systematic review and meta-analysis. Joint Bone Spine. 2018, in press. Acknowledgement: EMAS was funded by Novartis Pharma AG Disclosure of Interests: Christian Bindesboll Employee of: I currently work in Novartis Pharma AG Norway as listed in my affiliations, Marco Garrido-Cumbrera Consultant for: Honoraria from Novartis as steering committe of this survey, Gunnstein Bakland: None declared, Hanne Solveig Dagfinrud Consultant for: Honoraria from Novartis as a steering committee member on this survey

Background: In Norway encouraged by the health authorities non-medical switch from reference drug to biosimilar drug has been performed in most patients on biologic reference drugs with biosimilar drugs available, including etanercept. There is a need for real life data understanding the effect of biosimilar drugs when these drugs are introduced in clinical practice. Objectives: To explore drug survival for biosimilar SB4 etanercept in RA patients, both etanercept naive and non-medical switch patients, and compare with the etanercept reference drug. Methods: Preliminary 2 years drug survival data from one center in a 5 center study in Norway exploring drug survival for etanercept reference drug and biosimilar etanercept SB4 is presented. At this outpatient clinic RA patients as part of standard clinical care has been monitored systematically since 2003. Drug survival for SB4 etanercept, both the etanercept naive and the non-medical SB4 switch group, was compared with patients treated with the etanercept reference drug in the period 2003-2018. Baseline demographic, clinical and treatment data were retrieved and analyzed. Kaplan-Meier survival curves were used to explore 2 years drug survival. Survival differences between groups were tested using Breslow statistics. Results: At the outpatient clinic the number of RA patients treated with etanercept reference drug was 356, the number of patients treated with SB4 with no previous etanercept was 36 and the patients with a non-medical switch from reference etanercept to etanercept SB4 was 84. In the table below baseline demographics and disease measures are shown for the etanercept reference group, the non-medical SB4 switch group and the SB4 naive to etanercept group. Data in table are presented as percentage for group variables and as mean with standard deviation (SD) for continuous variables. Mean (95%CI) drug survival for the non-medical SB4 switch group was1.53 (1.38-1.68) years, for the SB4 group with no previous etanercept 1.23 (0.95-1.51) years and for etanercept reference group 1.38 (1.31-1.46) years. A statistically significant difference (p In the figure below Kaplan-Meier drug survival curves are shown. Conclusion: To the best of our knowledge this is the first data showing that drug survival of an etanercept biosimilar drug after a non-medical switch is higher than a historical cohort of etanercept reference drug. This is expected, since it is a selected group of etanercept responders. The interpretation of the results should be cautious, since only few patients are included in this first analysis. A larger number of patients from other participating out-patient clinics is planned to be included. Disclosure of Interests: Glenn Haugeberg Grant/research support from: For this study grant from Biogen, Consultant for: Medical Advisory boards for several companies, Paid instructor for: I have been paid for giving lectures for pharmaceutical companies and their employees, Speakers bureau: I have been paid for giving lectures in meetings organized by pharmaceutical companies, Bjorg Tilde Svanes Fevang: None declared, Gunnstein Bakland: None declared, Erik Rodevand: None declared, Andreas Diamantopoulos: None declared

Background: In the new millennium biologic therapies e.g. tumor necrosis factor inhibitors (TNFi) have played a major role improving clinical outcomes in rheumatoid arthritis (RA), psoriatic arthritis (PsA) and axial spondyloarthritis (ax-SpA). A major limitation in many countries for prescribing these drugs has been the high drug costs. The patent period for several of these TNFis e.g. infliximab, etanercept and adalimumab has ended and as a consequence biosimilar TNFis are now reaching the market. This has a cost saving potential for payers. In Norway, encouraged by the health authorities, non-medical switch from originator to biosimilar has been performed in most patients on biologic originator drugs with biosimilar drugs available, including etanercept. To the best of our knowledge no longer than one year real life experienced real life evidence data for non-medical switch from originator etanercept to biosimilar etanercept SB4 exist (ref.1). Objectives: To explore three-year drug survival for biosimilar SB4-etanercept in RA, PsA and ax-SpA patients with a non-medical switch from etanercept originator to SB4. Methods: At the participating outpatient clinics patients with RA, PsA and ax-SpA are monitored using a clinical computer system, as standard clinical care. Demographic, clinical and treatment data were retrieved from the computer system for patients who started treatment with biosimilar etanercept SB4 between January 2016 and January 2019. Kaplan-Meier survival curves were used to explore drug survival. Survival differences between groups were tested using Breslow statistics. Results: At the participating outpatient clinics since 2016 a total of 474 RA, 249 PsA and 320 ax-SpA patients had a non-medical switch from etanercept originator to biosimilar etanercept SB4. In RA, PsA and ax-SpA patients the percentage of women was 68.2%, 42.6% and 30.3%, the percentage of current smokers 17.0%, 12.8% and 19.6%, mean (SD) age was 63.0 (13.1), 58.2 (11.3), 53.1 (12.1) years and disease duration 16.8 (9.8), 16.1 (9.7), 17.7 (11.0) years, respectively. In RA 80.0% were anti-CCP positive and in PsA and ax-SpA 34.4% and 90.8% were HLAB27 positive. In the table selected disease measures at baseline are shown. No significant difference (p=0.97) in drug survival for SB4 was seen between RA, PsA and ax-SpA patients. Mean (95% CI) SB4 drug survival time (years) was for RA 2.3 (2.2-2.4), for PsA 2.3 (2.2-2.4) and for ax-SpA 2.4 (2.3-2.5). In the figure below Kaplan-Meier drug survival curves are shown. Men had a statistically significant longer mean drug survival than women (2.5 (2.4-2.6) vs 2.2 (2.1-2.3), p=0.001). Conclusion: Our long term real life data show that the majority of patients with a non-medical switch from originator etanercept to biosimilar etanercept SB4 remained on the drug. No significant difference in drug survival was seen between RA, PsA and ax-Spa patients. Men however had a significantly longer drug survival than women. Further analyses are needed to explore reasons for cessation across gender and patient groups. Reference: [1] Glintborg B et al. Ann Rheum Dis 2018;0:1-9 Disclosure of Interests: Glenn Haugeberg Grant/research support from: For this study grant from Biogen, Consultant for: Medical Advisory boards for several companies, Paid instructor for: I have been paid for giving lectures for pharmaceutical companies and their employees, Speakers bureau: I have been paid for giving lectures in meetings organized by pharmaceutical companies, Bjorg Tilde Svanes Fevang: None declared, Gunnstein Bakland: None declared, Erik Rodevand: None declared, Andreas Diamantopoulos: None declared

Introduction Ankylosing spondylitis (AS) is a lifelong condition where spinal inflammation causes chronic back pain and restriction of spinal function. While proinflammatory cytokines participate in the disease process, their relation with disease activity, spinal function, and quality of life is less well understood. Methods Cross-sectional study of serum levels of four inflammatory cytokines (IL-6, TNF, IL-23, and IL-17A) in AS patients not on biologics. Disease characteristics and simultaneous spinal function tests and patient-reported health measures (Bath Functional Index (BASFI), Dougados Functional Index (DFI), Modified Health Assessment Questionnaire (MHAQ), and routine laboratory parameters were recorded. The composite ASDAS-CRP score was used to classify disease activity as absent, low, or high. Results In 164 AS patients (age 46 years, 70.1% males, 90.9% HLAB27 positive, ASDAS-CRP 1.8), disease activity was classified as inactive in 14%, low in 54%, and high in 31%. ASDAS-CRP correlated well with MHAQ, DFI, BASFI, and spinal mobility across patients with low and high disease activity (all p 0.2). Conclusions A large proportion of AS not on biologics have active disease far into the disease course. This impacts negatively on quality of life, work ability, and spinal mobility. Serum cytokine levels are poor markers for these central disease features in AS management. Funding Abbott Norway AS and Arthritis Foundation of Western Australia. Electronic supplementary material The online version of this article (10.1007/s40744-019-0161-7) contains supplementary material, which is available to authorized users.

Objective To compare (1) golimumab drug survival and efficacy in bDMARD naive compared with non-naive rheumatoid arthritis (RA), psoriatic arthritis (PsA) and axial spondyloarthritis (ax-SpA) patients, (2) golimumab drug survival in RA and PsA patients treated with/without concomitant csDMARDs, (3) predictors of golimumab drug discontinuation. Methods Patients starting golimumab were included from the prospective observational multicenter Norwegian DMARD study. Drug survival was explored by Kaplan-Meier analyses with log rank test. Treatment responses were compared using ANCOVA. Univariate and multivariate Cox regression analyses were performed to identify predictors of golimumab discontinuation. Results We included 808 patients (163 RA, 266 PsA, 379 ax-SpA). Golimumab drug survival after 1/2/4 years were not significantly different between bDMARD naive and non-naive patients (all, p ≥ 0.12; RA, p ≥ 0.07; PsA, p ≥ 0.28; ax-SpA, p ≥ 0.61), nor between RA (p ≥ 0.10) and PsA (p ≥ 0.07) patients treated with vs. without csDMARD comedication. bDMARD naive compared with non-naive ax-SpA patients had better 3-month ASDAS/BASDAI/MHAQ responses (p ≤ 0.02). bDMARD naive compared with non-naive RA and PsA patients had a trend towards better treatment responses. Identified predictors of 4-year golimumab discontinuation were patient's global and female gender in patients overall and in subgroups of PsA and ax-SpA patients, and patient's global and CRP in RA. Conclusion Golimumab drug survival was not significantly different between bDMARD naive and non-naive RA, PsA and ax-SpA patients, nor between RA and PsA patients treated with vs. without concomitant csDMARDs. Treatment responses were significantly better for bDMARD naive than non-naive ax-SpA patients. Identified predictors of golimumab discontinuation were patient's global and female gender in patients overall and in subgroups of PsA and ax-SpA patients, and patient's global and CRP in RA.

Objective ANCA-associated vasculitides (AAV) have increased in prevalence since the 1980s. We aimed to investigate the incidence and prevalence of AAV during a 15-year period from 1999 to 2013 in Northern Norway, looking for variations during this period. Methods Patient records were retrieved from The Northern Norwegian Vasculitis Registry; in addition we searched all regional hospital databases. Patients diagnosed with AAV from 1999 through to 2013 were included. For prevalence data, patients residing in the area, but with AAV diagnosis prior to 1999, were also included. The diagnosis of AAV was based on the European Medicines Agency algorithm. Results We identified 140 cases; 88 were classified as granulomatosis with polyangiitis (GPA), 37 as microscopic polyangiitis (MPA) and 15 as eosinophilic granulomatosis with polyangiitis (EGPA). Adult (age ≥15 years) annual incidence rates per million were as follows: for GPA 15.6 (95% CI: 12.5, 19.2), MPA 6.5 (95% CI: 4.6, 9.0), EGPA 2.7 (95% CI: 1.5, 4.5) and overall AAV 24.7 (95% CI: 20.8, 29.2). Incidences of MPA and overall AAV showed an increasing trend (P Conclusion The incidence rate of GPA and the prevalence rates of GPA and EGPA are currently the highest reported. MPA increased significantly from a prior low incidence. The overall AAV annual incidence and prevalence are still increasing.

Background:Gastro-intestinal tract (GIT) symptoms is highly prevalent in patients with systemic sclerosis (SSc). The GIT-symptoms impact on the quality of life is significant, and available treatment alternatives are limited. Recently published articles show associations between gut microbiota changes and GIT-symptoms in SSc. We, therefore, performed a successful feasibility trial on faecal microbiota transplantation (FMT) in SSc patients using the single-donor bacterial culture “Anaerobic Cultivated Human Intestinal Microbiome (ACHIM)”. Based on the promising results from the feasibility trial, we aim to evaluate the safety and efficacy of FMT by ACHIM in SSc patients. (NCT04300426)Objectives:To design a clinical trial that explores the safety and efficacy of FMT in SSc patients.Methods:The ReSScue trial is a phase II, placebo-controlled, randomised 20-week, multicentre trial. The trial comprises three parts. In the induction phase (A1) lasting from week 0 to week 12, participants are randomised 1:1 to repeat infusions of 30 ml ACHIM or placebo at week 0 and 2 by gastro-duodenoscopy. In the maintenance phase (A2), all study participants will receive 30 ml ACHIM at week 12 and are followed continued blinded until week 20.For longer-term data on intervention effects and safety, the participant will be followed for a maximum extended monitoring period of 16 weeks (part B).The primary endpoint is change from baseline to week 12 in UCLA GIT scores on bloating or diarrhoea, depending on the worst symptom at baseline evaluated separately for each patient. Secondary endpoints are changes in UCLA GIT scores (bloating, diarrhoea and total) and safety measures.Results:We aim to enrol 70 SSc patients based on the power calculations for the primary endpoint “change in worst symptom from baseline to week 12”, with a considered drop out rate of 10%. This number of patients is expected to give a power of 80% of detecting a change in mean (p=0.05, two-sided) of -5.0 (or higher) if the relating standard deviation is 0.70 or lower. The patient screening started in September 2020, and we expect the study to be completed in May 2022.Conclusion:The ReSScue-study is to our knowledge the first FMT-study in SSc. This trial will assess the safety and efficacy of FMT in SSc patients with lower GI-symptoms, possibly leading to a novel treatment approach in SSc patients.Disclosure of Interests:Håvard Fretheim Grant/research support from: Received travel bursaries from Actelion, and remuneration from Bayer., Imon Barua: None declared, Vikas Sarna: None declared, Maylen N Carstens: None declared, Oliver Distler Speakers bureau: Below, Consultant of: Below, Grant/research support from: OD has/had consultancy relationship and/or has received research funding in the area of potential treatments for systemic sclerosis and its complications from (last three years): Abbvie, Acceleron Pharma, Amgen, AnaMar, Arxx, Baecon Discovery, Blade, Bayer, Boehringer Ingelheim, ChemomAb, Corbus, CSL Behring, Galapagos NV, Glenmark, GSK, Horizon (Curzion), Inventiva, iQvia, Italfarmaco, iQone, Kymera, Lilly, Medac, Medscape, Mitsubishi Tanabe Pharma, MSD, Novartis, Pfizer, Roche, Sanofi, Serodapharm, Topadur, Target Bioscience and UCB. Patent issued “mir-29 for the treatment of systemic sclerosis” (US8247389, EP2331143)., Dinesh Khanna Consultant of: Abbvie, Actelion/Janssen, Acceleron Pharma, Amgen, Bayer, Boehringer Ingelheim, CSL Behring, GSK, Horizon Pharmaceuticals, Mitsubishi Tanabe Pharma, Pfizer, Roche, Sanofi, United Therapeutics. DK is chief medical officer of Eicos Sciences, Inc., Grant/research support from: Abbvie, Actelion/Janssen, Acceleron Pharma, Amgen, Bayer, Boehringer Ingelheim, CSL Behring, GSK, Horizon Pharmaceuticals, Mitsubishi Tanabe Pharma, Pfizer, Roche, Sanofi, United Therapeutics. DK is chief medical officer of Eicos Sciences, Inc., Elizabeth Volkmann Consultant of: Boehringer Ingelheim, Grant/research support from: Corbus, Forbius, Boehringer Ingelheim, Øyvind Midtvedt Shareholder of: Son of owner of ACHIM., Henriette Didriksen Speakers bureau: Travel bursary - GSK, Alvilde Dhainaut: None declared, Anna-Kristine H Halse: None declared, Gunnstein Bakland: None declared, Inge Christoffer Olsen: None declared, Maiju E Pesonen: None declared, Øyvind Molberg: None declared, Anna-Maria Hoffmann-Vold Consultant of: Actelion, ARXX, Bayer, Boehringer Ingelheim, Medscape, Merck Sharp & Dohme, Lilly and Roche., Grant/research support from: Actelion, ARXX, Bayer, Boehringer Ingelheim, Medscape, Merck Sharp & Dohme, Lilly and Roche.

Background:Biosimilar drugs follow a tailored approval pathway that usually includes a Phase III comparative efficacy randomized controlled trial with a high internal but low external validity. Therefore, observational studies with high external validity are important to reassure patients and physicians that there are no clinically meaningful differences in effectiveness between a biosimilar and its reference drug. A EULAR Task Force systematic review and others have noted that recent comparative effectiveness studies often do not disclose applied analytical methods in sufficient detail, with many studies not adjusting for confounders nor accounting for attrition or missing data. 1,2Objectives:To apply the EULAR Points to Consider for Comparative Effectiveness Research (CER) in an analysis of reference etanercept (ETN) and SB4 biosimilar ETN in patients with rheumatoid arthritis (RA) treated in ordinary clinical practice in Norway.Methods:ETN-naÏve patients with RA starting ETN treatment between January 2010 and July 2018 at five centres in Norway were followed for at least 1 year; the 2 cohorts remained on either ETN or SB4 throughout. The primary outcome was DAS28 at Week 52. This CER has been designed to formally assess equivalence for DAS28, based on the accepted equivalence margin of 0.6.3 Conventional regression and propensity score (PS) models have been applied for the primary outcome evaluation of DAS28 at Week 52. Based on clinical knowledge, the confounders adjusted for in the step-wise PS model were age, gender, DAS28, order of biologics, and concomitant conventional synthetic disease-modifying anti-rheumatic drugs. A standardized difference (d) of Results:In the unmatched sample, there were 575 patients treated with reference ETN and 299 treated with SB4. Before PS matching, baseline mean (SD) DAS28 was different between the ETN and SB4 groups, 4.3 (1.2) vs 4.0 (1.3), (d) = 0.25. After PS matching, there were 176 RA patients in each group; baseline mean (SD) DAS28 was 4.1 (1.2) vs 4.1 (1.3), (d) = 0.05. At Week 52, the difference (mean [95% confidence interval (CI)]) between reference ETN and SB4 for primary outcome DAS28 at Week 52 was -0.02 (-0.33 to 0.29) in the unmatched analysis. Since the entire 95% CI is within the pre-defined equivalence margin of 0.6, equivalence at Week 52 has formally been shown. The analysis of the PS matched groups to Week 52 is ongoing and results will be presented in the poster.Conclusion:Our results show the importance of adopting proper analytical techniques when comparing a biosimilar with its reference product. A conventional regression model may not fully account for differences in key clinical measures (in this instance, disease activity) between the two groups at baseline, and therefore the Week 52 results might be biased. The propensity score matched model ensures comparability of the groups at baseline and therefore the validity of the Week 52 results should be more robust.References:[1]Cantini F and Benucci M. Mandatory, cost-driven switching from originator etanercept to its biosimilar SB4: possible fallout on non-medical switching. Ann Rheum Dis 2020; 79: e13.[2]Lauper K KJ, De Wit M, Fautrel B, et al. A Systematic Review to Inform the EULRA Points to Consider When Analysing and Reporting Comparative Effectiveness Research With Observational Data in Rheumatology. Annals of the Rheumatic Diseases 2020; 79:[3]Fransen J and van Riel PL. The Disease Activity Score and the EULAR response criteria. Clin Exp Rheumatol 2005; 23: S93-99.Acknowledgements:The authors wish to acknowledge Janet Addison and Ulrich Freudensprung of Biogen for their intellectual contributions to this abstract and Bjørg Tilde Fevang for providing data from Haukeland University Hospital in Bergen. Editorial support for the preparation of this abstract was provided by Excel Scientific Solutions (Fairfield, CT, USA); funding was provided by Biogen International GmbH.Disclosure of Interests:Glenn Haugeberg Grant/research support from: Biogen, Gunnstein Bakland: None declared, Erik Rødevand: None declared, Inger Johanne Widding Hansen: None declared, Andreas Diamantopoulos: None declared, Are Hugo Pripp: None declared

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

ObjectiveThe rheumatoid arthritis impact of disease (RAID) questionnaire comprises seven patient-important domains of disease impact (pain, function, fatigue, sleep disturbance, emotional well-being, physical well-being, coping). RAID was validated as a pooled-weighted score. Its seven individual items separately could provide a valuable tool in clinical practice to guide interventions targeting the patient’s experience of the disease. The aim was to separately assess the psychometric properties of each of the seven numeric rating scale (NRS) of the RAID (RAID.7).Material and methodsPost hoc analyses of data from the cross-sectional RAID study and from the Rainbow study, an open-label 12-week trial of etanercept in patients with RA. Construct validity of each NRS was assessed cross-sectionally in the RAID data set by Spearman’s correlation with the respective external instrument of reference. Using the rainbow data set, we assessed reliability through intraclass correlation coefficient between the screening and the baseline visits and responsiveness (sensitivity to change) by standardised response mean between baseline and 12 weeks.ResultsA total of 671 patients with RA with features of established disease were analysed, 563 and 108 from RAID and Rainbow, respectively. The NRS correlated moderately to strongly with the respective external instrument of reference (r=0.62–0.81). Reliability ranged from 0.64 (0.51–0.74) (pain) to 0.83 (0.76–0.88) (sleep disturbance) and responsiveness from 0.93 (0.73–1.13) (sleep disturbance) to 1.34 (1.01–1.64) (pain).ConclusionThe separate use of the individual NRS of RAID (RAID.7) is valid, feasible, reliable and sensitive to change, representing an opportunity to improve the assessment and treatment of disease impact with minimal questionnaire burden.Trial registration numberNCT00768053.

Endoplasmic reticulum aminopeptidase 1 (ERAP1) gene variants diminish the risk of developing ankylosing spondylitis (AS) through a reduction in ERAP1 activity. We investigated whether disease expression was altered in patients who developed AS despite the presence of two protective ERAP1 variants.We conducted a cross-sectional and longitudinal cohort study of patients with established AS (n = 334, 90% B27+, mean age at study 45 years) for whom clinical data and biological samples were collected during a research visit. Genotyping for the single nucleotide polymorphisms (SNPs) rs27044 and rs30187 was performed on genomic DNA by reverse transcription polymerase chain reaction (RT-PCR) with interleukin (IL)-6 and tumour necrosis factor (TNF) levels determined by a sandwich enzyme-linked immunosorbent assay (ELISA). Associations between genotypes and haplotypes, clinical and serological findings were analysed using SNPstats.Both SNPs were in strong linkage disequilibrium and formed three common haplotypes (C/C 0.65, G/T 0.30, and C/T 0.04). Haplotype C/T carried a lower risk for uveitis [odds ratio (OR) 0.32, p = 0.03] and elevated C-reactive protein (CRP) levels (OR 0.26, p = 0.04). There was no effect of ERAP1 haplotypes on cytokine levels or major outcomes after 8 years of follow-up.The ERAP1 rs27044/rs30187 haplotype C/T is associated with lower risk of extraspinal disease and systemic inflammation in Nordic AS patients but has no impact on IL-6 or TNF levels.

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

ObjectivesTo compare (1) Short Form-36 (SF-36) Physical Component Summary (PCS) and Mental Component Summary (MCS), scale scores and Short Form-6 dimensions (SF-6D) between patients with rheumatoid arthritis (RA) and patients with psoriatic arthritis (PsA) and Norwegian general population controls and (2) improvements in these measures between patients with RA and PsA.MethodsAnalyses of covariance were performed to compare SF-36 measures between first-time enrolled patients with RA (n=3898) and PsA (n=1515) from the prospective observational multicentre NORwegian-Disease Modifying Anti-Rheumatic Drug study (6 months follow-up) and general population controls (n=2323).ResultsIn age and gender-adjusted analyses, patients with PsA compared with patients with RA had similar PCS, MCS and SF-6D (p≥0.14), worse vitality and general health, but better physical functioning at 0/6 months (p≤0.03). With additional 28-joint disease activity scores adjustment as a proxy for joint inflammation, PCS, most scale scores and SF-6D were worse in patients with PsA than patients with RA at 0/3/6 months (p≤0.01). PCS was more impaired than MCS both in RA and PsA compared with general population controls (p≤0.001). Mean 3-month and 6-month improvements after disease-modifying anti-rheumatic drug treatment were larger in patients with RA than patients with PsA for bodily pain, vitality and mental health (p≤0.02).ConclusionsHealth-related quality of life was overall similar in patients with RA and patients with PsA—with a tendency to worse scores in PsA—and worse compared with Norwegian general population controls.

OBJECTIVE Variations in the IL-1 alpha (IL-A) gene increase the risk for ankylosing spondylitis (AS), but the pathway underlying this association is not fully understood. As IL-1A is primarily a regulatory cytokine, we investigated the influence of IL-1A gene variation on disease severity and cytokine expression in AS. METHODS This was a cross sectional study of tumor necrosis factor inhibitors (TNFi)-naive AS patients (n=334, 90% B27 +, age 45 years) fulfilling the modified New York criteria. We recorded demographics, clinical findings, spinal mobility, Bath AS Functional Index (BASFI), and routine lab findings. IL-1A genotyping for three AS-associated single nucleotide polymorphism (SNP; rs2856836, rs17561 and rs1894399) was performed using Taqman RT-PCR, with TNF, IL-6, IL-17A, and IL-23 levels measured using ELISA. Genotypic associations included logistic regression analysis for genotype (codominant model) and global haplotype (threshold 5%) associations with cytokine levels and clinical features. RESULTS The three variants were in near complete linkage disequilibrium and formed two only common haplotypes (ACC 67%, GAT 33%). The levels for TNF, IL-6, IL-17A, IL-23, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) were similar across genotypes and haplotypes (all p-values >0.4) as were the measures for spinal mobility and BASFI. The TAQ haplotype showed a borderline significant trend with reduced heart disease and mortality during follow-up. CONCLUSION IL-1A gene cluster variations do not have an impact on the clinical disease measures or cytokine levels in AS, suggesting that IL-1A has no direct role in AS.

Background Norwegian rheumatologists are encouraged to prescribe the lowest-priced biologic DMARDs according to the national tender system. Thus, non-medical switch from the originator drug to its biosimilar is extensively performed. There is a need for more real life data to clarify the clinical outcomes, dropout rates and reasons for these dropouts after a non-medical switch from the originator to biosimilar ETN. Objectives To explore drug survival and clinical outcomes in rheumatoid arthritis (RA) patients after a non-medical switch from the originator to biosimilar ETN (SB4) in ordinary outpatient clinics across Norway. Methods Herein we present preliminary data collected at one participating centre. Patients were monitored and data were collected by the use of a hospital clinical computer system GoTreatIT Rheuma. The computer system is also used for data collection for the Norwegian national arthritis registry, NorArtritt. Demographic, clinical and treatment data were retrieved (21st of January 2018) from the computer system for the time point of non-medical switch of ETN and the last follow up. Wilcoxon matched-pair signed rank test was used for comparison between the two-time points. Results Since April 2016 191 RA patients (mean age 60.8 years, 67% females) underwent a non-medical switch from originator to biosimilar ETN. Mean (SD) observation time for the 163 patients (85.3%) still on biosimilar ETN was 1.23 (0.46) yrs. 28 patients (14.7%) stopped treatment. Among them mean (SD) observation time for the 7 patients (3.7%) in remission was 0.53 (0.33) yrs, for the 10 patients (5.2%) reporting adverse events 0.44 (0.32) yrs and for the 11 patients (5.8%) reporting lack or loss of efficacy 0.44 (0.35) yrs. The adverse events reported was: 1 chest pain, 1 neuropathy, 1 GI reaction, 1 visual impairment, 1 infection, 2 joint stiffness (1 patient went back on ETN SB4) and 3 skin reactions. For all 191 patients no significant change (median [IQR]) from baseline to last observation was seen for DAS28 (2.1 [1.5–2.8] vs 1.9 [1.5–2.5], p=0.33), MHAQ (0.3 [0.0–0.7] vs 0.4 [0.1–0.6], p=0.62) and patient VAS global (20.0 [10.0–43.0] vs 25.0 [10.0–43.3] mm, p=0.73), whereas CRP improved significantly during follow up (2.0 [1.0–5.0] vs 1.0 [1.0–5.5] mg/dl, p=0.02). For the subgroup of RA patients who stopped treatment because of lack of efficacy a minor non-significant impairment was observed for DAS28 (2.0 [1.4–2.5] vs 2.6 [1.2–4.0], p=0.32), CRP (0.0 [0.0–6.0] vs 3.5 [0.8–13.3] mg/dl, p=0.66), MHAQ (0.1 [0.0–0.1] vs 0.5 [0.3–0.5], p=0.66) and patient VAS global (20.0 [10.0–30.0] vs 29.0 [17.0–58.5] mm, p=0.66). Conclusions Our preliminary data indicate that for the majority of patients, a non-medical switch from originator to biosimilar ETN (SB4) was well tolerated with no impairment in disease measures. Whether the reported adverse events were associated to the switch needs to be further studied. In patients who stopped the biosimilar because of lack of effect only a minor numerically increase in disease measures was seen. Our promising preliminary results need to be confirmed in a large scale study. Disclosure of Interest G. Haugeberg Shareholder of: DiaGraphIT AS, G. Bakland: None declared, E. Rodevand: None declared, B. T. Fevang: None declared, I. J. Hansen: None declared, A. Diamantopoulos: None declared