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ObjectivesTo define the instruments for the Assessment of SpondyloArthritis international Society–Outcomes Measures in Rheumatology (ASAS-OMERACT) core domain set for axial spondyloarthritis (axSpA).MethodsAn international working group representing key stakeholders selected the core outcome instruments following a predefined process: (1) identifying candidate instruments using a systematic literature review; (2) reducing the list of candidate instruments by the working group, (3) assessing the instruments’ psychometric properties following OMERACT filter 2.2, (4) selection of the core instruments by the working group and (5) voting and endorsement by ASAS.ResultsThe updated core set for axSpA includes seven instruments for the domains that are mandatory for all trials: Ankylosing Spondylitis Disease Activity Score and Numerical Rate Scale (NRS) patient global assessment of disease activity, NRS total back pain, average NRS of duration and severity of morning stiffness, NRS fatigue, Bath Ankylosing Spondylitis Function Index and ASAS Health Index. There are 9 additional instruments considered mandatory for disease-modifying antirheumatic drugs (DMARDs) trials: MRI activity Spondyloarthritis Research Consortium of Canada (SPARCC) sacroiliac joints and SPARCC spine, uveitis, inflammatory bowel disease and psoriasis assessed as recommended by ASAS, 44 swollen joint count, Maastricht Ankylosing Spondylitis Enthesitis Score, dactylitis count and modified Stoke Ankylosing Spondylitis Spinal Score. The imaging outcomes are considered mandatory to be included in at least one trial for a drug tested for properties of DMARD. Furthermore, 11 additional instruments were also endorsed by ASAS, which can be used in axSpA trials on top of the core instruments.ConclusionsThe selection of the instruments for the ASAS-OMERACT core domain set completes the update of the core outcome set for axSpA, which should be used in all trials.

Axial spondyloarthritis (axSpA) is a chronic inflammatory rheumatic disease that manifests primarily in the axial skeleton, initially mostly in the sacroiliac joints (SIJ), usually later spreading to the spine. The disease is characterised by inflammation and new bone formation which are mainly assessed by conventional radiography (CR) and magnetic resonance imaging (MRI). Tumour necrosis factor inhibitors (TNFi) and interleukin-17 antagonists have been shown to be efficacious and efficient in patients with axSpA. This treatment seems to also inhibit structural damage, for example, retard radiographic progression. Indeed, a reduction of new bone formation in the spine, as assessed by CR, has been reported to occur after at least 2 years of therapy with TNFi. Recently, a reduction of erosions and ankylosis in the SIJ has also been observed in axSpA patients treated with etanercept and filgotinib. In this narrative review, we discuss the limited significance of such findings.

Background and aimStriving for harmonisation of specialty training and excellence of care in rheumatology, the European League Against Rheumatism (EULAR) established a task force to develop points to consider (PtCs) for the assessment of competences during rheumatology specialty training.MethodsA systematic literature review on the performance of methods for the assessment of competences in rheumatology specialty training was conducted. This was followed by focus groups in five selected countries to gather information on assessment practices and priorities. Combining the collected evidence with expert opinion, the PtCs were formulated by the multidisciplinary task force, including rheumatologists, medical educationalists, and people with rheumatic and musculoskeletal diseases. The level of agreement (LoA) for each PtC was anonymously voted online.ResultsFour overarching principles and 10 PtCs were formulated. The overarching principles highlighted the importance of assessments being closely linked to the rheumatology training programme and protecting sufficient time and resources to ensure effective implementation. In the PtCs, two were related to overall assessment strategy (PtCs 1 and 5); three focused on formative assessment and portfolio (PtCs 2–4); three focused on the assessment of knowledge, skills or professionalism (PtCs 6–8); one focused on trainees at risk of failure (PtC 9); and one focused on training the trainers (PtC 10). The LoA (0–10) ranged from 8.75 to 9.9.ConclusionThese EULAR PtCs provide European guidance on assessment methods throughout rheumatology training programmes. These can be used to benchmark current practices and to develop future strategies, thereby fostering continuous improvement in rheumatology learning and, ultimately, in patient care.

ObjectivesSpinal MRI is used to visualise lesions associated with axial spondyloarthritis (axSpA). The ASAS MRI working group (WG) updated and validated the definitions for inflammatory and structural spinal lesions in the context of axSpA.MethodsAfter review of the existing literature on all possible types of spinal MRI pathologies in axSpA, the group (12 rheumatologists and two radiologists) consented on the required revisions of lesion definitions compared with the existing nomenclature of 2012. In a second step, using 62 MRI scans from the ASAS classification cohort, the proposed definitions were validated in a multireader campaign by global (absent/present) and detailed (inflammation and structural) lesion assessment at the vertebral corner (VC), vertebral endplate, facet joints, transverse processes, lateral and posterior elements. Intraclass correlation coefficient (ICC) was used for analysis.ResultsRevisions were made for both inflammatory (bone marrow oedema, BMO) and structural (fat, erosion, bone spur and ankylosis) lesions, including localisation (central vs lateral), extension (VC vs vertebral endplate) and extent (minimum number of slices needed), while new definitions were suggested for the type of lesion based on lesion maturity (VC monomorphic vs dimorphic). The most reliably assessed lesions were VC fat lesion and VC monomorphic BMO (ICC (mean of all 36 reader pairs/overall 9 readers): 0.91/0.92; 0.70/0.67, respectively.ConclusionsThe lesion definitions for spinal MRI lesions compatible with SpA were updated by consensus and validated by a group of experienced readers. The lesions with the highest frequency and best reliability were fat and monomorphic inflammatory lesions at the VC.

ObjectivesPatients with autoimmune inflammatory rheumatic diseases (AIRD) often have lower vaccination coverage rates compared with the general population, despite being disproportionately affected by infectious complications. We aim to systematically review the literature regarding vaccination willingness and hesitancy in AIRD.MethodsA scoping review was conducted in PubMed, EMBASE and the Cochrane Library in June 2021. Study selection was performed by two independent reviewers and data were extracted using a standardised form. Risk of bias was assessed using instruments from McMaster University. Identified barriers were categorised into the WHO’s measuring behavioural and social drivers (BeSD) of vaccination conceptual model.ResultsThe search yielded 1644 hits of which 30 publications were included (cross-sectional studies based on interviews (n=27) and intervention studies (n=3)). The majority of studies reported barriers to influenza and pneumococcal vaccination only (n=9) or in combination with another vaccination (n=8) from the patients’ perspective. Only one study assessed the view of rheumatologists. Coverage of domains matched to the BeSD model suggests a lack of awareness of infection risk by both patients and physicians. Patients mainly mentioned behavioural and social factors that negatively influenced their willingness to be vaccinated while physicians mentioned organisational deficits as major barriers.ConclusionsThe view on vaccination in patients with AIRD diverges between patients and rheumatologists. Our results show that in-depth counselling on vaccines is important for patients, whereas physicians need support in implementing specific immunisation recommendations. The themes identified provide a starting point for future interventions to improve vaccine rates in patients with AIRD.

No abstract available.

ObjectivesThe Assessment of SpondyloArthritis international Society (ASAS) MRI working group (WG) was convened to generate a consensus update on standardised definitions for MRI lesions in the sacroiliac joint (SIJ) of patients with spondyloarthritis (SpA), and to conduct preliminary validation.MethodsThe literature pertaining to these MRI lesion definitions was discussed at three meetings of the group. 25 investigators (20 rheumatologists, 5 radiologists) determined which definitions should be retained or required revision, and which required a new definition. Lesion definitions were assessed in a multi-reader validation exercise using 278 MRI scans from the ASAS classification cohort by global assessment (lesion present/absent) and detailed scoring (inflammation and structural). Reliability of detection of lesions was analysed using kappa statistics and the intraclass correlation coefficient (ICC).ResultsNo revisions were made to the current ASAS definition of a positive SIJ MRI or definitions for subchondral inflammation and sclerosis. The following definitions were revised: capsulitis, enthesitis, fat lesion and erosion. New definitions were developed for joint space enhancement, joint space fluid, fat metaplasia in an erosion cavity, ankylosis and bone bud. The most frequently detected structural lesion, erosion, was detected almost as reliably as subchondral inflammation (κappa/ICC:0.61/0.54 and 0.60/0.83) . Fat metaplasia in an erosion cavity and ankylosis were also reliably detected despite their low frequency (κappa/ICC:0.50/0.37 and 0.58/0.97).ConclusionThe ASAS-MRI WG concluded that several definitions required revision and some new definitions were necessary. Multi-reader validation demonstrated substantial reliability for the most frequently detected lesions and comparable reliability between active and structural lesions.

ObjectivesTo investigate patient characteristics predictive of response to secukinumab in patients with psoriatic arthritis (PsA) with axial manifestations.MethodsIn a post-hoc analysis from the MAXIMISE trial (NCT02721966) in patients with PsA and axial manifestations, we tested the hypothesis that the OR of the effect of treatment on the primary endpoint of the trial (Assessment of SpondyloArthritis international Society (ASAS) 20 responder status at week 12) would be different depending on 12 prespecified predictor variables. We applied a two-model logistic regression approach, a main effects and an interaction model.ResultsThe OR (95% CI) for ASAS20 response for the presence of nail dystrophy was 3.2 (95% CI 0.93 to 10.99) in the secukinumab 150 mg group and 5.0 (95% CI 1.47 to 17.19) in the secukinumab 300 mg group compared with the placebo group (p=0.029). Odds of being a responder were similar in men and women in the secukinumab groups, though men fared worse than women in the placebo group (p=0.039). Current smokers were less likely to be ASAS20 responders compared with never smokers regardless of the treatment group (p=0.589).ConclusionNail dystrophy was identified as a predictor of response to secukinumab in patients with PsA with axial manifestations in the MAXIMISE trial. These findings may be explained by the nail-entheseal concept as part of the axial phenotype in PsA .

ObjectiveStudying vertebral bone loss in radiographic axial spondyloarthritis (r-axSpA) has been challenging due to ectopic bone formation. We cross-sectionally analysed low-dose CT (ldCT) trabecular bone density Hounsfield units (HU) measurements and calculated inter-reader reliability at the vertebral level in patients with r-axSpA.MethodsLdCT scans of 50 patients with r-axSpA from the sensitive imaging in ankylosing spondylitis study, a multicentre 2-year prospective cohort were included. Trabecular bone HU taken from a region of interest at the centre of each vertebra (C3-L5) were independently assessed by two trained readers. HU mean (SD), and range were provided at the vertebral level, for each reader and centre separately. Inter-reader reliability and agreement were assessed using intraclass correlation coefficients (ICC; single measurements, absolute agreement, two-way mixed effects models); smallest detectable difference and Bland-Altman plots.ResultsOverall, 1100 vertebrae were assessed by each reader. HU values decreased from cranial to caudal vertebrae. For readers 1 and 2 respectively, the highest mean (SD) HU value was obtained at C3 (354(106) and 355(108)), and the lowest at L3 (153(65) and 150 (65)). Inter-reader reliability was excellent (ICC(2,1):0.89 to 1.00). SDD varied from 4 to 8. For most vertebrae, reader 1 scored somewhat higher than reader 2 (mean difference of scores ranging from −0.6 to 2.9 HU). Bland-Altman plots showed homoscedasticity.ConclusionLdCT measurement of HU is a feasible method to assess vertebral bone density in r-axSpA with excellent inter-reader reliability from C3 to L5. These results warrant further validation and longitudinal assessment of reliability.

BackgroundThe crystal-induced calcium pyrophosphate deposition disease (CPPD) clinically appearing as pseudogout differs from the mere radiographic finding of chondrocalcinosis (CC) but may cause symptoms resembling rheumatoid arthritis (RA).ObjectiveTo study the prevalence of CPPD and CC in rheumatic diseases focusing on differences between seropositive and seronegative RA.Patients and methodsIn a retrospective study design, we analysed records and radiographs of consecutive new patients presenting to our centre between January 2017 and May 2020. 503 patients were identified based on expert diagnoses: 181 with CPPD, 262 with RA, 142 seropositive (54.2%) and 120 seronegative RA, gout (n=30) and polymyalgia rheumatica (n=30), mean symptom duration ResultsThe majority of patients had only one rheumatological diagnosis (86.9%). Most patients with CPPD (92.6%) had radiographic CC, primarily in the wrists. The prevalence of CC was higher in seronegative (32.3%) than in seropositive RA (16.6%), respectively (pDiscussionCPPD and CC were more frequent in seronegative versus seropositive RA. Symmetry of arthritis and acuteness of attacks differentiated best between CPPD and RA but localisation of joint involvement did not. Co-occurrence of both diseases was frequently observed.

ObjectivesJanus kinase inhibitors (JAKi) have been approved for use in various immune-mediated inflammatory diseases. With five agents licensed, it was timely to summarise the current understanding of JAKi use based on a systematic literature review (SLR) on efficacy and safety.MethodsExisting data were evaluated by a steering committee and subsequently reviewed by a 29 person expert committee leading to the formulation of a consensus statement that may assist the clinicians, patients and other stakeholders once the decision is made to commence a JAKi. The committee included patients, rheumatologists, a gastroenterologist, a haematologist, a dermatologist, an infectious disease specialist and a health professional. The SLR informed the Task Force on controlled and open clinical trials, registry data, phase 4 trials and meta-analyses. In addition, approval of new compounds by, and warnings from regulators that were issued after the end of the SLR search date were taken into consideration.ResultsThe Task Force agreed on and developed four general principles and a total of 26 points for consideration which were grouped into six areas addressing indications, treatment dose and comedication, contraindications, pretreatment screening and risks, laboratory and clinical follow-up examinations, and adverse events. Levels of evidence and strengths of recommendations were determined based on the SLR and levels of agreement were voted on for every point, reaching a range between 8.8 and 9.9 on a 10-point scale.ConclusionThe consensus provides an assessment of evidence for efficacy and safety of an important therapeutic class with guidance on issues of practical management.

We read with interest the publication on COVID-19 outcomes related to hospitalisation of people with chronic inflammatory rheumatic diseases (CIRD) by Gianfrancesco et al .1 In our centre, we have taken a different approach by contacting 1495 patients with CIRD by telephone to ask for COVID-19 tests and symptoms. A total of 917 patients who agreed to participate (61%) was interviewed between 15 April and 15 June 2020: about 60% women, mean age 54, mean disease duration 12 years. Most had spondyloarthritis (SpA) including psoriatic arthritis (51%), 41% rheumatoid arthritis (RA) and 7% connective tissue diseases (CTD), mainly lupus. In RA, rheumatoid factor was found in 88%, anti-citrullinated protein antibodies (ACPA) in 77% and human leukocyte antigen (HLA) B27 in 73% of patients with axSpA, while 92% with CTD had antinuclear antibodies. Less than half of patients were vaccinated against pneumococci (43%) and influenca (47%). The German government started a national shutdown on 22 March 2020. To give some guidance to rheumatologists, the German Society of Rheumatology (DGRh) released recommendations on 29 April 2020.2 Our survey started about 2 weeks earlier. The care of our patients with CIRD is largely based on the ‘treat to …

Background:Pain is a debilitating symptom of ankylosing spondylitis (AS) and negatively impacts patient (pt) lives. Upadacitinib (UPA), a Janus kinase (JAK) inhibitor engineered for increased selectivity for JAK1 over JAK2, JAK3, and tyrosine kinase 2, 1 showed significant efficacy vs placebo (PBO) in the randomized phase 2/3 SELECT-AXIS 1 study in active AS.2Objectives:To evaluate the efficacy of UPA on multiple pain assessments through 64 weeks (wks).Methods:SELECT-AXIS 1 (NCT03178487) enrolled adults with active AS, who had an inadequate response, intolerance or contraindications to ≥2 NSAIDs, were biologic DMARD naive and met the modified New-York Criteria. Pts were randomized 1:1 to UPA 15 mg once daily (QD, n=93) or PBO (n=94) for 14 wks (Period 1), followed by open-label UPA 15 mg QD during 90-wk extension (Period 2); reported here are data through wk 64. Pain endpoints included the proportion of pts achieving ≥30%/≥50%/≥70% reduction in Pt’s Global Assessment (PGA) of pain on a 0–10 numeric rating scale (NRS), minimal clinically important difference (MCID, defined as ≥1 point reduction or ≥15% reduction from baseline [BL]) in PGA of pain, and much better improvement (MBI, defined as ≥2 point reduction and ≥33% reduction from BL) in PGA of pain. In addition, mean change from baseline in PGA of pain, BASDAI questions 2 (neck/back/hip pain) and 3 (peripheral pain/swelling), and pt’s assessment of back pain and nocturnal back pain NRS scores (NRS 0–10) were assessed. Non-responder imputation (binary endpoints) and mixed-effects model for repeated measurements (continuous endpoints) were used for missing data/dropouts in Period 1; as-observed analysis was used for Period 2.Results:A significantly higher proportion of pts receiving UPA vs PBO achieved reductions in all PGA of pain assessments as early as wk 2 that was sustained at all time points in Period 1; the only exception was ≥70% reduction in PGA of pain that was significant at wk 4 and sustained thereafter (Figure 1). For ≥30%/≥50%/≥70% reduction and MBI, the response rate increased over time with UPA; the difference for UPA vs PBO also continued to increase over time for ≥50% and ≥70% reduction endpoints. For MCID, an increase from BL to wk 2 was observed and plateaued thereafter. The mean change from BL in PGA of pain, BASDAI Q2, back pain, and nocturnal back pain NRS scores were significantly greater for UPA vs PBO at all time points in Period 1; BASDAI Q3 was significant at wk 8 and 14 (Figure 1). The effect of UPA on pain reduction was sustained through wk 64. PBO pts who switched to open-label UPA at wk 14 generally reached the same level of pain reduction as those initially randomized to UPA (Figure 1).Conclusion:In pts with active AS and an inadequate response/contraindication to NSAIDs, a greater proportion of patients treated with UPA achieved rapid, significant, and clinically meaningful reductions in pain vs PBO through 14 wks across multiple pain assessments. The reductions in pain were sustained over time, and pts who switched from PBO to UPA reached the same level of improvement as the continuous UPA group.References:[1]Parmentier JM, et al. BMC Rheumatology. 2018;2(23).[2]van der Heijde D, et al. Lancet. 2019;394(10214):2108-2117.Acknowledgements:AbbVie funded this study and participated in the study design, research, analysis, data collection, interpretation of data, reviewing, and approval of the publication. All authors had access to relevant data and participated in the drafting, review, and approval of this publication. No honoraria or payments were made for authorship. Medical writing support was provided by M Hovenden and J Matsuura of ICON plc and was funded by AbbVie.Disclosure of Interests:Atul Deodhar Speakers bureau: Novartis, Pfizer, AbbVie, Eli Lilly, UCB Pharma, GlaxoSmithKline, Consultant of: Novartis, Pfizer, AbbVie, Eli Lilly, UCB Pharma, GlaxoSmithKline, Grant/research support from: Novartis, Pfizer, AbbVie, Eli Lilly, UCB Pharma, GlaxoSmithKline, Xenofon Baraliakos Consultant of: Novartis, Pfizer AbbVie, Eli Lilly, UCB Pharma, Galapagos Janssen, Celgene and Amgen, Grant/research support from: Novartis, Pfizer AbbVie, Eli Lilly, UCB Pharma, Galapagos Janssen, Celgene and Amgen, Iain McInnes Consultant of: AbbVie, AstraZeneca, Boehringer Ingelheim, Bristol Myers, Celgene, Janssen, Leo, Lilly, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie, AstraZeneca, Boehringer Ingelheim, Bristol Myers, Celgene, Janssen, Leo, Lilly, Novartis, Pfizer, and UCB, Kurt de Vlam Speakers bureau: Celgene Eli Lilly, Galapagos, Novartis, and UCB, Consultant of: Celgene, Eli Lilly, Galapagos, Novartis, and UCB, Grant/research support from: Celgene and Galapagos, Louis Bessette Speakers bureau: Amgen, BMS, Janssen, UCB, AbbVie, Pfizer, Merck, Celgene, Lilly, Novartis, and Sanofi, Consultant of: Amgen, BMS, Janssen, UCB, AbbVie, Pfizer, Merck, Celgene, Lilly, Novartis, Sanofi, Gilead, Grant/research support from: Amgen, BMS, Janssen, UCB, AbbVie, Pfizer, Merck, Celgene, Lilly, Novartis, Sanofi, and Gilead, anna maniccia Shareholder of: AbbVie, Employee of: AbbVie, Ralph Lippe Shareholder of: AbbVie, Employee of: AbbVie, Christopher Saffore Shareholder of: AbbVie, Employee of: AbbVie, Tianming Gao Shareholder of: AbbVie, Employee of: AbbVie, In-Ho Song Shareholder of: AbbVie, Employee of: AbbVie, Andrew Ostor Consultant of: AbbVie, BMS, Roche, Janssen, Lilly, Novartis, Pfizer, UCB, Gilead, and Paradigm

Background:C-OPTIMISE was a phase 3b clinical trial investigating certolizumab pegol (CZP) maintenance dose continuation, reduction or withdrawal following achievement of sustained remission in patients with axial spondyloarthritis (axSpA). During the C-OPTIMISE maintenance period, the majority of patients randomised to CZP, either the full or reduced maintenance dose, did not experience disease flares. Conversely, in those who had CZP withdrawn, only a minority of patients remained flare-free.1Objectives:This post-hoc analysis evaluates disease activity and clinical markers of inflammation in patients who did not experience a disease flare following randomisation to CZP full maintenance dose, CZP reduced maintenance dose or placebo (PBO) during the maintenance period (Weeks 48–96) of C-OPTIMISE.Methods:C-OPTIMISE (NCT02505542) was a multicentre, double-blind, parallel-group, randomised phase 3b study with a 48-week open-label run-in period.1 Adult patients with early (3.5 at any visit. We report ASDAS, Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), and C-reactive protein (CRP) and fecal calprotectin levels during Weeks 48–96 in CZP- and PBO-randomised patients who did not experience a flare (i.e. completed Week 96 on randomised treatment). Missing data were imputed using last observation carried forward.Results:Of 313 patients entering the maintenance period at Week 48, 197 (62.9%) completed Week 96 on randomised treatment without experiencing a flare; of these, 89 (85.6%) and 84 (80.0%) patients were in the CZP 200 mg Q2W and CZP 200 mg Q4W arm, respectively, with only 24 (23.1%) patients randomised to PBO not experiencing a flare. Baseline characteristics of these patients are shown in the Table 1. During Weeks 48–96, disease activity (ASDAS, BASDAI) and CRP levels were comparable between the CZP full and reduced maintenance dose group, and lower in both CZP arms than in PBO (Figure 1 A–C). From Week 60 up to Week 96, PBO patients who did not flare had consistently higher mean ASDAS, BASDAI and CRP levels compared with CZP-randomised patients (Figure 1 A–C). Similarly, there was a greater increase in fecal calprotectin levels between Weeks 48 and 96 in the PBO arm compared with both CZP arms (Figure 1 D).Table 1.Baseline (Week 0) characteristics of patients who did not experience flares during the C-OPTIMISE maintenance periodPlacebo (n=24)CZP 200 mg Q4W (n=84)CZP 200 mg Q2W (n=89)Age (years), mean (SD)29.8 (7.4)32.9 (6.7)32.4 (7.2)Male, n (%)19 (79.2)69 (82.1)69 (77.5)Time since diagnosis (years)Mean (SD)2.0 (1.8)2.0 (1.7)2.5 (1.6)Median1.21.22.7Symptom duration (years)Mean (SD)2.7 (1.7)3.4 (1.9)3.9 (2.9)Median2.83.53.9ASDAS, mean (SD)3.4 (0.8)3.7 (0.8)3.7 (0.7)BASDAI, mean (SD)6.3 (1.1)6.6 (1.5)6.4 (1.4)CRP (mg/L), geometric mean6.287.887.35Fecal calprotectin (µg/g), mean (SD)71.8 (111.4)87.1 (110.5)81.0 (120.0)SD: standard deviation.Conclusion:Despite not meeting the threshold for a flare, consistently higher disease activity and increases in serologic and inflammatory biomarkers were observed in PBO-randomised patients who did not experience a flare during the C-OPTIMISE study compared to those who remained on CZP. These findings confirm that patients with axSpA who achieve sustained remission benefit from continued CZP treatment, either with the full or reduced maintenance dose, over treatment withdrawal.References:[1]Landewé R. Ann Rheum Dis 2020;79:920–8.Acknowledgements:This study was funded by UCB Pharma. Editorial services were provided by Costello Medical.Disclosure of Interests:Lianne S. Gensler Consultant of: AbbVie, Eli Lilly, Gilead, GSK, Novartis, Pfizer, UCB Pharma, Grant/research support from: Pfizer, Xenofon Baraliakos Speakers bureau: AbbVie, BMS, Chugai, Eli Lilly, Galapagos, Gilead, Novartis, Merck, Pfizer, UCB Pharma, Paid instructor for: AbbVie, BMS, Chugai, Eli Lilly, Galapagos, Gilead, Novartis, Merck, Pfizer, UCB Pharma, Consultant of: AbbVie, BMS, Chugai, Eli Lilly, Galapagos, Gilead, Novartis, Merck, Pfizer, UCB Pharma, Grant/research support from: AbbVie, Merck, Novartis, Lars Bauer Shareholder of: UCB Pharma, Employee of: UCB Pharma, Bengt Hoepken Shareholder of: UCB Pharma, Employee of: UCB Pharma, Thomas Kumke Shareholder of: UCB Pharma, Employee of: UCB Pharma, Mindy Kim Shareholder of: UCB Pharma, Employee of: UCB Pharma, Robert B.M. Landewé Speakers bureau: Abbott, Amgen, BMS, Centocor, Merck, Pfizer, Roche, Schering-Plough, UCB Pharma, Wyeth, Consultant of: Abbott, Ablynx, Amgen, AstraZeneca, BMS, Centocor, GSK, Merck, Novartis, Pfizer, Roche, Schering-Plough, UCB Pharma, Wyeth, Grant/research support from: Abbott, Amgen, Centocor, Novartis, Pfizer, Roche, Schering-Plough, UCB Pharma, Wyeth

Background:Axial, peripheral, and other disease manifestations often overlap between psoriatic arthritis (PsA) and ankylosing spondylitis (AS). Upadacitinib (UPA) is an oral Janus kinase inhibitor under evaluation for the treatment of PsA and AS.Objectives:To describe and compare baseline characteristics and UPA efficacy across 4 subgroups of patients (pts) from clinical trials: active PsA (with/without axial involvement) and active AS (with/without peripheral involvement).Methods:Baseline characteristics and efficacy of UPA in reducing axial and peripheral signs and symptoms were assessed via an integrated analysis across the 4 pt subgroups from the SELECT-PsA 1,1 SELECT-PsA 2,2 and SELECT-AXIS3 studies. Analyses of baseline characteristics included pts in the UPA 15 mg once daily (QD), UPA 30 mg QD, and placebo (PBO) groups; efficacy analyses included pts in the UPA 15 mg QD group only. Axial involvement in PsA (axial PsA) was determined by investigator assessment. Peripheral involvement in AS was defined based on presence of tender or swollen joints (TJC68 >0 or SJC66 >0), or presence of enthesitis at baseline (Maastricht Ankylosing Spondylitis Enthesitis Score >0).Results:2102 pts (UPA 15 mg; UPA 30 mg; PBO) were evaluated across the 4 subgroups (PsA [with/without axial involvement]: 626/1289; AS [with/without peripheral involvement]: 135/52). 33% of pts with PsA had axial PsA; 72% of pts with AS had peripheral symptoms. Pts with axial PsA had higher peripheral joint (TJC68 and SJC66) and skin (psoriasis) burden than pts with AS with peripheral involvement (pTable 1.Baseline demographics, medical history, and disease characteristicsMean (SD), unless otherwise specifiedPsA with axial involvementn=626PsA without axial involvementn=1289AS with peripheral involvementn=135AS without peripheral involvementn=52p-value(PsA with axial involvement versus AS with peripheral involvement)Male, n (%)300 (47.9)583 (45.2)88 (65.2)44 (84.6)0.0003Age, years50.7 (12.6)52.0 (12.0)46.6 (12.7)42.2 (11.4)0.0008Body mass index, kg/m230.3 (7.1)30.7 (6.8)a26.7 (4.9)26.8 (5.2)*Duration of disease symptoms, years11.2 (9.3)b10.4 (9.5)a14.6 (10.9)14.0 (10.6)0.0009Duration of disease since diagnosis, years7.7 (8.0)7.3 (8.0)7.0 (9.2)6.8 (8.4)0.3738TJC6823.6 (16.4)20.6 (14.6)5.3 (8.2)0*SJC6611.9 (9.0)11.2 (8.2)1.5 (3.2)0*Psoriasis, n (%)616 (98.4)1269 (98.4)7 (5.2)0*Uveitis, n (%)1 (0.2)5 (0.4)3 (2.2)1 (1.9)0.0191Inflammatory bowel disease, n (%)10 (1.6)13 (1.0)2 (1.5)2 (3.8)1.0000PhGA6.7 (1.7)6.5 (1.7)6.7 (1.5)c6.9 (1.7)b0.6960Pain, VAS 0–106.3 (2.0)b6.1 (2.2)d6.9 (1.6)a6.8 (1.7)a0.0002ASDAS(CRP)3.4 (1.0)e3.1 (1.0)f3.5 (0.7)a3.7 (0.8)a0.0351BASDAI (Total score)6.0 (2.1)e5.5 (2.2)f6.4 (1.6)6.3 (1.8)a0.0076BASDAI Q2 (Back pain)6.1 (2.7)e4.8 (3.2)f7.2 (1.7)7.2 (1.6)a*BASDAI Q3 (Peripheral pain/ swelling)6.3 (2.4)e6.0 (2.6)f5.9 (2.4)5.5 (2.4)a0.0747BASDAI Q4 (Tenderness)5.8 (2.6)e5.6 (2.7)f6.1 (2.5)5.7 (2.4)a0.3196*pData missing for an=1, bn=3, cn=6, dn=11, en=4, fn=14Conclusion:Pts with PsA with axial involvement and pts with active AS showed some differences in baseline characteristics but similar improvements versus placebo with UPA 15 mg QD.References:[1]McInnes I, et al. Ann Rheum Dis 2020;79(Suppl 1):16–17; 2. Genovese MC, et al. Ann Rheum Dis 2020;79(Suppl 1):139; 3. van der Heijde D, et al. Lancet 2019;394:2108–17.Acknowledgements:AbbVie funded this study; contributed to its design; participated in data collection, analysis, and interpretation of the data; and participated in the writing, review, and approval of the abstract. No honoraria or payments were made for authorship. Medical writing support was provided by Grant Thomas Kirkpatrick, MSc, of 2 the Nth (Cheshire, UK), and was funded by AbbVie.Disclosure of Interests:Xenofon Baraliakos Speakers bureau: AbbVie, Bristol-Myers Squibb, Celgene, Chugai, Eli Lilly, Galapagos, Gilead, MSD, Novartis, Pfizer, and UCB, Consultant of: AbbVie, Bristol-Myers Squibb, Celgene, Chugai, Eli Lilly, Galapagos, Gilead, MSD, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie, Bristol-Myers Squibb, Celgene, Chugai, Eli Lilly, Galapagos, Gilead, MSD, Novartis, Pfizer, and UCB, Atul Deodhar Speakers bureau: AbbVie, Amgen, Boehringer Ingelheim, Bristol-Myers Squibb, Eli Lilly, GSK, Janssen, Novartis, Pfizer, and UCB, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol-Myers Squibb, Eli Lilly, GSK, Janssen, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie, Eli Lilly, GSK, Novartis, Pfizer, and UCB, R Ranza Speakers bureau: AbbVie, Janssen, Novartis, and Pfizer, Consultant of: AbbVie, Janssen, Novartis, and Pfizer, Simona Rednic: None declared, francesco ciccia Speakers bureau: AbbVie, Bristol-Myers Squibb, Celgene, Novartis, Pfizer, UCB, and Werfen, Consultant of: AbbVie, Bristol-Myers Squibb, Celgene, MSD, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie, Celgene, Chugai, Pfizer, and UCB, Fabiana Ganz Shareholder of: May own stock or options in AbbVie, Employee of: AbbVie, Tianming Gao Shareholder of: May own stock or options in AbbVie, Employee of: AbbVie, Apinya Lertratanakul Shareholder of: May own stock or options in AbbVie, Employee of: AbbVie, In-Ho Song Shareholder of: May own stock or options in AbbVie, Employee of: AbbVie, Andrew Ostor Speakers bureau: AbbVie, Bristol-Myers Squibb, Eli Lilly, Gilead, MSD, Novartis, Pfizer, and Roche, Consultant of: AbbVie, Bristol-Myers Squibb, Eli Lilly, Gilead, MSD, Novartis, Pfizer, and Roche, Laura C Coates: None declared.

Background:The monoclonal antibody guselkumab (GUS; anti- IL-23p19-subunit) is approved to treat psoriatic arthritis (PsA). Post hoc analyses of DISCOVER-1&2 suggested that GUS may be effective in improving symptoms of axial manifestation of PsA.Objectives:Evaluate the efficacy of GUS across components of the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) in improving symptoms of axial manifestations of active PsA patients (pts) using data from Phase 3, randomized, placebo (PBO)-controlled studies.Methods:DISCOVER-1&2 enrolled pts with active PsA; pts were randomized to subcutaneous injections of guselkumab 100 mg every 4 weeks (Q4W) or at Wk0, 4, and Q8W, or PBO. These post hoc analyses included pts who were identified by the investigator as having axial symptoms and sacroiliitis (prior X-ray or MRI or screening X-ray). BASDAI scores were assessed at Wks 0, 8, 16, 24, and 52. Mean BASDAI component scores through Wk52 are reported by treatment group. Pooled data from the two studies are reported. Mean BASDAI component scores are reported using observed data; total BASDAI scores with missing components were set to missing. The proportion of pts achieving ≥50% improvement in BASDAI (BASDAI 50) was also determined; pts with missing data or who met the treatment failure criteria (discontinued study agent or used prohibited medications) were considered nonresponders at all subsequent timepoints.Results:These analyses included 312 pts from DISCOVER-1&2 (103 GUS Q4W, 91 GUS Q8W, 118 PBO); mean total BASDAI scores at Wk0 were 6.4, 6.5, and 6.6, respectively. Demographics and mean baseline BASDAI component scores (ie, fatigue, spinal pain, joint pain, enthesitis, qualitative morning stiffness, and quantitative morning stiffness) were similar across treatment groups (Table 1). In comparison with the total study population, this subgroup of pts had a higher mean C-reactive protein level at baseline and a higher proportion of pts with enthesitis and included a slightly higher proportion of males. Mean scores for all six BASDAI components, including spinal pain, decreased through Wk24 in GUS-treated pts, with separation from PBO observed as early as Wk8; improvements were maintained at Wk52. At Wk24, BASDAI 50 response rates were higher in the Q4W and Q8W groups vs PBO (38% and 40% vs 19%).1 At WK52, mean BASDAI component scores for PBO pts who crossed over to GUS Q4W at Wk24 were similar to those for pts who were randomized to GUS.2 A similar trend was observed for BASDAI50 response.Conclusion:Among PsA pts with axial symptoms and sacroiliitis (via investigator-confirmed imaging) in the DISCOVER-1&2 trials, GUS treatment resulted in lower mean scores for all six BASDAI components compared with PBO as early as Wk 8 and through Wk24, with mean scores maintained at Wk52.References:[1]Helliwell P, et al. Ann Rheum Dis. 2020; 79; Suppl 1.[2]Mease PJ, et al. Arthritis Rheumatol. 2020; 72 (suppl 10).Table 1.Baseline demographic and disease characteristics for patients who were identified by physicians as having symptoms consistent with spondylitis and had sacroiliitis confirmed via prior radiograph/MRI or screening radiographGUS Q4WGUS Q8WPlaceboPatients, n10391118Male, n (%)68 (66)54 (59)69 (59)Age, years44.9 ± 11.845.0 ± 10.745.3 ± 11.0BASDAIPatients, n9584110Score6.4 ± 1.76.5 ± 1.86.6 ± 1.5BASDAI ComponentsFatigue6.4 ± 2.06.7 ± 1.96.5 ± 1.9Spinal pain6.6 ± 2.16.5 ± 2.36.7 ± 2.0Joint pain6.3 ± 1.96.5 ± 2.26.8 ± 1.7Enthesitis6.3 ± 2.16.4 ± 2.26.3 ± 2.2Qualitative morning stiffness6.8 ± 2.16.7 ± 2.57.0 ± 2.0Quantitative morning stiffness6.2 ± 2.95.7 ± 2.96.1 ± 2.8Data are mean ± standard deviation unless otherwise noted.BASDAI, Bath ankylosing spondylitis disease activity indexDisclosure of Interests:Frank Behrens Speakers bureau: AbbVie, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Chugai, Eli Lilly, Galapagos, Genzyme, Gilead, Janssen, MSD, Novartis, Pfizer, Roche, Sanofi, and UCB, Consultant of: AbbVie, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Chugai, Eli Lilly, Galapagos, Genzyme, Gilead, Janssen, MSD, Novartis, Pfizer, Roche, Sanofi, and UCB, Grant/research support from: Celgene, Chugai, Janssen, Pfizer, and Roche, Philip J Mease Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, Galapagos, Gilead, GlaxoSmithKline, Janssen, Novartis, Pfizer, SUN, and UCB, Grant/research support from: AbbVie, Amgen, Bristol Myers Squibb, Eli Lilly, Galapagos, Gilead, Janssen, Novartis, Pfizer, SUN, and UCB, Philip Helliwell Consultant of: Galapagos, Janssen, Novartis, Grant/research support from: AbbVie, Janssen, Pfizer, May Shawi Shareholder of: Johnson & Johnson, Employee of: Janssen Global Services, Wim Noel Shareholder of: Johnson & Johnson, Employee of: Janssen Scientific Affairs, Soumya D Chakravarty Shareholder of: Johnson & Johnson, Employee of: Janssen Scientific Affairs, Alexa Kollmeier Shareholder of: Johnson & Johnson, Employee of: Janssen Research & Development, Xie L Xu Shareholder of: Johnson & Johnson, Employee of: Janssen Research & Development, Stephen Xu Shareholder of: Johnson & Johnson, Employee of: Janssen Research & Development, Yanli Wang Employee of: IQVIA providing statistical support (funded by Janssen), Xenofon Baraliakos Consultant of: AbbVie, Amgen, Bristol Myers Squibb, Eli Lilly, Galapagos, Gilead, Janssen, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie, Amgen, Bristol Myers Squibb, Eli Lilly, Galapagos, Gilead, Janssen, Novartis, Pfizer, and UCB.

Background:Coronavirus disease 2019 (COVID-19), has raised several questions in patients with immune-mediated inflammatory diseases (IMID). Whether the seroprevalence and factors associated with symptomatic COVID-19 are similar in IMID patients and in the general population is still unknown.Objectives:To assess the serological and clinical prevalence of COVID-19 in European IMID patients, along with the factors associated with its risk and the impacts the pandemic had on the IMID management.Methods:Prospective multicentre cross-sectional study among patients with five IMID (i.e. systemic lupus erythematous, Sjögren’s syndrome, rheumatoid arthritis, axial spondylarthritis or giant cell arteritis) from six tertiary-referral centers from France, Germany, Italy, Portugal, Spain and United Kingdom. Demographics, comorbidities, IMID, treatments, flares and COVID-19 details were collected. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) serological tests were systematically performed.Results:Between June 7 and December 8, 2020, 3028 patients were included (median age 58 years, 73.9% females). SARS-CoV-2 antibodies were detected in 166 (5.5%) patients. Symptomatic COVID-19 was seen in 122 patients (prevalence: 4.0%, 95% CI 3.4-4.8%); 23 (24.2%) of them were hospitalized and four (3.2%) died. In multivariate logistic regression analysis, symptomatic COVID-19 was more likely to be observed in patients with higher levels of C-reactive protein (OR: 1.18; 95% CI 1.05-1.33; p = 0.006), and increased with the number of IMID flares (OR: 1.27; 95% CI 1.02-1.58; p = 0.03). Conversely, it was less likely to occur in patients treated with biological therapy (OR: 0.51; 95% CI 0.32-0.82; p = 0.006). During the pandemic, at least one self-reported disease flare was seen in 654 (21.6%) patients. Also, 519 (20.6%) patients experienced changes in their treatment, with 125 of these (24.1%) being due to COVID-19.Conclusion:The SARS-CoV-2 prevalence in IMID patients over the study period seems to be similar to that of the general population1. The IMID inflammatory status seems to be independently associated with the development of COVID-19.References:[1]Pollán M, Pérez-Gómez B, Pastor-Barriuso R, Oteo J, Hernán MA, Pérez-Olmeda M, et al. Prevalence of SARS-CoV-2 in Spain (ENE-COVID): a nationwide, population-based seroepidemiological study. Lancet Lond Engl. 2020 Aug 22;396(10250):535–44.Disclosure of Interests:None declared.

Background:Bimekizumab (BKZ), a monoclonal antibody that selectively inhibits interleukin (IL)-17A and IL-17F, has demonstrated clinical efficacy and safety in patients with ankylosing spondylitis (AS) treated over a period up to 96 weeks.1,2Objectives:To report 3-year interim safety and efficacy of BKZ in patients with active AS from a phase 2b dose-ranging study (BE AGILE; NCT02963506) and its ongoing open-label extension (OLE; NCT03355573).Methods:BE AGILE study design has been described previously.1 Patients treated with BKZ 160 mg or 320 mg every 4 weeks (Q4W) at Week 48 in BE AGILE were eligible for OLE entry. All OLE patients received BKZ 160 mg Q4W. Treatment-emergent adverse events (TEAEs) are reported for the BE AGILE safety set (patients who received ≥1 dose of BKZ on study entry) for total exposure to BKZ across BE AGILE and the OLE. Efficacy outcomes are reported for the OLE full analysis set (patients who entered the OLE and had ≥1 dose of BKZ and ≥1 valid efficacy variable measurement in the OLE), and include: ASAS40, ASAS20, ASAS PR, ASDAS, ASDAS-CII, ASDAS-MI, ASDAS-ID (Results:262/303 (86%) patients randomised at BE AGILE study baseline completed Week 48 on BKZ 160 mg or 320 mg. At Week 48, 255/262 (97%) patients entered the OLE (full analysis set: 254); 219 patients had an efficacy assessment at Week 156. Over the 156 weeks, the exposure-adjusted incidence rate (EAIR) per 100 patient-years (PY) of TEAEs was 143.5, with an EAIR of 5.8 for serious TEAEs, 1.3 for serious infections, and 3.8 for Candida infections (Table 1). All Candida infections were mild or moderate; none were systemic or led to study discontinuation. Over 156 weeks, the EAIR of inflammatory bowel disease (1.2), anterior uveitis (0.8), and injection site reactions (0.5) remained low. Efficacy demonstrated at Week 48 in BE AGILE was maintained or improved up to Week 156 (Figure 1). Mean ASDAS improved from 3.9 at BE AGILE baseline to 2.0 and 1.8 at Weeks 48 and 156 respectively (by MI). At Week 156 in the NRI analyses, ASAS40 and ASAS PR were achieved by 62.6% (OC: 72.6%) and 32.7% (OC: 37.9%) patients respectively. ASDAS-ID and ASDAS Table 1.Safety for total exposure to BKZ across BE AGILE and the OLEBE AGILEWeeks 0–48BE AGILE + OLEWeeks 0–156n (%) [EAIR/100 PY]BKZ 160 mg(n=149;114.2 PY)BKZ 320 mg(n=150;119.6 PY)All BKZ(N=303;261.3 PY)All BKZ(N=303;781.0 PY)Any TEAE103 (69.1) [168.7]122 (81.3) [221.1]235 (77.6) [186.2]280 (92.4) [143.5]Serious TEAEs5 (3.4) [4.4]6 (4.0) [5.1]13 (4.3) [5.1]43 (14.2) [5.8]Key TEAEs of special monitoringSerious infections3 (2.0) [2.7]1 (0.7) [0.8]4 (1.3) [1.5]10 (3.3) [1.3]Candida infections10 (6.7) [9.1]9 (6.0) [7.9]19 (6.3) [7.5]28 (9.2) [3.8]Inflammatory bowel disease1 (0.7) [0.9]2 (1.3) [1.7]4 (1.3) [1.5]9 (3.0) [1.2]Anterior uveitis1 (0.7) [0.9]1 (0.7) [0.8]2 (0.7) [0.8]6 (2.0) [0.8]Study discontinuations due to TEAEs7 (4.7)10 (6.7)20 (6.6)38 (12.5)Drug-related TEAEs48 (32.2)54 (36.0)110 (36.3)149 (49.2)Deaths1 (0.7)01 (0.3)2 (0.7)TEAEs are reported for the BE AGILE safety set for total exposure to BKZ across BE AGILE and the OLE. There was one death in BE AGILE (cardiac arrest) and one in the OLE (road traffic accident); neither was considered treatment-related.Conclusion:The safety profile of BKZ in patients with AS was in line with previous observations.1.2 Patients treated with BKZ demonstrated sustained and consistent efficacy over 156 weeks.References:[1]van der Heijde D. Ann Rheum Dis 2020;79:595–604; 2. Baraliakos X. Arthritis Rheumatol 2020;72 (suppl 10).Acknowledgements:This study was funded by UCB Pharma. Editorial services were provided by Costello Medical.Disclosure of Interests:Désirée van der Heijde Consultant of: AbbVie, Amgen, Astellas, AstraZeneca, Bayer, BMS, Boehringer Ingelheim, Celgene, Cyxone, Daiichi, Eisai, Eli Lilly, Galapagos, Gilead, GSK, Janssen, Merck, Novartis, Pfizer, Regeneron, Roche, Sanofi, Takeda, UCB Pharma, Employee of: Director of Imaging Rheumatology, Atul Deodhar Speakers bureau: Janssen, Novartis, Pfizer, Consultant of: AbbVie, Amgen, BMS, Boehringer Ingelheim, Celgene, Eli Lilly, Gilead, GSK, Janssen, Novartis, Pfizer, UCB Pharma, Grant/research support from: AbbVie, Eli Lilly, GSK, Novartis, Pfizer, UCB Pharma, Lianne S. Gensler Consultant of: AbbVie, Eli Lilly, Gilead, GSK, Novartis, Pfizer, UCB Pharma, Grant/research support from: Pfizer, Denis Poddubnyy Speakers bureau: AbbVie, BMS, Eli Lilly, MSD, Novartis, Pfizer, UCB Pharma, Consultant of: AbbVie, Biocad, Eli Lilly, Gilead, GSK, MSD, Novartis, Pfizer, Samsung Bioepis, UCB Pharma, Grant/research support from: AbbVie, MSD, Novartis, Pfizer, Alan Kivitz Shareholder of: Pfizer, Novartis, Speakers bureau: Amgen, Eli Lilly, Pfizer, Novartis, Consultant of: Novartis, UCB Pharma, Maxime Dougados Consultant of: AbbVie, Eli Lilly, Novartis, Pfizer, UCB Pharma, Grant/research support from: AbbVie, Eli Lilly, Novartis, Pfizer, UCB Pharma, Natasha de Peyrecave Employee of: UCB Pharma, Marga Oortgiesen Employee of: UCB Pharma, Thomas Vaux Employee of: UCB Pharma, Carmen Fleurinck Employee of: UCB Pharma, Xenofon Baraliakos Speakers bureau: AbbVie, BMS, Chugai, Eli Lilly, Galapagos, Gilead, MSD, Novartis, Pfizer, UCB Pharma, Paid instructor for: AbbVie, BMS, Chugai, Eli Lilly, Galapagos, Gilead, MSD, Novartis, Pfizer, UCB Pharma, Consultant of: AbbVie, BMS, Chugai, Eli Lilly, Galapagos, Gilead, MSD, Novartis, Pfizer, UCB Pharma

Background:The oral Janus kinase 1 preferential inhibitor filgotinib (FIL) significantly improved Spondyloarthritis Research Consortium of Canada (SPARCC) magnetic resonance imaging (MRI) inflammation scores (bone marrow oedema) in the spine and sacroiliac joints vs placebo (PBO) in the Phase 2 TORTUGA trial (NCT03117270) in patients with active ankylosing spondylitis (AS).1Objectives:This post-hoc analysis evaluated the effects of FIL on Canada-Denmark (CANDEN) MRI measures of spinal inflammation and structural lesions in patients from the TORTUGA trial.Methods:TORTUGA was a PBO-controlled, multicentre, double-blind, randomised trial. Patients with active AS (as per modified New York classification criteria, with sacroiliitis confirmed by central reading) were treated with FIL 200 mg (n=58) or PBO (n=58) once daily for 12 weeks. MRI of the total spine was conducted at baseline and at treatment end. Scans were re-evaluated post-hoc by 2 independent experts (blinded to time point and assigned treatment) using the CANDEN method;2 inter-reader discrepancies were resolved by an independent adjudicator. Observed changes from baseline were evaluated using analysis of covariance, with factors for treatment, baseline value, and randomisation stratification by prior tumour necrosis factor inhibitor use. Least-squares (LS) mean changes from baseline and between-group differences with 95% confidence intervals (CI) were calculated; P values are nominal.Results:MRI scans from 88 patients (47 FIL, 41 PBO) with an evaluable scan at baseline and Week 12 (or early termination) were re-evaluated. Baseline characteristics were generally similar between patients with/without an MRI scan. Of those with MRI scans, mean total spine inflammation score (which ranges from 0–614) was higher, and mean ankylosis score (which ranges from 0–460) was lower, in the FIL vs PBO group at baseline. Total spine inflammation scores decreased from baseline with FIL but not with PBO (Figure and Table; P=0.0003 for between-group difference). Cumulative probability plots favoured FIL over PBO for change from baseline in subregion inflammation scores, including posterolateral elements (i.e. sum of lesions in ribs, transverse processes, spinous processes, soft tissue inflammation, and postero-lateral vertebral body), facet joint, and vertebral body. Total spine fat lesion scores numerically increased from baseline in the FIL but not PBO group (P=0.0878 for between-group difference; Table). There were no significant differences between groups for changes in erosion (P=0.1956) or ankylosis (P=0.3888) scores (Table).Table 1.Change from baseline at Week 12 in CANDEN total spine inflammation, total spine fat, total spine bone erosion, and ankylosis scoresTreatment groupnSample mean (SE)LS mean (SE)95% CI of treatment meanLS mean of group difference (SE)95% CI of group differenceBetween-group P valueTotal spine inflammation scoreFilgotinib47–4.98 (0.96)–4.40 (1.13)–6.65, –2.15–4.49 (1.21)–6.85, –2.120.0003Placebo410.29 (0.78)0.09 (1.13)–2.17, 2.34Total spine fat scoreFilgotinib471.01 (0.62)1.09 (0.66)–0.22, 2.401.18 (0.69)–0.18, 2.550.0878Placebo41–0.25 (0.19)–0.09 (0.66)–1.40, 1.21Total spine bone erosion scoreFilgotinib470.01 (0.02)0.07 (0.03)0.00, 0.140.05 (0.04)–0.02, 0.120.1956Placebo41–0.02 (0.03)0.02 (0.03)–0.04, 0.09Total ankylosis scoreFilgotinib470.30 (0.29)0.23 (0.31)–0.40, 0.850.28 (0.34)–0.37, 0.940.3888Placebo41–0.01 (0.08)–0.06 (0.31)–0.68, 0.56SE, standard errorConclusion:This is the first PBO-controlled trial to demonstrate a decrease in inflammatory activity with FIL, not only in the spinal vertebrae but also in the postero-lateral elements of the spine and facet joints. As expected in a 12-week study period, no changes in erosion or ankylosis were seen, while fat lesions showed a tendency to increase with FIL. Larger trials are needed to confirm these results.References:[1]van der Heijde D, et al. Lancet 2018;392:2378–87.[2]Krabbe S, et al. RMD Open 2019;5:e001057.Acknowledgements:The TORTUGA trial was sponsored by Galapagos NV (Mechelen, Belgium) and co-funded by Galapagos NV and Gilead Sciences, Inc. (Foster City, CA, USA). Medical writing support was provided by Debbie Sherwood BSc, CMPP (Aspire Scientific Ltd, Bollington, UK), and funded by Galapagos NV.Disclosure of Interests:Xenofon Baraliakos Consultant of: AbbVie, Bristol Myers Squibb, Celgene, Chugai, Eli Lilly, Galapagos, Hexal, Janssen, MSD, Novartis, Pfizer, Sandoz and UCB, Grant/research support from: AbbVie, Celgene, Novartis and UCB, Mikkel Østergaard Speakers bureau: AbbVie, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Orion, Pfizer, Roche, Sandoz, Sanofi and UCB, Consultant of: AbbVie, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Hospira, Janssen, Merck, Novartis, Novo Nordisk, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi and UCB, Grant/research support from: AbbVie, Bristol Myers Squibb, Celgene, Merck and Novartis, Robert B.M. Landewé Speakers bureau: AbbVie, Amgen, Bristol Myers Squibb, Janssen (formerly Centocor), Merck, Pfizer, Roche, Schering and UCB, Consultant of: AbbVie, Ablynx, Amgen, AstraZeneca, Bristol Myers Squibb, Celgene, Eli Lilly, Galapagos, Gilead, GlaxoSmithKline, Janssen, Merck, Novartis, Novo Nordisk, Pfizer, Roche, Schering, TiGenix and UCB, Grant/research support from: AbbVie, Amgen, Janssen (formerly Centocor), Novartis, Pfizer, Roche, Schering and UCB, Employee of: Director of Rheumatology Consultancy BV, William Barchuk Shareholder of: Gilead Sciences, Inc., Employee of: Currently employee of Gilead Sciences, Inc.; and former employee of AbbVie, Eli Lilly and Johnson & Johnson, Ke Liu Shareholder of: Gilead Sciences, Inc., Employee of: Gilead Sciences, Inc., Chantal Tasset Shareholder of: Galapagos, Employee of: Galapagos, Leen Gilles Employee of: Galapagos, Thijs Hendrikx Shareholder of: Galapagos, Employee of: Galapagos, Robin Besuyen Shareholder of: Galapagos, Employee of: Galapagos, Walter P Maksymowych Speakers bureau: AbbVie, Janssen, Novartis, Pfizer and UCB, Consultant of: AbbVie, Boehringer Ingelheim, Celgene, Eli Lilly, Galapagos, Gilead, Janssen, Novartis, Pfizer and UCB, Grant/research support from: AbbVie, Novartis, Pfizer and UCB, Employee of: Chief Medical Officer of CARE Arthritis Limited

ObjectivesTo compare the CT Syndesmophyte Score (CTSS) for low-dose CT (ldCT) with the modified Stoke Ankylosing Spondylitis Spine Score (mSASSS) for conventional radiographs (CR) in patients with ankylosing spondylitis (AS).MethodsPatients with AS in the Sensitive Imaging in Ankylosing Spondylitis cohort had lateral cervical and lumbar spine CR and whole spine ldCT at baseline and 2 years. CR and ldCT images were scored by two readers, paired by patient, blinded to time order, per imaging modality. For the total score analysis, we used average scores of readers per corner on CR or quadrant on ldCT. For the syndesmophyte analysis we used individual reader and consensus scores, regarding new or growing syndesmophyte at the same corner/quadrant.Results50 patients were included in the syndesmophyte analysis and 37 in the total score analysis. Mean (SD) status scores for mSASSS (range 0–72) and CTSS (range 0–552) at baseline were 17.9 (13.8) and 161.6 (126.6), and mean progression was 2.4 (3.8) and 17.9 (22.1). Three times as many patients showed new or growing syndesmophytes at ≥3 quadrants on ldCT compared with ≥3 corners on CR for individual readers; for consensus this increased to five times. In 50 patients, 36 new or growing syndesmophytes are seen on CR compared with 151 on ldCT, most being found in the thoracic spine.ConclusionsldCT, covering the whole spine, detects more progression in the form of new and growing syndesmophytes in patients with AS compared with CR, which is limited to the cervical and lumbar spine. Most progression occurred in the thoracic spine.

Background: In 2010 the latest ASAS-EULAR recommendations for ankylosing spondylitis and the ASAS recommendations for the use of TNF-inhibitors (TNFi) have been published. Since then new treatments for axial Spondyloarthritis (axSpA) have become available. Aim: To update and integrate the two sets[for full text, please go to the a.m. URL], 44. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh); 30. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh); 26. Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR)

Background:Axial spondyloarthritis (axSpA) is a chronic disease characterised by inflammation in the sacroiliac joints and spine, causing severe back pain and stiffness. Emerging evidence suggests chronic spinal inflammation may be associated with osteoproliferation leading to syndesmophyte formation and spinal ankylosis, with subsequent worsening of patient mobility and function.1Fatty lesions (FLs) on magnetic resonance imaging (MRI) T1 sequences are considered to be post-inflammatory precursors to these changes. Certolizumab pegol (CZP), an Fc-free, PEGylated tumour necrosis factor inhibitor (TNFi), has proven efficacy in treating the signs and symptoms of axSpA.2,3CZP has also been shown to decrease spinal and sacroiliac joint MRI inflammation, and limit radiographic progression of the spine over 4 years of treatment.4Objectives:To report the effect of early post-baseline (BL) inflammatory changes on fatty lesion prevalence over 4 years in a broad axSpA patient population treated with CZP.Methods:RAPID-axSpA (NCT01087762) was a phase 3 trial which was double-blind and placebo (PBO)-controlled to Week (Wk) 24, dose-blind to Wk 48 and open-label to Wk 204. CZP-randomised axSpA patients (Wk 0 CZP: 200 mg every 2 wks [Q2W] or 400 mg Q4W) continued their assigned dose throughout; PBO-randomised axSpA patients (Wk 0 PBO) received CZP from Wk 24, or if non-responders, from Wk 16 onwards. Blinded spinal MRI scans at Wks 0, 12, 48, 96 and 204 were assessed by 2 central readers to evaluate FL and inflammatory lesions in vertebral edges (VEs). Changes in FL prevalence are reported as odds ratios (OR; FL+/FL-) between time points or inflammation states, with nominal 95% confidence intervals (CI), for Wk 0 CZP. ORs were estimated from a logistic regression model for VE level data with random effects for patient and VE (within patient). The fixed model effects included time point, inflammatory status of VEs at BL and Wk 12, FL status at BL, and interactions if appropriate.Results:Of 325 axSpA patients, 89 and 47 initially randomised to CZP or PBO, respectively, had a BL and ≥1 post-BL MRI and therefore were eligible for these analyses. In these patients, a total of 3,127 of VEs were assessed at BL; inflammation was observed in 21.6% and FL in 29.3% of VEs, equating to mean counts of 5.0 and 6.7 per patient; 10.5% of VEs had both inflammation and FL at BL. At BL, FLs were relatively more often observed in inflamed VEs vs non-inflamed VEs: OR (95% CI) of 3.30 (1.94, 5.61). This difference increased over time, as the OR of FL at Wk 204 vs BL was 2.82 (1.70, 4.66) in VEs that were inflamed at BL compared with 1.08 (0.79, 1.48) in VEs that were not inflamed at BL (Figure 1A). Resolution of inflammation by Wk 12 appeared to lower the risk of FL prevalence over 4 years. When adjusted for BL VE status with respect to inflammation and FL, if inflammation prevailed at Wk 12, the OR of FL vs no FL was 1.80 (0.93, 3.49) at Wk 48, 2.54 (1.32, 4.91) at Wk 96 and 3.91 (1.87, 8.15) at Wk 204 (Figure 1B).Conclusion:This is the first report from a clinical interventional PBO-controlled study in a broad axSpA population showing that inflammation that prevailed after the start of TNFi treatment was associated with increased FL prevalence over 4 years. Reduction of inflammation by Wk 12 mitigated the risk of FL over the long-term, indicating the importance of early, effective and long-term treatment targeting inflammation. Similarly, a complete and persistent reduction of inflammation appears to be critical in these patients.References:[1]Maksymowych WP. Ann Rheum Dis 2013;72:23–8;2.Van der Heijde D. Rheumatology (Oxford) 2017;56:1498–509;3.Deodhar A. Arthritis Rheumatol 2019;71:1101–11;4.Van der Heijde D. Ann Rheum Dis 2018;77:699–705.Acknowledgments:This study was funded by UCB Pharma. Editorial services were provided by Costello Medical.Disclosure of Interests:Xenofon Baraliakos Grant/research support from: Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Consultant of: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Sebastian Kruse: None declared, Simone Auteri Shareholder of: UCB Pharma, Employee of: UCB Pharma, Natasha de Peyrecave Employee of: UCB Pharma, Tommi Nurminen Employee of: UCB Pharma, Thomas Kumke Employee of: UCB Pharma, Bengt Hoepken Employee of: UCB Pharma, Juergen Braun Grant/research support from: Abbvie (Abbott), Amgen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, Eli Lilly and Company, Medac, MSD (Schering Plough), Mundipharma, Novartis, Pfizer (Wyeth), Roche, Sanofi- Aventis, and UCB Pharma, Consultant of: Abbvie (Abbott), Amgen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, EBEWE Pharma, Eli Lilly and Company, Medac, MSD (Schering-Plough), Mundipharma, Novartis, Pfizer (Wyeth), Roche, Sanofi-Aventis, and UCB Pharma, Speakers bureau: Abbvie (Abbott), Amgen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, EBEWE Pharma, Eli Lilly and Company, Medac, MSD (Schering-Plough), Mundipharma, Novartis, Pfizer (Wyeth), Roche, Sanofi-Aventis, and UCB Pharma

Background:Patients with ankylosing spondylitis (AS) are burdened with decreased work productivity.1Ixekizumab (IXE), a high-affinity monoclonal antibody selectively targeting interleukin-17A, has been shown to improve disease signs and symptoms in 2 phase 3 trials assessing patients with active AS.2, 3Objectives:This study investigated the effect of IXE treatment for 52 weeks on work productivity and activity impairment as measured by absenteeism, presenteeism, overall work impairment, and activity impairment in patients with active AS.Methods:COAST-V (NCT02696785) and COAST-W (NCT02696798) were phase 3, multicenter, randomized, double-blind, placebo (PBO)-controlled (COAST-V active-controlled with adalimumab) trials investigating the efficacy of IXE every 4 weeks (Q4W) and every 2 weeks (Q2W) in 341 patients with active AS naïve to biologic disease-modifying antirheumatic drugs (bDMARDs; COAST-V) and in 316 patients who were inadequate responders or intolerant to 1 or 2 tumor necrosis factor inhibitors (TNFi; COAST-W). Patients receiving PBO were switched to IXE Q4W or Q2W at Week 16; patients receiving adalimumab (ADA) were switched to IXE Q4W or Q2W at Week 20. Data for IXE Q4W and Q2W were combined for PBO/IXE and ADA/IXE groups. Changes from baseline in work productivity were measured for those reporting full- or part-time work at Weeks 16 and 52 with the Work Productivity and Activity Impairment (WPAI) Questionnaire for Spondyloarthritis.Results:Compared to bDMARD-naïve patients (COAST-V), TNFi-experienced patients (COAST-W) were slightly older, had longer disease duration, reported less paid employment, and had greater scores for impaired work productivity, signifying more severe baseline disease. At Week 16, bDMARD-naïve patients treated with IXE Q4W or Q2W had significant improvements in activity impairment compared to placebo (pConclusion:Both bDMARD-naïve and TNFi-experienced patients with AS receiving IXE had greater improvements in aspects of work productivity compared to placebo. Improvements were sustained through Week 52.References:[1]Boonen, van der Linden. (2006).J Rheumatol Suppl.78:4-11.[2]Van der Heijde, et al. (2018)Lancet. 392(10163):2441-51.[3]Deodhar, et al. (2019)Arthritis Rheumatol.71(4):599-611.Disclosure of Interests:Helena Marzo-Ortega Grant/research support from: Janssen, Novartis, Consultant of: Abbvie, Celgene, Eli Lilly, Janssen, Novartis, Pfizer, UCB, Speakers bureau: Abbvie, Celgene, Eli Lilly, Janssen, Novartis, Pfizer, Takeda, UCB, Philip J Mease Grant/research support from: AbbVie, Amgen, Bristol-Myers Squibb, Janssen, Eli Lilly, Novartis, Pfizer, Sun Pharma, UCB Pharma, Consultant of: AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Janssen, Eli Lilly, Galapagos, Gilead, Novartis, Pfizer, Sun Pharma, UCB Pharma, Speakers bureau: AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Genentech, Janssen, Novartis, Pfizer, UCB Pharma, Proton Rahman Grant/research support from: Janssen and Novartis, Consultant of: Abbott, AbbVie, Amgen, BMS, Celgene, Lilly, Janssen, Novartis, and Pfizer., Speakers bureau: Abbott, AbbVie, Amgen, BMS, Celgene, Lilly, Janssen, Novartis, Pfizer, Victoria Navarro-Compán Consultant of: Abbvie, Lilly, Novartis, Pfizer, UCB, Speakers bureau: AbbVie, MSD, Lilly, Novartis, Pfizer, UCB, Vibeke Strand Consultant of: AbbVie, Amgen, Biogen, Celltrion, Consortium of Rheumatology Researchers of North America, Crescendo Bioscience, Eli Lilly, Genentech/Roche, GlaxoSmithKline, Hospira, Janssen, Merck, Novartis, Pfizer, Regeneron Pharmaceuticals, Inc., Sanofi, UCB, Maxime Dougados Grant/research support from: AbbVie, Eli Lilly, Merck, Novartis, Pfizer and UCB Pharma, Consultant of: AbbVie, Eli Lilly, Merck, Novartis, Pfizer and UCB Pharma, Speakers bureau: AbbVie, Eli Lilly, Merck, Novartis, Pfizer and UCB Pharma, Bernard Combe Grant/research support from: Novartis, Pfizer, Roche-Chugai, Consultant of: AbbVie; Gilead Sciences, Inc.; Janssen; Eli Lilly and Company; Pfizer; Roche-Chugai; Sanofi, Speakers bureau: Bristol-Myers Squibb; Gilead Sciences, Inc.; Eli Lilly and Company; Merck Sharp & Dohme; Pfizer; Roche-Chugai; UCB, James Cheng-Chung Wei Grant/research support from: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly, Janssen, Novartis, Pfizer Inc, UCB, Consultant of: AbbVie, Bristol-Myers Squibb, Celgene, Chugai, Eisai, Janssen, Novartis, Pfizer Inc, Sanofi-Aventis, UCB Pharma, Xenofon Baraliakos Grant/research support from: Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Consultant of: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Theresa Hunter Shareholder of: Eli Lilly and Company, Employee of: Eli Lilly and Company, David Sandoval Shareholder of: Eli Lilly and Company, Employee of: Eli Lilly and Company, Xiaoqi Li Shareholder of: Eli Lilly and Company, Employee of: Eli Lilly and Company, Baojin Zhu Shareholder of: Eli Lilly and Company, Employee of: Eli Lilly and Company, Louis Bessette Grant/research support from: AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Eli Lilly, Janssen, Merck, Novartis, Pfizer, Roche, Sanofi, UCB Pharma, Consultant of: AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Eli Lilly, Janssen, Merck, Novartis, Pfizer, Roche, Sanofi, UCB Pharma, Speakers bureau: AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Eli Lilly, Janssen, Merck, Novartis, Pfizer, Sanofi, Atul Deodhar Grant/research support from: AbbVie, Eli Lilly, GSK, Novartis, Pfizer, UCB, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myer Squibb (BMS), Eli Lilly, GSK, Janssen, Novartis, Pfizer, UCB, Speakers bureau: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myer Squibb (BMS), Eli Lilly, GSK, Janssen, Novartis, Pfizer, UCBFigure.Changes from baseline in Overall Work Impairment in A) bDMARD-naïve (COAST-V) and B) TNFi-experienced (COAST-W) patients and Activity Impairment in C) bDMARD-naïve and D) TNFi-experienced patients.

Background:For patients with rheumatoid arthritis (RA), long-term prevention of structural joint damage is a key treatment goal.1In the SELECT-EARLY and SELECT-COMPARE trials, upadacitinib (UPA), an oral JAK inhibitor, inhibited the progression of structural joint damage at 6 months and 1 year when used either as monotherapy or in combination with methotrexate (MTX) in patients (pts) with active RA.2Objectives:To describe the radiographic progression up to 2 years (96 wks) among pts with RA receiving UPA either as monotherapy or in combination with MTX.Methods:Both the SELECT-EARLY and SELECT-COMPARE phase 3, randomized controlled trials enrolled pts at high risk for progressive structural damage with baseline (BL) erosive joint damage and/or seropositivity.3,4In SELECT-EARLY, MTX-naïve pts (N=945) were randomized to UPA 15 mg or 30 mg once daily (QD) or MTX monotherapy. In SELECT-COMPARE, pts with an inadequate response to MTX (N=1629) were randomized to UPA 15 mg, placebo (PBO), or adalimumab (ADA) 40 mg every other wk, with all pts continuing background MTX; at wk 26, all pts receiving PBO were switched to UPA 15 mg, regardless of response. In both trials, mean changes from BL in modified Total Sharp Score (mTSS), joint space narrowing, and joint erosion as well as the proportion of pts with no radiographic progression (change in mTSS ≤0) were evaluated based on X-rays taken at wks 24/26, 48, and 96 for those patients in whom wk 96 X-rays were available. Data are reported as observed (AO).Results:BL demographics have been reported previously.3,4In the SELECT-EARLY study, at wk 96 UPA monotherapy (15 mg and 30 mg doses) significantly inhibited radiographic progression compared with MTX as measured by mean change in mTSS and by the proportion of patients with no radiographic progression (Figures 1 and 2). When patients who were rescued (MTX added to UPA or UPA added to MTX) were removed from the analysis, changes in mTSS from baseline remained similar. By the same measures, in SELECT-COMPARE, the degree of inhibition of structural progression observed was comparable between UPA and ADA. Following the switch of all PBO patients to UPA, the rate of progression slowed and was comparable to that observed in pts receiving UPA from BL. Among pts from both studies that had no radiographic progression at wk 24/26, >90% remained without radiographic progression at wk 48 and 96.Conclusion:UPA was effective in inhibiting the progression of structural joint damage through 2 years both in MTX-naïve patients receiving UPA monotherapy and MTX-inadequate responder patients receiving UPA in combination with MTX.References:[1]Smolen, et al.Ann Rheum Dis2017;76(6):960-77.[2]Peterfy, et al.Ann Rheum Dis2019;78(suppl 2):369-370.[3]Fleischmann, et al.Arthritis Rheumatol2019;71(11):1788-1800.[4]Van Vollenhoven, et al.Arthritis Rheumatol2018;70(suppl 10).Disclosure of Interests: :Charles Peterfy Consultant of: AbbVie, Acerta, Amgen, AstraZeneca, Bristol Myers Squibb, Centrexion, Daiichi Sankyo, Five Prime Therapeutics, Genentech, Gilead, Hoffman-La Roche, Janssen, Lilly USA, MedImmune, Merck, Myriad, Novartis, Plexxikon, Pfizer, Sanofi, Salix Santarus, Samsung, Samumed, Setpoint, Sorrento, UCB, Vorso, Employee of: founder and CEO of Spire Sciences, which provides imaging services to multiple pharmaceutical companies, Speakers bureau: Amgen, Vibeke Strand Consultant of: AbbVie, Amgen, Biogen, Celltrion, Consortium of Rheumatology Researchers of North America, Crescendo Bioscience, Eli Lilly, Genentech/Roche, GlaxoSmithKline, Hospira, Janssen, Merck, Novartis, Pfizer, Regeneron Pharmaceuticals, Inc., Sanofi, UCB, Mark C. Genovese Grant/research support from: Abbvie, Eli Lilly and Company, EMD Merck Serono, Galapagos, Genentech/Roche, Gilead Sciences, Inc., GSK, Novartis, Pfizer Inc., RPharm, Sanofi Genzyme, Consultant of: Abbvie, Eli Lilly and Company, EMD Merck Serono, Genentech/Roche, Gilead Sciences, Inc., GSK, Novartis, RPharm, Sanofi Genzyme, Alan Friedman Shareholder of: AbbVie Inc, Employee of: AbbVie Inc, Jose Jeffrey Enejosa Shareholder of: AbbVie, Employee of: AbbVie, Stephen Hall Grant/research support from: Abbvie, UCB, Janssen, Merck, Eduardo Mysler Grant/research support from: AbbVie, Amgen, Bristol Myers Squibb, Roche, Eli Lilly, Novartis, Janssen, Sanofi, and Pfizer., Speakers bureau: AbbVie, Amgen, Bristol Myers Squibb, Roche, Eli Lilly, Novartis, Janssen, Sanofi, and Pfizer, Patrick Durez Speakers bureau: AbbVie, Bristol-Myers Squibb, Celltrion, Eli Lilly, Pfizer, Sanofi, Xenofon Baraliakos Grant/research support from: Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Consultant of: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Tim Shaw Shareholder of: AbbVie, Employee of: AbbVie, Yanna Song Shareholder of: AbbVie Inc., Employee of: AbbVie Inc., Yihan Li Shareholder of: AbbVie, Employee of: AbbVie, In-Ho Song Shareholder of: AbbVie Inc., Employee of: AbbVie Inc.

Background:Although axial disease may affect up to 70% of patients (pts) with Psoriatic Arthritis (PsA), evidence on the efficacy of biologics in the treatment of axial manifestations in such pts is limited,1particularly as validated classification criteria for this subtype of PsA are not yet available. MAXIMISE (NCT02721966) is the first randomised controlled trial evaluating the efficacy of a biologic in the management of the axial manifestations of PsA and showed that secukinumab (SEC) 300 and 150 mg provided rapid and significant improvement in ASAS20 responses in these pts through week (Wk) 12.2Objectives:To present 52 wks efficacy results and imaging data from the MAXIMISE trial.Methods:This phase 3b, double-blind, placebo (PBO)-controlled, multicentre 52-wk trial included 498 pts (aged ≥18 years) with a diagnosis of PsA and classified by CASPAR criteria, spinal pain VAS score ≥ 40/100 and BASDAI score ≥ 4 despite use of at least two NSAIDs. Pts were randomised to SEC 300 mg (N=167) or SEC 150 mg (N=165) or PBO (N=166) wkly for 4 wks and every 4 wks thereafter. At Wk 12, PBO pts were re-randomised to SEC 300/150 mg. The primary endpoint was ASAS20 response with SEC 300 mg at Wk 12. The key secondary endpoint was ASAS20 response with SEC 150 mg at Wk 12. Wk 52 data are presented as observed. Bone marrow oedema of the entire spine and sacroiliac joints were assessed centrally with Berlin MRI scores at Baseline, Wk 12 and Wk 52.Results:Primary and key secondary endpoints were met; ASAS20 responses were sustained and increased further through Wk 52. 75%/79.7% of the PBO pts re-randomised at Wk 12 to SEC 300/150 mg achieved ASAS20 response at Wk 52 (Figure 1). ASAS40 responses at Wk 52 were 69.1% [SEC 300 mg], 64.5% [SEC 150 mg], 62.5% [PBO-SEC 300 mg], and 54.1% [PBO-SEC 150 mg]. At baseline, 59.5% [SEC 300 mg], 53.5% [SEC 150 mg] and 64.2% [PBO] of the pts had positive MRIs for the sacroiliac joints and/or the spine with Berlin MRI score ≥1. The reductions of Berlin MRI score for entire spine and sacroiliac joints were statistically significant for pts treated with SEC 300/150 mg vs. placebo (Figure 2a and b). There were no new or unexpected safety findings.Figure 1.ASAS20 Response over 52 Wks*Figure 2.Total Berlin MRI score for the Entire Spine and Sacroiliac Joints at Wk 12Conclusion:Secukinumab improved all evaluated ASAS responses through Wk 52 in PsA pts with axial manifestations and inadequate responses to NSAIDs and led to significant reduction of inflammatory MRI lesions in the spine and the Sacroiliac Joints. The safety profile of secukinumab through Wk 52 was consistent with previous reports.3-4References:[1]McInnes IB, et al.Lancet.2015;386(9999):1137–46.[2]Baraliakos X, et al.Arthritis Rheumatol. 2019;71 (suppl 10).[3]Langley RG, et al.N Engl J Med.2014;371:326–38.[4]Sieper J, et al.Ann Rheum Dis.2016;0:1–8.Acknowledgments:The study was sponsored by Novartis Pharma AG, Basel, Switzerland.Disclosure of Interests:Xenofon Baraliakos Grant/research support from: Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Consultant of: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Laure Gossec Grant/research support from: Lilly, Mylan, Pfizer, Sandoz, Consultant of: AbbVie, Amgen, Biogen, Celgene, Janssen, Lilly, Novartis, Pfizer, Sandoz, Sanofi-Aventis, UCB, Effie Pournara Shareholder of: Novartis, Employee of: Novartis, Sławomir Jeka Grant/research support from: AbbVie, Pfizer, Roche, Novartis, MSD, Sandoz, Eli Lilly, Egis, UCB, Celgene, Speakers bureau: AbbVie, Pfizer, Roche, Novartis, MSD, Sandoz, Eli Lilly, Egis, UCB, Celgene, Ricardo Blanco Grant/research support from: AbbVie, MSD, Roche, Consultant of: Abbvie, Eli Lilly, Pfizer, Roche, Bristol-Myers, Janssen, UCB Pharma and MSD, Speakers bureau: Abbvie, Eli Lilly, Pfizer, Roche, Bristol-Myers, Janssen, UCB Pharma. MSD, Salvatore D’Angelo Consultant of: AbbVie, Biogen, BMS, Celgene, Eli Lilly, MSD, Novartis, and UCB, Speakers bureau: AbbVie, BMS, Celgene, Eli Lilly, Novartis, Pfizer, and Sanofi, Georg Schett Speakers bureau: AbbVie, BMS, Celgene, Janssen, Eli Lilly, Novartis, Roche and UCB, Barbara Schulz Employee of: Novartis, Michael Rissler Shareholder of: Novartis, Employee of: Novartis, Kriti Nagar Employee of: Novartis, Chiara Perella Shareholder of: Novartis, Employee of: Novartis, Laura C Coates: None declared

Background:Ankylosing spondylitis (AS) is a chronic inflammatory disease of the axial skeleton associated with pain, stiffness, and disability.1Up to 66% of patients (pts) with AS may also have peripheral involvement, including swollen and tender joints (STJs),2,3which are associated with worse overall disease activity.4A previous analysis showed that secukinumab, a selective inhibitor of interleukin 17A, led to significant improvements in efficacy outcomes vs placebo, regardless of peripheral joint involvement.3However, the effect of secukinumab on symptoms of peripheral arthritis in pts with AS was not assessed.Objectives:The objective of this analysis was to assess changes in peripheral symptoms in pts with AS treated with secukinumab vs placebo.Methods:Data from pts with active AS and peripheral symptoms who were enrolled in MEASURE 1 (NCT01358175), 2 (NCT01649375), 3 (NCT02008916), and 4 (NCT02159053) were pooled in this post hoc, hypothesis-generating analysis. No adjustments for multiple comparisons were made. Pts with peripheral symptoms were identified by the presence of STJs, based on 44-joint counts at baseline (BL). Pts received subcutaneous (SC) secukinumab every 4 weeks at doses of 300 mg with an intravenous (IV) loading dose (MEASURE 3 only), 150 mg with an IV or SC loading dose, or placebo. Treatment response through Week 16 was assessed based on the proportions of pts who achieved improvements of 20%, 50%, 70%, or 100% in the number of swollen and number of tender joints and improvements in the BASDAI score for question 3 and Patient Global Assessment (PGA). Changes in the number of swollen and number of tender joints were assessed in pts with swollen or tender joints at BL, respectively.Results:This pooled analysis included 560 pts with AS and STJs at BL (Table). At Week 16, treatment with secukinumab led to significantly greater proportions of pts achieving reductions in the number of swollen (Fig 1A) or tender (Fig 1B) joints compared with placebo; the treatment effect was more pronounced in reduction of swollen joints. Furthermore, a greater proportion of secukinumab-treated pts achieved complete resolution of swollen or tender joints vs placebo (Fig 1). Secukinumab also led to significant improvements in peripheral pain/swelling (Fig 2A) and disease activity (Fig 2B) vs placebo, as assessed using BASDAI question 3 and the PGA, respectively.Table.Patient Characteristics at BaselineSecukinumabPlacebo (n = 252)300 mg (n = 52)150 mg (n = 256)Age, mean, y43.643.744.9Time since diagnosis, mean, y5.67.27.3Male, %63.562.157.5PGA of Disease Activity, mean, mm73.471.770.1BASDAI question 3, mean6.36.66.4Swollen 44-joint count, mean1.92.62.5Tender 44-joint count, mean7.17.87.9Conclusion:In parallel with its previously reported efficacy in axial symptoms,3secukinumab led to significant improvements in symptoms of peripheral arthritis in pts with AS. Significant improvements were seen in both tender and swollen joints.References:[1]Braun J, Sieper J.Lancet. 2007;369:1379-1390.[2]de Winter JJ, et al.Arthritis Res Ther. 2016;18:196.[3]Mease P, et al.Arthritis Rheumatol. 2019;71(suppl 10):1553.[4]de Winter JJ, et al.RMD Open. 2019;5:e000802.Acknowledgments:This study was funded by Novartis Pharmaceuticals Corporation, East Hanover, NJ. The authors thank Amos Race, PhD, of ArticulateScience LLC, Hamilton, NJ, USA, for providing medical writing/editorial support, which was funded by Novartis Pharmaceuticals Corporation, East Hanover, NJ, USA, in accordance with Good Publication Practice (GPP3) guidelines (http://www.ismpp.org/gpp3).Disclosure of Interests:Philip J Mease Grant/research support from: Abbott, Amgen, Biogen Idec, BMS, Celgene Corporation, Eli Lilly, Novartis, Pfizer, Sun Pharmaceutical, UCB – grant/research support, Consultant of: Abbott, Amgen, Biogen Idec, BMS, Celgene Corporation, Eli Lilly, Novartis, Pfizer, Sun Pharmaceutical, UCB – consultant, Speakers bureau: Abbott, Amgen, Biogen Idec, BMS, Eli Lilly, Genentech, Janssen, Pfizer, UCB – speakers bureau, Atul Deodhar Grant/research support from: AbbVie, Eli Lilly, GSK, Novartis, Pfizer, UCB, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myer Squibb (BMS), Eli Lilly, GSK, Janssen, Novartis, Pfizer, UCB, Speakers bureau: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myer Squibb (BMS), Eli Lilly, GSK, Janssen, Novartis, Pfizer, UCB, Renato Calheiros Shareholder of: Novartis, Employee of: Novartis, Xiangyi Meng Shareholder of: Novartis, Employee of: Novartis, Todd Fox Shareholder of: Novartis, Employee of: Novartis, Xenofon Baraliakos Grant/research support from: Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Consultant of: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen

Background:Bimekizumab (BKZ), a monoclonal antibody that selectively neutralises interleukin (IL)-17A and IL-17F, is a potential therapeutic option in ankylosing spondylitis (AS).Objectives:To report 48-week (wk) patient-reported outcomes (PROs) in patients (pts) with AS treated with BKZ in a phase 2b dose-ranging study (BE-AGILE;NCT02963506).Methods:Pts with active AS (Bath AS Disease Activity Index [BASDAI] ≥4; spinal pain ≥4 [0–10]), fulfilling modified New York criteria (central reading), and inadequate response/intolerance to NSAIDs were randomised according to the study design (Figure 1). PROs included spinal pain, fatigue (BASDAI Q1), morning stiffness (mean of BASDAI Q5 + 6), Bath AS Functional Index (BASFI), Medical Outcomes Study (MOS) Sleep Problems Index II and AS Quality of Life questionnaire (ASQoL). Efficacy is reported for pts initially randomised to placebo (PBO) or BKZ 160/320 mg every 4 weeks (Q4W); treatment-emergent adverse events (TEAEs) are reported for pts who received ≥1 dose of study drug (Safety Set).Results:Of 303 pts, 181 were randomised to PBO or BKZ 160/320 Q4W mg at Wk 0; 179/181 completed Wk 12 and 161/181 completed Wk 48. At Wk 12, improvements in pain, fatigue, morning stiffness, BASFI, sleep and ASQoL were greater in BKZ pts vs PBO pts. Responses were further improved or maintained to Wk 48, with no meaningful differences between BKZ 160 mg and 320 mg (Table 1). Serious TEAEs occurred in 13/303 (4.3%) pts (Table 2), which included 2 major adverse cardiac events considered not related to study drug. Oral candidiasis occurred in 16 (5.3%) pts.Table 1.PRO efficacy endpoints to Week 48 (multiple imputation)Mean (SD)WkPBO – BKZ 160 mg(n=24)PBO – BKZ 320 mg(n=36)BKZ 160 mg(n=58)BKZ 320 mg(n=61)Spinal pain06.9 (1.4)7.0 (1.9)6.6 (2.0)7.3 (1.5)CfB12-1.5 (1.6)-0.7 (1.7)-2.6 (2.2)-3.6 (2.4)48-3.7 (2.0)-3.7 (2.6)-3.8 (2.4)-4.7 (2.1)Fatigue06.4 (1.7)6.8 (1.6)6.4 (1.7)6.4 (1.9)CfB12-0.7 (2.5)-1.0 (1.7)-2.1 (2.2)-2.1 (2.5)48-2.7 (2.2)-2.8 (2.4)-3.1 (2.1)-3.3 (2.4)Morning stiffness06.9 (1.7)6.7 (2.0)6.5 (1.8)6.6 (2.1)CfB12-1.5 (1.7)-1.1 (1.5)-2.8 (2.0)-3.4 (2.7)48-3.9 (2.2)-3.6 (2.4)-3.9 (2.2)-4.4 (2.4)BASFI05.8 (1.8)5.5 (2.2)5.5 (2.2)5.9 (2.0)CfB12-1.0 (2.1)-0.3 (1.7)-1.7 (1.8)-2.2 (2.0)48-2.9 (2.2)-2.4 (2.2)-2.5 (2.0)-2.9 (2.2)MOS Sleep Problems Index II045.5 (8.1)45.3 (7.9)46.9 (7.5)47.2 (9.4)CfB122.1 (8.3)1.8 (6.8)5.6 (6.7)6.8 (7.5)487.6 (8.7)8.0 (9.1)6.5 (6.1)8.0 (7.9)ASQoL08.4 (4.7)9.2 (4.7)8.4 (4.3)8.7 (4.3)CfB12-1.3 (5.5)-1.3 (3.7)-3.5 (4.3)-4.6 (4.8)48-4.2 (5.6)-5.3 (5.6)-4.9 (4.1)-5.4 (4.8)CfB: change from baselineTable 2.Overview of TEAEs to Week 48 (Safety Set; N=303)n (%)BKZ 160 mg(n=149)BKZ 320 mg(n=150)All BKZ [a](N=303)Any TEAE103 (69.1)122 (81.3)235 (77.6)Drug-related TEAEs48 (32.2)54 (36.0)110 (36.3)Serious TEAEs5 (3.4)6 (4.0)13 (4.3)Discontinuations due to TEAEs7 (4.7)10 (6.7)20 (6.6)[a] Includes TEAEs for 16 and 64 mg BKZConclusion:Pts with active AS demonstrated rapid and sustained improvements in PROs, sleep and quality of life over 48 wks of BKZ treatment. BKZ was generally well tolerated with no unexpected safety findings versus previous studies.Acknowledgments:This study was funded by UCB Pharma. Editorial services were provided by Costello Medical.Disclosure of Interests: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, Lianne S. Gensler Grant/research support from: Pfizer, Novartis, UCB, Consultant of: AbbVie, Eli Lilly, GSK, Novartis, UCB, Atul Deodhar Grant/research support from: AbbVie, Eli Lilly, GSK, Novartis, Pfizer, UCB, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myer Squibb (BMS), Eli Lilly, GSK, Janssen, Novartis, Pfizer, UCB, Speakers bureau: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myer Squibb (BMS), Eli Lilly, GSK, Janssen, Novartis, Pfizer, UCB, Xenofon Baraliakos Grant/research support from: Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Consultant of: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Denis Poddubnyy Grant/research support from: AbbVie, MSD, Novartis, and Pfizer, Consultant of: AbbVie, Bristol-Myers Squibb, Eli Lilly, MSD, Novartis, Pfizer, Roche, UCB, Speakers bureau: AbbVie, Bristol-Myers Squibb, Eli Lilly, MSD, Novartis, Pfizer, Roche, UCB, Alan Kivitz Shareholder of: AbbVie, Amgen, Gilead, GSK, Pfizer Inc, Sanofi, Consultant of: AbbVie, Boehringer Ingelheim, Flexion, Genzyme, Gilead, Janssen, Novartis, Pfizer Inc, Regeneron, Sanofi, SUN Pharma Advanced Research, UCB, Paid instructor for: Celgene, Genzyme, Horizon, Merck, Novartis, Pfizer, Regeneron, Sanofi, Speakers bureau: AbbVie, Celgene, Flexion, Genzyme, Horizon, Merck, Novartis, Pfizer Inc, Regeneron, Sanofi, Mary Katherine Farmer Employee of: UCB Pharma, Dominique Baeten Employee of: UCB Pharma, Nadine Goldammer Employee of: UCB Pharma, Jason Coarse Employee of: UCB Pharma, Marga Oortgiesen Employee of: UCB Pharma, Maxime Dougados Grant/research support from: AbbVie, Eli Lilly, Merck, Novartis, Pfizer and UCB Pharma, Consultant of: AbbVie, Eli Lilly, Merck, Novartis, Pfizer and UCB Pharma, Speakers bureau: AbbVie, Eli Lilly, Merck, Novartis, Pfizer and UCB Pharma

Background:Guselkumab (GUS), an interleukin-23 inhibitor, was efficacious in reducing signs and symptoms of active psoriatic arthritis (PsA) in patients (pts) in two phase 3 trials (DISCOVER-1 and DISCOVER-2).Objectives:To evaluate the efficacy of GUS in PsA pts with imaging-confirmed axial involvement consistent with sacroiliitis in DISCOVER-1&2.Methods:In DISCOVER-1, 381 pts with active PsA (≥ 3 swollen joints, ≥ 3 tender joints; C-reactive protein ≥ 0.3mg/dL despite standard therapies) and in DISCOVER-2, 739 pts with active PsA (≥ 5 swollen joints, ≥ 5 tender joints, CRP ≥ 0.6mg/dL despite standard therapies) were randomized 1:1:1 to GUS 100mg Q4W, GUS 100mg Q8W (Wk0, Wk4, then Q8W), or PBO. This analysis included pts with sacroiliitis at baseline who had either documented imaging confirmation of sacroiliitis in the past or pelvic X-ray confirmation of sacroiliitis at screening (pooled data from DISCOVER-1&2) based on investigators’ judgment of presence/absence of sacroiliitis. Efficacy was assessed by BASDAI score, BASDAI50, modified BASDAI (mBASDAI; excludes Q#3), spinal pain (BASDAI Q#2), ASDAS-CRP score, and ASDAS responses of inactive disease (Results:312 pts presented with axial involvement (PBO, n= 118; GUS q8w, n = 91; GUS q4w, n = 103). The LS mean changes from baseline to wk24 in BASDAI, spinal pain, mBASDAI, and ASDAS-CRP were greater in the two GUS groups vs PBO (Table). Greater proportions of GUS-treated pts achieved BASDAI50 (Table) and ASDAS responses of inactive disease, major improvement, and clinically important improvement (Figure) at wk24 vs PBO.Conclusion:GUS improved axial symptoms over 24 weeks in active PsA patients with imaging-confirmed sacroiliitis.Table.Efficacy of GUS in PsA patients with axial involvement at week 24.aPBO(n=118)GUS 100 mg every 8 weeks(n=91)GUS100 mg every 4 weeks(n=103)LS Mean change in BASDAI-1.35-2.67*-2.68*LS Mean change in spinal painb-1.30-2.73*-2.48*BASDAI50c, %21/110 (19.1%)34/84 (40.5%)**36/95 (37.9%)**LS Mean change in modified BASDAId-1.13-2.16*-2.18*LS Mean change in ASDAS-CRP-0.71-1.43*-1.46*aPts with axial involvement consistent with sacroiliitis at baseline and either a history of imaging confirmation or pelvic X-ray at screening (pooled data from DISCOVER-1 & 2)bQuestion 2 of the BASDAI.cPts with BASDAI > 0 at baseline.dExcludes question 3 of the BASDAI.Unadjusted p-values as noted: *p < 0.001, ** p < 0.01Acknowledgments:NoneDisclosure of Interests:Philip Helliwell: None declared, Dafna D Gladman Grant/research support from: AbbVie, Amgen Inc., BMS, Celgene Corporation, Janssen, Novartis, Pfizer, UCB – grant/research support, Consultant of: AbbVie, Amgen Inc., BMS, Celgene Corporation, Janssen, Novartis, Pfizer, UCB – consultant, Denis Poddubnyy Grant/research support from: AbbVie, MSD, Novartis, and Pfizer, Consultant of: AbbVie, Bristol-Myers Squibb, Eli Lilly, MSD, Novartis, Pfizer, Roche, UCB, Speakers bureau: AbbVie, Bristol-Myers Squibb, Eli Lilly, MSD, Novartis, Pfizer, Roche, UCB, Philip J Mease Grant/research support from: AbbVie, Amgen, Bristol-Myers Squibb, Janssen, Eli Lilly, Novartis, Pfizer, Sun Pharma, UCB Pharma, Consultant of: AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Janssen, Eli Lilly, Galapagos, Gilead, Novartis, Pfizer, Sun Pharma, UCB Pharma, Speakers bureau: AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Genentech, Janssen, Novartis, Pfizer, UCB Pharma, Xenofon Baraliakos Grant/research support from: Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Consultant of: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Alexa Kollmeier Shareholder of: Johnson & Johnson, Employee of: Janssen Research & Development, LLC, Elizabeth C Hsia Shareholder of: Johnson & Johnson, Employee of: Janssen Research & Development, LLC, Xie L Xu Shareholder of: Johnson & Johnson, Employee of: Janssen Research & Development, LLC, Shihong Sheng Shareholder of: Johnson & Johnson, Employee of: Janssen Research & Development, LLC, Prasheen Agarwal Shareholder of: Johnson & Johnson, Employee of: Janssen Research & Development, LLC, Bei Zhou Shareholder of: Johnson & Johnson, Employee of: Janssen Research & Development, LLC, Soumya D Chakravarty Shareholder of: Johnson & Johnson, Employee of: Janssen Scientific Affairs, LLC, May Shawi Shareholder of: Johnson & Johnson, Employee of: Janssen Research & Development, LLC, Chetan Karyekar Shareholder of: Johnson & Johnson, Consultant of: Janssen, Employee of: Janssen Global Services, LLC. Previously, Novartis, Bristol-Myers Squibb, and Abbott Labs., Atul Deodhar Grant/research support from: AbbVie, Eli Lilly, GSK, Novartis, Pfizer, UCB, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myer Squibb (BMS), Eli Lilly, GSK, Janssen, Novartis, Pfizer, UCB, Speakers bureau: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myer Squibb (BMS), Eli Lilly, GSK, Janssen, Novartis, Pfizer, UCB, 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:Axial spondyloarthritis (axSpA) is clinically characterized by chronic inflammatory back pain and by inflammatory and structural changes in the sacroiliac joint (SIJ) as assessed by magnetic resonance imaging (MRI). Several studies have reported high rates of bone marrow edema (BME) suggestive of inflammatory SIJ changes in up to 20% of individuals in the general population Objectives:To compare the influence of age on the prevalence of inflammatory and structural MRI changes in the SIJ of patients with chronic low back pain diagnosed with axSpA or non-SpA.Methods:MRIs of the SIJ of patients referred for differential diagnosis of back pain who were finally diagnosed with axSpA or not by experienced rheumatologists, were evaluated using semi-coronal STIR and T1-weighted MRI sequences. All images were scored blinded to, age, sex and diagnosis for the occurrence of BME, FL, erosions and ankylosis on the level of SIJ-quadrants (SIJ-Q). Patient groups were built based on decade of age (until 29, 30-39, 40-49 and ≥50 years).Results:A total of 309 patients (175 axSpA and 134 non-SpA) with complete MRI sets were included in the analysis. The mean age was 38.5±11.4 and 43.4±13.8, 66.9% and 35.8% were male, the mean CRP was 1.6±2.4 and 1.1±2.1mg/dl and the median back pain symptom duration was 48 and 60 months, respectively. The number of SIJ-Q with BME and erosions was significantly higher in axSpA vs. non-SpA independent of the age group (Table 1). In comparison, with exception of the patients in the oldest population (≥50 years), the number of SIJ-Q with FL and the number of patients with at least one FL was not different between subgroups, while the number of erosions and FL but not BME was higher in both groups with increasing age. In the univariate analysis, only female sex was significantly associated with higher occurrence of FL.Conclusion:Despite a relatively high prevalence in non-SpA patients, BME and erosions were significantly more frequent in axSpA independent of age, while the presence of FL was not different between groups. FL and erosions are increasingly found in older age groups independent of diagnosis. These data are relevant for the interpretation of MRI findings in the SIJ of patients suspicious of axSpA.Table 1.Comparison of MRI findings between axSpA and non-SpA patients at different age groupsDisclosure of Interests:None declared.

Background:In patients with spondyloarthritis (SpA), root joint diseases (RJD), i.e. hip or shoulder involvement, may be associated with a distinct disease phenotype compared to those with other affected joints. The ASAS-PerSpA study (PERipheral involvement in SPondyloArthritis) [1], offers a unique opportunity to study the phenotypes of patients with RJD in a global cohort.Objectives:Primary objective was to compare the clinical characteristics of SpA patients with and without RJD. Secondary objectives were to compare the prevalence of RJD across the different SpA subtypes and the different regions of the world, compare the severity of axial disease as well as the disease burden in SpA patients with and without RJD.Methods:This is a post-hoc analysis of the ASAS-PerSpA study, which included 4,465 patients with any subtype of SpA (axial SpA (axSpA), peripheral SpA (pSpA), psoriatic arthritis (PsA), inflammatory bowel disease associated SpA (IBD-SpA), reactive arthritis (ReA) and Juvenile SpA (Juv-SpA)) according to the rheumatologist’s diagnosis. RJD was defined as a positive answer by the investigator to the following question: “Do you consider that the patient has ever suffered from RJD (e.g. hip, shoulder) related to SpA?” In case of a positive answer, a potential specific treatment (e.g. Total Articular Replacement) was investigated. The patient’s characteristics were compared between those with and without RJD involvement, using Chi-2 or Fisher exact test for the categorical variables and t-test for the continuous variables. Two separate multivariable stepwise binary logistic regression analyses were conducted to identify factors associated with the dependent variables “hip involvement” and “shoulder involvement”.Results:RJD occurred in 1,503 patients (33.7%), with more prevalent hip (24.2%) than shoulder (13.2%) involvement. The prevalence of RJD as a group was the highest in Juv-SpA (52.7%), followed by pSpA (44.3%) and axSpA (33.9%). The highest prevalence of RJD was found in Asia and the lowest in Europe and North America. Among patients with hip involvement, 6.0% had a history of hip replacement (highest in the Middle East and North Africa and Latin America); among patients with shoulder involvement, 0.8% had a history of shoulder replacement. Hip had a distinct pattern of associations compared to shoulder involvement (Figure 1). Hip involvement was significantly associated with the SpA main diagnosis (highest in pSpA, lowest in PsA), younger age at first SpA symptom, lower prevalence of family history of psoriasis, positive HLA-B27, occiput-to-wall distance>0, and treatment with cs-DMARDs and b-DMARDs. Shoulder involvement was associated with the SpA main diagnosis (highest in Juv-SpA and pSpA, lowest in axSpA), older age at first SpA symptom, higher prevalence of enthesitis, dactylitis, tender joints count, IBD, occiput-to-wall distance>0, EQ5D score and treatment with cs-DMARDs.Conclusion:Hip involvement was more prevalent than shoulder involvement in patients with SpA, and had a distinct phenotype resembling axial disease whereas shoulder involvement was mostly associated with features of peripheral disease. Hip and shoulder involvement should be analyzed separately in future studies rather than under the RJD entity.References:[1]Lopez-medina, C. et al. Prevalence and Distribution of Peripheral Musculoskeletal Manifestations in Axial Spondyloarthritis, Peripheral Spondyloarthritis and Psoriatic Arthritis: Results of the International, Cross-sectional ASAS-PerSpA Study. RMD Open; 2021;7:e001450.Disclosure of Interests:None declared

Background:Carpal tunnel syndrome (CTS) is the most common nerve compression syndrome and a common extra-articular manifestation of rheumatoid arthritis (RA). Different causes of CTS are known, among them inflammatory and non-inflammatory pathologies. Electroneurography (ENG) of the median nerve, the method of choice to diagnose CTS, measures impairment of nerve conduction velocity without explaining its underlying cause. However, because the electrical stimulation is often not well tolerated, ENG results may come out inconclusive. Using greyscale ultrasonography (GS-US) provides anatomic information including a structural representation of the carpal tunnel.Objectives:To investigate the performance of nerve GS-US in the diagnosis of CTS in patients with RA.Methods:Consecutive patients with active RA under suspicion of CTS presenting to a large rheumatologic center were included. Both hands were examined by an experienced neurologist including ENG and a GS-US (ML linear probe with 6-15 Hz) of the median nerve. An established grading system for ENG (1), and an established system for GS-US based on cut-offs for the nerve cross sectional area (CSA) [mild: 0,11-0,13cm2, moderate: 0,14-0,15 cm2, severe: > 0,15 cm2 CTS (2)] were used. In addition, the Boston Carpal Tunnel Syndrome Questionnaire (BCTSQ) was used to assess CTS symptoms (3).Results:Both hands of 58 patients with active RA (n=116) and clinical suspicion of CTS (in 38 cases bilaterally) were included. After clinical examination, CTS was suspicious in 96 hands (82.8%), and 59 of all hands had a final diagnosis of CTS (50.9%). Of the latter, 43 hands (72.9%) had a positive ENG and 16 (27.1%) a positive GS-US finding only, while 30 hands (50.8%) were positive in both examinations.There was a good correlation of the cross-sectional area (CSA) as well as the CSA-ratio to the ENG findings: the larger the CSA, the more severe was the CTS as assessed by ENG (Spearman’s rho=0.554; pIn the 46 hands positive in GS-US, tenosynovial hypertrophy of the flexor tendons was detected in 19 hands (41.3%), 7 of which (36.8%) also showed an additional cystic mass. In these 19 patients, clinical complains were more severely present than in patients with non-inflammatory CTS, as assessed by the BCTSQ with a total score of 68.8±13.4 vs. 59.3±13.7, respectively (p=0.007).Conclusion:In patients with active RA and clinical complains of CTS, ultrasound examinations provide additional information about inflammation which is helpful for a diagnosis of CTS. Thus, ENG and nerve GS-US should be used complementary for a diagnostic workup of CTS in RA patients with a suspicion of CTS. Power-Doppler may further improve the diagnostic performance of GS-US.References:[1]Padua L et al. Acta Neurol Scand 1997; 96:211–217[2]El Miedany et al., Rheumatology (Oxford). 2004 Jul; 43(7):887-895[3]Levine DW et al. J Bone Joint Surg Am 1993; 75: 1585-1592Figure 1.BCTSQ scores in patients with diagnosis of CTS and absence or presence of RA-related tenosynovial hypertrophyDisclosure of Interests:None declared

Background:Psoriatic arthritis (PsA) is a heterogeneous disease with variability of response to different therapeutic modalities.1 Identifying potential demographic and disease characteristics as predictors of treatment response may define personalised treatment optimisation strategies.2–3Objectives:This post-hoc exploratory analysis of the MAXIMISE trial4 investigated the differential treatment effect of demographics and baseline characteristics as predictive factors in biologic naïve patients with active PsA and symptoms of active spinal disease.Methods:The full analysis set (FAS) comprised of all patients from the randomised set assigned to study treatment, fulfilling the predefined clinical criteria for active axial disease and for whom Assessment of SpondyloArthritis International Society (ASAS) 20 data were available at Week 12. The research hypothesis was that the odds ratio associated with the effect of treatment on ASAS20 responder status at Week 12 would be different depending on 12 pre-specified predictor variables. A logistic regression model was initially fitted to the FAS that included 12 pre-specified covariates. A second logistic regression model was then fitted to the FAS that allowed for all 12 pre-specified variables to interact with treatment.5 The log-likelihood of the two fitted models were compared using a likelihood ratio test at a pre-specified significance level of 20% (i.e. P-value ≤0.20) to test whether any of the predefined variables interacted with treatment. If the above test was statistically significant at the 20% level of statistical significance the variables of the second model were formally examined to determine whether the overall effect of treatment is not applicable. Three forest plots were produced, one for each treatment group. Hypothesis tests were employed to determine the strength of evidence for each individual variable.Results:The likelihood ratio test provided evidence against the assumption that the overall effect of treatment is applicable to all patients (P-value = 0.08). Notably, the odds of being an ASAS20 responder if nail dystrophy is present at baseline were 3 times greater in the secukinumab 150 mg group and 5 times greater in the 300 mg group compared with placebo (interaction P-value = 0.029). Although males fare worse than females in the placebo group, in the secukinumab 150 mg and 300 mg treatment groups the odds of being a responder were similar to females (interaction P-value = 0.039). Current smokers were less likely to be ASAS20 responders compared to never smokers regardless of treatment group (interaction P-value = 0.589) (Figure 1). Age, CRP level, Berlin MRI spine/SIJ score, time since first axial signs, number of swollen joints, new bone formation and BMI did not show a differential treatment effect on ASAS20 responses.Conclusion:Of the 12 baseline variables of a unique population of 473 PsA patients with active axial disease diagnosed by clinical criteria, our analyses showed evidence of a differential treatment effect most notably for nail dystrophy suggesting that the presence of nail dystrophy may predict a better response to secukinumab in PsA patients with axial manifestations.References:[1]Coates LC, Helliwell PS. Clin Med (Lond). 2017;17(1):65–70.[2]Watson DS, et al. BMJ. 2019;364:l886.[3]Hügle M, et al. Rheumatol Adv Pract. 2020;4(1):rkaa005.[4]Baraliakos X, et al. Ann Rheum Dis. Published Online First: 17 Dec 2020. doi:10.1136/annrheumdis-2020-218808.[5]Peto R, et al. Br J Cancer. 1977;35(1):1–39.Figure 1.Forest plots of the adjusted odds ratio by treatment using interaction modelDisclosure of Interests:Xenofon Baraliakos Speakers bureau: AbbVie, BMS, Celgene, Chugai, MSD, Novartis, Pfizer, and UCB., Consultant of: AbbVie, BMS, Celgene, Chugai, Galapagos, Gilead, MSD, Novartis, Pfizer, and UCB., Grant/research support from: AbbVie, and Novartis., Effie Pournara Shareholder of: Novartis, Employee of: Novartis, Laure Gossec Consultant of: AbbVie, Amgen, BMS, Biogen, Celgene, Gilead, Janssen, Lilly, Novartis, Pfizer, Samsung Bioepis, Sanofi-Aventis, and UCB., Grant/research support from: Amgen, Lilly, Janssen, Pfizer, Sandoz, Sanofi, and Galapagos., Helena Marzo-Ortega Consultant of: Janssen, Novartis, AbbVie, Celgene, Lilly, Pfizer, Takeda and UCB., Grant/research support from: Janssen, Novartis, AbbVie, Celgene, Lilly, Pfizer, Takeda and UCB., Philip J Mease Speakers bureau: AbbVie, Amgen, Genentech, Janssen, Lilly, Merck, Novartis, Pfizer and UCB., Consultant of: AbbVie, Amgen, BMS, Boehringer Ingelheim, Galapagos, Celgene, Genentech, Gilead, Janssen, Lilly, Novartis, Pfizer, SUN Pharma, and UCB., Grant/research support from: AbbVie, Amgen, BMS, Celgene, Galapagos, Genentech, Gilead, Janssen, Lilly, Merck, Novartis, Pfizer, SUN, and UCB., Roisin White Shareholder of: Novartis, Employee of: Novartis, Eamonn O’Brien Shareholder of: Novartis, Employee of: Novartis, Barbara Schulz Employee of: Novartis, Laura C Coates Speakers bureau: AbbVie, Amgen, Biogen, Celgene, Gilead, Eli Lilly, Janssen, Medac, Novartis, Pfizer, and UCB., Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Eli Lilly, Gilead, Janssen, Novartis, Pfizer, and UCB., Grant/research support from: AbbVie, Amgen, Celgene, Eli Lilly, Pfizer, and Novartis.

Background:Axial spondyloarthritis (axSpA) is characterized by development of structural damage in the spine, assessed by conventional radiographs (CR). The modified Stokes Ankylosing Spondylitis Scoring System (mSASSS) includes all the SpA-relevant CR findings and is the most frequently used scoring system for quantification of spinal structural damage in patients (pts) with axSpA. Radiographic progression over 2 years using mean mSASSS progression, scored by a blinded ‘paired’ (sets of CRs of the same patient) approach, is considered as a key treatment outcome reflecting structural progression in clinical trials. However, this approach has been accompanied by questions about the influence of pts showing mSASSS ‘improvement’, indicating possible disappearance of syndesmophytes over time, something ‘naturally unexpected’.Objectives:To investigate the performance of mSASSS in assessing spinal radiographic damage and progression in axSpA pts using different approaches of CR evaluations.Methods:Complete sets (cervical and lumbar CRs) from the German SpA Inception Cohort (GESPIC) at baseline and after 2 years were blinded to all clinical and demographic characteristics and then scored using the mSASSS by 5 different experienced readers, 2 blinded and 3 unblinded to the timepoint of CR performance. The final mSASSS score was calculated as a mean of 2 (blinded) or 3 (unblinded) readers. Descriptive statistics, cumulative probability plots and shift analyses (agreement of 2/2 readers in the blinded and 2/3 readers in the unblinded group) were performed for each reader group.Results:A total of 210 pts (mean age 37.3y, 51% male, 79% HLA-B27+) with non-radiographic (n=115) and radiographic (n=95) axSpA at baseline were included. The mean mSASSS at baseline was 4.3±8.3 vs. 3.4±7.9, while the mean progression was 0.7±2.3 vs.1.0±1.9 mSASSS units for the blinded vs. the unblinded group, respectively (Figure). On the patient level, progression of ≥2 mSASSS units was found in 30 (14.3%) vs. 37 (17.6%) pts in the blinded vs. the unblinded group, while agreement between groups was seen in 179 (85.2%) pts, 18 (8.9%) pts for progression and 161 (76.7%) for no progression.Figure 1.Cumulative probability plot for mean mSASSS scores (all scores) in blinded (A) and unblinded (B) and ‘definite’ scores in blinded (C) and unblinded (D) scoring approachIn the analysis of ‘definite’ CR findings (only scores of 2=syndesmophytes or 3=ankylosis), the mean mSASSS score at baseline was 3.3±8.0 vs. 2.6±7.2 and the mean radiographic progression was 0.6±2.4 vs. 0.8±2.1 mSASSS units for the blinded vs. the unblinded group, respectively (Figure). On the patient level, progression was found in 37 (17.6%) vs. 33 (15.7%) pts in the blinded vs. the unblinded group, while agreement between groups was seen in 188 (89.5%) pts, 24 (11.3%) for progression and in 164 (78.1%) pts for no progression.In the shift analysis, mSASSS worsening was found in 35 (0.8%) and mSASSS ‘improvement’ in only 4 (0.1%) out of a total of 4.373 vertebral edges (VE) analyzed in the blinded and in 109 (2.2%) and 2 (0.04%), respectively, out of a total of 4.914 VE analyzed in the unblinded group (Table). The majority of progression was found for the development of ‘definite’ signs of progression in both the blinded (25/35, 71.4%) and the unblinded (61/109, 56%) group, while more VE showing ‘minor’ (only scores of 1=sclerosis, squaring, erosion) signs of progression were found in the unblinded (48/109, 44%) vs. to the blinded (10/25, 28.6%) group.Conclusion:Despite lower mean baseline mSASSS, higher mean mSASSS progression was found using the unblinded approach, while in the shift analysis the unblinded approach was also more specific, confirming the absence of ‘improvement’ of radiographic damage over time. These results were similar in the analysis on the patient’s level. The scoring approach and the influence of ‘minor’ radiographic changes should be taken into account for avoiding the so-called ‘background noise’ in the evaluation of mSASSS.Acknowledgements:GESPIC was initially supported by the BMBF. As a consequence of the funding reduction by BMBF according to schedule in 2005 and stopped in 2007, complementary financial support has been obtained also from Abbott, Amgen, Centocor, Schering–Plough, and Wyeth. Starting from 2010, the core GESPIC cohort was supported by AbbVie.Table 1.Shift analysis of the blinded and unblinded reading approach on the basis of VE.Disclosure of Interests:None declared

Background:There is evidence that drug retention rates to adalimumab (ADA) in patients (pts.) with chronic inflammatory rheumatic diseases (CIRD) are impaired by loss of efficacy and adverse events, and that about 50% of users had discontinued ADA within 5 years (1). With the introduction of ADA biosimilars in October 2018, non-medical switching from originator to ADA biosimilars is now increasingly part of daily practice in rheumatologic care.Objectives:The aim was to study treatment trajectories over two years in pts. with CIRD receiving originator ADA.Methods:Pts. with CIRD on originator ADA who switched to ADA biosimilar from October 2018 onwards were identified and followed until 2020. Disease activity (ASDAS), physical function (HAQ, BASFI), and changes in treatment were documented every 3 months. The four predefined treatment trajectories “continued ADA biosimilar therapy”, “back-switch to originator ADA therapy”, “switch to other biological (b) disease modifying anti-rheumatic drug (DMARD) therapy”, and “stopped bDMARD therapy /death /drop out” were used to compare characteristics of pts. with different trajectories.Results:A total of 111 CIRD pts. on treatment with originator ADA were switched to ADA biosimilar (Table 1). The majority of pts. 75 continued therapy with ADA biosimilar (Figure 1 next page) while 16% switched back to originator ADA, 7% switched to a different bDMARD, and 9% either stopped treatment (n=9) or died (n=1). Pts. who continued ADA biosimilar were more frequently male, older or with a longer disease duration than those who switched therapy back to originator ADA and those who switched to a different bDMARD (Table 1). The previous duration on originator ADA treatment was increased in patients who continued ADA biosimilar compared to those who switched therapy back to originator ADA and those who switched to a different bDMARD. There was more functional impairment (HAQ, BASFI) and higher disease activity (ASDAS) in pts. who switched compared to those who continued ADA biosimilar therapy (Table 1). Treatment with csDMARDs and glucocorticoids was increased in pts. who continued ADA biosimilar therapy, while pts. who switched therapy had more previous bDMARD therapies (Table 1).Table 1.Characteristics of patients at baseline for the entire group and stratified by treatment trajectoryTotal groupN=111 (100%)Treatment trajectorycontinued ADA biosimilar therapyN=75 (67.6%)back-switch to originator ADA therapyN=18 (16.2%)switch to different bDMARD therapyN=8 (7.2%)no bDMARD therapy /death /drop outN=10 (9.0%)Age, y51.2 (14.5)51.5 (13.6)50.6 (16.8)43.5 (9.5)56.4 (19.0)Women, No. (%)46 (41.4)27 (36.0)9 (50.0)6 (75.0)4 (40.0)RA23 (20.7)17 (22.7)2 (11.1)1 (12.5)3 (30.0)axSpA68 (61.3)47 (62.7)11 (61.1)6 (75.0)4 (40.0)PsA15 (13.5)7 (9.3)4 (22.2)1 (12.5)3 (30.0)Other diagnoses5 (4.5)4 (5.3)1 (5.6)0 (0.0)0 (0.0)Disease duration, median (IQR), y5.0 (2.0-8.0)5.0 (2.0-9.0)3.5 (2.0-6.0)2.0 (1.0-5.5)4.5 (2.0-8.0)Duration previous originator ADA therapy40.7 (27.7)45.3 (27.8)35.0 (25.2)20.3 (24.7)32.3 (25.1)DAS283.0 (1.0)2.9 (1.0)3.4 (1.0)-3.3 (1.2)CRP, median (IQR), mg/L0.2 (0.1-0.3)0.1 (0.1-0.2)0.2 (0.0-0.5)0.2 (0.2-1.3)0.3 (0.2-0.4)HAQ score1.3 (0.8)1.1 (0.7)1.7 (0.8)-1.8 (1.0)ASDAS2.2 (1.1)2.0 (1.0)3.0 (1.2)2.7 (0.9)2.3 (0.2)BASFI3.5 (2.6)3.0 (2.5)5.4 (2.4)3.4 (1.6)5.4 (1.6)+values are given as mean (SD)Conclusion:Two thirds of pts. who switched to ADA biosimilar remained on this therapy for 2 years. As many as 16% of pts. switched back to ADA originator. Whether or to what degree this was influenced by nocebo effects needs further study. The same is true for the effect of functional impairment – it would be interesting to know whether this was due to inflammation or structural damage.References:[1]Neovius M et al. Ann Rheum Dis 2015; 74:354-360[2]The study was funded by Hexal Germany.Figure 1.Treatment trajectories of ADA therapy in patients with CIRD during two years ADA: adalimumab; bDMARD: biological disease modifying anti-rheumatic drug.Disclosure of Interests:None declared

Background:The best treatment options of patients with chronic inflammatory rheumatic diseases (CIRD) in the pandemic have not been completely clear, especially in the beginning of the lockdown. Whether and to which degree pandemic-related therapy changes have occurred, has not been studied in detail.Objectives:To study the behaviour of patients with CIRD initially facing the COVID 19 pandemic related to their disease status and medication.Methods:Patients with CIRD were contacted by telephone to assess their health status and ask for changes in medication. Standardized assessment tools were used to assess disease activity, depression and anxiety. High disease activity was assumed if RADAI-5 ≥ 3.2 and BASDAI ≥ 4. Anxiety (HADS-A) and depression (HADS-D) of patients were assessed using HADS. A score < 8 was taken as indication of no major problem in this regard.Results:A total of 886 patients was interviewed between April 15 and June 15 of 2020. Here we report on 550 patients with complete information on standard assessments (62%). About 60% were female, mean age 54.4±13.7, mean disease duration 12.2±10.5 years. Most had spondyloarthritis (SpA, n=287) including axial SpA (axSpA, n=172) and psoriatic arthritis (PsA, n=116), in total 52.2%, while 40.2% had rheumatoid arthritis (RA, n=221), and 7.6% connective tissue diseases (CTD, n=42). Most RA patients were on methotrexate (48.8%), while 43.8% took glucocorticoids. In addition, 61.0% of patients were on bDMARDs, mostly on TNF inhibitors (59.6%). More SpA than RA patients were on bDMARDs: 71.0% vs 49.7% respectively. A recent change in medication was reported by 182 patients (33.1%): 89 with RA (40.2%), 88 with SpA (30.6%) and 5 with CTD (11.9%). Half of those who changed (n=92; 50.5%) admitted that the change was mainly made due to fear of the pandemic (16.7% of all patients). Altogether, significantly more patients changed bDMARDs (68.5%) than csDMARDs (57.3%). The data of patients who changed vs patients who didn’t change is shown in the Table 1, including subgroup analyses. The median HADS scores were < 8.Table 1.RA and SpA patients who changed and who did not change their medicationGroup (N) / ReasonNActive disease (%)HADS-D≥ 8 (%)HADS-A≥ 8 (%)bDMARD therapy (%)Rheumatoid arthritis221134 (60.6)76 (35.0) [4]94 (43.3) [4]110 (50.9) [5]Spondyloarthritis287130 (45.4)83 (29.5) [6]109 (38.8) [6]204 (72.6) [6] Pa (RA vs SpA)0.2280.354Patients did not change their medication Rheumatoid arthritis (%)132 (59.7)84 (63.6)46 (35.9) [4]58 (45.3) [4]62 (48.4) [4] Spondyloarthritis (%)199 (69.3)88 (44.2)58 (30.1) [6]69 (35.8) [6]137 (71.0) [6] P (RA vs SpA)0.0310.3580.101Patients changed their medication Rheumatoid arthritis89 (40.3)50 (56.2)30 (33.7)36 (40.4)48 (54.5) [1] P (vs no change)0.3310.8460.5670.457 Reason[9] Pandemic41 (51.3)15 (36.6)11 (26.8)14 (34.1)24 (60.0) [1] Inactive disease23 (28.8)12 (52.2)6 (26.1)10 (43.5)12 (52.2) Active disease b16 (20.0)14 (87.5)6 (37.5)7 (43.8)7 (43.8) P (reasons)0.0030.6870.6870.526 Spondyloarthritis88 (30.7)42 (47.7)25 (28.4)40 (45.5)67 (76.1) P (vs no change)0.6730.8890.1570.451 Reason[6] Pandemic50 (61.0)22 (44.0)13 (26.0)22 (44.0)42 (84.0) Inactive disease15 (18.3) 7 (46.7)4 (26.7)7 (46.7)10 (66.7) Active disease b17 (20.7)11 (64.7)6 (35.3)6 (35.3)11 (64.7) P (reasons)0.3310.7560.7740.156 P (RA vs SpA)0.0310.2940.9500.6030.004Data are presented as numbers (percentage proportions; across rows except for column N) or medians (interquartile ranges). Missing values are in square brackets.a P values calculated using χ2 test or Mann-Whitney rank sum test.b Self-reported claim of disease activity.Conclusion:Two thirds of patients did not change medication but one third changed. A relatively high number of patients did so due to fear of the pandemic, mostly those on biologics. There were no major differences between RA and SpA. Anxiety and depression do not seem to play an important role for the decision to change medication (Table 1 below).Disclosure of Interests:None declared

Background:The timeframe for maximum treatment response varies across patients with radiographic axial spondyloarthritis (r-axSpA). Understanding which patients may benefit from additional time on treatment could influence treatment decisions.Objectives:This post-hoc analysis aims to determine the percentage of patients, previously exposed to TNFi, who progressed from ASAS20 at week 16 to ASAS40 response at week 52 with ixekizumab (IXE) treatment and to explore factors that may associate with additional improvement after 16 weeks.Methods:Patients who achieved Assessment of SpondyloArthritis International Society (ASAS)20 at week 16 from COAST-W (NCT02696798), a Phase 3, randomized, double-blind, placebo-controlled trial, in tumour necrosis factor inhibitor (TNFi)-experienced patients who fulfilled the ASAS criteria for r-axSpA, were analysed. Patients treated with IXE 80 mg Q4W were categorized according to their ASAS response at week 52: sustaining ASAS20 but not reaching an ASAS40 response or achieving ASAS40. Patient demographics and disease characteristics at baseline were analysed by descriptive statistics, and the individual components determining ASAS response at baseline and at week 52 are provided.Results:At week 16, 22.8% (n=26/114) of patients achieved ASAS20 but not ASAS40; of these, 2 patients discontinued the study before week 52. Amongst the patients who continued through week 52, 50% (12/24) of patients achieved ASAS40; the other 50% sustained their ASAS20 response. Patients who achieved ASAS40 at week 52 were older, had longer disease duration, were less likely to be HLA-B27 positive, and had worse BASDAI and BASFI scores at baseline (Table 1, part a). Achieving ASAS40 appeared to depend most on the Patient Global Assessment of Disease Activity and spinal pain score over time (Table 1, part b).Table 1.a) Demographics and Characteristics at Baseline (week 0) and b) Descriptive observed data for the individual components of the ASAS response criteria at week 52, mean (SD)a)IXEQ4WPatients sustaining an ASAS20 but not reaching an ASAS40 response at week 52 (n=12)Patients achieving an ASAS40 response at week 52 (n=12)Age, years47.3 (13.3)49.6 (12.3)Duration of symptoms since axSpA onset, years16.4 (9.2)18.6 (12.6)HLA B27 positive, n (%)12 (100)9 (75)Current tobacco use, n (%)4 (33.3)1 (8.3)ASDAS Score4.0 (1.0)4.2 (1.1)BASDAI Score7.4 (1.2)7.8 (1.7)Serum CRP concentration (mg/L)23.0 (47.1)28.0 (66.0)Spinal Pain due to Ankylosing Spondylitis (NRS)8.2 (0.8)8.5 (1.6)Patient Global Assessment of Disease Activity (NRS)7.8 (1.3)8.6 (1.2)BASFI7.1 (1.4)7.4 (2.3)BASDAI stiffness score7.1 (1.5)7.6 (2.2)b)IXEQ4WPatient Global Assessment of Disease Activity (NRS)5.5 (1)3.2 (1.3)Spinal Pain due to Ankylosing Spondylitis (NRS)5.6 (1)3 (1.9)BASFI5.0 (1.5)3.7 (2.1)BASDAI stiffness score4.1 (1.4)3.4 (2.3)Values are mean (SD) unless stated otherwiseASAS= Assessment of SpondyloArthritis International Society; ASDAS= Ankylosing Spondylitis Disease Activity Score; axSpa = axial spondyloarthritis; BASDAI= Bath Ankylosing Spondylitis Disease Activity Index; BASFI= Bath Ankylosing Spondylitis Functional Index; CRP= C-reactive protein; HLA= human leucocyte antigen; NRS = numeric rating scale; SD= standard deviationConclusion:For patients with r-axSpA previously exposed to TNFis and showing modest response to IXE over 16 weeks, longer exposure to IXE may be required to achieve ASAS40.Acknowledgements:The authors would like to acknowledge Philana Fernandes, an employee of Eli Lilly, for her editorial and writing support.Disclosure of Interests:Xenofon Baraliakos Speakers bureau: Abbvie, BMS, Chugai, Celgene, Eli Lilly, Pfizer, Galapagos, UCB, MSD, Consultant of: Abbvie, BMS, Chugai, Celgene, Eli Lilly, Pfizer, Galapagos, UCB, MSD, Grant/research support from: Abbvie, Celgene, MSD, Atul Deodhar Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Giliad, GlaxoSmith & Kline, Janssen, Novartis, Pfizer, UCB, Grant/research support from: AbbVie, Boehringer Ingelheim, Eli Lilly, GlaxoSmith & Kline, Novartis, Pfizer, UCB, Soyi Liu Leage Employee of: Eli Lilly, Yves Schymura Employee of: Eli Lilly, Rebecca Bolce Shareholder of: Eli Lilly, Employee of: Eli Lilly, David Sandoval Shareholder of: Eli Lilly, Employee of: Eli Lilly, Jessica A. Walsh Consultant of: AbbVie, Novartis, Eli Lilly, UCB, Amgen & Pfizer, Grant/research support from: AbbVie, Pfizer, Merck, Joachim Sieper Speakers bureau: Abbvie, Janssen, Eli Lilly and Novartis, Consultant of: Abbvie, Janssen, Eli Lilly and Novartis.

Background:Bimekizumab (BKZ), a monoclonal antibody that selectively inhibits interleukin (IL)-17A and IL-17F, has demonstrated clinical efficacy and safety in patients with ankylosing spondylitis (AS) treated over a period up to 96 weeks.1,2Objectives:To report 3-year interim patient-reported outcomes (PROs) in patients with active AS treated with BKZ in a phase 2b dose-ranging study (BE AGILE; NCT02963506) and its open-label extension (OLE; NCT03355573).Methods:BE AGILE study design has been described previously.1 Patients treated with BKZ 160 mg or 320 mg every 4 weeks (Q4W) at Week 48 in BE AGILE were eligible for OLE entry. All OLE patients received BKZ 160 mg Q4W. Outcome measures are reported for the OLE full analysis set (patients who entered the OLE and had ≥1 dose of BKZ and ≥1 valid efficacy variable measurement in the OLE), and include: BASDAI, BASDAI50 responder rate, BASFI, fatigue (BASDAI Q1), morning stiffness (mean of BASDAI Q5 + 6), total spinal pain (numeric rating scale [NRS]), SF-36 PCS and MCS, and ASQoL. Missing data were imputed using multiple imputation (MI; based on the missing at random assumption) for continuous variables and non-responder imputation (NRI) for dichotomous variables.Results:262/303 (86%) patients randomised at BE AGILE study baseline (BL) completed Week 48 on BKZ 160 mg or 320 mg, of whom 255/262 (97%) entered the OLE (full analysis set: 254). From baseline to Week 48 in BE AGILE, BKZ-treated patients showed clinically relevant improvements in disease activity (BASDAI, BASDAI50), physical function (BASFI), fatigue, morning stiffness, spinal pain, and quality of life (SF-36 PCS and MCS, ASQoL) (Figure 1). Group-level improvements in all reported continuous efficacy measures exceeded published minimally important difference (MID), minimum clinically important improvement (MCII), and/or minimum clinically important difference (MCID) thresholds (Figure 1).3,4 Efficacy in all reported outcome measures was maintained or continued to improve from Week 48 to Week 144 or 156 (Figure 1).Conclusion:BKZ treatment was associated with sustained and consistent efficacy in patients with active AS over 3 years, including patient-reported disease activity, physical function, fatigue, morning stiffness, spinal pain, and quality of life.References:[1]van der Heijde D. Ann Rheum Dis 2020;79:595–604.[2]Baraliakos X. Arthritis Rheumatol 2020;72 (suppl 10).[3]Ogdie A. Arthritis Care Res 2020;72 (S10):47–71.[4]Maruish ME. User’s manual for the SF-36v2 Health Survey (3rd ed). 2011; Lincoln, RI: QualityMetric Incorporated.Acknowledgements:This study was funded by UCB Pharma. Editorial services were provided by Costello Medical.Disclosure of Interests:Xenofon Baraliakos Speakers bureau: AbbVie, BMS, Chugai, Eli Lilly, Galapagos, Gilead, MSD, Novartis, Pfizer, UCB Pharma, Paid instructor for: AbbVie, BMS, Chugai, Eli Lilly, Galapagos, Gilead, MSD, Novartis, Pfizer, UCB Pharma, Consultant of: AbbVie, BMS, Chugai, Eli Lilly, Galapagos, Gilead, MSD, Novartis, Pfizer, UCB Pharma, Maxime Dougados Consultant of: AbbVie, Eli Lilly, Novartis, Pfizer and UCB Pharma, Grant/research support from: AbbVie, Eli Lilly, Novartis, Pfizer and UCB Pharma, Karl Gaffney Speakers bureau: AbbVie, Eli Lilly, Novartis, UCB Pharma, Consultant of: AbbVie, Eli Lilly, Novartis, UCB Pharma, Grant/research support from: AbbVie, Gilead, Eli Lilly, Novartis, UCB Pharma, Raj Sengupta Speakers bureau: AbbVie, Biogen, Celgene, MSD, Novartis, UCB Pharma, Consultant of: AbbVie, Biogen, Celgene, Eli Lilly, MSD, Novartis, UCB Pharma, Grant/research support from: AbbVie, Celgene, UCB Pharma, Marina Magrey Consultant of: AbbVie, Eli Lilly, Novartis, Pfizer, UCB Pharma, Grant/research support from: AbbVie, UCB Pharma, Natasha de Peyrecave Employee of: UCB Pharma, Marga Oortgiesen Employee of: UCB Pharma, Thomas Vaux Employee of: UCB Pharma, Carmen Fleurinck Employee of: UCB Pharma, Valerie Ciaravino Employee of: UCB Pharma, Atul Deodhar Speakers bureau: Janssen, Novartis, Pfizer, Consultant of: AbbVie, Amgen, BMS, Boehringer Ingelheim, Celgene, Eli Lilly, Gilead, GSK, Janssen, Novartis, Pfizer, UCB Pharma, Grant/research support from: AbbVie, Eli Lilly, GSK, Novartis, Pfizer, UCB Pharma

Background:Imaging guidance gives the opportunity to visualize a needle or other instrument when performing interventions on musculoskeletal sites in patients with rheumatic and musculoskeletal diseases (RMDs). Studies assessing the role of imaging guided procedures have been performed, however, no consensus has been made yet about when and which imaging techniques to use for these interventions.Objectives:To inform a EULAR taskforce on the current literature on different imaging techniques, procedures and materials to guide interventions on musculoskeletal sites in RMD patients.Methods:Prospective and retrospective studies published in English and comparing either palpation or imaging guided interventions in patients with RMDs were included. MEDLINE, EMBASE, the Cochrane Library and Epistemonikos were searched through October 2021. Risk of bias (RoB) was assessed using the Cochrane RoB tool for randomized trials version 2 (ROB2), the RoB tool for Non-Randomized Studies of Interventions (ROBINS-I) and the appraisal tool for cross-sectional studies (AXIS).Results:Sixty-six studies, with moderate to high RoB, consisting of 49 randomized controlled trials, three prospective cohort studies and 14 retrospective studies were included.Fifty-one studies compared one imaging technique against either another imaging technique, or palpation-guided interventions. Most of the studies were on peripheral joints (47/51), while data on joints of the axial skeleton were scare and heterogeneous (4/51). For peripheral joints, ultrasound (US) was the most studied imaging technique (49/51), followed by fluoroscopy (10/51). Results revealed a higher accuracy and safety (including procedural pain) of US or fluoroscopy compared to palpation- guided interventions. Data on other imaging techniques was scarce (computed tomography: n=3, arthroscopy: n=1) and the results heterogeneous. Results of studies comparing different imaging techniques (12/51) did not favor one imaging method over another.Three studies comparing different materials used for imaging guided interventions were found (e.g. automatic vs manual syringes), showing little evidence for one material being superior to another one.Fifteen studies were found comparing different imaging guided procedures (e.g. intraarticular vs periarticular injections). Overall, studies indicated an advantage of targeted vs. not targeted interventions (intraarticular vs periarticular or intraepineurial vs extraepineurial injections) concerning pain levels, while the comparison of different puncture sites to inject (e.g. ulnar vs midline carpal tunnel injection) was inconclusive.Conclusion:Imaging guidance, especially US, performs favorably for interventions at the peripheral joints compared to palpation-guided interventions, concerning accuracy and safety. Data for the axial skeleton are scarce. Imaging guided targeted interventions may lead to better outcomes than non-targeted interventions.Disclosure of Interests:None declared.

We would like to thank our colleagues from Taiwan for their interest in our work and their comments.1 The Study of Health in Pomerania (SHIP) cohort is a population-based epidemiological study which was designed to investigate common risk factors, subclinical disorders and manifest diseases with no interest in one specific disease but rather in data relevant for the prevalence and incidence of common diseases and their risk factors. Importantly, this was the first population-based cohort study worldwide which included whole-body MRI, which raised our interest many years ago. We appreciate the comments of our colleagues from Taiwan on potentially better methods to assess MRI lesions suggestive of axial spondyloarthritis (axSpA). In general, we agree that the STIR sequence, in combination with a T1-weighted sequence, is currently the best method to identify axSpA-related lesions in sacroiliac joints (SIJs)2 and the spine. As a matter of fact, in our study, short tau inversion recovery (STIR) sequences for the evaluation of the SIJs were used. For the evaluation of spinal MRIs, T1 and T2 …

We thank Wei et al 1 for their correspondence on the recently published European League Against Rheumatism (EULAR) recommendations for the management of psoriatic arthritis (PsA).2 The authors of this correspondence raise some interesting points. The first point relates to the role of cyclosporine A (CsA) in the treatment of patients with psoriatic disease. The authors mention that this drug is often used in Asia, in particular in skin psoriasis. They suggest that CsA could be proposed for PsA. While CsA is recommended for the management of skin psoriasis, …

Background:A single switch from an originator to a biosimilar product has been shown to be safe and effective in the treatment of rheumatic musculoskeletal diseases (RMDs). The availability of biosimilars has created a financial incentive to encourage switching to cheaper products (“non-medical switch”). This is naturally associated with multiple switches. However, the effect of multiple switching between biosimilars of the same reference product has not been thoroughly investigated to date.Objectives:To assess the effectiveness and safety of systematic non-medical switching from innovator etanercept (ETN) to biosimilar ETN (SB4) and successive to another biosimilar ETN (GP2015) in adult patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA) or axial spondyloarthritis (axSpA) in a real-life setting.Methods:This retrospective study was performed in a tertiary center in adult patients with RA, PsA or axSpA who had been treated with the innovator ETN and who had been switched to two ETN biosimilars for economic reasons thereafter. The first switch from innovator ETN to the first biosimilar ETN occurred between February-May 2017 and the second switch from the first to the second biosimilar ETN occurred between September-December 2017. The end of the observation period was October 2019. Disease activity, function and adverse events (AE) were regularly assessed, and any changes in outcome were recorded during the follow-up period. The scores documented at week 12 week after the second switch were taken as primary outcome.A total of 100 patients (54 RA, 27 axSpA, 19 PsA, mean age 54.3±15.1, 46% male) who switched twice to those ETN biosimilars over a follow-up period of 21.1±7.4 months were included. The retention rate after the second ETN biosimilar switch was 89% about 6 months after the second switch. While 2 patients were lost to follow-up and 1 patient died (cardiac arrest), 7 patients discontinued due to inefficacy or AE, including one pancreatic cancer. One patient was withdrawn due to pregnancy. Overall, 14 AEs were reported in 8 patients. Among them, 4 patients switched back to originator etanercept in month 6, 1 patient re-administered GP2015 successfully in month 3 after suffering from mucosal erosions and in 3 patients another mode of action was prescribed. The scores at week 12 of both, disease activity and function, remained unchanged (Table 1).Table 1.Patient characteristicsAssessmentBaseline(n=100)SB4 Follow-up 12 weeks(n=100)SB 4 Follow-up 24 weeks(n=100)Second switch to GP2015(n=100)GP2015 Follow-up 12 weeks(n=97)GP2015 Follow-up 24 weeks(n=89)RADAS283,0 (1,2)2,9 (1,4)3,1 (1,2)2,8 (1,4)3,4 (2,5)3,0 (1,4)HAQ1,4 (0,8)1,6 (0,9)1,0 (0,9)1,5 (0,8)1,5 (0,8)1,6 (0,9)PsADAS283,8 (1,4)1,9 (1,4)2,8 (1,5)3,1 (1,1)4,5 (2,6)3,6 (2,6)HAQ1,2 (0,9)1,0 (0,9)0,9 (0,9)1,0 (0,8)1,0 (0,9)1,2 (0,8)axSpABASDAI5,1 (2,7)4,5 (2,6)5,1 (3,8)4,1 (2,2)4,6 (2,5)4,3 (2,4)ASDAS3,4 (0,8)2,5 (0,8)2,7 (0,8)3,2 (1,8)2,7 (1,2)2,5 (0,9)BASFI4,4 (2,7)4,3 (2,7)4,3 (3,2)4,6 (2,6)4,5 (2,7)4,8 (3,0)*Values are mean ± standard deviationDisclosure: Hexal funded this researchConclusion:The retention rate after multiple switches from innovator ETN to two ETN biosimilars was close to 90%. No major changes in disease activity and function were observed in all three indications.

Background:The clinical efficacy of tumor necrosis factor inhibitors (TNFi) in patients with axial spondyloarthritis (axSpA) is well established but its effect on new bone formation is still unclear (1). Positron emission tomography (PET) using bone-seeking18F-Fluoride [18F]F in combination with magnetic resonance imaging ([18F]F /MRI) has been shown to depict not only bone marrow edema (BME) but also shows the quantity of tracer uptake in the late phase of perfusion suggestive of remodeling and osteoblastic activity, not only in radiographic axSpA (r-axSpA) (2).Objectives:Assess the effect of TNFi on bone remodeling processes in the axial skeleton of r-axSpA patients using [18F]F/MRI prior (baseline, BL) and 4 months after (follow-up, FU) treatment.Methods:Patients (11 male, 5 female, mean age 38.6±12.0 years) with clinically active r-axSpA (BASDAI>4, failure of NSAIDs, no previous biologics) prospectively underwent 3-Tesla and [18F]F PET/MRI (40 minutes after injection of a mean activity of 157 MBq [18F]F). Images of the SIJ (n=16 patients) and the whole spine (n=10 patients) were performed at BL and FU. Three readers (1 for [18F]F/MRI and 2 for conventional MRI) evaluated all images independently and blinded to timepoint allocation. Only lesions on which all readers agreed on were used for further analyses. Inflammation (bone marrow edema, BME), structural lesions (fat deposition (FD), sclerosis, erosions and ankylosis) and focal [18F]F uptake were recorded on the level of SIJ (SIJ-Q) and vertebral quadrants (V-Q), with each SIJ or vertebral body consisting of 4 VQs (superior and inferior sacral and iliac for the SIJ, and superior and inferior, anterior and posterior for the vertebral bodies).Results:A total of 128 SIJ-Q and 920 VQs were analyzed at both BL and FU. In the SIJs, 75 (58.6%), 120 (93.8%), 69 (53.9%), 99 (77.3%) and 16 (12.5%) SIJ-Q showed BME, FD, sclerosis, erosions and ankylosis, while 111 (86.7%) SIJ-Q showed focal [18F]F-uptake at BL. Association with increased [18F]F-uptake was found most frequently in SIJ-Q with BME (70/75 SIJ-Q, 93.3%), sclerosis (65/69 SIJ-Q, 94.2%) and FD (105/120 SIJ-Q, 87.5%). At FU, 37 SIJ-Q still showed BME (improvement by 50.7%), while almost no changes were observed in chronic lesions. In comparison, improvement of focal [18F]F-uptake was found in all lesion combinations, with improvement of focal [18F]F-lesions associated with BME by 62.9%, with sclerosis by 33.8% and with FD by 22.9% of SIJ-Q.In the spine, only 41 (4.5%), 61 (6.6%), 14 (1.5%) V-Q showed BME, FD and sclerosis, respectively, while 77 V-Q (8.4%) showed focal [18F]F-uptake. An association to increased [18F]F-uptake was found most frequently with sclerosis (7/14 V-Q, 50%) and FD (25/61 V-Q, 41%). At FU, 12 V-Q still showed BME (improvement by 70.7%), while, similar to SIJ, almost no changes were observed in the chronic lesions. The largest improvement was found in focal [18F]F-lesions associated with BME 81.8% and with FD by 22.9% of V-Q.Conclusion:In this first prospective study on whole spine and SIJ [18F]F/MRI in patients with r-axSpA, a significant decrease of osteoblastic activity was observed over 4 months of continuous anti-TNF treatment. The effect of treatment was observed not only at sites with inflammatory lesions (BME) but also at sites with pre-existing chronic structural lesions, while some osteoblastic activity remained visible at 4 months. These data support a short-term effect of anti-TNF treatment on osteoblastic activity, while the long-term effects need to be further studied.References:[1]Van der Heijde D et al, Ann Rheum Dis 2017[2]Buchbender C et al, J Rheumatol 2015This work was supported by an unrestricted Grant by MSD GmbH, GermanyDisclosure of Interests:Xenofon Baraliakos Grant/research support from: Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Consultant of: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Styliani Tsiami: None declared, Christoph Rischpler: None declared, Nils-Martin Bruckmann: None declared, Wolfgang Fendler: None declared, Julian Kirchner: None declared, Ken Hermann: None declared, Lino Sawicki: None declared, Juergen Braun Grant/research support from: Abbvie (Abbott), Amgen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, Eli Lilly and Company, Medac, MSD (Schering Plough), Mundipharma, Novartis, Pfizer (Wyeth), Roche, Sanofi- Aventis, and UCB Pharma, Consultant of: Abbvie (Abbott), Amgen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, EBEWE Pharma, Eli Lilly and Company, Medac, MSD (Schering-Plough), Mundipharma, Novartis, Pfizer (Wyeth), Roche, Sanofi-Aventis, and UCB Pharma, Speakers bureau: Abbvie (Abbott), Amgen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, EBEWE Pharma, Eli Lilly and Company, Medac, MSD (Schering-Plough), Mundipharma, Novartis, Pfizer (Wyeth), Roche, Sanofi-Aventis, and UCB Pharma

Background:Filgotinib, an oral selective Janus kinase (JAK) 1 inhibitor, reduced disease activity and improved symptoms and inflammation of the sacroiliac joint (SIJ) and spine in patients with active axial ankylosing spondylitis (AxSpA) in the Phase 2 TORTUGA trial (NCT03117270).1The effects of JAK inhibitors on structural lesions in active AxSpA are unknown and optimal methods for image analysis of structural disease progression are not established.Objectives:The aim of this post hoc analysis was to evaluate the effects of filgotinib on magnetic resonance imaging (MRI) measures of structural changes in the SIJ in patients from the TORTUGA trial, as assessed by Spondyloarthritis Research Consortium of Canada (SPARCC) SIJ Structural Scores (SSS).Methods:TORTUGA was a multicenter, double-blind, randomized trial of 116 patients with active AxSpA treated with filgotinib 200 mg (n=58) or placebo (n=58) once daily for 12 weeks. MRI was conducted at baseline and Week 12 (or early discontinuation visit). MRIs were re-evaluated post hoc by two independent experts (blinded to time point and assigned treatment) to determine SPARCC SSS; inter-reader discrepancies were resolved by an independent adjudicator. Observed changes from baseline were evaluated using analysis of covariance with factors for treatment, baseline value, and randomization stratification. Least-squares mean changes from baseline and between-group differences with 95% confidence intervals were calculated.Results:MRI scans from 87 patients with an evaluable MRI at baseline and Week 12 (or early termination visit) were re-evaluated (48 filgotinib, 39 placebo). Erosion scores decreased in the filgotinib group and increased in the placebo group (p=0.02 for between-group difference; Table 1; Figure 1a). Backfill scores increased in the filgotinib group but not in the placebo group (p=0.005; Table 1; Figure 1b). There was no statistically significant between-group difference in SSS total ankylosis (p=0.46) or fat lesion (p=0.17) changes from baseline (Table 1).Table 1.Summary of Spondyloarthritis Research Consortium of Canada Sacroiliac Joint Structural Scores.ScoreMean (SD) BL scoreLSM change from BL (95% CI) at Week 12LSM group difference at Week 12 (95% CI)Erosion FIL 200 mg3.38 (5.34)–0.46 (–1.31, 0.40)–1.01 (–1.87, –0.16) PBO2.62 (3.76)0.56 (–0.31, 1.42)[p=0.02]Backfill FIL 200 mg1.02 (1.99)0.76 (0.07, 1.45)1.02 (0.32, 1.72) PBO1.35 (2.59)–0.26 (–0.97, 0.45)[p=0.005]Fat metaplasia FIL 200 mg4.19 (6.06)0.37 (–0.23, 0.97)0.43 (–0.18, 1.03) PBO4.35 (5.44)–0.06 (–0.67, 0.56)[p=0.17]Ankylosis FIL 200 mg9.58 (8.15)0.14 (–0.02, 0.30)0.06 (–0.10, 0.22) PBO9.83 (8.45)0.08 (–0.08, 0.25)[p=0.46]BL, baseline; CI, confidence interval; FIL, filgotinib; LSM, least-squares mean; PBO, placebo; SD, standard deviationConclusion:In addition to previously reported decreases in SPARCC inflammation, filgotinib was associated with significant reduction in SIJ erosion scores and increase in backfill scores at Week 12 of the TORTUGA trial, versus placebo. Long-term effects are to be determined.References:[1]van der Heijde D, et al. Lancet 2018;392:2378–87.Acknowledgments:We thank Robert Lambert for his review of the MRI scans in the role of adjudicator. The TORTUGA trial was sponsored by Galapagos NV and co-funded by Galapagos NV and Gilead Sciences. Medical writing support was provided by Hannah Mace MPharmacol, CMPP (Aspire Scientific Ltd, Bollington, UK) and funded by Galapagos NV (Mechelen, Belgium).Disclosure of Interests:Walter P. Maksymowych Grant/research support from: AbbVie, Novartis, Pfizer, and UCB, Consultant of: AbbVie, Boehringer Ingelheim, Celgene, Eli Lilly, Galapagos, Janssen, Novartis, Pfizer, and UCB, Employee of: Chief Medical Officer of CARE Arthritis Limited, Speakers bureau: AbbVie, Janssen, Novartis, Pfizer, and UCB, 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, Robert B.M. Landewé Consultant of: AbbVie; AstraZeneca; Bristol-Myers Squibb; Eli Lilly & Co.; Galapagos NV; Novartis; Pfizer; UCB Pharma, William Barchuk Shareholder of: Gilead Sciences Inc and Eli Lilly, Employee of: Current employee of Gilead Sciences Inc and a former employee of AbbVie, Eli Lilly, and Johnson & Johnson, Ke Liu Shareholder of: Gilead Sciences Inc (stockholder), Employee of: Gilead Sciences Inc, Chantal Tasset Shareholder of: Galapagos (share/warrant holder), Employee of: Galapagos, Leen Gilles Consultant of: Galapagos, Thijs Hendrikx Shareholder of: Galapagos (share/warrant holder), Employee of: Galapagos, Robin Besuyen Shareholder of: Galapagos, Employee of: Galapagos, Xenofon Baraliakos Grant/research support from: Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Consultant of: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen

Background:Early diagnosis and treatment are important for the management of inflammatory rheumatic diseases (RMD). However, the availability of rheumatologists is limited in most European countries and selection strategies lack sensitivity and/or specificity.Objectives:To evaluate a triage strategy that offers the possibility to see patients within 4 weeks for short term appointments in order to check the probability of an inflammatory RMD and the necessity to further evaluate the patients in due time.Methods:Physician’s and patient’s information who called our tertiary rheumatology department´s outpatient clinic for a date in the triage system were included in this analysis. The time to first appointment as assessed by a nurse (Step 1), the short evaluation by a rheumatologist in the triage (Step 2) and the patient´s complaints and the diagnoses after an extensive diagnostic evaluation (Step 3) were documented.Results:In a period of 9 months in 2018, a total of 982 patients presented. A total of 62 patients (6.3%) were considered urgent (appointment within 3 days), while 240 (24.4%) were appointed within 4 weeks at Step 2. Of the former 46 (19.2%), and of the latter 151 patients (62.9%) were diagnosed with inflammatory RMD at Step 3.In total, 334 patients (34.0%) were diagnosed with inflammatory RMD at Step 3, including 126 with RA (37.7%), 71 with axSpA/PsA (21.3%), 95 with connective tissue disease/vasculitis (28.4%) and 20 with gout (6.0%). The diagnosis suspected in Step 2 was confirmed in Step 3 in 77.9% of cases. In 217 patients, the diagnosis suspected in Step 2 was not confirmed in Step 3. Of them, 34 (15.7%) had unclear findings at Step 2 but an inflammatory RMD was found at Step 3, while 148 (68.2%) had a suspected inflammatory RMD at Step 2 but this was not confirmed at Step 3.The most frequent musculoskeletal complaint at the time point of referral was pain in small peripheral joints (hands and/or feet) in 858 patients (87.4%), in large peripheral joints (knees, shoulders and/or hips) in 780 patients (79.4%) and back pain in 682 patients (69.5%). Fever, night sweats and unclear weight loss was reported by 50 patients (5.1%), while 210 patients (24.5%) presented with findings suspicious of inflammatory RMD such as elevated CRP of unclear origin, and 43 patients (4.8%) because of a threat of organ damage such as unclear elevation of creatinine, as reported by the referring physician. In addition, 167 patients (17.0%) had received glucocorticoids prior to referral, 87 (52.1%) of which finally did not receive the diagnosis of inflammatory RMD at Step 3, while 737 patients (75.1%) were receiving NSAIDs prior to referral.Conclusion:In this prospective evaluation of a triage system where all patients were pre-screened by a nurse and were seen within 4 weeks by a rheumatologist, clinical differentiation could be performed timely due to a successfully structured triage system. The initially suspected diagnosis was finally confirmed in ≥75% of cases, while ≥1/3 of patients had a definite inflammatory RMD.This work was supported by an unrestricted Grant from AbbvieDisclosure of Interests:Xenofon Baraliakos Grant/research support from: Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Consultant of: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Imke Redeker: None declared, Maria Zacharopoulou: None declared, Styliani Tsiami: None declared, Konstantia Tsiaousi: None declared, Doris Morzeck: None declared, Juergen Braun Grant/research support from: Abbvie (Abbott), Amgen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, Eli Lilly and Company, Medac, MSD (Schering Plough), Mundipharma, Novartis, Pfizer (Wyeth), Roche, Sanofi- Aventis, and UCB Pharma, Consultant of: Abbvie (Abbott), Amgen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, EBEWE Pharma, Eli Lilly and Company, Medac, MSD (Schering-Plough), Mundipharma, Novartis, Pfizer (Wyeth), Roche, Sanofi-Aventis, and UCB Pharma, Speakers bureau: Abbvie (Abbott), Amgen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, EBEWE Pharma, Eli Lilly and Company, Medac, MSD (Schering-Plough), Mundipharma, Novartis, Pfizer (Wyeth), Roche, Sanofi-Aventis, and UCB Pharma

Background:The Assessment of SpondyloArthritis international Society (ASAS) has defined separate core sets for: i) symptom-modifying anti-rheumatic drugs (SM-ARD), ii) clinical record keeping, and iii) disease-controlling anti-rheumatic therapy (DC-ART). These all include the following domains: ‘physical function’, ‘pain’, ‘spinal mobility’, ‘spinal stiffness’ and ‘patient global assessment’ (PGA). The core set for clinical record keeping further includes the domains ‘peripheral joints’ and ‘acute phase reactants’, and the core set for DC-ART further includes the domains ‘fatigue’, ‘spine/hip radiographs’.Objectives:To assess the effect of interventions for each of the 9 axSpA core domains.Methods:We investigated the efficacy across all interventions included in Cochrane reviews according to the core outcome set for axSpA, as reported in these eligible axSpA trials. We combined data using the standardized mean difference (SMD) to meta-analyze outcomes involving similar constructs. By meta-regression analysis, we examined the effect for each of the nine separate SMD measures on the primary endpoint across all trials.Results:Among 85 articles screened, we included 43 trials with 63 randomized comparisons. Mean (SD) number of core outcomes domains measured for SM-ARD trials was 4.2 (1.7). 6 trials assessed all 5 proposed domains. Mean (SD) for number of core outcome domains for DC-ART trials was 5.8 (1.7). Unfortunately, no trials assessed all 9 domains. 8 trials were judged to have high risk of selective outcome reporting. The most responsible core domains for achieving success in meeting the primary objective per trial were pain; OR (95% CI) 5.19 (2.28, 11.77) and PGA; OR (95% CI) 1.87 (1.14, 3.07).Conclusion:Overall outcome reporting was good for SM-ARD trials, and poor for DC-ART trials. None of the DC-ART trials assessed all 9 domains. Outcome-reporting bias and ‘missing data’ should be reduced by implementing the endorsed ASAS/OMERACT outcome domains in all clinical trials. Our findings suggest that PGA and pain likely provide a holistic assessment of disease beyond “objective measures” of spinal inflammation.Disclosure of Interests:Rikke Asmussen Andreasen: None declared, Lars Erik Kristensen Consultant of: UCB Pharma (Advisory Board), Sannofi (Advisory Board), Abbvie (Advisory Board), Biogen (Advisory Board), Speakers bureau: AbbVie, Amgen, Biogen, Bristol-Myers Squibb,Celgene, Eli Lilly, Gilead, Forward Pharma, Janssen Pharmaceuticals, MSD, Novartis, Pfizer, and UCB Pharma, Xenofon Baraliakos Grant/research support from: Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Consultant of: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Vibeke Strand Consultant of: AbbVie, Amgen, Biogen, Celltrion, Consortium of Rheumatology Researchers of North America, Crescendo Bioscience, Eli Lilly, Genentech/Roche, GlaxoSmithKline, Hospira, Janssen, Merck, Novartis, Pfizer, Regeneron Pharmaceuticals, Inc., Sanofi, UCB, Philip J Mease Grant/research support from: Abbott, Amgen, Biogen Idec, BMS, Celgene Corporation, Eli Lilly, Novartis, Pfizer, Sun Pharmaceutical, UCB – grant/research support, Consultant of: Abbott, Amgen, Biogen Idec, BMS, Celgene Corporation, Eli Lilly, Novartis, Pfizer, Sun Pharmaceutical, UCB – consultant, Speakers bureau: Abbott, Amgen, Biogen Idec, BMS, Eli Lilly, Genentech, Janssen, Pfizer, UCB – speakers bureau, Maarten de Wit Grant/research support from: Dr. de Wit reports personal fees from Ely Lilly, 2019, personal fees from Celgene, 2019, personal fees from Pfizer, 2019, personal fees from Janssen-Cilag, 2017, outside the submitted work., Consultant of: Dr. de Wit reports personal fees from Ely Lilly, 2019, personal fees from Celgene, 2019, personal fees from Pfizer, 2019, personal fees from Janssen-Cilag, 2017, outside the submitted work., Speakers bureau: Dr. de Wit reports personal fees from Ely Lilly, 2019, personal fees from Celgene, 2019, personal fees from Pfizer, 2019, personal fees from Janssen-Cilag, 2017, outside the submitted work., Torkell Ellingsen: None declared, Inger Marie Jensen Hansen: None declared, Jamie Kirkham: None declared, George Wells: None declared, Peter Tugwell: None declared, Lara Maxwell: None declared, Maarten Boers: None declared, Kenneth Egstrup: None declared, Robin Christensen Grant/research support from: Dr. Christensen reports non-financial support from Board membership, grants from Consultancy (AbbVie, Amgen, Axellus A/S, Biogen, Bristol-Myers Squibb, Cambridge Weight Plan, Celgene, Eli Lilly, Hospira, MSD, Norpharma, Novartis, Orkla Health, Pfizer, Roche, Sobi, Takeda), personal fees from Employment (Research Unit for Musculoskeletal Function and Physiotherapy, Institute of Sports Science and Clinical Biomechanics, University of Southern Denmark), non-financial support from Expert testimony, grants from Grants/grants pending (Axellus A/S, AbbVie, Cambridge Weight Plan, Janssen, MSD, Mundipharma, Novartis, and Roche), grants from Payment for lectures including service on speakers bureaus (Abbott, Amgen, Axellus, Bayer HealthCare Pharmaceuticals, Biogen Idec, Bristol-Myers Squibb, Cambridge Weight Plan, Ipsen, Janssen, Laboratoires Expanscience, MSD, Mundipharma, Norpharma, Novartis, Pfizer, Roche, Rottapharm-Madaus, Sobi, and Wyeth), grants from Payment for manuscript preparation (Axellus, Bristol-Myers Squibb, and Cambridge Weight Plan, Aleris-Hamlet (via Norpharma)), non-financial support from Patents (planned, pending or issued), non-financial support from Royalties, grants from Payment for development of educational presentations (Bristol-Myers Squibb, MSD, Pfizer), non-financial support from Stock/stock options, grants from Travel/accommodations/meeting expenses unrelated to activities listed (Abbott, AbbVie, Axellus, Biogen, Bristol-Myers Squibb, Cambridge Weight Plan, Celgene, Laboratoires Expanscience, Norpharma, Novartis, Pfizer, Roche, Rottapharm-Madaus, and Wyeth), non-financial support from Other (err on the side of full disclosure), outside the submitted work; and I am involved in many health-care initiatives and research that could benefit from wide uptake of this publication (including Cochrane, OMERACT, IDEOM, RADS, and the GRADE Working Group).Musculoskeletal Statistics Unit, The Parker Institute is grateful for the financial support received from public and private foundations, companies and private individuals over the years. The Parker Institute is supported by a core grant from the Oak Foundation; The Oak Foundation is a group of philanthropic organizations that, since its establishment in 1983, has given grants to not-for-profit organizations around the world.., Consultant of: Dr. Christensen reports non-financial support from Board membership, grants from Consultancy (AbbVie, Amgen, Axellus A/S, Biogen, Bristol-Myers Squibb, Cambridge Weight Plan, Celgene, Eli Lilly, Hospira, MSD, Norpharma, Novartis, Orkla Health, Pfizer, Roche, Sobi, Takeda), personal fees from Employment (Research Unit for Musculoskeletal Function and Physiotherapy, Institute of Sports Science and Clinical Biomechanics, University of Southern Denmark), non-financial support from Expert testimony, grants from Grants/grants pending (Axellus A/S, AbbVie, Cambridge Weight Plan, Janssen, MSD, Mundipharma, Novartis, and Roche), grants from Payment for lectures including service on speakers bureaus (Abbott, Amgen, Axellus, Bayer HealthCare Pharmaceuticals, Biogen Idec, Bristol-Myers Squibb, Cambridge Weight Plan, Ipsen, Janssen, Laboratoires Expanscience, MSD, Mundipharma, Norpharma, Novartis, Pfizer, Roche, Rottapharm-Madaus, Sobi, and Wyeth), grants from Payment for manuscript preparation (Axellus, Bristol-Myers Squibb, and Cambridge Weight Plan, Aleris-Hamlet (via Norpharma)), non-financial support from Patents (planned, pending or issued), non-financial support from Royalties, grants from Payment for development of educational presentations (Bristol-Myers Squibb, MSD, Pfizer), non-financial support from Stock/stock options, grants from Travel/accommodations/meeting expenses unrelated to activities listed (Abbott, AbbVie, Axellus, Biogen, Bristol-Myers Squibb, Cambridge Weight Plan, Celgene, Laboratoires Expanscience, Norpharma, Novartis, Pfizer, Roche, Rottapharm-Madaus, and Wyeth), non-financial support from Other (err on the side of full disclosure), outside the submitted work; and I am involved in many health-care initiatives and research that could benefit from wide uptake of this publication (including Cochrane, OMERACT, IDEOM, RADS, and the GRADE Working Group).Musculoskeletal Statistics Unit, The Parker Institute is grateful for the financial support received from public and private foundations, companies and private individuals over the years. The Parker Institute is supported by a core grant from the Oak Foundation; The Oak Foundation is a group of philanthropic organizations that, since its establishment in 1983, has given grants to not-for-profit organizations around the world.., Speakers bureau: Dr. Christensen reports non-financial support from Board membership, grants from Consultancy (AbbVie, Amgen, Axellus A/S, Biogen, Bristol-Myers Squibb, Cambridge Weight Plan, Celgene, Eli Lilly, Hospira, MSD, Norpharma, Novartis, Orkla Health, Pfizer, Roche, Sobi, Takeda), personal fees from Employment (Research Unit for Musculoskeletal Function and Physiotherapy, Institute of Sports Science and Clinical Biomechanics, University of Southern Denmark), non-financial support from Expert testimony, grants from Grants/grants pending (Axellus A/S, AbbVie, Cambridge Weight Plan, Janssen, MSD, Mundipharma, Novartis, and Roche), grants from Payment for lectures including service on speakers bureaus (Abbott, Amgen, Axellus, Bayer HealthCare Pharmaceuticals, Biogen Idec, Bristol-Myers Squibb, Cambridge Weight Plan, Ipsen, Janssen, Laboratoires Expanscience, MSD, Mundipharma, Norpharma, Novartis, Pfizer, Roche, Rottapharm-Madaus, Sobi, and Wyeth), grants from Payment for manuscript preparation (Axellus, Bristol-Myers Squibb, and Cambridge Weight Plan, Aleris-Hamlet (via Norpharma)), non-financial support from Patents (planned, pending or issued), non-financial support from Royalties, grants from Payment for development of educational presentations (Bristol-Myers Squibb, MSD, Pfizer), non-financial support from Stock/stock options, grants from Travel/accommodations/meeting expenses unrelated to activities listed (Abbott, AbbVie, Axellus, Biogen, Bristol-Myers Squibb, Cambridge Weight Plan, Celgene, Laboratoires Expanscience, Norpharma, Novartis, Pfizer, Roche, Rottapharm-Madaus, and Wyeth), non-financial support from Other (err on the side of full disclosure), outside the submitted work; and I am involved in many health-care initiatives and research that could benefit from wide uptake of this publication (including Cochrane, OMERACT, IDEOM, RADS, and the GRADE Working Group).Musculoskeletal Statistics Unit, The Parker Institute is grateful for the financial support received from public and private foundations, companies and private individuals over the years. The Parker Institute is supported by a core grant from the Oak Foundation; The Oak Foundation is a group of philanthropic organizations that, since its establishment in 1983, has given grants to not-for-profit organizations around the world.

Background:SpA has historically been a difficult clinical diagnosis, especially early diagnosis. Two imaging techniques that address this problem are magnetic resonance imaging (MRI) and Single-Photon Emission Computed Tomography-Computed Tomography (SPECT-CT). Their accuracies have not been adequately compared.Objectives:The purpose of this study is to compare the sensitivities and specificities of SPECT-CT and MRI in SpA.Methods:This retrospective study assessed all patients who underwent SPECT-CT of the sacroiliac joint to assess for SpA. The results of SPECT-CT were compared against MRI for all patients in the cohort who underwent an MRI within 4 weeks of the SPECT-CT. A diagnosis of SpA in the discharge summary was considered the reference standard, and was based on a combination of clinical scenario, response to therapy, imaging,, patient history or lab index.Results:200 patients (173 men; average 22±4 years of age) were included SpA was diagnosed in 189 (AS patients=99 and excluded in 11. SPECT-CT and MRI had similar (P >0 .05;k ¼ 0.74) sensitivities (0.94 vs 0.94),specificities (1.00 vs 1.00),positive predictive values (1.00 vs 1.00),negative predictive values (0.94 vs 0.80),and accuracies (0.97 vs 0.95) when compared to the reference standard.Conclusion:Although MRI remains the initial modality of choice in early diagnosing SpA, SPECT-CT appears diagnostically equivalent and should be considered a viable supplementary or alternative imaging modality particularly if there is contra-indication or inaccessibility to MRI.References:[1]Taurog J D, Chhabra A, Colbert R A. Ankylosing Spondylitis and Axial Spondyloarthritis[J]. N Engl J Med, 2016,375(13):1303.[2]van der Linden S, Valkenburg H A, Cats A. Evaluation of diagnostic criteria for ankylosing spondylitis. A proposal for modification of the New York criteria[J]. Arthritis Rheum, 1984,27(4):361-368.[3]Ward M M, Deodhar A, Gensler L S, et al. 2019 Update of the American College of Rheumatology/Spondylitis Association of America/Spondyloarthritis Research and Treatment Network Recommendations for the Treatment of Ankylosing Spondylitis and Nonradiographic Axial Spondyloarthritis[J]. Arthritis Rheumatol, 2019,71(10):1599-1613.[4]Boonen A, Sieper J, van der Heijde D, et al. The burden of non-radiographic axial spondyloarthritis[J]. Semin Arthritis Rheum, 2015,44(5):556-562.[5]Sieper J, Rudwaleit M, Baraliakos X, et al. The Assessment of SpondyloArthritis international Society (ASAS) handbook: a guide to assess spondyloarthritis[J]. Ann Rheum Dis, 2009,68 Suppl 2:i1-i44.[6]Bermo M, Behnia S, Fair J, et al. Review of Extraskeletal Activity on Tc-99m Methylene Diphosphonate Bone Scintigraphy and Value of Cross-Sectional and SPECT-CT Imaging Correlation[J]. Curr Probl Diagn Radiol, 2018,47(5):324-332.[7]Ward M M, Deodhar A, Akl E A, et al. American College of Rheumatology/Spondylitis Association of America/Spondyloarthritis Research and Treatment Network 2015 Recommendations for the Treatment of Ankylosing Spondylitis and Nonradiographic Axial Spondyloarthritis[J]. Arthritis Rheumatol, 2016,68(2):282-298.[8]Abdelhafez Y G, Hagge R J, Badawi R D, et al. Early and Delayed 99mTc-MDP SPECT/CT Findings in Rheumatoid Arthritis and Osteoarthritis[J]. Clin Nucl Med, 2017,42(11):e480-e481.Figure 1.An 20-years-old man with 5 years of low back pain and spine malformation. (A) SPECT-CT showed an abnormal concentration of radioactivity in SIJ. (B–C) In SIJ, MRI showed a high signal on T1-WI, and a high signal on STIR.Figure 2.An 37-year-old man with 20 years of low back pain and spine malformation. (A) SPECT-CT showed an abnormal concentration of radioactivity in SIJ. (B–C) In SIJ, MRI showed a high signal on T1-WI, and a low signal on STIR.Disclosure of Interests:Qing Han: None declared, Zhaohui Zheng: None declared, Kui Zhang: None declared, Zheng Yu: None declared, Fengfan Yang: None declared, Qiang Liang: None declared, Ping Zhu: None declared, Xenofon Baraliakos Grant/research support from: Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Consultant of: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen

Background:Axial spondyloarthritis (axSpA) is a potentially severe chronic inflammatory disease with impact on function and quality of life. About 20-30% of axSpA patients show symptoms of depression or are diagnosed with depression [1]. Depression may influence outcome, especially patient reported outcomes.Objectives:To assess differences in baseline characteristics and outcome parameters between patients with and without symptoms of depression using WHO-5 score.Methods:RABBIT-SpA is a prospective longitudinal cohort study including axSpA patients enrolled at start of a new conventional treatment (including NSAID) or bDMARD. WHO-5 score was used to identify depressive symptoms categorised into 3 groups using validated cut-offs: moderate to severe depressive symptoms 50. Baseline values of patients categorised as having moderate to severe depressive symptoms were compared with the rest of the patients using t-test. Spearman correlation coefficient was calculated to analyse the relationship between WHO-5 score and other outcome parameters.Results:A total of 848 axSpA patients were included in this analysis (table 1). Moderate to severe depressive symptoms were found in 221 patients (30%), 226 (31%) had mild depressive symptoms and 285 (39%) reported a good well-being. Percentages of patients with inflammatory back pain, peripheral arthritis or enthesitis as well as the number of affected joints (44 JC) and entheseal sites (using SPARCC) were higher in the group of patients with moderate to severe depressive symptoms.Table 1.ParameterWHO-5 (Moderate severeN=221WHO-5 (29-50/>50)Mild/well-beingN=511Age, mean43.844.1Female, n (%)100 (45.2)229 (44.8)Disease duration, years, mean6.86.5Inflammatory back pain, n (%)195 (88.6)416 (81.6)Enthesitis, n (%)49 (22.3)78 (15.4)Peripheral arthritis (44 JC), n (%)64 (29.1)134 (26.3)Uveitis, n (%)45 (20.4)76 (15)IBD, n (%)13 (5.9)31 (6.1)Psoriasis, n (%)35 (15.8)58 (11.4)CRP positive (≥5mg/l), n (%)115 (59)243 (55.1)HLA-B27, n (%)151 (72.6)354 (74.2)BMI≥30, n (%)66 (30)117 (23.6)Comorbidities ≥3, n (%)50 (22.6)89 (17.4)Current smoking, n (%)102 (47.2)185 (36.7)All analysed outcome parameters (e.g. ASDAS, ASAS-HI, BASDAI, BASFI, patient global, physician global, pain, sleep) were significantly worse in the group of patients with moderate to severe depressive symptoms versus the other patients (table 2). This includes physician-reported, patient-reported and composite scores.Table 2.ParameterWHO-5 (Moderate severeN=221WHO-5 (29-50/>50)Mild/well-beingN=511p-valuePhysGA (NRS 0-10)6.2 (1.6)5.4 (1.9)0.0001ASDAS6.1 (1.6)4.2 (1.8)0.0001BASDAI (NRS 0-10)3.5 (0.8)2.9 (0.9)0.0001BASFI (NRS 0-10)5.5 (2.2)3.2 (2.2)0.0001ASAS-HI (0-17)9.8 (3.1)5.8 (3.1)0.0001PatGA (NRS 0-10)7 (1.8)5.4 (2.3)0.0001PatPain (NRS 0-10)6.9 (1.9)5.2 (2.3)0.0001PatSleep (NRS 0-10)7.2 (2.4)4.6 (2.9)0.0001Results are presented as mean ± SD.WHO-5 was highly correlated with all outcome parameters regardless of gender. Figure 1 shows the correlation of BASDAI and WHO-5 stratified for gender.Figure 1.Conclusion:Almost one third (30%) of axSpA patients in this analysis reported scores indicative of depressive symptoms and depression. The strong correlation of WHO-5 scores with patient and physician reported outcomes may be relevant for the management of patients with axSpA.References:[1]Redeker I, et al. Ann Rheum Dis 2018;0:1–8. doi:10.1136Acknowledgments:RABBIT-SpA is supported by a joint, unconditional grant from AbbVie, Amgen, Janssen-Cilag, Lilly, MSD, Mylan, Novartis, Pfizer, and UCB.Disclosure of Interests:Anne Regierer Speakers bureau: Novartis, Celgene, Janssen-Cilag, Anja Weiß: None declared, Xenofon Baraliakos Grant/research support from: Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Consultant of: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Denis Poddubnyy Grant/research support from: AbbVie, MSD, Novartis, and Pfizer, Consultant of: AbbVie, Bristol-Myers Squibb, Eli Lilly, MSD, Novartis, Pfizer, Roche, UCB, Speakers bureau: AbbVie, Bristol-Myers Squibb, Eli Lilly, MSD, Novartis, Pfizer, Roche, UCB, Ilka Schwarze: None declared, Juergen Braun Grant/research support from: Abbvie (Abbott), Amgen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, Eli Lilly and Company, Medac, MSD (Schering Plough), Mundipharma, Novartis, Pfizer (Wyeth), Roche, Sanofi- Aventis, and UCB Pharma, Consultant of: Abbvie (Abbott), Amgen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, EBEWE Pharma, Eli Lilly and Company, Medac, MSD (Schering-Plough), Mundipharma, Novartis, Pfizer (Wyeth), Roche, Sanofi-Aventis, and UCB Pharma, Speakers bureau: Abbvie (Abbott), Amgen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, EBEWE Pharma, Eli Lilly and Company, Medac, MSD (Schering-Plough), Mundipharma, Novartis, Pfizer (Wyeth), Roche, Sanofi-Aventis, and UCB Pharma, Joachim Sieper Consultant of: AbbVie, Boehringer Ingelheim, Eli Lilly and Company, Janssen, Merck, Novartis, Pfizer, Roche, and UCB Pharma, Speakers bureau: AbbVie, Boehringer Ingelheim, Eli Lilly and Company, Janssen, Merck, Novartis, Pfizer, Roche, and UCB Pharma, Angela Zink Speakers bureau: AbbVie, Amgen, BMS, Gilead, Hexal, Janssen, Lilly, MSD, Pfizer, Roche, Sanofi Aventis, UCB, Anja Strangfeld Speakers bureau: AbbVie, BMS, Pfizer, Roche, Sanofi-Aventis

Background:Hip joint lesion are the main cause of disability in patients with Ankylosing Spondylitis(AS) in western China. Seriously affect the quality of life of patients.The early clinical characteristics of hip joint disease are not typical, the disease is insidious, and the radiological diagnosis is delayed.The main prevention is early screening and early diagnosis.Objectives:This study attempted to find out the main characteristics and related factors in different groups of AS combine with hip joint lesion in western China.Methods:A-First evaluation:How many patients have 1) active SIJ changes on MRI. 2) chronic SIJ changes (each for erosion, clerosis, ankylosis, or any of those) on MRI. 3) a combination of active changes and chronic changes (each for erosion, sclerosis, ankylosis, or any of those) on MRI. 4) active hip changes on MRI. 5) chonic hip changes (erosion, effusion any of those) on MRI. 6) a combination of active changes and chronic hanges (erosion, effusion any of those) on MRI. B-Then, combination SIJ / hip. 7) active SIJ changes on MRI and in parallel active hip changes on MRI. 8) chronic (see above) SIJ changes on MRI and in parallel active hip changes on MRI. 9) chronic (see above) SIJ changes on MRI and in parallel chronic (see above) hip changes on MRI. 10) chronic (see above) SIJ changes on MRI and in parallel any (active or chronic) hip changes on MRI. C-Then, characterization of these groups with non-imaging findings. Characteristics of groups 7-10 above, for age, sex, Disease duration, Hip pain, Joint pain, enthesitis, Diarrhea, uveitis, ASDAS-CRP, BASDAI, BASFI, BASMI, Pat. Global, CRP, ESR, Harris Score, HLA-B27.Results:Retrospective analysis total 558 SpA patients (mean age 29, mean duration 5 years). 1) HIP-Active+Chronic group (N=288, AS=151) vs SIJ+HIP-Active group (N=241, AS=138): hip pain (pConclusion:Hip joint lesion are closely related to sacroiliac joint lesion and HLA-B27 positive in AS. Hip pain is the main clinical manifestation of hip joint lesion in AS. Hip joint lesion may lead to function declines, disease activity in AS.References:[1]Vander C B, Munoz-Gomariz E, Font P, et al. Hip involvement in ankylosing spondylitis:epidemiology and risk factors associated with hip replacement surgery[J]. Rheumatology (Oxford), 2010,49(1):73-81.[2]Sieper J, Rudwaleit M, Baraliakos X, et al. The Assessment of SpondyloArthritis international Society (ASAS) handbook: a guide to assess spondyloarthritis[J]. Ann Rheum Dis, 2009,68 Suppl 2:i1-i44.[3]Ward M M, Deodhar A, Akl E A, et al. American College of Rheumatology/Spondylitis Association of America/Spondyloarthritis Research and Treatment Network 2015 Recommendations for the Treatment of Ankylosing Spondylitis and Nonradiographic Axial Spondyloarthritis[J]. Arthritis Rheumatol, 2016,68(2):282-298.Disclosure of Interests:Qing Han: None declared, Zhaohui Zheng: None declared, Kui Zhang: None declared, Zheng Yu: None declared, Fengfan Yang: None declared, Qiang Liang: None declared, Ping Zhu: None declared, Xenofon Baraliakos Grant/research support from: Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Consultant of: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen

Background:Assessment and monitoring of disease activity and functioning is of major importance for the course of axial spondyloarthritis (axSpA). This is equally important for patient monitoring in daily routine as also for tight control strategies. Even though there is evidence that a closer monitoring of patients is better than routine care, more intensive treatment schedules are often not realized in daily practice for several reasons including shortage of time and personal resources. Using application software devices (apps) in clinical routine for the recording of disease-specific patient reported outcomes (PRO) may facilitate monitoring and improve clinical decision processes but there is a lack of data on the use of apps.Objectives:To investigate the use of such App technology in respect to usability, feasibility and equivalence of data in daily care of patients with axSpA. In more detail, it will be first determined how many patients are capable and ready to use the technology in a routine setting. Furthermore, the usage and behavior of patients using the app will be studied, the usability of the app and the equivalence of the collected parameters as well as the adherence to the documentation of disease activity over time.Methods:Patients diagnosed with axSpA were consecutively included in this ongoing monocentric prospective cohort study. In addition to patient and disease characteristics, information on previous experience with digital health apps was collected. Patients were asked to submit BASDAI and BASFI scores regularly every 2 weeks. The free to use AxSpA Live App is available for Android and iOS as a Class I certified medical device.Results:Out of 103 axSpA patients asked, 69 patients with axSpA (mean age 41.5 ± 11.3, 58% male, 76.8% use of bDMARDs, BASDAI 4.3 ± 2.0, BASFI 3.8 ± 2.5) out of 103 patients (67%) agreed to use participate, while 5 did not have a smartphone, 1 was unable to download the app for technical reasons, 28 reported other personal reasons). Of the 69, 62 patients (89.9%) reported using electronic media frequently and had used digital health apps (mean apps used 1.0 ± 1.3) in everyday life before. There were no systematic differences between pain levels documented on paper or by app at baseline (ICC 0.9 (95%CI 0.82 – 0.93). Out of 55 patients who completed week 2, only 33 patients (60%) used the App regularly to transmit their BASDAI/BASFI responses within the first two weeks (60%). Patients who started a new drug treatment because of high disease activity, reported BASDAI values more often than patients without a treatment change within a follow-up period of 5.5± 2.4 weeks (Table).Conclusion:The majority of patients with axSpA were able to use the AxSpA Live App. Most patients report scores regularly. The current disease activity seems to influence the adherence to reporting.Patients without change in their medication (n=53)Patients with change in their medication (n=16)Age, years42.0 (11.9)39.8 (9.3)Sex, male (%)62.343.8BASDAI, baseline4.1 (2.1)4.9 (1.7)BASFI, baseline3.8 (2.6)3.8 (2.3)Time of follow-up, in weeks5.4 (2.4)5.6 (2.5)Number of transmitted BASDAI values at week 222 (41%)11 (69%)Median number of transmitted BASDAI values during follow up1.0(3.6)1.5 (1.4)This work was supported by an unrestricted Grant by Novartis Pharma GmbH, GermanyAcknowledgments:n/aDisclosure of Interests:Uta Kiltz Grant/research support from: AbbVie, Amgen, Biogen, Novartis, Pfizer, Consultant of: AbbVie, Biocad, Eli Lilly and Company, Grünenthal, Janssen, Novartis, Pfizer, UCB, Speakers bureau: AbbVie, MSD, Novartis, Pfizer, Roche, UCB, Robin Kempin: None declared, Anna Schlegel: None declared, Xenofon Baraliakos Grant/research support from: Grant/research support from: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Consultant of: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, UCB and Werfen, Styliani Tsiami: None declared, Bjoern Buehring Grant/research support from: GE/Lunar, Kinemed, Consultant of: Gilead, Abbvie, Lilly, GE/Lunar, Janssen, Amgen, Speakers bureau: UCB, David Kiefer Grant/research support from: Novartis, Juergen Braun Grant/research support from: Abbvie (Abbott), Amgen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, Eli Lilly and Company, Medac, MSD (Schering Plough), Mundipharma, Novartis, Pfizer (Wyeth), Roche, Sanofi- Aventis, and UCB Pharma, Consultant of: Abbvie (Abbott), Amgen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, EBEWE Pharma, Eli Lilly and Company, Medac, MSD (Schering-Plough), Mundipharma, Novartis, Pfizer (Wyeth), Roche, Sanofi-Aventis, and UCB Pharma, Speakers bureau: Abbvie (Abbott), Amgen, BMS, Boehringer, Celgene, Celltrion, Centocor, Chugai, EBEWE Pharma, Eli Lilly and Company, Medac, MSD (Schering-Plough), Mundipharma, Novartis, Pfizer (Wyeth), Roche, Sanofi-Aventis, and UCB Pharma