Explore the vast range of titles available.

Background:There is evidence of subclinical activity in psoriatic arthritis (PsA) patients in remission detected by power Doppler ultrasound (PDUS), which represent a risk factor for relapse [1].Objectives:The study aimed to evaluate subclinical ultrasound changes in patients with PsA who reached the therapeutic target with biological therapy.Methods:This cross-sectional study included patients from the Romanian Registry of Rheumatic Diseases, with Disease Activity Index for Psoriatic Arthrititis (DAPSA) < 14, undergoing biological therapy. Clinical and musculoskeletal ultrasound examinations were performed. PDUS scanning protocol included bilateral evaluation of hands and feet joints for synovitis and bilateral assessment of elbow lateral epicondyle, quadriceps insertion, distal patella tendon insertion, and Achilles enthesis for enthesitis. Enthesitis and synovitis were defined using the OMERACT criteria [2] and they were considered active if they exhibited at least a score 1 for PDUS signal.Results:The study included 44 patients: mean age of 55.2 ± 15.2 years; 52.3% women; 36.4% obesity; 29.5% smokers; mean PsA duration of 15.4 ± 9.1 years; average psoriasis duration of 22.9 ± 13.0 years; 1 patient with PsA sine psoriasis; mean DAPSA of 4.5 ± 3.0. In total 15.9% of patients had active synovitis and 18.2% had active enthesitis. Only 12.5% of the active ultrasound enthesitis were painful on palpation. The comparison of clinical and PDUS findings at entheseal level showed a sensitivity of 12.5%, a specificity of 95.1% for clinical examination and an overall agreement of 93.2%. The probability of observing positive ultrasound changes in patients with painful enthesis was 2.5 times higher than in those with painless enthesis.Conclusion:A high proportion of active synovitis and enthesitis was detected in PsA patients considered within the therapeutic target. Clinical examination may be used as a guide for selecting the anatomic sites to scan, and patients with positive PDUS findings should be considered at risk of relapse.REFERENCES:[1] Ruta S et al. J Rheumatol. 2017; 44 (7): 1018-1023.[2] Bruyn GA, et al OMERACT Ultrasound Working Group.J Rheumatol. 2019 Oct;46(10):1388-1393.Acknowledgements:NIL.Disclosure of Interests:Mihaela Agache speaking fees in meetings sponsored by Abbvie, Novartis, Pfizer, Luminita Enache: None declared, Corina Mogosan speaking fees in meetings sponsored by Abbvie, Lilly, Novartis, Pfizer, Claudiu Popescu speaker fees from Abbvie, Norvartis, Pfizer, Emilio Filippucci speaking fees in meetings sponsored by Abbvie, Amgen, Bristol-Myers Squibb, Janssen-Cilag, Lilly, Novartis, Pfizer and UCB Pharma, Catalin Codreanu Support for clinical studies: AbbVie, Ewopharma, Lilly, Novartis, PfizerSpeaker fees & consultancy: AbbVie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis, Pfizer, Sandoz.

BackgroundSystemic lupus erythematosus (SLE) is a chronic, multisystemic autoimmune disease of unknown etiology. A defining characteristic is its immunological anomalies such as the production of antinuclear antibodies (ANA). Polymorphic clinical manifestations, the absence of pathognomonic signs and the absence of specific laboratory tests for SLE, make the diagnosis difficult. Although they have been developed for the homogenization of patients included in clinical trials, the SLE 2019 EULAR (European Alliance of Associations for Rheumatology)/ACR (American College of Rheumatology) classification criteria [1] can serve as a guide or diagnostic verification in individual cases from current medical practice.ObjectivesThe study assessed the characteristics and consistency of the diagnosis and classification of SLE in order to measure a potential patient pool for inclusion in clinical trials.MethodsThe study retrospectively evaluated the conformity of the 2019 EULAR/ACR classification criteria in patients discharged from a single-center tertiary university rheumatology center between February 2020 and February 2022, diagnosed with SLE according to their attending rheumatologists and identified by international classification of diseases (ICD10) codes. Normally-distributed continuous variables are reported as “mean ± standard deviation”. The correlation of continuous variables was studied with Spearman tests. Differences of continuous variables between nominal dichotomous subgroups were evaluated with Mann Whitney tests. Statistics were considered significant if p < 0.05.ResultsThe study included 146 patients, of whom 92.5% were women, with an average age of 48.3 ± 13.3 years. Approximatively 7.5% of patients had negative ANA (including at repeated measurements) and 12.3% had an unknown ANA status. The method for determining ANA was ELISA (enzyme-linked immunosorbent assay; 75.3%), indirect immuno-fluorescence (2.7%) or undetermined (21.9%). Men scored a significantly higher median number of classification points than women (i.e., 21 points versus 16 points; p = 0.020) and they had a higher prevalence of class 3/4 nephritis (18.2% versus 3.0%; p = 0.014), pleuritis/pericarditis (36.4% versus 14.8%; p = 0.064) and oral ulcers (27.3% versus 9.6%; p = 0.072). Only 63.7% of SLE diagnoses also met the 2019 EULAR/ACR classification criteria. The most common manifestations not complying with these classification criteria were proteinuria (59.5% discordance), thrombocytopenia (13.6% discordance) and joint involvement (9.3% discordance). The median number of classification points correlated significantly with the median titer of ANA (rho = 0.301; p = 0.001) measured by ELISA.ConclusionDiagnostic reality includes ANA-negative SLE, which should be further investigated. In clinical practice, ANA are preferably determined by ELISA and their titer seems to be proportionally associated with more classifiable SLE clinical characteristics. Clinical trials have a maximum eligible SLE population of 63.7% of patients to whom additional inclusion/exclusion criteria could be applied.Reference[1]Aringer et al. Arthritis Rheumatol. 2019; 71 (9), 1400-1412.Acknowledgements:NIL.Disclosure of InterestsNone Declared.

Psychiatric comorbidities are frequent extra-articular manifestations in rheumatoid arthritis (RA) and depression is the most common [1]. A 2013 study estimated that 16.8 % of RA patients suffer from major depressive disorder, being more prevalent than diabetes, Parkinson's disease or cancer [2-3]. Patients with RA have constitutional symptoms, frequently encountered in depression, like fatigue, weight loss, insomnia and lack of appetite. The overlap of depression in inflammatory immune mediated diseases is recognized for some time [4]. Studies show that immune mediated inflammation affects and modulates neurogenesis, neurotransmission, neuroendocrine activity and neuroplasticity [5]. Depression has important effects on RA patients: worse prognosis, pain, fatigue, functional deficit, more comorbidities, higher rate of mortality, increased healthcare resource utilization and lowered quality of life [6]. The scope of this article is to highlight the importance of managing depression in RA. The primary objective was to estimate the prevalence of depression in a cohort of RA patients. The secondary objective was to describe the phenotypic characteristics of RA patients with depression. RA patients from the Center of Rheumatic Diseases in Bucharest were included in the study if they were at least 18 years-old and if they had two or three follow-ups, after 2019. The protocol included collection of demographical, clinical and biological data. Prevalence of depression is derived from patients' medical history, known depression. Demographical characteristics and RA phenotype were compared between the two groups. Disease activity was estimated with DAS28 and its components, tender joint count, swollen joint count, CRP and were followed over time to compare disease activity between patients with known depression and patients without depression. We collected data from 203 patients with RA, among whom 37 were known with depression, generating a prevalence of 18.2%. A meta-analysis from 2013 reported that 16.8 % patients with RA suffer from a major depression disorder [1]. Most of the patients with depression were women (87.2%). Female sex is a potential risk factor for depression [7]. The prevalence of active smoking among the depression subgroup was higher (8.1%, 1.8%, p = 0.041). Depression is a known risk factor for negative behaviors like smoking [8]. Patients had a longer disease duration (in median, 13 years compared to 10 years, p = 0.059) and also the seropositivity prevalence was lower. In 2022 a correlation between depression and seronegative RA was found [9]. DAS28 and the components of DAS28 were higher in the depression RA subgroup; DAS28 was higher at all time points (p < 0.001). Higher tender joint count was expected (p < 0.001), but swollen joint count was also higher among depressive RA patients (p < 0.001), as well as CRP (p = 0.009, Figure 1). Depression is prevalent among RA patients and it has an important impact on the quality of life; so depressive symptoms should be addressed in clinical practice. The correlation between the prognosis of rheumatic disease and depression is strong, regardless of the direction of causality. The assessment of depression could be a psychomarker for assessing RA prognosis. DAS28 is used to make therapeutic decisions, so given that depression scores increase DAS28, it follows that they also influence therapeutic decisions. [1] Morf H et al. Clin Rheumatol 2021, 40(5):1779-1787. [2] Overman CL et al. Arthritis Care Res (Hoboken) 2014, 66(5):671-678. [3] Jamshidi T et al. Open Access Rheumatol 2019, 11:53-59. [4] Nerurkar L et al. Lancet Psychiatry 2019, 6(2):164-173. [5] Muller N et al. Mol Psychiatry 2007, 12(11):988-1000. [6] Yilmaz V et al. Eur J Rheumatol 2017, 4(2):127-132. [7] Kim SY et al. Rheumatology (Oxford) 2020 Aug 1;59(8):1889-1897. [8] Englbrecht M et al. PLoS One 2019, 14(5):e0217412. [9] Kwiatkowska B et al. Reumatologia 2018, 56(4):219-227. NIL. None Declared. [Display omitted]

Summary Findings from this 5-year phase 3 study of postmenopausal women with osteoporosis showed that bazedoxifene was associated with an overall favorable safety and tolerability profile, with no evidence of endometrial or breast stimulation. Overall, the results at 5 years were consistent with those seen at 3 years. Introduction We report safety and tolerability findings from a 5-year randomized, double-blind, phase 3 study of bazedoxifene in postmenopausal women with osteoporosis. Methods In the core study, healthy postmenopausal women with osteoporosis (N = 7,492; mean age, 66.4 years) were randomized to daily doses of bazedoxifene 20 or 40 mg, raloxifene 60 mg, or placebo for 3 years. During the 2-year study extension, the raloxifene 60-mg treatment arm was discontinued after the 3-year database was finalized, and subjects receiving bazedoxifene 40 mg were transitioned in a blinded manner to bazedoxifene 20 mg (bazedoxifene 40-/20-mg group) after 4 years. Safety and tolerability data are reported for subjects in the bazedoxifene 20- and 40-/20-mg and placebo groups; efficacy findings are reported elsewhere. Results A total of 3,146 subjects in the bazedoxifene 20- and 40-mg and placebo groups were enrolled in the extension study (years 4 and 5). Overall, the 5-year incidence of adverse events (AEs), serious AEs, and discontinuations due to AEs were similar among groups. The incidence of hot flushes and leg cramps was higher with bazedoxifene compared with placebo. Venous thromboembolic events, primarily deep vein thrombosis, were more frequently reported in the bazedoxifene groups compared with the placebo group. Reports of cardiac disorders and cerebrovascular events were few and evenly distributed among groups. Bazedoxifene showed a neutral effect on the breast and endometrium. Conclusion Bazedoxifene was associated with an overall favorable safety and tolerability profile in postmenopausal women with osteoporosis over 5 years of therapy, consistent with findings at 3 years.

Background:The increasing availability of biosimilars has strongly reduced bDMARD costs, although drug prices vary considerably across countries. The introduction of biosimilars can be seen as an opportunity to reduce costs and improve access to bDMARDs, particularly for countries with lower socioeconomic status. However, it is unknown whether there is an equal penetration of biosimilars to the drug market in countries with different socioeconomic status.Objectives:To study the ratio between biosimilar and bio-originator use in rheumatoid arthritis (RA) patients in countries worldwide, and relate this to country-level socioeconomic status.Methods:Data on biosimilar use and bio-originator use were collected from 18 countries worldwide, from 2015 to 2022. Data were collected on abatacept, adalimumab, etanercept, certolizumab, infliximab, tocilizumab, rituximab and golimumab. For France, only data from TNFi initiators were available. Data were derived from several registries and cohorts: Data sources varied from single hospital cohorts to country-level bDMARD registries. Data on the representativeness of each data source compared to the total RA population of a country were unavailable. Additional data on the availability of biosimilars and regulations regarding their use were collected by a short questionnaire. Data on ‘gross domestic product (GDP) per capita based on power purchasing parity’ and ‘country income category’ as proxies for socioeconomic status were derived from publicly available data from the World Bank. Main outcome was the prevalent % biosimilar use per year [n patients biosimilar/ (n patients biosimilar + n patients bio-originator)*100]. Data are presented graphically. A linear regression analysis was performed to determine the association between GDP per capita and the % biosimilar use.Results:According to the questionnaire data, in 2022 biosimilars were available in each country, except for Nigeria. In most countries biosimilars were available for 4 bio-originators, except for Turkey (2), Mexico and Japan (3). Switching to a biosimilar was reported to be mandatory in Italy, Canada and Denmark and recommended in Norway, Finland, Portugal, Romania, France, Spain and Sweden.The proportion of biosimilar use per year per country is shown in Figure 1. In the majority of countries, the proportion of biosimilar use increased over time. In 2022, the most recent time point, the proportion of biosimilar use ranged from 0% in Nigeria and South-Africa to 90% in Denmark and 100% in France (France based on TNFi initiators only). Biosimilar use in lower middle- and upper middle-income countries was <10% during all years. Linear regression analyses showed a statistically significant negative association between GDP per capita and % biosimilar use from 2016 till 2022 (Table 1). For example in 2022, per 10.000 IntI$ increase in GDP per capita, the % biosimilar use in a country increased with 5.9 (95% CI 0.93; 11.0).Conclusion:In the past 6 years biosimilar use increased, but with major differences in biosimilar uptake between countries. In the included countries with lowest socioeconomic status, biosimilar uptake in 2022 was close to or equal to 0, which was in some cases explained by a total lack of availability. Whereas biosimilars are not by definition less costly than bio-originators for individual hospitals, the introduction of biosimilars does introduce price competition which lowers bDMARD prices in general. This lower penetration of biosimilars in countries with lower socioeconomic status therefore seems to contribute to further inequity in bDMARD availability worldwide.REFERENCES:NIL.Table 1.Association between GDP per capita (international $, per 10.000) and % of biosimilars used in a country per yearB (95% CI)20151.1 (-0.75; 2.8)20162.1 (0.71; 3.5)20173.4 (1.2; 5.6)20184.3 (1.5; 7.0)20194.8 (0.85; 8.7)20205.1 (0.82; 9.5)20215.5 (0.82; 10.3)20225.9 (0.93; 11.0)Linear regression outcomes. Coefficients can be interpreted as % increase in biosimilar use in a country per 10.000 IntI$ increase in GDP per capita.Acknowledgements:NIL.Disclosure of Interests:Sytske Anne Bergstra Benecke, ASPIRE grant from Pfizer, Denis Mongin: None declared, Lene Dreyer L. Dreyer has received research grant (paid to her institution) from BMS and Abbvie outside the current manuscript. She is member of the steering committee of the Danish Rheumatology Quality Registry (DANBIO, DRQ), which receives public funding from the hospital owners and funding from pharmaceutical companies., Dan Nordström BMS, Lilly, MSD, Novartis, Pfizer, UCB, MSD, Kichul Shin Novartis, Astellas, AbbVie, BMS, and Yuhan, Denis Choquette: None declared, Manuel Pombo-Suarez consulting and/or speaking from GSK, Janssen, Merck Sharp & Dohme, Novartis and Pfizer., María Julieta Gamba: None declared, Raphaèle Seror GSK, Bristol Myer Squib, Boerhinger and Janssen; Amgen, Pfizer and Roche. travel fees from Amgen and GSK., Catalin Codreanu Speaker fees & consulting: AbbVie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis, Pfizer, Sandoz, UCB, Jakub Zavada speaker fees & consulting: Abbvie, Akord, Astra Zeneca, Eli-Lilly, Novartis, Pfizer, SobiC., Ana Maria Rodrigues Amgen, AbbVie and Novartis, Amgen, AstraZeneca, Novartis, AbbVie, Pfizer, MSD, Lilly, Boehringer Ingelheim, Bente Glintborg Pfizer, AbbVie, Sandoz, Merete Lund Hetland Medac, Novartis, Pfizer, Sandoz, AbbVie, BMS, Eli Lilly, MSD, Pfizer, Sandoz, Novartis, Vijaya Rivera Terán Apopharma, Carolina Isnardi Received research funding to Argentine Society of Rheumatology from AbbVie, Pfizer and Elea Phoenix, Florenzo Iannone Consulting and/or speaking from Abbvie, Amgen, AstraZeneca, BMS, Galapagos, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, UCB, Carlos Enrique Toro-Gutierrez AbbVie, Astra Zeneca, Biopas, Janssen and Lilly, Deshire Alpizar-Rodriguez scientific advisor GSK Mexico, Courage Uhunmwangho: None declared, Riette du Toit: None declared, Axel Finckh Speaker honoraria or consultancies: AbbVie, Astra-Zeneca, Eli-Lilly, GSK, MSD, Pfizer., Received research funding to HUG Hospital from AbbVie, BMS, Galapagos, Eli-Lilly, Pfizer., Tore K. Kvien Janssen, Sandoz, Grünenthal, UCB. Fees for consulting: AbbVie, Galapagos, Janssen, Pfizer, Sandoz, Data monitoring committee: AbbVie, Received research funding to Diakonhjemmet Hospital from AbbVie, BMS, Novartis, Pfizer and UCB., Kim Lauper Speaker honoraria or consultancies: Pfizer, Received research funding to the institution from AbbVie, Galapagos, Eli-Lilly, Pfizer.

BackgroundThe impact of radiographic status on real-world secukinumab treatment effectiveness in axial spondyloarthritis (axSpA) patients is unknown.ObjectivesTo compare the treatment effectiveness of secukinumab in radiographic (r-) vs. non-radiographic (nr-) axSpA patients treated in routine care across Europe.MethodsProspectively collected data on secukinumab-treated axSpA patients with known radiographic status followed in routine care in the EuroSpA collaboration [1] were pooled from 9 countries. Patients were listed as r-axSpA if registered to fulfil the modified New York [2] or the radiographic ASAS classification [3] criteria. If patients were registered to fulfil neither criterion or if they did not fulfil one criterion and the other was unknown, patients were registered as nr-axSpA.Patient-reported outcome (PRO) remission rates including pain (VAS≤20), Bath Ankylosing Spondylitis Disease Activity (BASDAI≤20) and Functional Index (BASFI≤ 20) (all in the form of 0–100 visual analogue scale), and Ankylosing Spondylitis Disease Activity Score-CRP (ASDAS inactive disease <1.3) after 6, 12 and 24 months of secukinumab treatment were calculated.Remission rates in r-axSpA vs. nr-axSpA patients were compared by logistic regression analyses in an unadjusted model (MODEL1), a model adjusted for age/gender (MODEL2) and a model adjusted for age/gender/country/previous bDMARD (yes/no)/baseline CRP/years since diagnosis to secukinumab initiation (MODEL3). For MODEL3, parameter estimates (CRP) from 100 imputed data sets were pooled using Multivariate Imputation by Chained Equations.ResultsPatients with r-axSpA had longer disease duration at secukinumab initiation, were more frequently males and HLA-B27 positive compared to nr-axSpA patients. PROs at baseline were largely similar between groups, while CRP and ASDAS-CRP were higher in r-axSpA patients. A higher percentage of nr-axSpA patients had received previous bDMARDs compared to r-axSpA patients.Crude PRO remission rates at 6/12/24-months were significantly lower in nr-axSpA compared to r-axSpA patients (Table 1, Figure 1 (MODEL1)) as were percentages of patients in ASDAS inactive disease (Table 1). However, when adjusting for age/gender (MODEL2) the difference in PROs diminished, and when adjusting for multiple possible confounders (MODEL3), no significant differences were found between the two groups (Figure 1). Differences in percentages of patients in ASDAS inactive disease in r-axSpA vs. nr-axSpA patients were almost unaffected by adjustments (Figure 1).ConclusionWhile crude remission rates in European secukinumab-treated patients followed in routine care were higher in r-axSpA compared to nr-axSpA patients, this difference disappeared after adjusting for multiple confounders, and, thus, appeared to be related to other factors than radiographic status.References[1]https://eurospa.eu/[2]van der Linden et al. Arthritis Rheum 1984.[3]Rudwaleit et al. Ann Rheum Dis 2009.Table 1.Baseline characteristics and remission rates for European secukinumab treated r- and nr-axSpA patients.Radiographic axSpA (n=899)Non-radiographic axSpA (n=236)BASELINEValue (%/ median (IQR))N availableValue (%/ median (IQR))N availableAge (years)47 (38–55)89946 (36–55)236Male (%)6189936236HLA–B27 pos (%)8075455214Years from diagnosis7 (3–14)8864 (2–8)231bDMARD naïve (%)4089926236Pain (VAS, 0-100)70 (55–85)61470 (51–80)128BASDAI (0-100)64 (50–76)68567 (49–76)139BASFI (0-100)55 (35–73)47654 (30–73)118CRP (mg/L)16 (5–31)6805 (2–15)151ASDAS–CRP4.0 (3.2–4.7)6233.6 (2.9–4.2)123FOLLOW-UPRemission rates(6m/ 12m/ 24m)N available(6m/ 12m/ 24m)Remission rates(6m/ 12m/ 24m)N available(6m/ 12m/ 24m)Pain remission (≤ 20), (%)39.2/ 46.1/ 47.7523/ 360/ 17422.8/ 25.0/ 27.6114/ 76/ 29BASDAI remission (≤ 20), (%)37.6/ 41.2/ 49.7603/ 408/ 19721.9/ 19.3/ 19.4128/ 83/ 31BASFI remission (≤ 20), (%)31.4/ 36.2/ 40.9376/ 240/ 11024.1/ 28.2/ 33.3108/ 71/ 27ASDAS inactive disease (<1.3), (%)11.4/ 12.5/ 18.9559/ 383/ 1906.5/ 5.7/ 7.7108/ 70/ 26AcknowledgementsNovartis Pharma AG for supporting the EuroSpA collaboration.Disclosure of InterestsSara Nysom Christiansen Speakers bureau: BMS, Novartid and GE, Grant/research support from: Novartis, Simon Horskjær Rasmussen: None declared, Mikkel Østergaard Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi, UCB, Consultant of: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi, UCB, Brigitte Michelsen Grant/research support from: Novartis, Karel Pavelka Speakers bureau: Pfizer, MSD, BMS, UCB, Amgen, Egis, Roche, AbbVie, Consultant of: Pfizer, MSD, BMS, UCB, Amgen, Egis, Roche, AbbVie, Catalin Codreanu Speakers bureau: AbbVie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis, Pfizer, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis, Pfizer, Adrian Ciurea Speakers bureau: AbbVie, Novartis, Bente Glintborg Grant/research support from: Pfizer, Abbvie, BMS, Maria Jose Santos Speakers bureau: Abbvie, AstraZeneca, Lilly, Novartis, Pfizer, İsmail Sari: None declared, Ziga Rotar Speakers bureau: Abbvie, Novartis, MSD, Medis, Biogen, Eli Lilly, Pfizer, Sanofi, Lek, Janssen, Consultant of: Abbvie, Novartis, MSD, Medis, Biogen, Eli Lilly, Pfizer, Sanofi, Lek, Janssen, Björn Gudbjornsson Speakers bureau: Novartis and Nordic Pharma, Consultant of: Novartis and Nordic Pharma, Jakub Zavada Speakers bureau: Abbvie, Elli-Lilly, Sandoz, Novartis, Egis, UCB., Consultant of: Abbvie, Elli-Lilly, Sandoz, Novartis, Egis, UCB., Corina Mogosan: None declared, Michael J. Nissen Speakers bureau: AbbVie, Eli Lilly, Janssens, Novartis, Pfizer, Consultant of: AbbVie, Eli Lilly, Janssens, Novartis, Pfizer, Anne Gitte Loft Speakers bureau: AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, UCB, Consultant of: AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, UCB, Anabela Barcelos Speakers bureau: Abbvie, Janssen, Novartis, Consultant of: Abbvie, Lilly and Novartis, Yesim Erez: None declared, Katja Pirkmajer Speakers bureau: Abbvie, Novartis, MSD, Medis, Eli Lilly, Pfizer, Lek, Janssen, Consultant of: Abbvie, Novartis, Medis, Eli Lilly, Pfize, Boehringer Ingelheim, Gerdur Gröndal: None declared, Merete Lund Hetland Speakers bureau: Pfizer, Medac, Sandoz, Grant/research support from: Abbvie, Biogen, BMS, Celltrion, Eli Lilly, Janssen Biologics B.V, Lundbeck Fonden, MSD, Medac, Lykke Midtbøll Ørnbjerg Grant/research support from: Novartis.

Background:The safety profile of Janus kinase inhibitors (JAKi), particularly concerning infection risks, remains a critical concern in patients with rheumatoid arthritis (RA). Initial pivotal trials and subsequent safety trials[1] showed increased incidences of opportunistic infections and herpes zoster (HZ). However, real-world data on the incidence and severity of these infections continues to be an area of active study.Objectives:To assess the incidence of infections (any and serious) and HZ in RA patients treated with JAKi, compared to other biologic agents in a large multi-country real-world population.Methods:We studied patients from 14 RA registers across Europe and Québec, starting JAKi, TNF-inhibitors (TNFi) or bDMARDs with other modes of action (OMA). Investigated outcomes included all infections, serious infections (requiring hospitalisation, intravenous treatment or resulting in death), all infections excluding HZ, and HZ. Infections were linked to treatments within 3 months of cessation (1 year after initiation for rituximab) or until follow-up loss, death, or study end. Incidence rates (IR) per 100 patient-years (PY) with 95% confidence intervals (CI) were computed. Poisson regressions with propensity score weighting (including country, disease-, patient-characteristics, and comorbidities, see Figure 1) were performed within each individual register and combined using random-effect meta-analysis to obtain adjusted incidence rate ratios (aIRR) with 95% CI.Results:Over the 54’905 treatment initiations considered in 36’838 patients with a mean patient follow-up of 2.8 years, 7’070 incident infections were reported of which 1’379 were considered as serious and 352 were HZ. Crude incidence of any infection was lower for TNFi (7.0/100 PY) than for JAKi (9.0/100 PY) and OMA (10.6/100 PY). The adjusted Poisson regression found no significant difference in the incidence of any infections (aIRR = 1.13; 95% CI [0.91; 1.40]) or serious infections (aIRR = 0.99; 95% CI [0.71; 1.39]) between JAKi vs TNFi. However, the incidence of any infection was higher for OMA vs TNFi (aIRR = 1.20; 95% CI [1.09; 1.32]; Figure 1). Compared to TNFi, incidence of HZ was significantly higher for JAKi (aIRR = 2.27; 95% CI [1.71; 3.02]), but not for OMA (aIRR = 1.07; 95% CI [0.74; 1.55]).Conclusion:In a real-world study with 14 RA registers and all available JAKi, we found no significantly higher risk of infections, either any or serious, in RA patients treated with JAKi compared to TNFi. However, there was a higher risk of any infections with OMA. Compared to TNFi, the incidence of HZ was significantly higher in patients receiving JAKi. Planned subgroup analyses will focus on at-risk populations, specific medications, and infection types to guide treatment choices.REFERENCES:[1] DOI:10.1056/NEJMoa2109927.Table 1.Baseline characteristicsJAKi(tofacitinib (30%), baricitinib (44%), upadacitinib (21%), filgotinib (5%))n = 13’374OMA(rituximab (33%), tocilizumab (32%), abatacept (24%), sarilumab (7%), other (4%))n = 16’482TNFi(etanercept (40%), adalimumab (30%), golimumab (8%), certolizumab (9%), infliximab (5%), unspecified (7%))n = 25’049Treatment duration, years (median [IQR])1.4 [0.6; 2.7]1.2 [0.4; 2.6]1.3 [0.6; 2.8]Age, years (mean (SD))58.3 (12.2)60.5 (12.4)57.2 (13.3)Female (%)78.375.875.5Disease duration, years (median [IQR])11.0 [5.4; 18.4]11.9 [6.0; 20.0]8.4 [3.7; 16.0]Seropositivity (%)80.784.877.2Previous b/ts DMARD (%)020.216.144.6124.125.927.9219.422.413.5≥ 336.335.713.9Concomitant csDMARD (%)49.551.960.0Concomitant GC (%)44.242.034.4CRP, mg/L (mean (SD))11.3 (21.2)12.2 (27.0)11.4 (21.5)CDAI (mean (SD))25.0 (13.7)22.2 (14.0)23.7 (13.9)DAS 28 (mean (SD))4.7 (1.5)4.3 (1.7)4.6 (1.6)HAQ (mean (SD))1.2 (0.7)1.2 (0.8)1.1 (0.7)BMI (mean (SD))27.1 (5.8)27.3 (6.0)27.3 (6.3)Tobacco (ever) (%)36.038.738.5csDMARDs = conventional synthetic DMARDs, GC = glucocorticoids, CRP = C-reactive protein, CDAI = Clinical Disease Activity Index, DAS 28 = Disease Activity Score 28, HAQ = Health Assessment Questionnaire, BMI = Body Mass Index.Acknowledgements:NIL.Disclosure of Interests:Romain Aymon: None declared, Denis Mongin: None declared, Benoit Gilbert: None declared, Romain Guemara: None declared, Denis Choquette Abbvie, Amgen, Pfizer, Sandoz and Tevapharm, Abbvie, Amgen, Celltrion, Eli Lilly, Fresenius-Kabi, INESSS, Jamppharma, Pfizer, Sandoz and Tevapharm, Rhumadata is supported through grants from Abbvie, Amgen, Fresenius-Kabi, Eli Lilly, Pfizer, Sandoz and Tevapharm, Catalin Codreanu Abbvie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis, Pfizer, AbbVie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis, Pfizer, Irini Flouri: None declared, Doreen Huschek: None declared, Kimme Hyrich: None declared, Florenzo Iannone Abbvie, BMS, Celgene, Eli Lilly, Galapagos, Janssen, MSD, Novartis, Pfizer, SOBI, Roche and UCB, Abbvie, BMS, Celgene, Eli Lilly, Galapagos, Janssen, MSD, Novartis, Pfizer, SOBI, Roche and UCB, Lianne Kearsley-Fleet: None declared, Tore K. Kvien AbbVie, Amgen, Celltrion, Gilead, Grünenthal, Novartis, Pfizer, Sandoz, UCB, AbbVie, Amgen, Celltrion, Gilead, Grünenthal, Novartis, Pfizer, Sandoz, UCB, Burkhard F. Leeb Eli-Lilly, Pfizer, Astropharma, Biogen, Celgene, Eli-Lilly, Pfizer, AbbVie, Biogen, Celgene, Dan Nordström Abbvie, BMS, Lilly, MSD, Novartis, Pfizer, Roche, UCB, Karel Pavelka: None declared, Manuel Pombo-Suarez Janssen, Merck Sharp & Dohme, Novartis and Sanofi Genzyme, Sella Aarrestad Provan: None declared, Ana Maria Rodrigues Amgen, Pfizer, Astrazeneca, Novartis, Roche and Nordic pharma, Amgen, Pfizer, Astrazeneca, Novartis, Roche and Nordic pharma, Reuma.pt is supported througth grants from Abbvie, Bristol Myers Squibb, Lilly, MSD, Novartis, Pfizer, Boehringer Ingelheim, Astrazeneca and Amgen, Ziga Rotar Abbive, Amgen, Biogen, Eli Lilly, Medis, Mediasi, Novartis, Sandoz, Pfizer, MSD, Sanofi, Roche, SOBI, Abbive, Amgen, Biogen, Eli Lilly, Medis, Mediasi, Novartis, Sandoz, Pfizer, MSD, Sanofi, Roche, SOBI, Prodromos Sidiropoulos AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, Amgen and UCB, AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, Amgen and UCB, AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, Amgen and UCB, Anja Strangfeld Abbvie, Amgen, BMS, Celltrion, MSD, Lilly, Pfizer, Roche, UCB, AbbVie, Amgen, BMS, Celltrion, Fresenius Kabi, Galapagos, Hexal, Lilly, MSD, Pfizer, Samsung Bioepis, Sanofi Aventis, Viatris Sante, and UCB, and previously Roche. The German Biologics Register RABBIT is supported by a joint unconditional grant from these companies., Nina Trokovic: None declared, Jakub Zavada Abbvie, Elli-Lilly, Sandoz, Novartis, Egis, UCB, Sanofi, Astra Zeneca, Sobi, Abbvie, Elli-Lilly, Sandoz, Novartis, Egis, UCB, Sanofi, Astra Zeneca, Sobi, Delphine Sophie Courvoisier: None declared, Axel Finckh AbbVie, Eli-Lilly, Novartis, MSD, Pfizer, UCB, BMS, Eli-Lilly, Pfizer, AbbVie, BMS, Eli-Lilly, Galapagos, Pfizer, Kim Lauper Pfizer, AbbVie, Eli-Lilly, Galapagos and Pfizer.

Objective: To assess methods to calculate achieving and sustaining remission in a double blind randomised trial in patients with RA who received etanercept, methotrexate, or an etanercept/methotrexate combination. Methods: Remission was defined as DAS <1.6, DAS28 <2.6, and ACR70 response. Sustaining remission was analysed in three ways: (a) analysis of sustained DAS remission, DAS28 remission, or ACR70 response continuously for 6 months; (b) analysis of sustained remission appraised through a continuity rewarded scoring system, which is the weighted sum of all intervals in the study in which patients are in DAS or DAS28 remission; or (c) longitudinal modelling of remission odds using generalised estimating equations. Results: Significantly more patients treated with the etanercept/methotrexate combination reached DAS remission (37%) than those treated with either methotrexate (14%) or etanercept (18%) alone (p<0.01). Results for DAS28 and for the ACR70 response were similar. Agreement between DAS remission and DAS28 remission was good, but agreement between either of these and the ACR70 response was less. Patients in DAS or DAS28 remission had a lower level of disease activity (fewer active joints, lower ESR) than those achieving ACR70 response; the converse was seen using pain VAS. The three methods were comparable for sustainability of remission and showed significant advantage for combination therapy, which increased the number and durability of remission periods. Conclusions: DAS and DAS28 remission results were similar for assessing achieving and sustaining remission in RA, frequently differing from patients classified as ACR70 responders. The three methods of examining duration of remission produced comparable results.

Background:In psoriatic arthritis (PsA), the assessment of TNFi treatment outcomes primarily focuses on the improvement in the number of affected joints, disregarding their specific locations. Transcriptomic variances identified in synovial fibroblasts (SF) from various joint sites in rheumatoid arthritis translated into joint-specific SF phenotypes with distinct characteristics and responsiveness to cytokines. These findings suggest that various joints may potentially respond differently to specific immunosuppressive treatments.Objectives:To investigate whether joints at different anatomical locations might respond differently to TNFi treatment in patients with PsA.Methods:PsA patients starting a first TNFi between 2000 and 2022 in eight European registries met the following additional inclusion criteria: age ≥18 years, TNFi initiation as monotherapy or added to methotrexate, and at least one swollen joint out of 28 at treatment start (baseline). The primary outcome was time to the first resolution of joint swelling on the individual joint level, assessed at baseline and at 6, 12, 18, and 24 months. Hazard ratios (HR) for resolution comparing different joint locations were estimated using interval-censored mixed-effects Cox proportional hazards models. The nested data structure was accounted for by including a random effect for the country and the patient. Analyses were adjusted for age and sex.Results:A total of 1729 patients with 8397 swollen joints at baseline met the inclusion criteria. The proportion of women was 54%. The proportion of patients on concomitant methotrexate was 77%. The mean (SD) age was 49.4 (12.1) years, and the symptom duration 9.0 (8.6) years. The mean number of swollen and tender joints at baseline was 4.8 (4.1) and 7.4 (6.0), respectively, with a mean disease activity score using the C-reactive protein (DAS28-CRP) of 4.7 (1.0). The proportion of patients with joint swelling at specified locations at baseline is depicted in Figure 1. Concerning the upper limb and using the response of the proximal interphalangeal joint of the third digit (PIP3) as a reference, a significantly higher rate of resolution of joint swelling was observed for the elbow and the shoulder (HR 1.80, 95% CI 1.29-2.51 and HR 1.56, 95% CI 1.08-2.26, respectively) (Figure 2). In contrast, a lower rate of resolution of joint swelling was found for the wrist in relation to the PIP3 joint (HR 0.68, 95% CI 0.56-0.82, Figure 2). No evidence for a difference in resolution of joint swelling was found for the knee in comparison to the elbow (HR 0.78, 95% CI 0.51-1.20).Figure 1.Proportion of the 1729 PsA patients with joint swelling at specified locations at initiation of TNFi.Figure 2.Interval-censored mixed-effects Cox proportional hazards model estimating HRs and 95% CI for resolution of joint swelling of joints along the upper limb after initiation of a first TNF inhibitor in PsA patients (N=953). The numbers in brackets at each site refer to the number of swollen joints and the number of patients. MCP3 = metacarpophalangeal joint of digit 3; PIP3 = proximal interphalangeal joint of digit 3.Conclusion:The clinical response of articular inflammation to a TNFi in PsA, in terms of time to the first resolution of joint swelling, appears to depend on joint location. This suggests that local factors, such as differences in mechanical factors or synovial fibroblast phenotypes, might impact treatment effectiveness at specific joints. Future analyses exploring whether joint specific responses in PsA are associated with distinct therapeutic modes of action are warranted.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of Interests:Adrian Ciurea: None declared, Seraphina Kissling: None declared, Andrea Goetschi: None declared, Lykke Midtbøll Ørnbjerg Research grant from Novartis, Simon Horskjær Rasmussen Research grant from Novartis, Bálint Tamási: None declared, Burkhard Moeller Speakers bureau: Eli-Lilly, Janssen, Novartis, Pfizer, Grant/research support: Amgen, Michael J. Nissen Speaker fees from AbbVie, Amgen, Eli Lilly, Janssens, Novartis, Pfizer, Consulting fees from AbbVie, Eli Lilly, Janssens, Novartis, Pfizer, Research grants from Novartis and Pfizer, Bente Glintborg Research grants from Pfizer, AbbVie, BMS, Sandoz, Anne Gitte Loft Speaking and/or consulting fees from AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, UCB, Speaking and/or consulting fees from AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, UCB, Research grant from Novartis, João Madruga Dias: None declared, Paula Valente: None declared, Almut Scherer Employed by Bristol-Myers-Squib in 2007-2008, René Braem: None declared, Karel Pavelka Consultant: AbbVie, UCB, Pfizer, Eli Lilly, Celltrion, MSD, and Novartis, Jakub Zavada Speakers bureau: AbbVie, Elli-Lilly, Sandoz, Novartis, Egis, UCB, Sanofi, Astra Zeneca, Sobi, Bjorn Gudbjornsson Speaking fees from Novartis and Nordic-Pharma, Consulting fees from Novartis, Olafur Palsson: None declared, Gareth T. Jones Speaker fee from Janssen, Research grants (paid to employer) from AbbVie, Pfizer, UCB, Amgen, GSK, Gary J. Macfarlane Research grant from GSK, Catalin Codreanu Speaker fees from AbbVie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis, Pfizer, Consultancy fees from AbbVie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis, Pfizer, Corina Mogosan Speaker fees from AbbVie, Boehringer Ingelheim, Ewopharma, Lilly, Novartis, Pfizer, Vappu Rantalaiho Speakers bureau: Novartis, Viatris, Consultant: Pfizer, Ritva Peltomaa Consultant: AbbVie, Boehringer, Celltrion, Fresenius, Lilly, UCB, Isabel Castrejon Speaker and/or consultancy fees from BMS, Eli-Lilly, Galapagos, Gilead, Janssen, Novartis, MSD, Pfizer, GSK, Speaker and/or consultancy fees from BMS, Eli-Lilly, Galapagos, Gilead, Janssen, Novartis, MSD, Pfizer, GSK, Ziga Rotar Speakers bureau: Abbvie, Amgen, Novartis, MSD, Medis, Biogen, Eli Lilly, Pfizer, Sanofi, Lek, Janssen, Consultant: Abbvie, Novartis, Eli Lilly, Pfizer, Janssen, SOBI, Swixx BioPharma, AstraZeneca, Brigitte Michelsen Consulting fees from Novartis, Research grant from Novartis (paid to employer). Centre for treatment of Rheumatic and Musculoskeletal Diseases (REMEDY) is funded as a Centre for Clinical Treatment Research by The Research Council of Norway (project 328657), Florenzo Iannone Consulting and/or speaking from Abbvie, Amgen, AstraZeneca, BMS, Galapagos, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, UCB, Consulting and/or speaking from Abbvie, Amgen, AstraZeneca, BMS, Galapagos, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, UCB, Research grant from BMS, Galapagos, Pfizer, Francesca Cozzini Speaker fees from Eli Lilly, Janssen, BMS, Pfizer, Galapagos, Boehringer-Ingheleim, Consultation fees from Eli Lilly, Janssen, BMS, Pfizer, Galapagos, Boehringer-Ingheleim, Research grant from BMS, Johan K Wallman Speaker fees from AbbVie, Amgen, Research support from AbbVie, Amgen, Eli Lilly, Novartis, Pfizer, Irene van der Horst-Bruinsma Speaker and/or consultancy fees from UCB. Fees received for Lectures from BMS, AbbVie, Pfizer, MSD, UCB, Consultant for Abbvie, UCB, MSD, Novartis, Lilly, Unrestricted Grants received for investigator initiated studies from MSD, Pfizer, AbbVie, UCB., Oliver Distler: None declared, Mikkel Østergaard Speaker and/or consultancy fees from Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi, UCB, Speaker and/or consultancy fees from Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi, UCB, Research grants from Abbvie, BMS, Merck, Novartis and UCB, Merete Lund Hetland Speaker for Pfizer, Medac, Sandoz (no personal income, institution), Advisory Board Abbvie (No personal income, paid to institution). Prev. chaired the steering committee of the Danish Rheumatology Quality Registry (DANBIO, DRQ), which receives public funding from the hospital owners and funding from pharmaceutical companies., Research grants (institution) from Abbvie, Biogen, BMS, Celltrion, Eli Lilly, Janssen Biologics B.V, Lundbeck Fonden, MSD, Medac, Pfizer, Roche, Samsung Biopies, Sandoz, Novartis, Nordforsk, Raphael Micheroli Honoraria for lectures or presentations from AbbVie, Eli Lilly, Janssen, Gilead, and Pfizer, Caroline Ospelt: None declared.

Background:Several predictors of treatment response to tumour necrosis factor inhibitors (TNFi) have been reported in axial spondyloarthritis (axSpA). However, data on predictors of treatment response to secukinumab, a fully human IgG1 monoclonal antibody targeting interleukin-17A (IL-17A), are sparse.Objectives:In axSpA patients initiating secukinumab, we aimed to identify predictors at treatment start (baseline) of achieving low disease activity (LDA) at 6 months and treatment continuation at 12 months.Methods:The study was conducted within the European Spondyloarthritis (EuroSpA) Research Collaboration Network. From 11 European registries, patients with axSpA who initiated secukinumab as a first IL-17A inhibitor between 2015 and 2020, and who had available data on 6-month Ankylosing Spondylitis Disease Activity Score with C-reactive protein (ASDAS-CRP) and Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), were included. Logistic regression analyses on multiply imputed data (30 imputed datasets) were performed to determine baseline predictors for ASDAS-CRP LDA (<2.1), BASDAI LDA (<4), and treatment continuation. We considered 19 baseline variables as potential predictors. For each outcome, predictors were selected by applying variable selection separately in 30 imputed datasets. A single model across the imputed datasets was determined by selecting predictors that wear statistically significant in at least half of the 30 separate models. Once the set of predictors was selected, the model was fitted to all imputed datasets and the model estimates were pooled.Results:A total of 1,174 axSpA patients initiating secukinumab were included. At baseline, patients had a median (IQR) age of 47 (38-55) years, were predominantly male (53%), Human Leucocyte Antigen (HLA)-B27 positive (80%), and had radiographic axSpA (83%). The median (IQR) ASDAS-CRP and BASDAI were 3.8 (3.0-4.5) and 6.5 (4.9-7.7), respectively. Among the patients, 28%/20%/52% had previously received 0/1/≥2 biologic/targeted synthetic disease-modifying anti-rheumatic drugs (b/tsDMARDs), respectively. Non-radiographic axSpA (a negative predictor) was the only baseline predictor for all 3 outcomes. Additional baseline predictors for achieving ASDAS-CRP and BASDAI LDA were HLA-B27 positivity and higher Physician Global Assessment scores (PhGA) as positive predictors, and current smoking, number of previous b/tsDMARDs, higher Health Assessment Questionnaire (HAQ) score and higher BASDAI as negative predictors. CRP >10mg/L showed inconsistent results across outcomes. In addition, history of psoriasis and secukinumab start year (2018-2020) were predictors for BASDAI LDA and treatment continuation, respectively (see Table 1).Conclusion:Having non-radiographic disease was a negative predictor of obtaining LDA at 6 months and remaining on treatment at 12 months in European axSpA patients initiating secukinumab. Other predictors included both objective, subjective and lifestyle variables, underscoring the complex mechanisms of real-world drug effectiveness.Table 1.baseline predictors in multivariable analyses for ASDAS LDA and BASDAI LDA at 6 months, and treatment continuation at 12 months on secukinumabBaseline predictorsASDAS-CRP LDA at 6 months*OR (95% CI)BASDAI LDA at 6 months*OR (95% CI)Treatment continuation at 12 months*OR (95% CI)n/N (%) of patients achieving the outcome345/1,174 (29.4%)545/1,174 (46.4%)618/1,174 (52.6%)Current smokers0.62 (0.43 - 0.87)0.67 (0.48 - 0.93)HLA-B27 positive1.44 (0.95 - 2.17)1.83 (1.20 - 2.78)Non-radiographic axSpA0.60 (0.37 - 0.98)0.71 (0.44 - 1.12)0.73 (0.48 - 1.11)History of psoriasis1.78 (1.07 - 2.97)Secukinumab start year (2018-2020)0.60 (0.46 - 0.78)Number of previous b/tsDMARDs0.82 (0.74 - 0.92)0.82 (0.74 - 0.91)CRP (>10 mg/L)0.52 (0.35 - 0.76)1.37 (0.97 - 1.95)Fatigue (0-10)0.91 (0.81 - 1.03)HAQ (0-3)0.57 (0.39 - 0.82)0.63 (0.45 - 0.88)PhGA (0-10)1.11 (1.00 - 1.23)1.19 (1.07 - 1.32)BASDAI (0-10)0.83 (0.75 - 0.91)0.80 (0.70 - 0.92)*Gross domestic product per capita was a priori forced into the models to adjust for socio-economic differences between registries.REFERENCES:NIL.Acknowledgements:Novartis is acknowledged for providing funds to establish the research consortium.Disclosure of Interests:Marion Pons Research grant from Novartis (paid to the employer), Stylianos Georgiadis Research grant from Novartis, Mikkel Østergaard Speaker and/or consultancy fees from Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi, UCB, Speaker and/or consultancy fees from Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi, UCB, Research grants from Abbvie, BMS, Merck, Novartis and UCB, Zohra Faizy Ahmadzay Research grant from Novartis (paid to the employer), Simon Horskjær Rasmussen Research grant from Novartis (paid to the employer), Sara Nysom Christiansen Research grant from Novartis (paid to the employer), Katja Perdan Pirkmajer Abbvie, Novartis, MSD, Medis, Eli Lilly, Pfizer, Lek, Janssen, Abbvie, Novartis, Medis, Eli Lilly, Pfize, Boehringer Ingelheim, Ziga Rotar Abbvie, Amgen, Novartis, MSD, Medis, Biogen, Eli Lilly, Pfizer, Sanofi, Lek, Janssen, Abbvie, Novartis, Eli Lilly, Pfizer, Janssen, SOBI, Swixx BioPharma, AstraZeneca, Daniela Di Giuseppe: None declared, Johan K Wallman Speaker fees from AbbVie, Amgen, Research support from AbbVie, Amgen, Eli Lilly, Novartis, Pfizer, Bjorn Gudbjornsson Speaking fees from Novartis and Nordic-Pharma, Consulting fees from Novartis, Ólafur Pálsson: None declared, Florenzo Iannone consulting and/or speaking from Abbvie, Amgen, AstraZeneca, BMS, Galapagos, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, UCB, consulting and/or speaking from Abbvie, Amgen, AstraZeneca, BMS, Galapagos, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, UCB, Research grant from BMS, Galapagos, Pfizer, Bente Glintborg Research grants from Pfizer, Abbvie, BMS, Sandoz, Anne Gitte Loft Speaking and/or consulting fees from AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, UCB, Speaking and/or consulting fees from AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, UCB, Research grant from Novartis, Karel Pavelka AbbVie, UCB, Pfizer, Eli Lilly, Celltrion, MSD, and Novartis, Jakub Zavada Abbvie, Elli-Lilly, Sandoz, Novartis, Egis, UCB, Sanofi, Astra Zeneca, Sobi, Michael J. Nissen Speaker fees from AbbVie, Amgen, Eli Lilly, Janssens, Novartis, Pfizer, Consulting fees from AbbVie, Eli Lilly, Janssens, Novartis, Pfizer, Research grants from Novartis and Pfizer, Adrian Ciurea: None declared, Helena Santos Consulting and/or speaking fees from Abbvie, Celgene, Pfizer, UCB, Viatris, Consulting and/or speaking fees from Abbvie, Celgene, Pfizer, UCB, Viatris, Research grant from Sociedade Portuguesa de Reumatologia, Marie Helena Fernandes Lourenco: None declared, Brigitte Michelsen Consulting fees from Novartis, Research grant from Novartis (paid to employer). Centre for treatment of Rheumatic and Musculoskeletal Diseases (REMEDY) is funded as a Centre for Clinical Treatment Research by The Research Council of Norway (project 328657), Pawel Mielnik GALAPAGOS, Isabel Castrejon Speaker and/or consultancy fees from BMS, Eli-Lilly, Galapagos, Gilead, Janssen, Novartis, MSD, Pfizer, GSK, Speaker and/or consultancy fees from BMS, Eli-Lilly, Galapagos, Gilead, Janssen, Novartis, MSD, Pfizer, GSK, Laura Kuusalo Abbvie, Lilly, Medac, Orion, Pfizer, UCB, Gilead, Pfizer, Vappu Rantalaiho Novartis, Viatris, Pfizer, Gary J. Macfarlane Research grant form GSK, Karin Laas Abbvie, Johnson and Johnson, Novartis, Pfizer, Irene van der Horst-Bruinsma UCB, Consultant for Abbvie, UCB, MSD, Novartis, Lilly, Unrestricted Grants received for investigator initiated studies from MSD, Pfizer, AbbVie, UCB. Fees received for Lectures from BMS, AbbVie, Pfizer, MSD, UCB, Marleen van de Sande Speakers fee: Novartis, UCB, Janssen, Consultant for Novartis, Abbvie, Eli Lilly UCB, Grant/research support: UCB, Janssen, Novartis, Eli Lilly, Catalin Codreanu Speaker and consultancy fees from AbbVie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis, Pfizer, Speaker and consultancy fees from AbbVie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis, Pfizer, Corina Mogosan Speaker fees from AbbVie, Boehringer Ingelheim, Ewopharma, Lilly, Novartis, Pfizer, İsmail Sari: None declared, Merete Lund Hetland Speaker for Pfizer, Medac, Sandoz (no personal income, institution), Advisory Board Abbvie (No personal income, paid to institution). Prev. chaired the steering committee of the Danish Rheumatology Quality Registry (DANBIO, DRQ), which receives public funding from the hospital owners and funding from pharmaceutical companies., Research grants (institution) from Abbvie, Biogen, BMS, Celltrion, Eli Lilly, Janssen Biologics B.V, Lundbeck Fonden, MSD, Medac, Pfizer, Roche, Samsung Biopies, Sandoz, Novartis, Nordforsk, Lykke Midtbøll Ørnbjerg Research grant from Novartis.