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ObjectiveTo describe psoriatic arthritis (PsA) flares and their effect on patient-reported outcomes (PROs).MethodsCross-sectional surveys of rheumatologists/dermatologists and their patients with PsA were conducted in France, Germany, Italy, Spain, the United Kingdom, and the United States, capturing data on physician-reported patient flare status, demographics, PsA severity, and clinical outcomes. Patient-completed surveys captured data on PROs: 5-level EuroQol 5-dimension, Work Productivity and Activity Impairment questionnaire, Health Assessment Questionnaire–Disability Index, and 12-item Psoriatic Arthritis Impact of Disease questionnaire. Patients were compared by flare status using parametric and nonparametric tests. Multivariate regression was used to identify flare associations. Multivariate logistic regression adjusted for patient demographics and physician specialty assessed the effect of flare status.ResultsAmong 2238 patients (586 from the US, 1652 from Europe) managed by 572 physicians, physician-reported flare was present for 168 patients (7.5%), and self-reported flare was present for 95 patients (10% of available data). Mean (SD) flare count over 12 months was 2.2 (4.9), lasting on average 16.4 (16.2) days. Flare status was linked to worse PROs. Patients who had not flared in the last 12 months or had never flared had a higher quality of life, lower overall work impairment, and a lower degree of disability compared with patients who were currently experiencing a flare (all;P< 0.01).ConclusionActively experiencing a flare adversely affected QOL, disability, and work productivity. PsA flares should be routinely assessed and managed in clinical care.

Objectives Evaluate effects of long-term bimekizumab treatment on patient-reported outcome (PRO) measures, symptoms and the impact of PsA on patients. Methods Patients with active PsA were enrolled into BE ACTIVE, a 48-week randomised controlled trial (NCT02969525). After Week 48, patients could enter a 104-week open-label extension (NCT03347110), receiving bimekizumab 160 mg every four weeks. PRO measures assessed included arthritis pain visual analogue scale (VAS), PsA Impact of Disease (PsAID)-9, 36-Item Short Form Survey (SF-36) and HAQ-Disability Index (HAQ-DI). Results were analysed as mean (S.E.M.) changes from baseline (CfB) from Week 0 to the end of the open-label extension (3 years) and as percentage of patients reaching patient-acceptable symptom state (PASS) for global impact (PsAID-9 total score ≤4) and normal function (HAQ-DI total score Results In 206 patients (mean age 49.3 years, 51.0% male), completion rate was high; 161 (78.2%) patients completed Week 152. Bimekizumab treatment was associated with long-term sustained improvements in pain [arthritis pain VAS CfB; Week 48: −29.9 (1.9); Week 152: −32.0 (1.9)] and fatigue [PsAID-9 fatigue CfB; −2.4 (0.2); −2.7 (0.2)]. High percentages of patients achieved acceptable symptom state (PsAID-9 PASS: 75.2%; 65.0%) and normalised function (HAQ-DI Conclusions Bimekizumab treatment was associated with long-term sustained improvements in pain and fatigue, reducing overall impact of PsA on patients. Physical function and quality of life improved up to 3 years. Trial registration ClinicalTrials.gov, https://clinicaltrials.gov, NCT02969525, NCT03347110.

Background/Aims Guselkumab, a human monoclonal antibody targeting the interleukin-23 p19 subunit, demonstrated joint and skin efficacy in patients with PsA in the Phase III DISCOVER-1/-2 trials. MDA, a multi-domain composite outcome, is a clinically relevant measure of therapeutic response in PsA. However, response dynamics and the effect of individual domains on achieving MDA are not well understood. This analysis aimed to characterise MDA response clusters according to domain changes over time and identify potential baseline predictors in patients with PsA receiving guselkumab. Methods Data from bio-naïve patients with active PsA receiving guselkumab 100 mg every 4 or 8 weeks were pooled across DISCOVER-1/-2. Unsupervised machine learning using the time-series K-means clustering algorithm was performed to identify clusters according to MDA domain responses over 52 weeks. Missing data were not imputed. Results This analysis included 571 of 669 patients receiving guselkumab and distinguished four response clusters (C1-4; Table 1). Mean age and body mass index were similar across clusters; C3 had a lower proportion of female patients vs. other clusters. Relative to C3, a high burden of baseline disease was observed in C4 across clinical measures and PROs, and across PROs only in C2. Through Week 52, mean values for all MDA domains showed continuous improvement across clusters (Table 1). MDA response rates were highest in C3, in which all individual domain thresholds were rapidly approached, and lowest in C4. In C1 and C2, improvement in clinical measures paralleled that of C3; both met the PASI threshold and showed substantial reduction in SJC. PROs appeared to take longer to improve but did so earlier in C1 than C2. Improvements were slowest in C4, though still substantial given the high baseline disease burden. Conclusion Machine learning differentiated four clusters of patients with PsA receiving guselkumab based on response patterns in individual MDA domains. Response may differ due to baseline disease burden, especially in patients with high pain, PtGA and functional disability scores. These results offer an innovative, complementary approach to identifying treatment response patterns across diverse clusters of bio-naïve patients with PsA, which may facilitate clinical decision-making. Disclosure A. Zabotti: Member of speakers’ bureau; AbbVie, Amgen, Janssen, Lilly, Novartis and UCB. Grants/research support; Novartis. S. Ohrndorf: Other; Speaker fees or travel expense reimbursements from AbbVie, BMS, Janssen, Novartis and Pfizer. W. Tillett: Other; Research funding, consulting, speaker fees and/or honoraria from AbbVie, Amgen, Celgene, GlaxoSmithKline, Janssen, Lilly, MSD, Novartis, Pfizer and UCB. M. Neuhold: Other; Former employee of Janssen and is now an employee of Takeda Pharmaceuticals International AG. M. van Speybroeck: Shareholder/stock ownership; Employee of Janssen and owns stocks in Johnson & Johnson. E. Theander: Other; Former employee of Janssen. C. Contré: Other; Former employee of Janssen and is now an employee of Chiesi. M. Sharaf: Shareholder/stock ownership; Employee of Janssen and owns stocks in Johnson & Johnson. M. Shawi: Shareholder/stock ownership; Employee of Janssen and owns stocks in Johnson & Johnson. M. Perate: Shareholder/stock ownership; Employee of Janssen and owns stocks in Johnson & Johnson. A. Kollmeier: Shareholder/stock ownership; Employee of Janssen and owns stocks in Johnson & Johnson. P. Richette: Other; Received fees from AbbVie, Amgen, Celgene, Janssen, Lilly, MSD, Novartis, Pfizer and UCB.

Background/Aims Although continuous composite measures of disease activity for PsA assessment exist, more feasible abbreviated measures are needed for routine screening. The 3VAS and 4VAS scores, developed by abridging the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) Composite Exercise (GRACE) measure, are the first short multidimensional composite measures specifically for routine PsA care. 3VAS/4VAS showed superior performance vs. several established composite measures using small datasets. However, GRAPPA members recommended further testing of 3VAS/4VAS in observational and trial datasets. Methods This post hoc analysis used pooled data through W24 from all treatment groups in the DISCOVER 1/2 and COSMOS studies. Correlation of 3VAS/4VAS with DAPSA, PASDAS, PhGA and PtGA was assessed with Pearson’s correlation coefficient, minimal important difference (MID) with four distribution-based methods and minimal detectable change (MDC) with the standard formula (Table 1). Clinically relevant thresholds for low, moderate and high disease activity were estimated with receiver operating characteristic analysis and DAPSA (≤4, >4-≤14, >14-≤28, >28), PASDAS (≤1.9, >1.9-≤3.2, >3.2-1-≤3, >3-≤6, >6 cm) as anchors. Results This analysis included 1405 patients: 51.3% were male, with a mean (sd) age of 47.1 (11.8) and PsA duration of 6.4 (6.5) years. The mean baseline 3VAS, 4VAS, DAPSA, PASDAS, PhGA and PtGA scores reflected high disease activity levels (Table 1). Through W24, 3VAS and 4VAS showed very strong correlation with PtGA (r3VAS=0.92, r4VAS=0.94) and PASDAS (r3VAS=0.81, r4VAS=0.82), strong with PhGA (r3VAS=0.77, r4VAS=0.74) and moderate-to-strong with DAPSA (r3VAS=0.59, r4VAS=0.61). Calculated MIDs were 0.9 for 3VAS and 0.9 for 4VAS; MDCs were 3.3 for 3VAS and 3.2 for 4VAS (Table 1). Cut-off values for low, moderate and high disease activity were 2.0, 3.4 and 4.9 for 3VAS, and 2.1, 3.5 and 5.1 for 4VAS. Conclusion Using a large pooled clinical trial dataset of patients with active PsA, we have calculated clinically relevant thresholds for improvement, as well as disease activity thresholds, for 3VAS and 4VAS. These estimates are generally comparable to those previously reported and may facilitate setting treatment targets and screening disease activity in routine care when resources are limited or in remote patient monitoring. Disclosure W. Tillett: Other; Received research funding, consulting, speaker fees and/or honoraria from AbbVie, Amgen, Celgene, GlaxoSmithKline, Janssen, Lilly, MSD, Novartis, Pfizer and UCB. L. Coates: Consultancies; AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Gilead, Galapagos, Janssen, Novartis, Pfizer and UCB. Member of speakers’ bureau; AbbVie, Amgen, Biogen, Celgene, Eli Lilly, Galapagos, Gilead, Janssen, Medac, Novartis, Pfizer and UCB. Grants/research support; AbbVie, Amgen, Celgene, Eli Lilly, Janssen, Novartis, Pfizer and UCB. Other; National Institute for Health Research (NIHR) Clinician Scientist award. The research was supported by the NIHR Oxford Biomedical Research Centre, The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health, We acknowledge the support of the NIHR Clinical Research Network. M. Vis: Other; Received research grants and consulting or speaker fees from AbbVie, Amgen, Eli Lilly, Janssen, Novartis, Pfizer, UCB and the Dutch Arthritis Foundation. J. Merola: Consultancies; Consultant and/or investigator for AbbVie, Arena, Biogen, Bristol Myers Squibb, Dermavant, Lilly, Janssen, Novartis, Pfizer, Sun Pharma and UCB Pharma. E. Soriano: Consultancies; AbbVie, Janssen, Novartis and Roche. Member of speakers’ bureau; AbbVie, Amgen, Bristol Myers Squibb, Eli Lilly, Janssen, Novartis, Pfizer, Roche and UCB. Grants/research support; AbbVie, Janssen, Novartis, Pfizer, Roche and UCB. M. Perate: Shareholder/stock ownership; Employee of Janssen and owns stocks in Johnson & Johnson. M. Shawi: Shareholder/stock ownership; Employee of Janssen and owns stocks in Johnson & Johnson. M. Zimmermann: Shareholder/stock ownership; Employee of Janssen and owns stocks in Johnson & Johnson. E. Rampakakis: Consultancies; Employee of JSS Medical Research; paid consultant of Janssen. M. Sharaf: Shareholder/stock ownership; Employee of Janssen and owns stocks in Johnson & Johnson. P. Nash: Other; Received grants for research and clinical trials and honoraria for advice and lectures on behalf of AbbVie, Boehringer-Ingelheim, Gilead/Galapagos, GSK, Janssen, Lilly, MSD, Novartis, Pfizer, Samsung,. P.S. Helliwell: Consultancies; AbbVie, Amgen, Novartis and Janssen. Other; Fees for educational services from AbbVie, Amgen, Novartis and Janssen.

Background/Aims Upadacitinib (UPA), an oral Janus kinase (JAK) inhibitor, demonstrated efficacy and safety in patients (pts) with psoriatic arthritis (PsA) and prior inadequate response or intolerance to ≥ 1 biologic disease-modifying antirheumatic drug (bDMARD) at week (wk) 56 in the phase 3 SELECT-PsA 2 study. We aimed to evaluate the efficacy and safety of UPA at wk 104 from the ongoing long-term extension of SELECT-PsA 2. Methods Pts were randomized to UPA 15 mg (UPA15), UPA 30 mg (UPA30), or placebo (PBO) for 24 wks; PBO pts were then switched to UPA15 or UPA30. For continuous UPA treatment groups, efficacy endpoints at wk 104 were analyzed using non-responder imputation (NRI) and as observed (AO) (binary endpoints) or mixed-effect model repeated measures (MMRM) and AO (continuous endpoints). Treatment-emergent adverse events (TEAEs) were summarized for pts who received ≥1 dose of study drug using visit-based cut-off at wk 104. Results A total of 641 pts received ≥1 dose of study drug. At wk 104, 38.4% of all patients had discontinued study drug, with the highest discontinuation observed in patients randomized to PBO at baseline (all PBO: 46.7%). The most common reasons for discontinuation were lack of efficacy (UPA15: 12.3%, UPA30: 8.7%, all PBO: 21.7%) and adverse event (UPA15: 10.9%, UPA30: 13.3%, all PBO: 12.7%). The proportion of UPA pts that achieved ACR20/50/70, MDA, PASI75/90/100, and resolution of dactylitis and enthesitis were generally similar, or further improved, with 104 wks of treatment vs 56 wks. Similarly, mean change from baseline in HAQ-DI, patient’s assessment of pain, BASDAI, and ASDAS was improved with UPA treatment. At 104 wks of therapy, clinical responses were largely similar with UPA15 and UPA30. Generally, safety data at wk 104 were consistent with that reported at wk 56. Rates of serious infection, herpes zoster, hepatic disorder, anemia, neutropenia, lymphopenia, and CPK elevation remained numerically higher with UPA30 vs UPA15, while rates of malignancies, MACE, and VTE were similar for both UPA groups. One death was reported with UPA15 (unexplained due to lack of information; however, the patient had recently been diagnosed with ovarian cancer) and two with UPA30 (pancytopenia and COVID-19 pneumonia). Conclusion In PsA pts with prior inadequate response or intolerance to ≥ 1 bDMARD, clinical responses were maintained with UPA15 and UPA30 up to two years of treatment. No new safety signals were identified in this long-term extension. Disclosure P.J. Mease: Consultancies; Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol-Myers Squib, Celgene, Eli Lilly, Galapagos, Genentech, Gilead, GSK, Janssen, Novartis, Pfizer, Sun Pharma, and UCB. Member of speakers’ bureau; Speakers bureau: AbbVie, Amgen, Boehringer Ingelheim, Bristol-Myers Squib, Celgene, Eli Lilly, Galapagos, Genentech, Gilead, GSK, Janssen, Novartis, Pfizer, Sun Pharma, and UCB. Grants/research support; Grant/research support from: AbbVie, Amgen, Boehringer Ingelheim, Bristol-Myers Squib, Celgene, Eli Lilly, Galapagos, Genentech, Gilead, GSK, Janssen, Novartis, Pfizer, Sun Pharma, and UCB. A. Setty: Shareholder/stock ownership; Financial Disclosures: Employee of AbbVie and may hold stock or options. K. Papp: Consultancies; Consultant of: AbbVie, Akros, Allergan, Almirall, Amgen, Arcutis, Avillion, Bausch Health, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Dermavant, Dermira, Eli Lilly, Galderma, Genentech/Roche. Member of speakers’ bureau; Speakers bureau: AbbVie, Akros, Allergan, Almirall, Amgen, Bausch Health, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Dermavant, Dermira, Eli Lilly, Galderma, Genentech/Roche, Janssen, Kyowa. Grants/research support; Grant/research support from: AbbVie, Akros, Allergan, Almirall, Amgen, Arcutis, Avillion, Bausch Health, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Dermavant, Dermira, Eli Lilly, Galderma, G. F. Van den Bosch: Consultancies; Consultant of: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly, Galapagos, Gilead, Janssen, Merck, Novartis, Pfizer, and UCB. Member of speakers’ bureau; Speakers bureau: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly, Galapagos, Gilead, Janssen, Merck, Novartis, Pfizer, and UCB. S. Tsuji: Consultancies; Consultant of: AbbVie, Eli Lilly, Janssen, Novartis, and UCB. Member of speakers’ bureau; Speakers bureau: AbbVie, Eli Lilly, Janssen, Novartis, and UCB. Grants/research support; Grant/research support from: AbbVie, Eli Lilly, Janssen, Novartis, and UCB. M. Keiserman: Consultancies; Consultant of: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly, Janssen, Novartis, Pfizer, Roche, and UCB. Member of speakers’ bureau; Speakers bureau: AbbVie, Bristol Myers Squibb, Celgene, Eli Lilly, Janssen, Novartis, Pfizer, Roche, and UCB. Grants/research support; Grant/research support from: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly, Janssen, Novartis, Pfizer, Roche, and UCB. X. Bu: Shareholder/stock ownership; Financial Disclosures: Employee of AbbVie and may hold stock or options. L. Chen: Shareholder/stock ownership; Financial Disclosures: Employee of AbbVie and may hold stock or options. R. Mccaskill: Shareholder/stock ownership; Financial Disclosures: Employee of AbbVie and may hold stock or options. E. Mcdearmon-Blondell: Shareholder/stock ownership; Financial Disclosures: Employee of AbbVie and may hold stock or options. P. Wung: Shareholder/stock ownership; Financial Disclosures: Employee of AbbVie and may hold stock or options. W. Tillett: Consultancies; Consultant of: AbbVie, Amgen, Celgene, Eli Lilly, MSD, Novartis, Pfizer, and UCB. Member of speakers’ bureau; Speakers bureau: AbbVie, Amgen, Celgene, Eli Lilly, Janssen, Novartis, Pfizer, and UCB. Grants/research support; Grant/research support from: AbbVie, Celgene, Eli Lilly, and Janssen.

ObjectivesPsoriatic arthritis (PsA) phenotypes are typically defined by their clinical components, which may not reflect patients’ overlapping symptoms. This post hoc analysis aimed to identify hypothesis-free PsA phenotype clusters using machine learning to analyse data from the phase III DISCOVER-1/DISCOVER-2 clinical trials.MethodsPooled data from bio-naïve patients with active PsA receiving guselkumab 100 mg every 8/4 weeks were retrospectively analysed. Non-negative matrix factorisation was applied as an unsupervised machine learning technique to identify PsA phenotype clusters; baseline patient characteristics and clinical observations were input features. Minimal disease activity (MDA), disease activity index for psoriatic arthritis (DAPSA) low disease activity (LDA) and DAPSA remission at weeks 24 and 52 were evaluated.ResultsEight clusters (n=661) were identified: cluster 1 (feet dominant), cluster 2 (male, overweight, psoriasis dominant), cluster 3 (hand dominant), cluster 4 (dactylitis dominant), cluster 5 (enthesitis, large joints), cluster 6 (enthesitis, small joints), cluster 7 (axial dominant) and cluster 8 (female, obese, large joints). At week 24, MDA response was highest in cluster 2 and lowest in clusters 3, 5 and 6; at week 52, it was highest in cluster 2 and lowest in cluster 5. At weeks 24 and 52, DAPSA LDA and remission were highest in cluster 2 and lowest in clusters 4 and 6, respectively. All clusters improved with guselkumab treatment over 52 weeks.ConclusionsUnsupervised machine learning identified eight PsA phenotype clusters with significant differences in demographics, clinical features and treatment responses. In the future, such data could help support individualised treatment decisions.

ObjectivesPsoriasis and psoriatic arthritis (PsA) are independently associated with comorbidities, including obesity and metabolic syndrome, which may impact treatment outcomes. This study aimed to assess baseline differences between patients with plaque psoriasis alone and those with concomitant PsA, and to investigate the impact of these characteristics on ustekinumab (UST) persistence and outcomes.Methods9057 patients receiving UST or conventional systemic disease-modifying antirheumatic drugs were selected from the British Association of Dermatologists Biologic and Immunomodulators Register. The psoriasis and PsA cohorts were compared at baseline. Time to discontinuation during 10-year follow-up was assessed using multivariable Cox regression and Kaplan–Meier analyses, stratifying for interacting covariates and PsA status. Generalised linear mixed models assessed the impact of baseline characteristics on Psoriasis Area and Severity Index (PASI) and Dermatology Life Quality Index over time.ResultsGreater comorbidity burden, including hypertension, diabetes, obesity and depression, and greater inability to work were observed in the PsA cohort than in the psoriasis cohort. PsA (HR 1.98), female sex (HR for male sex 0.72) and depression (HR 1.21) were associated with shorter UST persistence. PsA showed a differential association with UST persistence by PASI strata and prior biologic exposure. Quality of life was negatively impacted by depression and PsA.ConclusionsThe negative impact of comorbidities on treatment persistence identified in this study emphasises the need for patient-centric, multidisciplinary care in screening for and managing comorbidities in psoriasis and PsA treatment. Psychological support and lifestyle management of modifiable risk factors, including obesity, should be considered.

OBJECTIVES To examine concurrent validity and discrimination of modified minimal disease activity (mMDA) criteria in peripheral spondyloarthritis (pSpA) following OMERACT filter principles and determine predictors of mMDA response. METHODS Four mMDA versions were derived in the ABILITY-2 study using the SPondyloArthritis Research Consortium of Canada (SPARCC) or Leeds Enthesitis Index (LEI) but excluding psoriasis. To assess concurrent validity, mMDA versions were correlated with Peripheral SpondyloArthritis Response Criteria (PSpARC) remission, Ankylosing Spondylitis Disease Activity Score for inactive disease (ASDAS ID), and physician global. Treatment discrimination was assessed between adalimumab and placebo at week 12. Multiple logistic regression was used to determine baseline predictors of long-term mMDA responses and sustained mMDA. RESULTS The four mMDA versions showed a stronger positive correlation with PSpARC remission (rtet >0.95) versus ASDAS ID (rtet >0.75) at week 12 and years 1-3 and were able to show discrimination (p

INTRODUCTION: The phase 3 DISCOVER-2 trial evaluated the effect of guselkumab on impaired work productivity and nonwork activity in biologic-naïve patients with psoriatic arthritis (PsA).METHODS: Adults with active PsA were randomized (1:1:1) to guselkumab 100 mg every 4 weeks (Q4W), guselkumab 100 mg at weeks 0 and 4 and then every 8 weeks (Q8W), or placebo (with crossover to guselkumab Q4W at week 24). Least squares mean change from baseline in Work Productivity and Activity Impairment Questionnaire for PsA (WPAI-PsA) domains and employment were assessed by treatment group. Multivariate analysis of data from weeks 0 through 24 assessed independent associations between PsA clinical features and WPAI-PsA domains.RESULTS: In total, 738 patients were evaluated (guselkumab Q4W n = 245; guselkumab Q8W n = 248; placebo n = 245). At week 24, improvements (reduced impairment) in presenteeism (Q4W -20.1%, Q8W -19.6%, placebo -10.5%), work productivity (Q4W -20.1%, Q8W -19.2%, placebo -10.6%), and nonwork activity (Q4W -20.5%, Q8W -21.2%, placebo -9.9%) were greater in guselkumab-treated versus placebo-treated patients. At week 52, following placebo crossover at week 24, improvements were similar among groups. Baseline absenteeism was minimal and did not change in any group. By week 52, 23.1-25.9% of guselkumab-treated patients who were unemployed at baseline were employed. All WPAI-PsA domains were positively associated with C-reactive protein level, fatigue, and pain. All domains except absenteeism were positively associated with enthesitis and Psoriasis Area and Severity Index score. Age was negatively associated with presenteeism and work productivity loss, female sex and tender joint count were positively associated with nonwork activity impairment, and dactylitis was positively associated with presenteeism.CONCLUSION: Both guselkumab regimens reduced work productivity loss and nonwork activity impairment in patients with active PsA. Association of work productivity loss and nonwork activity impairment with PsA joint and skin features suggests that improvement in both features is beneficial for optimizing improved work productivity loss and nonwork activity impairment.TRIAL REGISTRATION: ClinicalTrials.gov identifier, NCT03158285.

OBJECTIVES: To characterize the evolving demographics of participants recruited to phase III randomised controlled trials (RCTs) of biologic/targeted synthetic disease-modifying anti-rheumatic drugs (b/tsDMARDs) in peripheral psoriatic arthritis (PsA).METHODS: We conducted a systematic review of EMBASE, MEDLINE, and the Cochrane Database of Clinical Trials (CENTRAL) to identify all placebo-controlled phase III RCTs of b/tsDMARDs in peripheral PsA published up to 1 June 2022. Data extracted included inclusion criteria, date of initiation, countries in which studies were conducted, age, sex, race, disease duration, swollen joint count, tender joint count, Health Assessment Questionnaire - Disability Index, Psoriasis Area and Severity Index, and radiographic damage scores. Trends over time were evaluated using descriptive statistics.RESULTS: 34 eligible RCTs from 33 reports were included. The proportion of female participants increased over time with females representing 29.0-43.7% of participants in studies initiated in 2000-2004 which increased to 46.0-58.8% in 2015-2019. While the number of countries included in RCTs increased significantly from 1-8 countries (2000-2004) to 2-46 (2015-2019), the proportion of white participants changed marginally from 90.0-98.0% (2000-2004) to 80.9-97.3% (2015-2019). The SJC and TJC decreased from 13.9 to 24.6 respectively (2000-2004), to 7.0-13.9 and 12.9-24.9 (2015-2019). Baseline CRP and HAQ-DI remained stable.CONCLUSION: Despite the expansion of countries from which PsA RCT participants were recruited from, non-white participants continue to be under-represented. Improving diversity in patient representation is imperative to further our understanding of PsA phenotypes, proteogenomics, socioeconomic determinants, and treatment effects, to advance the care of all patients with psoriatic disease.

Background Psoriatic arthritis (PsA) is a chronic, heterogeneous, immune-mediated disease manifesting as a spectrum of possible inflammatory signs and symptoms. Clinicians need therapeutic choices that work across all active PsA disease domains, as well as practical information about efficacy of available treatments for individual domains in specific groups of patients. The objective of this study was to evaluate the effect of prior tumor necrosis factor inhibitor (TNFi) exposure on the efficacy of secukinumab across PsA core domains. Methods Data were pooled from 2049 participants with PsA in four phase 3 studies (FUTURE 2–5). Efficacy at week 16 was evaluated for each GRAPPA-OMERACT PsA core domain using nonresponder imputation for musculoskeletal disease activity and Psoriasis Area and Severity Index scores or as-observed data for other outcomes. For each measure, comparisons with placebo were made separately in the TNFi-naive and TNFi-inadequate responder/intolerant (TNF-IR) cohorts. Results Treatment with secukinumab improved PsA disease activity across all disease domains regardless of previous TNFi use, although TNFi-naive patients experienced numerically greater benefits in most outcomes. Among patients treated with secukinumab 300 mg, 41.5% and 24.4% of TNFi-naive patients (P, Plain Language Summary Psoriatic arthritis (PsA) is a long-term disease that can affect a patient’s joints, skin, lower back, physical function, mental health, productivity, and other areas. Drugs called tumor necrosis factor inhibitors (TNFis) can be used to treat PsA, although not all patients benefit from TNFis and many seek other treatment options. These patients, known as TNFi-inadequate responders (TNF-IR), have PsA that is difficult to treat. Another treatment option is secukinumab, a drug that blocks a molecule called interleukin-17 that is involved in PsA. Doctors need to know how different drugs work for treating PsA signs and symptoms in different groups of patients, including TNF-IR patients and those who have never received TNFis (TNFi-naive patients). This study used data from 2049 patients in four different PsA clinical trials (FUTURE 2–5) to see how well secukinumab worked at treating different signs and symptoms of PsA in TNFi-naive and TNF-IR patients. After 16 weeks of treatment, patients who took secukinumab saw greater improvements across all measured PsA signs and symptoms than those who took placebo. This was true for both TNFi-naive and TNF-IR patients. TNFi-naive patients seemed to benefit slightly more than TNF-IR patients—especially in their joint symptoms—although this study was not designed to judge the significance of these differences. These results suggest that secukinumab would be an effective first treatment option for patients with PsA. Since secukinumab improves the skin, joints, and other affected areas, it can be useful in treating the whole patient who has psoriatic disease. Supplementary Information The online version contains supplementary material available at 10.1007/s40744-021-00337-5.

Introduction Upadacitinib is a Janus kinase inhibitor under investigation in patients with psoriatic arthritis (PsA). This study assessed the 56-week efficacy and safety of upadacitinib in patients with PsA and an inadequate response or intolerance to biologic therapy. Methods In the phase 3 SELECT-PsA 2 study, patients were randomized to 56 weeks of blinded treatment with oral upadacitinib 15 or 30 mg once daily, or placebo switched to upadacitinib 15 or 30 mg once daily at week 24. Efficacy endpoints included the proportion of patients achieving 20/50/70% improvement in American College of Rheumatology criteria (ACR20/50/70), 75/90/100% improvement in Psoriasis Area and Severity Index (PASI75/90/100), and minimal disease activity. Safety was assessed throughout the study. Results Of 641 patients who received ≥ 1 dose of study drug, 479 (74.7%) completed 56 weeks of treatment. Improvements in the proportion of patients achieving ACR20/50/70, PASI75/90/100, and minimal disease activity were maintained with both doses of upadacitinib through 56 weeks. Week 56 results for patients who switched from placebo to upadacitinib at week 24 were similar to those for patients originally randomized to the upadacitinib groups. The exposure-adjusted event rate for serious infections was 2.6 and 6.1 events/100 patient-years in the upadacitinib 15 and 30 mg groups, respectively. Herpes zoster occurred more frequently with upadacitinib 30 versus 15 mg; most cases were non-serious. Conclusion In patients with PsA who had an inadequate response or intolerance to biologic therapy, the efficacy of upadacitinib was maintained over 56 weeks with no new significant safety signals observed. Trial registration NCT03104374. Electronic supplementary material The online version of this article (10.1007/s40744-021-00305-z) contains supplementary material, which is available to authorized users.

Objectives The aim of this study was to explore the use of Bayesian networks (BNs) to understand the relationships between musculoskeletal symptoms and the development of PsA in people with psoriasis. Methods Incident cases of psoriasis were identified for 1998 to 2015 from the UK Clinical Research Practice Datalink. Musculoskeletal symptoms (identified by Medcodes) were concatenated into primary groups, each made up of several subgroups. Baseline demographics for gender, age, BMI, psoriasis severity, alcohol use and smoking status were also extracted. Several BN structures were composed using a combination of expert knowledge and data-oriented modelling based on: (i) primary musculoskeletal symptom groups; (ii) musculoskeletal symptom subgroups and (iii) demographic variables. Predictive ability of the networks using the area under the receiver operating characteristic curve was calculated. Results Over one million musculoskeletal symptoms were extracted for the 90 189 incident cases of psoriasis identified, of which 1409 developed PsA. The BN analysis yielded direct relationships between gender, BMI, arthralgia, finger pain, fatigue, hand pain, hip pain, knee pain, swelling, back pain, myalgia and PsA. The best BN, achieved by using the more site-specific musculoskeletal symptom subgroups, was 76% accurate in predicting the development of PsA in a test set and had an area under the receiver operating characteristic curve of 0.73 (95% CI: 0.70, 0.75). Conclusion The presented BN model may be a useful method to identify clusters of symptoms that predict the development of PsA with reasonable accuracy. Using a BN approach, we have shown that there are several symptoms which are predecessors of PsA, including fatigue, specific types of pain and swelling.

The phase 3 DISCOVER-2 trial evaluated the effect of guselkumab on impaired work productivity and nonwork activity in biologic-naïve patients with psoriatic arthritis (PsA).Adults with active PsA were randomized (1:1:1) to guselkumab 100 mg every 4 weeks (Q4W), guselkumab 100 mg at weeks 0 and 4 and then every 8 weeks (Q8W), or placebo (with crossover to guselkumab Q4W at week 24). Least squares mean change from baseline in Work Productivity and Activity Impairment Questionnaire for PsA (WPAI-PsA) domains and employment were assessed by treatment group. Multivariate analysis of data from weeks 0 through 24 assessed independent associations between PsA clinical features and WPAI-PsA domains.In total, 738 patients were evaluated (guselkumab Q4W n = 245; guselkumab Q8W n = 248; placebo n = 245). At week 24, improvements (reduced impairment) in presenteeism (Q4W -20.1%, Q8W -19.6%, placebo -10.5%), work productivity (Q4W -20.1%, Q8W -19.2%, placebo -10.6%), and nonwork activity (Q4W -20.5%, Q8W -21.2%, placebo -9.9%) were greater in guselkumab-treated versus placebo-treated patients. At week 52, following placebo crossover at week 24, improvements were similar among groups. Baseline absenteeism was minimal and did not change in any group. By week 52, 23.1-25.9% of guselkumab-treated patients who were unemployed at baseline were employed. All WPAI-PsA domains were positively associated with C-reactive protein level, fatigue, and pain. All domains except absenteeism were positively associated with enthesitis and Psoriasis Area and Severity Index score. Age was negatively associated with presenteeism and work productivity loss, female sex and tender joint count were positively associated with nonwork activity impairment, and dactylitis was positively associated with presenteeism.Both guselkumab regimens reduced work productivity loss and nonwork activity impairment in patients with active PsA. Association of work productivity loss and nonwork activity impairment with PsA joint and skin features suggests that improvement in both features is beneficial for optimizing improved work productivity loss and nonwork activity impairment.ClinicalTrials.gov identifier, NCT03158285.

Background/Aims Guselkumab (GUS), a human monoclonal antibody targeting the interleukin-23p19-subunit, has demonstrated efficacy at Week 24 (W24) in the Phase IIIb COSMOS clinical trial of patients with active psoriatic arthritis (PsA) and inadequate response or intolerance to one or two tumour necrosis factor inhibitors (TNFis). This post hoc analysis aimed to identify predictors of minimal disease activity (MDA) with GUS at W24 in this population. Methods Multiple logistic regression analysis was performed to identify potential predictors of MDA with GUS at W24 in TNFi-refractory patients with PsA; odds ratios, 95% confidence intervals and p-values were calculated. Baseline characteristics assessed as predictors included sex, body mass index (BMI), C-reactive protein (CRP), other medication use and disease duration; clinical features included tender and swollen joint counts (TJC/SJC), affected joint location, dactylitis, enthesitis, spondylitis, Psoriasis Area Severity Index (PASI) score and psoriasis (PsO) localisation (Table). Missing data for MDA at W24 were imputed as non-response; missing baseline values were imputed for two patients. Results Patients (n = 187; female, 54.6%; mean disease duration, 8.3 years) had mean TJC 0-68 and SJC 0-66 of 21.0 and 10.3, respectively, mean PASI score of 11.6, and mean BMI of 28.9; 67.9% had enthesitis and 35.8% had dactylitis at baseline. One prior TNFi had been received by 88.2% of patients, with two received by 11.8%. At W24, 17.1% (32/187) of patients achieved MDA. Wrist involvement (p = 0.031) and scalp PsO (p = 0.049) were positive predictors of MDA. Women were significantly less likely to achieve MDA vs. men; other negative predictors included hand small joints or shoulder involvement and hand/foot PsO (all p < 0.05). Age, BMI, CRP, TJC/SJC, HAQ-DI, PASI, spondylitis, enthesitis, dactylitis, other medication and number of prior TNFis were not predictive of MDA (Table). Conclusion Baseline characteristics and clinical features may be positively (wrist involvement, scalp PsO) or negatively (female sex, hand small joints or shoulder involvement, hand/foot PsO) associated with achieving MDA with GUS at W24 in a TNFi-refractory population. Though the low patient number limits the generalisability of this analysis, assessment of Week 48 data may further elucidate potential predictors of MDA after longer-term treatment. Disclosure W. Tillett: Other; William Tillett has received research grants and consulting or speaker fees from AbbVie, Amgen, Celgene, Eli Lilly, Janssen, MSD, Novartis, Pfizer and UCB. S. Ohrndorf: Other; Sarah Ohrndorf has received fees from AbbVie, BMS, Janssen, Novartis and Pfizer. J. Ramírez: Other; Julio Ramírez has received consulting or speaker fees from AbbVie, Amgen, Eli Lilly, Janssen, Novartis and UCB. M. Neuhold: Other; Marlies Neuhold is an employee of Janssen and owns stocks in Johnson & Johnson. R. Wapenaar: Other; Robert Wapenaar is an employee of Janssen and owns stocks in Johnson & Johnson. E. Theander: Other; Elke Theander is an employee of Janssen and owns stocks in Johnson & Johnson. C. Contre: Other; Christine Contre is an employee of Janssen and owns stocks in Johnson & Johnson. M. Sharaf: Other; Mohamed Sharaf is an employee of Janssen and owns stocks in Johnson & Johnson. M. Shawi: Other; May Shawi is an employee of Janssen and owns stocks in Johnson & Johnson. M. Vis: Other; Marijn Vis has received research grants and consulting or speaker fees from AbbVie, Amgen, Eli Lilly, Janssen, Novartis, Pfizer, UCB and the Dutch Arthritis Foundation.

Background/Aims There are regional variations in access to biologic disease modifying anti-rheumatic drugs (bDMARDs) for patients with rheumatoid arthritis in the UK, with relative under-treatment according to established best practice. Similar concerns exist for access to biologic therapies for patients with psoriatic arthritis (PsA). In this study we set out to understand regional variations in access to bDMARDS for the treatment of PsA in England. Methods Formularies are mandated to be published by the National Institute for Health and Care Excellence (NICE). ValueBase, a personalised business intelligence company specialising in healthcare, tracks every change for every drug on every published formulary every day with data from January 2017 in 184 formularies. The Availability Index (AI) is used to standardise individual formulary listing differences. It is scored from 0-100 and calculated by dividing the ‘base score’ for prescribing initiators by the ‘prescribing position’. The ‘base score’ values included 0 (not recommended), 5 (unlisted/under review), 30 (restricted availability), 45 (specialist/hospital only), 65 (initiated by specialist, continued in primary care) and 100 (all prescribers). We would expect the optimal score to be > 45 as these are specialist medications. The ‘prescribing position’ included where the drug is ranked on the formulary (e.g., first line). Results For anti-TNFa, the mean AI was 45 ([standard deviation] SD 16, minimum 0, maximum 100). For the IL-17 inhibitors, the mean AI was 48 (SD 17, the minimum 0, maximum 100). For the IL-23 inhibitors, the mean AI was 48 (SD 18, minimum 30, maximum 100). For the JAK inhibitors, the mean AI was 24 (SD 22, minimum 0, maximum AI 50). For the other monoclonal antibodies, the mean AI was 45 (SD 14, minimum 0, maximum 100). The rate of formulary adoption for new drugs approved since 2016 varied considerably (Table 1). Conclusion There are regional variations in access to bDMARDs for treatment of PsA in England. Such differences have also been demonstrated in other countries (e.g., Sweden) and call for further improvement towards delivering equitable PsA care, both nationally and internationally. Disclosure A. Vivekanantham: None. L. Coates: None. W. Tillett: Consultancies; WRT has received research funding, consulting, or speaker fees from Abbvie, Amgen, Celgene, Eli Lilly, Janssen, MSD, Novartis, Pfizer and UCB.

Background/Aims Bimekizumab (BKZ), a monoclonal IgG1 antibody that selectively inhibits interleukin (IL)-17F and IL17A, has demonstrated an acceptable safety profile with improvements in joint and skin outcomes to 3 years in patients with active psoriatic arthritis (PsA). Psoriatic Arthritis Response Criteria (PsARC) response data can help relate clinical trial data to UK clinical practice. We report PsARC response rates to 3 years in patients with active PsA from the phase 2b 48-week (wk) dose-ranging study BE ACTIVE (NCT02969525) and its open-label extension (OLE)(NCT03347110). Methods In BE ACTIVE, patients were randomised (1:1:1:1:1) to placebo, BKZ 16mg, BKZ 160mg (with or without 320mg loading dose), or BKZ 320mg, every 4 wks (Q4W). At Wk12, patients assigned to placebo or BKZ 16mg were reassigned (1:1) to dose-blind BKZ 160mg or 320mg Q4W; other patients remained on their original dose. From Wk48 all patients received open-label BKZ 160mg Q4W. We report PsARC to Wk152 and maintenance of response among patients with PsARC response at Wk12, for the full analysis set (FAS). Data are reported as observed and with NRI. Results 206 patients were randomised at baseline in BE ACTIVE and included in the FAS. 181 patients entered the OLE and 161 completed the OLE. 157 patients had calculable PsARC response at Wk152. At Wk12, PsARC response (NRI) was achieved by 125/206, including placebo: 33.3% (14/42), BKZ 16mg: 56.1% (23/41), 160mg: 73.2% (60/82), 320mg: 68.3% (28/41) (Table). At Wk48 and Wk152, 78.2% (161/206) and 68.0% (140/206) patients were PsARC responders, respectively. Of the 125 PsARC responders at Wk12, 88.8% (111/125) also met PsARC at Wk48 and 74.4% (93/125) were PsARC responders at Wk152 (NRI). Over 152 wks, the exposure-adjusted incidence rate per 100 patient-years was 126.4 for all treatment-emergent adverse events (TEAEs), 4.1 for serious TEAEs, 0.7 for serious infections and 4.6 for Candida infections. Conclusion A numerically higher proportion of patients achieved PsARC response in all BKZ-treated groups at Wk12, compared with placebo. The PsARC response rate was sustained through 3 years. Nearly three-quarters of patients who achieved PsARC at Wk12 were also PsARC responders at Wk152. No new safety signals were observed. Disclosure W. Tillett: Consultancies; WT has received consulting fees from AbbVie, Amgen, Celgene, Eli Lilly, Janssen, MSD, Novartis, Pfizer and UCB Pharma. Honoraria; WT has received honoraria from AbbVie, Amgen, Celgene, Eli Lilly, Janssen, MSD, Novartis, Pfizer and UCB Pharma. Grants/research support; WT has received research grants from AbbVie, Amgen, Celgene, Eli Lilly, Janssen, MSD, Novartis, Pfizer and UCB Pharma. I.B. McInnes: Consultancies; IBM has received consulting fees from AbbVie, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Eli Lilly, Janssen, Novartis, UCB Pharma. Honoraria; IBM has received honoraria from AbbVie, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Eli Lilly, Janssen, Novartis, UCB Pharma. Grants/research support; IBM has received research support from Boehringer Ingelheim, BMS, Celgene, Janssen and UCB Pharma. D. McGonagle: Consultancies; DM has received consulting fees from AbbVie, Celgene, Janssen, Merck, Novartis, Pfizer and UCB Pharma. Honoraria; DM has received honoraria from AbbVie, Celgene, Janssen, Merck, Novartis, Pfizer and UCB Pharma. Member of speakers’ bureau; DM has been on speaker’s bureau for AbbVie, Celgene, Janssen, Merck, Novartis, Pfizer and UCB Pharma. Grants/research support; DM has received grants/research support from AbbVie, Celgene, Janssen, Merck, Pfizer and Novartis. D.R. Jadon: Consultancies; DRJ has received consultancy fees from AbbVie, Amgen, Biogen, BMS, Celgene, Celltrion, Eli Lilly, Fresenius Kabi, Galapagos, GSK, Janssen, Merck, Novartis, Pfizer, Roche, Sandoz, Sanofi and UCB Pharma. Grants/research support; DRJ has received research grants from AbbVie, Amgen, Biogen, BMS, Celgene, Celltrion, Eli Lilly, Fresenius Kabi, Galapagos, GSK, Janssen, Merck, Novartis, Pfizer, Roche, Sandoz, Sanofi, UCB Pharma. B. Ink: Corporate appointments; BI is an employee of UCB Pharma. Shareholder/stock ownership; BI is a shareholder of GSK and UCB Pharma. D. Assudani: Corporate appointments; DA is an employee of UCB Pharma. Shareholder/stock ownership; DA is a shareholder of UCB Pharma. J. Coarse: Corporate appointments; JC is an employee of UCB Pharma. Shareholder/stock ownership; JC is a shareholder of UCB Pharma. J. Eells: Corporate appointments; JE is an employee of UCB Pharma. Shareholder/stock ownership; JE is a shareholder of UCB Pharma. L.C. Coates: Consultancies; LCC has received consulting fees from AbbVie, Amgen, Biogen, Boehringer Ingelheim, Celgene, Domain, Eli Lilly, Gilead and Janssen. Member of speakers’ bureau; LCC has been on speaker’s bureau for AbbVie, Amgen, Biogen, Celgene, Eli Lilly, Gilead, GSK, Janssen, Medac, Novartis, Pfizer and UCB Pharma. Grants/research support; LCC has received grants/research support from AbbVie, Amgen, Celgene, Eli Lilly, Gilead, Janssen, Novartis, Pfizer and UCB Pharma.

Background Many patients with psoriatic arthritis do not reach minimal disease activity (MDA) on methotrexate alone. This phase 4 open-label study aimed to compare attainment of MDA following introduction of adalimumab with methotrexate escalation in patients with psoriatic arthritis who do not reach MDA after an initial methotrexate course (≤15 mg every week). Methods CONTROL was a phase 4, randomised, two-part, open-label study conducted in 14 countries and 46 sites. We recruited patients with confirmed active psoriatic arthritis, naive to biologic disease-modifying antirheumatic drugs, with an inadequate response to 15 mg or less of methotrexate. In part 1, patients were randomly assigned (1:1) to receive either methotrexate 15 mg (oral or subcutaneous) every week with the addition of adalimumab 40 mg (subcutaneously) every other week (adalimumab plus methotrexate group) or methotrexate (oral or subcutaneous) escalation up to 25 mg every week (escalated methotrexate group). Randomisation was done using Interactive Response Technology and stratified by the duration of methotrexate treatment (≤3 months and >3 months). In this open-label study there was no masking; participants, people giving the interventions, those assessing outcomes, and those analysing the data were aware of group assignment. The primary endpoint was the proportion of patients who reached MDA at 16 weeks. After 16 weeks (part 2), patients who reached MDA (responders) had their current therapy maintained or modified, wheras patients who did not reach MDA (non-responders) had their therapy escalated until 32 weeks. The primary endpoint in part 2 was the proportion of patients who reached MDA at 32 weeks, analysed in all patients who received one or more doses of study drug. The study is registered with ClinicalTrials.gov, NCT02814175. Findings Between Aug 5, 2016, and March 19, 2020, 245 of 287 patients initially assessed were enrolled in the study (50% men and 50% women; 92% of patients were White). 123 patients were randomly assigned to receive adalimumab plus methotrexate and 122 patients to receive escalated methotrexate. All 245 patients were included in the primary analysis, and 227 completed part 1 and entered part 2. A significantly higher proportion of patients reached MDA at 16 weeks in the adalimumab plus methotrexate group (51 [41%] patients) compared with the escalated methotrexate group (16 [13%] patients; p

Objective.To determine the risk of a diagnosis of osteoarthritis (OA) in patients with psoriatic arthritis (PsA) compared to patients with psoriasis and a general population cohort.Methods.Incident PsA patients aged 18–89 years at diagnosis were identified from the United Kingdom Clinical Practice Research Datalink between 1998 and 2014. All patients with PsA were matched to 2 cohorts of patients, both at a 1:4 ratio. The first cohort included patients with psoriasis (and no PsA) and the second was a general population cohort (with no psoriasis or PsA). The baseline prevalence of OA was calculated for each study cohort. The incidence of OA was calculated, and adjusted relative risks (RRadj) were calculated using conditional Poisson regression.Results.We identified 6783 incident PsA patients. The baseline prevalence of OA ranged from 22.1% (95% CI 21.1–23.1) in the PsA cohort to 12.6% (95% CI 12.2–13.0) and 11.0% (95% CI 10.6–11.3) in the psoriasis and general population cohorts, respectively. The incidence of OA was significantly higher in the PsA cohort compared to the psoriasis and general population cohorts after adjusting for BMI (RRadj 1.68, 95% CI 1.46–1.93, and RRadj 1.86, 95% CI 1.62–2.14, respectively).Conclusion.An increased risk of OA was observed in patients with PsA compared to patients with psoriasis alone and those in the general population. Further work is needed to determine whether this reflects a true increase in OA risk or misdiagnosed PsA, and the extent to which it can be explained by differences in the opportunity for OA diagnosis between cohorts.

OBJECTIVE: To determine health perceptions of patients with rheumatic diseases in the early phase of the coronavirus disease 2019 (COVID-19) pandemic.METHODS: Rheumatology patients at a single center received via text message the Australian Rheumatology Association COVID-19 information sheet and an invitation to participate in a deidentified survey. Patient concerns regarding risks conferred by their rheumatologic disease or medications, impact of receiving the information sheet on the likelihood of staying on medication, and acceptance of telehealth were ascertained.RESULTS: A total of 2,630 patients received the text message, and the survey response rate was 21% (n = 550). The mean ± SD age of the participants was 52 ± 15.2 years, and 75.3% were female. Participants' highest ranked concern was that their medications would increase the severity of their COVID-19 symptoms (76.1%). The highest levels of concern were seen in patients taking combination conventional synthetic disease-modifying antirheumatic drugs (DMARDs) and/or a biologic/targeted synthetic DMARD. There was no association between prednisolone dose and concern. While 63% of patients planned to continue their antirheumatic medications, a further 30% were more likely to continue taking their medications because of receiving the information. Telehealth was acceptable to 98.4% of patients, but 28.1% felt this was only appropriate while infection control measures were in place.CONCLUSION: Concerns regarding the risk of COVID-19 among patients taking antirheumatic drugs are common. Proactive dissemination of information is needed to address misconceptions related to medication risk, improve medication adherence, and minimize the risk of flares. Telehealth is acceptable to most patients during the COVID-19 pandemic.