ANTIPHOSPHOLIPID ANTIBODIES AND VASCULAR THROMBOSIS IN PATIENTS WITH THE MOST SEVERE FORMS OF COVID-19

BackgroundThe presence of antiphospholipid antibodies (aPL) has been observed in patients with COVID-19 (1,2), suggesting that they may be associated with deep vein thrombosis, pulmonary embolism, or stroke in severe cases (3). Antiphospholipid syndrome (APS) is a systemic autoimmune disorder and the most common form of acquired thrombophilia globally. At least one clinical criterion, vascular thrombosis (arterial, venous or microthrombosis) or pregnancy morbidity and at least one laboratory criterion- positive aPL two times at least 12 weeks apart: lupus anticoagulant (LA), anticardiolipin (aCL), anti-β2-glycoprotein 1 (anti-β2GPI) antibody, have to be met for international APS classification criteria(4). Several reports also associate anti-phosphatidylserine/prothrombin antibodies (aPS/PT) with APS.ObjectivesTo combine clinical data on arterial/venous thrombosis and pregnancy complications before and during hospitalisation with aPL laboratory findings at 4 time points (hospital admission, worsening of COVID-19, hospital discharge, and follow-up) in patients with the most severe forms of COVID-19 infection.MethodsPatients with COVID-19 pneumonia were consequetively enrolled, as they were admitted to the General hospital Pancevo. Exclusion criteria were previous diagnosis of inflammatory rheumatic disease and diagnosis of APS. Clinical data were obtained from the medical records. Laboratory results, including LA, aCL, anti-β2GPI, and aPS/PT antibodies were taken at hospital admission, worsening (defined as cytokine storm, connection of the patient to the respirator, use of the anti-IL-6 drug- Tocilizumab), at hospital discharge and at 3-months follow-up and sent to University Medical Centre Ljubljana, Slovenia for analysis. Statistics was performed by using SPSS 21.Results111 patients with COVID-19 pneumonia were recruited;7 patients died during hospitalisation (none were aPL-positive on admission and at the time of worsening), 3 due to pulmonary artery embolism. All patients were treated according to a predefined protocol which included antibiotics, corticosteroids, anticoagulation therapy and specific comorbidity drugs;patients with hypoxia were supported with oxygen. During hospitalisation, pulmonary artery thrombosis occurred in 5 patients, one was aPL-positive at all time points (was diagnosed with APS), others were negative. In addition, 9/101 patients had a history of thrombosis (5 arterial thrombosis (coronary and cerebral arteries), none of whom was aPL-positive on admission and at follow-up, and 4 venous thrombosis, one of which was aPL-positive at all time points and received an APS diagnosis). Among 9/101 patients with a history of thrombosis, 55.6% were transiently positive at the time of discharge, compared to patients without prior thrombosis, in whom 26.1% were transiently positive at the hospital release (p=0.074). Two patients had a history of pregnancy complications (both had miscarriage after 10th week of gestation), but did not have aPL positivity at any time point.ConclusionAlthough aPL was expected to be associated with vascular disease in the most severe forms of COVID-19, all patients that have died in our cohort were aPL negative. At hospital discharge, 56% of patients with a history of arterial or venous thrombosis had positive aPL that became negative at the 3-months follow-up (were transienlty positive), which should be considered when prescribing therapy after hospitalisation.References[1]Trahtemberg U, Rottapel R, Dos Santos CC, et al. Anticardiolipin and other antiphospholipid antibodies in critically ill COVID-19 positive and negative patients. Annals of the Rheumatic Diseases 2021;80:1236-1240.[2]Stelzer M, Henes J, Saur S. The Role of Antiphospholipid Antibodies in COVID-19. Curr Rheumatol Rep. 2021;23(9):72-4.[3]Xie Y, Wang X, Yang P, Zhang S. COVID-19 complicated by acute pulmonary embolism. Radiology: Cardiothoracic Imaging 2020: 2: e200067.[4]Miyakis S, Lockshin MD, Atsumi T, Branch DW, Brey RL, et al. J.Thromb.Haemost. 2006;4: 295-306.Acknowledgements:NIL.Disclosure of nterestsNone Declared.

MUSCULOSKELETAL DISORDERS DURING COVID-19 INFECTION: A SURVEY OF HEALTHCARE WORKERS

BackgroundCOVID-19 infection has revealed a considerable number of extra-pulmonary manifestations, especially rheumatological. The detection of these manifestations, which herald the infection, is of great value in the early diagnosis of the disease, especially in health care workers (HCWs) who are at considerable risk of infection. Although myalgia is a common clinical feature of COVID-19, other musculoskeletal disorders (MSDs) have been rarely described.ObjectivesTo describe MSDs during SARS-COV2 infection in HCWs.MethodsProspective descriptive study conducted at the department of occupational pathology and fitness for work of Charles Nicolle Hospital in Tunis, having included the HCWs affected by COVID-19 during the period from 01 September 2020 to 28 February 2021. Data collection was carried out by regular telephone follow-up during the containment period using a pre-established form.ResultsDuring the study period, 656 HCWs were infected with SARS COV 2, of whom 134 (20.4%) had at least one musculoskeletal event. The mean age was 42±9 years with a sex ratio (M/F) of 0.2. The most represented occupational category was nurses (33.6%) followed by health technicians (23.1%). The median professional length of service was 12 [7;20] years. The presence of comorbidity was noted in 58.2% of HCWs. A pre-existing osteoarticular disease was found in 8.2% of cases. Obesity was noted in 25.4% of the population. Active smoking was reported by 14.3% of respondents. A known vitamin D deficiency was noted in 16.5% of patients. Spinal pain was the most reported MSD, present in 87.3% of cases. Low back pain was the most frequent spinal pain (56.7%) followed by back pain (37.4%) and neck pain (5.9%). MSDs of the lower limbs were found in 12.7% of patients. They were represented by gonalgia in 11.9% of cases, ankle pain in 5.2% of cases and hip pain in 4.3% of cases. MSDs of the upper limbs were described by 7.5% of the patients, 92.5% of whom presented with shoulder pain. The median duration of MSDs during COVID-19 was 5 [3;8] days. These manifestations were persistent on return to work in 21.1% of cases.ConclusionKnowledge of the frequency and consequences of musculoskeletal manifestations related to COVID-19 infection is of great importance, particularly in HCWs, in order to optimise management and ensure a rapid return to work.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsNone Declared.

AUTOANTIBODIES RELATED TO RHEUMATIC DISEASES AFTER COVID-19 INFECTION

BackgroundSARS-CoV-2(Severe acute respiratory syndrome coronavirus 2) has been circulating worldwide for three years. It mainly causes upper respiratory tract infection, which can manifest as pulmonary infection and even respiratory distress syndrome in severe cases. Different autoantibodies can be detected in patients infected with COVID-19.ObjectivesTo explore autoantibodies related to rheumatic diseases after COVID-19 infection.MethodsNinety-eight inpatients were tested for antinuclear antibodies (ANA), antibodies to extractable nuclear antigens(ENA), anti-neutrophil cytoplasmic antibodies（ANCA), anticardiolipin antibodies,a-β2GPI (IgG/IgM). They were from a tertiary hospital in Guangzhou during the COVID-19 epidemic. Data were described statistically.ResultsNinety-eight hospitalized patients were tested for relevant antibodies. The average age was 50.64±19.54;67 (68.4%) were male, 64 (65.3%) were COVID-19 positive, 90 (90.9%) had rheumatic diseases, and 56 of them were COVID-19 positive patients with rheumatic diseases.There were 76 patients tested for antinuclear antibodies;29 （38.16%）were negative, 18 （23.68%）had a 1/80 titre, and 29（28.16%） had a titre greater than 1:80. The 31 covid patients were positive for ANA. In the high-titer group, 19 patients with rheumatic diseases were positive for COVID-19, and 12 patients had an exacerbation of the rheumatic diseases (6 of whom had previously had pulmonary fibrosis). Of 31 covid patients, only two were non-rheumatic patients, and both were elderly, aged 85 and 100, respectively.Fifty-six patients had ENA results, and 29 for positive antibodies, 8 for ds-DNA antibodies, 2 for anti-Sm antibodies, 6 for anti-nucleosome antibodies, 12 for anti-U1RNP antibodies, 2 for anti-Scl-70 antibodies, 12 for anti-SS-A antibodies, 3 for anti-mitochondrial M2 antibodies, 2 for anti-centromere antibodies, 1 for anti-Po antibodies, and one for anti-Jo-1 antibody. All 56 patients had rheumatic diseases, and no new patients were found.There were 62 patients with ANCA data. P-ANCA was positive in 12 cases(19.35%), and MPO-ANCA was positive in 2 cases. An 85-year-old non-rheumatic COVID-19 patient was P-ANCA positive. She had a history of hypertension, colon cancer, CKD3, coronary heart disease, and atrial flutter.In the anticardiolipin antibodies group, there were 62 patients;only 6 were positive, and 2 were rheumatic patients infected with COVID-19. Antiphospholipid antibodies were detected in 33 patients, and a-β2GPI was tested in one patient, an 82-year-old COVID-19 patient with gout, diabetes, and cerebral infarction in the past. We did not find a statistical difference in the above results.ConclusionWe have not found a correlation between SARS-CoV-2 and serum autoantibodies of rheumatic immune diseases. It needs large samples and an extended follow-up to research.AcknowledgementsThis work was supported by Scientific and Technological Planning Project of Guangzhou City [202102020150], Guangdong Provincial Basic and Applied Basic Research Fund Project [2021A1515111172], National Natural Science Foundation of China Youth Fund [82201998] and Third Affiliated Hospital of Sun Yat-Sen University Cultivating Special Fund Project for National Natural Science Foundation of China [2022GZRPYQN01].Disclosure of Interestsone declared.

PSYCHOLOGICAL DISTRESS OVER 12 MONTHS POST-DIAGNOSIS IN A NATIONAL EARLY INFLAMMATORY ARTHRITIS COHORT

BackgroundIn inflammatory arthritis patients, the concomitant decline of their mental wellbeing is an increasing concern[1,2]. It is important to not only describe the trajectory of psychological distress in early disease stages, but also understand which clinical outcome measures are most associated with these changes.ObjectivesUsing data from the National Early Inflammatory Arthritis Audit (NEIAA), we assessed trends in psychological wellbeing over 12 months after initial diagnosis and mapped these against clinical outcomes to identify significant associations.MethodsNEIAA collects data from patients referred with suspected early inflammatory arthritis in rheumatology services in England and Wales. We used data provided by 20,472 patients eligible for follow-up (diagnosis of inflammatory arthritis) between May 1st, 2018, and April 1st, 2022. Data items included baseline demographics e.g., age and gender, and clinical variables e.g., rheumatic disease comorbidity index (RDCI), DAS28, and patient reported outcomes.Psychological distress was measured by the sum score of Patient Health Questionnaire Anxiety and Depression Screener (PHQ4ADS). Using mixed effects regression models, we analysed the co-variability of PHQ4ADS with demographic factors and clinical outcomes over 12 months. Time was included as a dummy-coded covariant.ResultsThe analysis included 36% of patients (7,378 out of 20,472) who completed the baseline patient outcome survey. In this cohort, PHQ4ADS scores decreased from a baseline average of 4.7 (CI: [4.6, 4.8]) to 2.62 (CI: [2.5, 2.8]) at 12 months post-diagnosis. The proportion of patients screening positive decreased from 50.0% (CI: [48.9, 51.1]) at baseline to 23.8% (CI: [21.8, 25.9]) at 12 months.At baseline, psychological distress correlated significantly with age, gender, ethnicity, RDCI, prior depression diagnosis, and baseline DAS28 (Figure 1). No significant correlations were found between psychological distress and working diagnosis, seropositivity, or the assessment being recorded after the start of the COVID-19 pandemic. Younger ages were nonlinearly associated with higher distress levels (coefficient per decade: -0.006;p<0.001;CI: [-0.009, -0.003]) (Figure 1a). Distress levels in females were higher than that of males (coefficient: 0.5;p<0.001;CI: [0.4, 0.7]) (Figure 1b). White patients reported lower PHQ4ADS scores compared to non-white patients (coefficient: -0.7;p<0.001;CI: [-1.0, -0.4]) (Figure 1c). Higher distress levels were also associated with higher RDCI (coefficient: 0.2;p<0.001;CI: [0.1, 0.3]) and prior diagnosis of depression (coefficient: 1.8;p<0.001;CI: [1.5, 2.2]) (Figure 1d, 1e). Furthermore, higher baseline DAS28 scores correlated with more severe psychological distress (coefficient: 0.8;p<0.001;CI: [0.7, 0.8]) (Figure 1f).By 12-months, psychological distress decreased significantly overall, which correlated significantly with ethnicity (coefficient: 0.8;p=0.005;CI: [0.3, 1.4]) and baseline DAS28 (coefficient: -0.5;p<0.001;CI: [-0.6, -0.4]). Compared to white patients, the reduction was significantly greater for non-white patients, but the level of distress was no longer different at 12 months (Figure 1c). While those with higher baseline DAS28 showed a greater reduction in psychological distress, the distress levels remained higher at 12 months (Figure 1f).Figure 1.Changes in psychological distress correlated with age, gender, ethnicity, RDCI, prior depression diagnosis, and baseline DAS28.[Figure omitted. See PDF]ConclusionIn this early inflammatory arthritis cohort, mental health burden was high. Age, gender, ethnicity, RDCI, prior depression diagnosis and baseline DAS28 significantly correlated with psychological distress at baseline. Supporting mental health should be a focus of clinical care for this population and it may be beneficial to use an approach that is culturally valid for non-white patients and accounts for multimorbidity.References[1]Euesden, J, et al. Psychosomatic medicine 79.6 (2017): 638.[2]Lwin, MN, et al. Rheumatology and therapy 7.3 (2020): 457-471.AcknowledgementsThe authors would like to thank the Healthcare Quality Improvement Partnership (HQIP) as the commisioner of NEIAA, British Society for Rheumatology as the audit providers, Net Solving as the audit platform developers, and the Wellcome Trust (ST12406) for funding to support L.Z..Disclosure of InterestsLucy Zhao: None declared, James Galloway Speakers bureau: Has received honoraria from AbbVie Celgene, Chugai, Gillead, Janssen, Eli Lilly, Pfizer, Roche, and UCB, Jo Ledingham: None declared, Sarah Gallagher: None declared, Neena Garnavos: None declared, Paul Amlani-Hatcher: None declared, Nicky Wilson: None declared, Lewis Carpenter Consultant of: Statistical consultancy for Pfizer, Kirsty Bannister: None declared, Sam Norton Speakers bureau: Has received honoraria from Janssen and Pfizer.

IMPACT OF THE COVID-19 PANDEMIC ON SEPTIC ARTHRITIS MANAGEMENT

BackgroundSince 2020, the SARS-Cov-2 pandemic has disrupted the organization of healthcare systems worldwide.ObjectivesThis study aimed to assess the impact of this pandemic on septic arthritis management in a tertiary rheumatology department.MethodsIt was a single-center descriptive case-control study, which included patients hospitalized for septic arthritis between January 2018 and December 2021, whose diagnosis was retained after positive bacterial growthor on culture on according to presumptive criteria. Our patients were divided into two groups: G1: patients hospitalized during the COVID-19 pandemic (2020-2021), and G2: patients hospitalized during a similar period before the COVID-19 pandemic (2018-2019). In both groups, septic arthritis prevalence was calculated, socio-demographic characteristics, risk factors, clinical, paraclinical, and therapeutic data were collected. COVID-19 status was reported in the G1.ResultsTwenty-two patients were enrolled: G1 (n = 15), G2 (n = 7). The prevalence of septic arthritis was 0.77% and 0.36% respectively. The median age was 54.6±12.25 and 54.29±21.81 years old respectively. Diabetes was found in 26, 7% in G1 and 28.6% in G2. During the pandemic, arthropathy and oral corticosteroids use were noted in 53.3% and 28.6% of patients versus 26.7% and 14.3% in G2. The diagnosis delay and the prior use of antibiotic therapy were more significant in G1: 14.08[7-30] d versus 6.5[3.25-19.25] d, and 46.7% versus 14.3%. The knee was the most common localization in both groups. Other joints were affected in G1: shoulder (n = 2), hip (n = 1), and sacroiliac (n = 1). The most common germ was staphylococcus aureus. The duration of hospitalization and duration of antibiotic therapy in G1 and G2 were 26.07±9.12d versus 27.43±10.87d and 50±10d versus 48±25.79d, respectively. Concerning COVID-19 status, 33.3% of patients in G1 have received their vaccination and no recent SARS-Cov2 infection was noted before hospitalization. During the pandemic, synovectomy was required in three patients, one of whom was also transferred to intensive care for septic shock (two of these three patients are being followed for rheumatoid arthritis, and only one has never been vaccinated against COVID-19).ConclusionDuring the COVID-19 pandemic, the prevalence of septic arthritis in our department was higher and the diagnosis was delayed. Duration of hospitalization was not impacted, however, atypical localisations, prior use of antibiotics, recourse to synovectomy, and transfer to intensive care were reported. These results suggest an inadequate and difficult access to healthcare services during the lockdown, as well as an impact of social distancing on the immune system [1, 2]. More studies are needed to confirm these findings.References[1]Robinson E. Pires et al, What Do We Need to Know about Musculoskeletal Manifestations of COVID-19? A Systematic Review, JBJS Rev. 2022 Jun 3;10(6)[2]Pantea Kiani et al, Immune Fitness and the Psychosocial and Health Consequences of the COVID-19 Pandemic Lockdown in The Netherlands: Methodology and Design of the CLOFIT Study, Eur J Investig Health Psychol Educ. 2021 Feb 20;11(1):199-218Acknowledgements:NIL.Disclosure of InterestsNone Declared.

RHEUMATOID ARTHRITIS FLARE FOLLOWING COVID-19 VACCINATION IN MALAYSIAN POPULATION AND ITS ASSOCIATED RISK FACTORS

BackgroundFlare of Rheumatoid Arthritis (RA) following COVID-19 vaccination has been reported with a low occurrence observed in those patients with disease remission. However, no local data is available in our multi-ethnic Malaysian population.ObjectivesTo evaluate the prevalence of RA flare in Malaysian patients following COVID-19 vaccination and its associated risk factors.MethodsThis was a cross-sectional study assessing RA flare based on patient-reported disease flare through self-administered questionnaires and physician-reported flare. Patient self-reported disease flare was defined as ‘a sudden worsening of rheumatology condition or arthritis within 1 month post-vaccination' while physician-reported flare was defined as ‘an increment of disease activity score 28-joint documented within 3 months post-vaccination‘ from either a scheduled or unscheduled clinic visit. A total of 186 RA patients attended the rheumatology clinic in Hospital Putrajaya from May to July 2022 who completed the primary COVID-19 vaccination under the Malaysian National Vaccination Programme were recruited. Demographic data, disease parameters including serology for rheumatoid factor (RF) and anti-citrullinated peptide antibodies (ACPA), cessation of disease modifying anti-rheumatic drugs (DMARDs) around vaccination, type of vaccines and adverse events were examined using descriptive and univariate analyses.ResultsMajority (93%) of RA patients enrolled were female with a mean age of 58 years old (standard deviation, SD 12.2) and mean disease duration was 12 years (SD 7.7). More than half were seropositive (66% RF, 63% ACPA) with 47.4% had double seropositivity (RF and ACPA positive). All patients received DMARDs with the majority (71%) were on methotrexate (MTX), 21.5% were on leflunomide, 17.7% on other DMARDs, with a small proportion (14%) of patients were receiving prednisolone. Only 4.8% of patients were on biologics or targeted synthetic disease modifying anti-rheumatic drugs. Half of the patients were in remission prior to vaccination. 62% of patients received Pfizer-BioNTech vaccine as the primary vaccine, followed by Sinovac-CoronaVac (24.6%) and Oxford-AstraZeneca (13.4%) vaccines. A booster dose had been administered to 80% of patients, of which 88.7% was Pfizer-BioNTech vaccine. MTX therapy were discontinued in 39.4% of patients (n=52) post-vaccination for a week duration. The prevalence of RA flare was only 12.9% (n=24) in which 14 were self-reported and 10 were physician-reported flares (4 severe flare, 6 mild-moderate flare). Flare rates were higher during the first and second dose of vaccination with 29.2% respectively, and only 12.5% were reported after booster vaccination. Common vaccine adverse effects were fever (16.8%), myalgia (8.6%) and arthralgia (6.4%). There were no significant differences in the occurrence of flare post-vaccination between age, gender, disease activity prior to vaccination, types of vaccine, usage of MTX and prednisolone, and discontinuation of MTX post-vaccination. Although seropositivity did not exhibit statistically significant flare rate post vaccination, sub-analysis revealed four times higher rate of flare in those who has double positivity compared to seronegative RA patients (12% vs 4%).ConclusionPrevelance of RA flare post-COVID-19 vaccination in Malaysian RA population is low. No significant associated risk factors were identified although double seropositivity appeared to have higher number of flares.References[1]Bixio, R., Bertelle, D., Masia, M., Pistillo, F., Carletto, A. and Rossini, M. (2021), Incidence of Disease Flare After BNT162b2 Coronavirus Disease 2019 Vaccination in Patients With Rheumatoid Arthritis in Remission. ACR Open Rheumatology, 3: 832-833.[2]Li X, Tong X, Yeung WWY, Kuan P, Yum SHH, Chui CSL, Lai FTT, Wan EYF, Wong CKH, Chan EWY, Lau CS, Wong ICK. Two-dose COVID-19 vaccination and possible arthritis flare among patients with rheumatoid arthritis in Hong Kong. Ann Rheum Dis. 2022 Apr;81(4):564-568.Acknowledgements:NIL.Disclosure of InterestsNone Declared.

IMPAIRED HEALTH-RELATED QUALITY OF LIFE IN PATIENTS WITH IDIOPATHIC INFLAMMATORY MYOPATHIES: A CROSS-SECTIONAL ANALYSIS FROM AN INTERNATIONAL E-SURVEY

BackgroundComprehensive and large-scale assessment of health-related quality of life in patients with idiopathic inflammatory myopathies (IIMs) worldwide is lacking. The second COVID-19 vaccination in autoimmune disease (COVAD-2) study [1] is an international, multicentre, self-reported e-survey assessing several aspects of COVID-19 infection and vaccination as well as validated patient-reported outcome measures (PROMs) to outline patient experience in various autoimmune diseases (AIDs), with a particular focus on IIMs.ObjectivesTo investigate physical and mental health in a global cohort of IIM patients compared to those with non-IIM autoimmune inflammatory rheumatic diseases (AIRDs), non-rheumatic AIDs (NRAIDs), and those without AIDs (controls), using Patient-Reported Outcome Measurement Information System (PROMIS) global health data obtained from the COVAD-2 survey.MethodsDemographics, AID diagnoses, comorbidities, disease activity, treatments, and PROMs were extracted from the COVAD-2 database. The primary outcomes were PROMIS Global Physical Health (GPH) and Global Mental Health (GMH) scores. Secondary outcomes included PROMIS physical function short form-10a (PROMIS PF-10a), pain visual analogue scale (VAS), and PROMIS Fatigue-4a scores. Each outcome was compared between IIMs, non-IIM AIRDs, NRAIDs, and controls. Factors affecting GPH and GMH scores in IIMs were identified using multivariable regression analysis.ResultsA total of 10,502 complete responses from 1582 IIMs, 4700 non-IIM AIRDs, 545 NRAIDs, and 3675 controls, which accrued as of May 2022, were analysed. Patients with IIMs were older [59±14 (IIMs) vs. 48±14 (non-IIM AIRDs) vs. 45±14 (NRAIDs) vs. 40±14 (controls) years, p<0.001] and more likely to be Caucasian [82.7% (IIMs) vs. 53.2% (non-IIM AIRDs) vs. 62.4% (NRAIDs) vs. 34.5% (controls), p<0.001]. Among IIMs, dermatomyositis (DM) and juvenile DM were the most common (31.4%), followed by inclusion body myositis (IBM) (24.9%). Patients with IIMs were more likely to have comorbidities [68.1% (IIMs) vs. 45.7% (non-IIM AIRDs) vs. 45.1% (NRAIDs) vs. 26.3% (controls), p<0.001] including mental disorders [33.4% (IIMs) vs. 28.2% (non-IIM AIRDs) vs. 28.4% (NRAIDs) vs. 17.9% (controls), p<0.001].GPH median scores were lower in IIMs compared to NRAIDs or controls [13 (interquartile range 10–15) IIMs vs. 13 (11–15) non-IIM AIRDs vs. 15 (13–17) NRAIDs vs. 17 (15–18) controls, p<0.001] and PROMIS PF-10a median scores were the lowest in IIMs [34 (25–43) IIMs vs. 40 (34–46) non-IIM AIRDs vs. 47 (40–50) NRAIDs vs. 49 (45–50) controls, p<0.001]. GMH median scores were lower in AIDs including IIMs compared to controls [13 (10–15) IIMs vs. 13 (10–15) non-IIM AIRDs vs. 13 (11–16) NRAIDs vs. 15 (13–17) controls, p<0.001]. Pain VAS median scores were higher in AIDs compared to controls [3 (1–5) IIMs vs. 4 (2–6) non-IIM AIRDs vs. 2 (0–4) NRAIDs vs. 0 (0–2) controls, p<0.001]. Of note, PROMIS Fatigue-4a median scores were the highest in IIMs [11 (8–14) IIMs vs. 8 (10–14) non-IIM AIRDs vs. 9 (7–13) NRAIDs vs. 7 (4–10) controls, p<0.001].Multivariable regression analysis in IIMs identified older age, male sex, IBM, comorbidities including hypertension and diabetes, active disease, glucocorticoid use, increased pain and fatigue as the independent factors for lower GPH scores, whereas coexistence of interstitial lung disease, mental disorders including anxiety disorder and depression, active disease, increased pain and fatigue were the independent factors for lower GMH scores.ConclusionBoth physical and mental health are significantly impaired in patients with IIMs compared to those with non-IIM AIDs or those without AIDs. Our results call for greater attention to patient-reported experience and comorbidities including mental disorders to provide targeted approaches and optimise global well-being in patients with IIMs.Reference[1]Fazal ZZ, Sen P, Joshi M, et al. COVAD survey 2 long-term outcomes: unmet need and protocol. Rheumatol Int. 2022;42:2151–58.AcknowledgementsThe authors a e grateful to all respondents for completing the questionnaire. The authors also thank The Myositis Association, Myositis India, Myositis UK, the Myositis Global Network, Cure JM, Cure IBM, Sjögren's India Foundation, EULAR PARE for their contribution to the dissemination of the survey. Finally, the authors wish to thank all members of the COVAD study group for their invaluable role in the data collection.Disclosure of InterestsAkira Yoshida: None declared, Yuan Li: None declared, Vahed Maroufy: None declared, Masataka Kuwana Speakers bureau: Boehringer Ingelheim, Ono Pharmaceuticals, AbbVie, Janssen, Astellas, Bayer, Asahi Kasei Pharma, Chugai, Eisai, Mitsubishi Tanabe, Nippon Shinyaku, Pfizer, Consultant of: Corbus, Mochida, Grant/research support from: Boehringer Ingelheim, Ono Pharmaceuticals, Naveen Ravichandran: None declared, Ashima Makol Consultant of: Boehringer-Ingelheim, Parikshit Sen: None declared, James B. Lilleker: None declared, Vishwesh Agarwal: None declared, Sinan Kardes: None declared, Jessica Day Grant/research support from: CSL Limited, Marcin Milchert: None declared, Mrudula Joshi: None declared, Tamer A Gheita: None declared, Babur Salim: None declared, Tsvetelina Velikova: None declared, Abraham Edgar Gracia-Ramos: None declared, Ioannis Parodis Grant/research support from: Amgen, AstraZeneca, Aurinia Pharmaceuticals, Eli Lilly, Gilead Sciences, GlaxoSmithKline, Janssen Pharmaceuticals, Novartis, and F. Hoffmann-La Roche, Elena Nikiphorou Speakers bureau: Celltrion, Pfizer, Sanofi, Gilead, Galapagos, AbbVie, Eli Lilly, Consultant of: Celltrion, Pfizer, Sanofi, Gilead, Galapagos, AbbVie, Eli Lilly, Grant/research support from: Pfizer, Eli Lilly, Ai Lyn Tan Speakers bureau: AbbVie, Gilead, Janssen, Eli Lilly, Novartis, Pfizer, UCB, Consultant of: AbbVie, Gilead, Janssen, Eli Lilly, Novartis, Pfizer, UCB, Arvind Nune: None declared, Lorenzo Cavagna: None declared, Miguel A Saavedra Consultant of: AbbVie, GlaxoSmithKline, Samuel Katsuyuki Shinjo: None declared, Nelly Ziade Speakers bureau: AbbVie, Boehringer-Ingelheim, Eli Lilly, Janssen, Pfizer, Roche, Consultant of: AbbVie, Boehringer-Ingelheim, Eli Lilly, Janssen, Pfizer, Roche, Grant/research support from: AbbVie, Boehringer-Ingelheim, Eli Lilly, Janssen, Pfizer, Roche, Johannes Knitza: None declared, Oliver Distler Speakers bureau: AbbVie, Amgen, Bayer, Boehringer Ingelheim, Janssen, Medscape, Novartis, Consultant of: 4P-Pharma, AbbVie, Acceleron, Alcimed, Altavant, Amgen, AnaMar, Arxx, AstraZeneca, Baecon, Blade, Bayer, Boehringer Ingelheim, Corbus, CSL Behring, Galderma, Galapagos, Glenmark, Gossamer, iQvia, Horizon, Inventiva, Janssen, Kymera, Lupin, Medscape, Merck, Miltenyi Biotec, Mitsubishi Tanabe, Novartis, Prometheus, Redxpharma, Roivant, Sanofi, Topadur, Grant/research support from: AbbVie, Amgen, Boehringer Ingelheim, Kymera, Mitsubishi Tanabe, Novartis, Roche, Hector Chinoy Grant/research support from: Eli Lilly, UCB, Vikas Agarwal: None declared, Rohit Aggarwal Consultant of: Mallinckrodt, Octapharma, CSL Behring, Bristol Myers-Squibb, EMD Serono, Kezar, Pfizer, AstraZeneca, Alexion, Argenx, Boehringer Ingelheim (BI), Corbus, Janssen, Kyverna, Roivant, Merck, Galapagos, Actigraph, Abbvie, Scipher, Horizontal Therapeutics, Teva, Biogen, Beigene, ANI Pharmaceutical, Nuvig, Capella, CabalettaBio, Grant/research support from: Bristol Myers-Squibb, Pfizer, Mallinckrodt, Janssen, Q32, EMD Serono, Boehringer Ingelheim, Latika Gupta: None declared.

REDUCED HEALTH-RELATED QUALITY OF LIFE USING PROMIS IN PATIENTS WITH SYSTEMIC SCLEROSIS: A CROSS-SECTIONAL ANALYSIS FROM THE INTERNATIONAL COVAD-2 E-SURVEY

BackgroundThe second COVID-19 vaccination in autoimmune disease (COVAD-2) study [1] is an international, multicentre, self-reported e-survey designed to evaluate several facets covering COVID-19 infection and vaccination as well as validated patient-reported outcome measures (PROMs) in a variety of autoimmune diseases (AIDs), including systemic sclerosis (SSc). Detailed assessment of the health-related quality of life (HRQOL) and its drivers in patients with SSc is lacking.ObjectivesTo assess physical and mental health in a global cohort of SSc patients in comparison with non-SSc autoimmune inflammatory rheumatic diseases (AIRDs), non-rheumatic AIDs (NRAIDs), and those without AIDs (controls) using Patient-Reported Outcome Measurement Information System (PROMIS) global health data from the COVAD-2 survey.MethodsThe COVAD-2 database was used to extract demographics, AID diagnosis, comorbidities, disease activity, current therapies, and PROMs. PROMIS global physical health (GPH), global mental health (GMH) scores, PROMIS physical function short form-10a (PROMIS PF-10a), pain visual analogue scale (VAS), and PROMIS Fatigue-4a scores were compared between SSc, non-SSc AIRDs, NRAIDs, and controls. Outcomes were also compared between diffuse cutaneous SSc (dcSSc) vs limited cutaneous SSc (lcSSc). Multivariable regression analysis was performed to identify factors influencing GPH and GMH scores in SSc.ResultsA total of 10,502 complete responses from 276 SSc, 6006 non-SSc AIRDs, 545 NRAIDs, and 3675 controls as of May 2022 were included in the analysis. Respondents with SSc were older [SSc vs. non-SSc AIRDs vs. NRAIDs vs. controls: 55 (14) vs. 51 (15) vs. 45 (14) vs. 40 (14) years old, mean (SD), p < 0.001]. Among patients with SSc, 129 (47%) had dcSSc and 147 (53%) had lcSSc. SSc patients reported a significantly higher prevalence of ILD [SSc vs. non-SSc AIRDs vs. NRAIDs vs. controls: 30.4% vs. 5.5% vs. 1.5% vs. 0.2%, p < 0.001], and treatment with MMF [SSc vs. non-SSc AIRDs vs. NRAIDs vs. controls: 26.4% vs. 9.5% vs. 1.1% vs. 0%, p < 0.001].Patients with SSc had lower GPH and PROMIS PF-10a scores [SSc vs. non-SSc AIRDs vs. NRAIDs vs. controls: 13 (11–15) vs. 13 (11–15) vs. 15 (13–17) vs. 17 (15–18), median (IQR), p < 0.001;39 (33–46) vs. 39 (32–45) vs. 47 (40–50) vs. 49 (45–50), p < 0.001, respectively] and higher Pain VAS and PROMIS Fatigue-4a scores compared to those with NRAIDs or controls [SSc vs. non-SSc AIRDs vs. NRAIDs vs. controls: 3 (2–5) vs. 3 (1–6) vs. 2 (0–4) vs. 0 (0–2), p < 0.001;11 (8–14) vs. 11 (8–14) vs. 9 (7–13) vs. 7 (4–10), p < 0.001, respectively]. Patients with AIDs including SSc had lower GMH scores compared to controls [SSc vs. non-SSc AIRDs vs. NRAIDs vs. controls: 12.5 (10–15) vs. 13 (10–15) vs. 13 (11–16) vs. 15 (13–17), p < 0.001].Among SSc patients, GPH, GMH, and PROMIS PF-10a scores were lower in dcSSc compared to lcSSc [dcSSc vs. lcSSc: 12 (10–14) vs. 14 (11–15), p < 0.001;12 (10-14) vs. 13 (10-15), p<0.001;38 (30–43) vs. 41 (34–47), p < 0.001, respectively]. Pain VAS and PROMIS Fatigue-4a scores were higher in dcSSc compared to lcSSc [4 (2–6) vs. 3 (1–5), p < 0.001;12 (8–15) vs. 9 (8–13), p < 0.001, respectively].The independent factors for lower GPH scores in SSc were older age, Asian ethnicity, glucocorticoid use, and higher pain and fatigue scales, while mental health disorders and higher pain and fatigue scales were independently associated with lower GMH scores.ConclusionIn a global cohort, patient-reported physical and mental health were significantly worse in patients with SSc in comparison to those with non-SSc AIDs and without AIDs. Our findings support the critical need for more attention to patient's subjective experiences including pain and fatigue to improve the HRQOL in patients with SSc.Reference[1]Fazal ZZ, Sen P, Joshi M, et al. COVAD survey 2 long-term outcomes: unmet need and protocol. Rheumatol Int. 2022;42: 2151–58.Acknowledgements:NIL.Disclosure of InterestsKeina Yomono: None declared, Yuan Li: None dec ared, Vahed Maroufy: None declared, Naveen Ravichandran: None declared, Akira Yoshida: None declared, Kshitij Jagtap: None declared, Tsvetelina Velikova Speakers bureau: Pfizer and AstraZeneca, Parikshit Sen: None declared, Lorenzo Cavagna: None declared, Vishwesh Agarwal: None declared, Johannes Knitza: None declared, Ashima Makol: None declared, Dey Dzifa: None declared, Carlos Enrique Toro Gutierrez: None declared, Tulika Chatterjee: None declared, Aarat Patel: None declared, Rohit Aggarwal Consultant of: Bristol Myers-Squibb, Pfizer, Genentech, Octapharma, CSL Behring, Mallinckrodt, AstraZeneca, Corbus, Kezar, Abbvie, Janssen, Kyverna Alexion, Argenx, Q32, EMD-Serono, Boehringer Ingelheim, Roivant, Merck, Galapagos, Actigraph, Scipher, Horizon Therepeutics, Teva, Beigene, ANI Pharmaceuticals, Biogen, Nuvig, Capella Bioscience, and CabalettaBio, Grant/research support from: Bristol Myers-Squibb, Pfizer, Genentech, Octapharma, CSL Behring, Mallinckrodt, AstraZeneca, Corbus, Kezar, Abbvie, Janssen, Kyverna Alexion, Argenx, Q32, EMD-Serono, Boehringer Ingelheim, Roivant, Merck, Galapagos, Actigraph, Scipher, Horizon Therepeutics, Teva, Beigene, ANI Pharmaceuticals, Biogen, Nuvig, Capella Bioscience, and CabalettaBio, Latika Gupta: None declared, Masataka Kuwana Speakers bureau: Abbvie, Asahi-Kasei, Astellas, Boehringer-Ingelheim, Chugai, Eisai, MBL, Mochida, Nippon Shinyaku, Ono Pharmaceuticals, Tanabe-Mitsubishi, Consultant of: Astra Zeneka, Boehringer-Ingelheim, Chugai, Corbus, GSK, Horizon, Tanabe-Mitsubishi, Grant/research support from: Boehringer-Ingelheim, Vikas Agarwal: None declared.

LONG-TERM AND BOOSTER VACCINATION RESPONSES IN PATIENTS WITH GIANT CELL ARTERITIS AND POLYMYALGIA RHEUMATICA

BackgroundVaccination remains essential in preventing morbidity of SARS-CoV-2 infections. We previously showed that >10mg/day prednisolone and methotrexate use were associated with reduced antibody concentrations four weeks after primary vaccination in patients with giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) [1].ObjectivesHere, we performed a follow-up study to measure the decay of antibody concentrations over time and the immunogenicity of SARS-CoV-2 booster vaccination.MethodsGCA/PMR patients included in the primary vaccination (BNT162b2 or ChAdOx1) study were asked again to donate blood samples six months after primary vaccination (n=24) and one month after booster vaccination (n=46, BNT162b2 or mRNA1273). Data were compared to that of age-, sex-, and vaccine-matched controls (n=58 and n=42, respectively).ResultsAntibody concentrations decreased faster over time in GCA/PMR patients than in controls, but this decrease was not associated with treatment during primary vaccination. Post-booster antibody concentrations were comparable between patients and controls. Antibody concentrations post booster vaccination associated strongly with antibody concentrations post primary vaccination, but not with treatment during booster vaccination. However, the fold-change of post-booster vaccination showed a slight negative correlation with the post-primary vaccine antibodies.ConclusionThese results indicate that patients with impaired vaccine responses after primary vaccination, have slightly stronger increases in humoral immunity after booster vaccination, but this is not enough to reach a similar protection. The decrease in humoral immunity, and subsequent increase after booster vaccination, is likely not impacted by prednisolone or methotrexate treatment. Rather, these treatments put the patients at an immunogenic disadvantage during primary SARS-CoV-2 vaccination, which is not fully repaired by a single booster vaccination. This longitudinal study in GCA/PMR patients stresses the importance of repeat booster vaccination for patients that used >10mg/day prednisolone or methotrexate during primary vaccination.Reference[1]van Sleen Y, van der Geest, Kornelis SM, Reitsema RD, Esen I, Terpstra JH, Raveling-Eelsing E, et al. Humoral and cellular SARS-CoV-2 vaccine responses in patients with giant cell arteritis and polymyalgia rheumatica. RMD open 2022;8(2):e002479.Figure 1.Acknowledgements:NIL.Disclosure of InterestsYannick van Sleen: None declared, Kornelis van der Geest Speakers bureau: Speaker fees from Roche, Grant/research support from: Grant support from Abbvie, Annemarie Buisman: None declared, Maria Sandovici: None declared, Debbie van Baarle: None declared, Elisabeth Brouwer: None declared.

THE KINETICS OF HUMORAL AND CELLULAR RESPONSES AFTER THE BOOSTER DOSE OF COVID-19 VACCINE IN INFLAMMATORY ARTHRITIS PATIENTS

BackgroundImpaired immunogenicity of COVID-19 vaccinations in inflammatory arthritis (IA) patients results in diminished immunity. However, optimal booster vaccination regimens are still unknown, due to unstudied kinetics of the immune response after booster vaccinations.ObjectivesThis study aimed to assess the kinetics of humoral and cellular responses in IA patients after the COVID-19 booster.MethodsIn 29 IA patients and 16 healthy controls (HC) humoral responses (level of IgG antibodies) and cellular responses (IFN-γ production) were assessed before (T0), after 4 weeks (T1), and after more than 6 months (T2) from the booster vaccination with BNT162b2.ResultsIA patients, but not HC, showed lower anti-S-IgG concentration and IGRA fold change at T2 compared to T1 (p=0.026 and p=0.031). Furthermore, in IA patients the level of cellular response at T2 returned to the pre-booster level (T0). All immunomodulatory drugs, except IL-6 and IL-17 inhibitors for the humoral and IL-17 inhibitors for the cellular response, impaired the immunogenicity of the booster dose at T2. However, none of the immunomodulatory drugs affected the kinetics of both humoral and cellular responses (measured as the difference between response rates at T1 and T2).ConclusionOur study showed impaired kinetics of both humoral and cellular responses after the booster dose of the COVID-19 vaccine in IA patients, which, in the case of cellular response, did not allow the vaccination effect to be maintained for more than 6 months. Repetitive vaccination with subsequent booster doses seems to be necessary for IA patients.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsNone Declared.

EVALUATION OF RESPONSE TO ADJUVANTED RECOMBINANT ZOSTER VACCINATION IN PATIENTS WITH RHEUMATOID ARTHRITIS RECEIVING UPADACITINIB: RESULTS FROM A RANDOMIZED TRIAL SUB-STUDY

BackgroundUpadacitinib (UPA) is an oral JAK inhibitor (JAKi) approved for the treatment of RA. JAKi have been associated with an elevated risk of herpes zoster (HZ) in patients (pts) with RA. The adjuvanted recombinant zoster vaccine (RZV, Shingrix) was shown to be well-tolerated and effective in preventing HZ in adults aged ≥ 50 years.[1] The efficacy and safety of RZV have not been studied in pts with RA while on UPA in combination with MTX.ObjectivesTo assess the immunogenicity of RZV in pts with RA receiving UPA 15 mg once daily (QD) with background MTX.MethodsEligible adults aged ≥ 50 years with RA enrolled in the ongoing SELECT-COMPARE phase 3 trial (NCT02629159) received two RZV doses, administered at the baseline and week (wk) 12 visits. Pts should have been on stable doses of UPA 15 mg QD and background MTX for ≥ 8 wks before the first vaccination and ≥ 4 wks after the second vaccination. Antibody titers were collected pre-vaccination (baseline), 4 wks post-dose 1 vaccination (wk 4), and 4 wks post-dose 2 vaccination (wk 16). The primary endpoint was the proportion of pts with a humoral response to RZV defined as ≥ 4-fold increase in pre-vaccination concentration of anti-glycoprotein E [gE] titer levels at wk 16. Secondary endpoints included humoral response to RZV at wk 4 and the geometric mean fold rise (GMFR) in anti-gE antibody levels at wks 4 and 16. Cell-mediated immunogenicity to RZV was an exploratory endpoint evaluated by the frequencies of gE-specific CD4+ [2+] T cells (CD4+ T cells expressing ≥ 2 of 4 activation markers: IFN-γ, IL-2, TNF-α, and CD40 ligand) measured by flow cytometry at wks 4 and 16 in a sub-cohort of pts.ResultsOf the 95 pts who received ≥ 1 RZV dose, 93 (98%) received both RZV doses. Pts had a mean (standard deviation) age of 62.4 (7.5) years. The median (range) disease duration was 11.7 (4.9–41.6) years and duration of UPA exposure was 3.9 (2.9–5.8) years. At baseline, all but 2 pts were receiving concomitant MTX and half (50%) were taking an oral corticosteroid (CS) at a median daily dose of 5.0 mg. One pt discontinued UPA by wk 16. Blood samples were available from 90/93 pts. Satisfactory humoral responses to RZV occurred in 64% (95% confidence interval [CI]: 55–74) of pts at wk 4 and 88% (81–95) at wk 16 (Figure 1). Age (50–< 65 years: 85% [95% CI: 75–94];≥ 65 years: 94% [85–100]) and concomitant CS (yes: 87% [77–97];no: 89% [80–98]) use at baseline did not affect humoral responses at wk 16. GMFR in anti-gE antibody levels compared with baseline values were observed at wks 4 (10.2 [95% CI: 7.3–14.3]) and 16 (22.6 [15.9–32.2]). Among the sub-cohort of pts, nearly two-thirds achieved a cell-mediated immune response to RZV (wk 4: n = 21/34, 62% [95% CI: 45–78];wk 16: n = 25/38;66% [51–81]). Within 30 days post-vaccination of either RZV dose, no serious adverse events (AEs) (Table 1) or HZ were reported. AEs that were possibly related to RZV were reported in 17% of pts. One death occurred more than 30 days after wk 16 due to COVID-19 pneumonia.ConclusionMore than three-quarters (88%) of pts with RA receiving UPA 15 mg QD on background MTX achieved a satisfactory humoral response to RZV at wk 16. In a subgroup of pts, two-thirds (66%) achieved a cell-mediated immune response to RZV at wk 16. Age and concomitant CS use did not negatively affect RZV response.Reference[1]Syed YY. Drugs Aging. 2018;35:1031–40.Table 1. Safety Results Through 30-Days Post-RZV Vaccination in UPA-Treated PatientsEvent, n (%)UPA 15 mg QD (N = 95)Any AE38 (40%)AE with reasonable possibility of being related to UPAa13 (14%)AE with reasonable possibility of being related to RZVa16 (17%)Severe AEb1 (1%)Serious AE0AE leading to discontinuation of UPA0Death0AE, adverse event;QD, once daily;RZV, adjuvanted recombinant zoster vaccine;UPA, upadacitinib.aAs assessed by the investigator.bHypersensitivity.AcknowledgementsAbbVie funded this study and participated in the study design, research, analysis, data collection, interpretation of data, review, and approval of the . All authors had access to relevant data and participated in the drafting, review, and approval of this publication. No honoraria or payments were made for authorship. Medical writing support was provided by Julia Zolotarjova, MSc, MWC, of AbbVie.Disclosure of InterestsKevin Winthrop Consultant of: AbbVie, AstraZeneca, BMS, Eli Lilly, Galapagos, Gilead, GSK, Novartis, Pfizer, Regeneron, Roche, Sanofi, and UCB, Grant/research support from: AbbVie, AstraZeneca, BMS, Eli Lilly, Galapagos, Gilead, GSK, Novartis, Pfizer, Regeneron, Roche, Sanofi, and UCB, Justin Klaff Shareholder of: AbbVie, Employee of: AbbVie, Yanxi Liu Shareholder of: AbbVie, Employee of: AbbVie, CONRADO GARCIA GARCIA: None declared, Eduardo Mysler Speakers bureau: AbbVie, Amgen, AstraZeneca, BMS, Eli Lilly, GlaxoSmithKline, Pfizer, Roche, and Sandoz, Consultant of: AbbVie, Amgen, AstraZeneca, BMS, Eli Lilly, GlaxoSmithKline, Pfizer, Roche, and Sandoz, Alvin F. Wells Consultant of: AbbVie, Amgen, BMS, Eli Lilly, Novartis, Pfizer, and Sanofi, Xianwei Bu Shareholder of: AbbVie, Employee of: AbbVie, Nasser Khan Shareholder of: AbbVie, Employee of: AbbVie, Michael Chen Shareholder of: AbbVie, Employee of: AbbVie, Heidi Camp Shareholder of: AbbVie, Employee of: AbbVie, Anthony Cunningham Consultant of: GSK, Merck Sharp & Dohme, and BioCSL/Sequirus.

THE SWEDISH OSTEOARTHRITIS REGISTRY. TRENDS IN SWEDISH OSTEOARTHRITIS HEALTH CARE BETWEEN 2008- 2021

BackgroundIn 2012 the Swedish national guidelines for osteoarthritis (OA) were published. The guidelines implicit that all patients with OA should obtain information and supervised exercise as first-line intervention and that OA is a clinical, not radiological diagnosis. The Swedish OA registry contains data which measure compliance to the guidelines since 2008 [2].ObjectivesTo describe the trends over time from 2008 to 2021 for patients who have received first-line interventions for hip and knee OA in Sweden and adherence of the healthcare staff to the national guidelines.MethodsDescriptive registry-based study including patients with hip or knee OA who participated in first-line interventions including education and exercise. Data were extracted from the Swedish OA registry between January 1st, 2008, and December 31, 2021. The registry contains patient-reported outcomes and physiotherapist-reported outcomes. In this study the following physiotherapist-reported outcomes were described over time: radiological examination before first-line intervention, if the first-line intervention was given the first time the patient seek health care caused of OA, which explanation patients had been given about their disease, intake of painkillers before the start of first-line intervention and the percent who got supervised exercise >10 times according to the guidelines of OA in Sweden. The following patient-reported outcomes were described over time: mean BMI at the first visit, and mean age at the first visit. To be included in the study, participants had to meet the following criteria: i) clinical diagnosis of OA, with hip or knee OA as the most symptomatic joint, ii) provided 3-month follow-up.ResultsA total of 175 764 participants with hip or knee OA were included in the study.The trends from 2008-2021 showed that the proportion of patients who had a radiological examination before entering the first-line intervention decreased from 97 % to 65 % in men and from 95% to 62 % in women. The proportion of patients who get assess to first-line intervention the first time they seek for their symptoms increased from 4 % to 10 % both in men and women. People that get the correct information about OA increased from 15% to 40 %, and patients that get the explanation that OA was a tear and wear disease decreased from 30 % to 5%. The mean BMI (28) is unchanged over time. The mean age increased from 64 years to 67 years between 2008-2020 but decreased during the covid-19 pandemic to 64 years. The percentage that was given supervised exercise more than 10 times was constant between 2012-2020 at 30 % but decreased during the covid-19 pandemic to 20%.ConclusionThe results implicit that the implementation of a supported OA self-management program in Sweden has been successful and changed the care given to patients with OA in Sweden. However, the national guidelines for OA, have still not been fully implemented. We need to keep implementing the guidelines so all patients with OA get the first-line intervention at the right time.References[1]Anon. (2012). Nationella riktlinjer för rörelseorganens sjukdomar 2012 - stöd för styrning och ledning. Socialstyrelsen.[2]Thorstensson CA, Garellick G, Rystedt H, Dahlberg LE. Better Management of Patients with Osteoarthritis: Development and Nationwide Implementation of an Evidence-Based Supported Osteoarthritis Self-Management Programme. Musculoskeletal Care. 2015 Jun;13(2):67-75. doi: 10.1002/msc.1085. Epub 2014 Oct 24. PMID: 25345913.Acknowledgements:NIL.Disclosure of InterestsNone Declared.

THE PREVALENCE AND INCIDENCE OF PSORIASIS AND PSORIATIC ARTHRITIS IN ENGLAND FROM 2009-2019: AN OBSERVATIONAL STUDY USING PRIMARY CARE DATA

BackgroundPsoriasis (PsO) and psoriatic arthritis (PsA) can greatly impact quality of life and result in substantial personal and societal costs. Complete and up to date data on the prevalence and incidence of these conditions and whether these change over time and vary by age is important for healthcare service planning so that specialist care and funding can be appropriately allocated.ObjectivesTo determine the prevalence and incidence of PsO and PsA in males and females from 2009-2019 across all age groups in England.MethodsWe used Clinical Practice Research Datalink AURUM, a primary care electronic health record database, including 20% of the English population. The codes used to identify patients with PsO and PsA were selected by rheumatologists and dermatologists and cross-checked with published code lists from other studies to ensure inclusion of all relevant codes. All included patients must have data for at least 1 year before their diagnosis. The annual incidence and point prevalence were calculated from 2009-2019 and stratified by age/sex. The study period ended in 2019 to avoid COVID-19 pandemic affecting results.ResultsThe prevalence of PsO and PsA in males and females increased annually, peaking in 2019 (PsO males 2.41% [95% confidence interval (CI) 2.40, 2.42];PsO females 2.60% [95% CI 2.59-2.61];PsA males 0.20% [95% CI 0.20-0.20];PsA females 0.21% [95% CI 0.21- 0.22]), as illustrated in Table 1. In 2019, the prevalence of PsO and PsA was highest in the over 65 years age group;PsO 4.25% [95% CI 4.22-4.28] and PsA 0.38% [95% CI 0.37-0.38]. The annual incidence (per 100,000 person years) of PsO has gradually decreased in males (from 168 (164-171) in 2009 to 148 (145-151) in 2019) but in females it has been stable with a slight annual decrease (from 180 (177-184) in 2009 to 173 (170-176) in 2019). The annual incidence for PsA has increased in both males and females (13 (12-14) in 2009 and 15 (14-16) in 2019 for males and 12 (11-13) in 2009 and 18 (17-19) in 2019 for females).ConclusionThe increasing prevalence of PsO and PsA highlights the importance of organising healthcare services to meet this need, particularly in the elderly population.ReferencesNIL.Table 1.Prevalence of PsO and PsA from 2009-2019 in EnglandYear20092010201120122013201420152016201720182019Population (n)1073383110910802110318501118036711343299112249341137842211657996119336261223432512420998PsO (n)216841229106239819250667259988268032276804286499295712304568311104PsO prevalence (%, 95%CI)-Male1.98 (1.96-1.99)2.06 (2.05- 2.07)2.13 (2.12-2.14)2.19 (2.18-2.20)2.24 (2.23- 2.25)2.33 (2.32- 2.34)2.37 (2.36- 2.38)2.39 (2.38- 2.40)2.40 (2.39- 2.41)2.40 (2.39- 2.42)2.41 (2.40- 2.42)-Female2.07 (2.05- 2.08)2.14 (2.13- 2.16)2.22 (2.21- 2.23)2.29 (2.28- 2.31)2.35 (2.33- 2.36)2.45 (2.43- 2.46)2.50 (2.49- 2.51)2.53 (2.52- 2.54)2.56 (2.54- 2.57)2.58 (2.56- 2.59)2.60 (2.59- 2.61)PsO incidence (100,000 person years)-Male168 (164-171)158 (155- 162)161 (158-165)153 (150-157)161 (157- 164)156 (153- 159)155 (152- 159)154 (151- 157)153 (150-156)150 (147-153)148 (145-151)-Female180 (177-184)176 (172-179)181 (177-184)171 (167-174)175 (171-178)176 (172-180)179 (176-183)178 (174-181)177 (174-181)174 (170-177)173 (170-176)PsA (n)1444515443164681752218545196182072021994232572451425683PsA prevalence (%, 95%CI)-Male0.14 (0.14- 0.14)0.15 (0.14- 0.15)0.15 (0.15- 0.16)0.16 (0.16- 0.16)0.17 (0.16- 0.17)0.18 (0.17- 0.18)0.18 (0.18- 0.19)0.19 (0.18- 0.19)0.19 (0.19- 0.20)0.20 (0.19- 0.20)0.20 (0.20- 0.20)-Female0.13 (0.13- 0.13)0.14 (0.13- 0.14)0.15 (0.14- 0.15)0.15 (0.15- 0.16)0.16 (0.16- 0.16)0.17 (0.17- 0.18)0.18 (0.18- 0.18)0.19 (0.19- 0.19)0.20 (0.19- 0.20)0.20 (0.20- 0.21)0.21 (0.21- 0.22)PsA incidence (100,000 person years)-Male13 (12- 14)12 (11- 13)13 (12- 14)12 (11- 13)13 (12-14)14 (13- 15)14 (13- 15)14 (13-15)1514-16)14(13- 15)15 (14-16)-Female12 (11- 13)13 (12- 14)13 (12- 14)14 (13-15)14 (13-15)15 (14-16)17 (16- 18)16 (15- 17)17 (16- 18)18 (17-19)18 (17-19)Acknowledgements:NIL.Disclosure of InterestsArani Vivekanantham: None declared, Edward Burn: None dec ared, Marta Pineda-Moncusí: None declared, Sara Khalid Grant/research support from: SK has received research grant funding from the UKRI and Alan Turing Institute outside this work. SK's research group has received grant support from Amgen and UCB Biopharma., Daniel Prieto-Alhambra Grant/research support from: DPA's department has received grant/s from Amgen, Chiesi-Taylor, Lilly, Janssen, Novartis, and UCB Biopharma. His research group has received consultancy fees from Astra Zeneca and UCB Biopharma. Amgen, Astellas, Janssen, Synapse Management Partners and UCB Biopharma have funded or supported training programmes organised by DPA's department., Laura Coates Speakers bureau: LC has been paid as a speaker for AbbVie, Amgen, Biogen, Celgene, Eli Lilly, Galapagos, Gilead, Janssen, Medac, Novartis, Pfizer and UCB., Consultant of: LC has worked as a paid consultant for AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Gilead, Galapagos, Janssen, Novartis, Pfizer and UCB., Grant/research support from: LC has received grants/research support from AbbVie, Amgen, Celgene, Eli Lilly, Novartis and Pfizer.

SAFETY OUTCOMES IN PATIENTS (PTS) WITH RHEUMATOID ARTHRITIS (RA) TREATED WITH FILGOTINIB (FIL) IN FILOSOPHY: INTERIM RESULTS FROM A PROSPECTIVE OBSERVATIONAL STUDY

BackgroundConsideration is needed when using Janus kinase (JAK) inhibitors to treat RA in pts aged ≥65 years or those with cardiovascular (CV) risk factors. The JAK1 preferential inhibitor FIL was generally well tolerated in clinical trials[1];safety has not been determined in a real-world setting.ObjectivesTo report baseline characteristics and up to 6-month safety data from the first 480 pts treated with FIL in the FILOSOPHY study (NCT04871919), and in two mutually exclusive subgroups based on age and CV risk.MethodsFILOSOPHY is an ongoing, phase 4, non-interventional, European study of pts with RA who have been prescribed FIL for the first time and in accordance with the product label in daily practice. Baseline characteristics and the incidence of select adverse events (AEs) are assessed in pts aged ≥65 years and/or with ≥1 CV risk factor (Table 1), and in those aged <65 years with no CV risk factors.ResultsAs of the end of June 2022, 480 pts had been treated: 441 received FIL 200 mg and 39 received FIL 100 mg. Of the 480 pts, 148 (30.8%) were aged ≥65 years;332 (69.2%) were aged <65 years. In total, 86 (17.9%) were former smokers, 81 (16.9%) were current smokers and 203 (42.3%) were non-smokers (data were missing for 110 pts [22.9%]). In addition to smoking, the most frequent CV risk factors included a history of hypertension (32.3%), a history of dyslipidemia (10.2%) and a family history of myocardial infarction (8.5%;Table 1).23 pts (4.8%) discontinued treatment due to AEs. Of the 354 pts aged ≥65 years or with ≥1 CV risk factor, infections affected 64 pts (18.1%), 34 (9.6%) had COVID-19, 2 (0.6%) had herpes zoster, and cardiac disorders (angina pectoris, atrial fibrillation, palpitations and tachycardia) affected 5 pts (1.4%);no cases of malignancies were observed. In the subgroup aged <65 years and with no CV risk factors (n=126), infections occurred in 18 pts (14.3%) (9 [7.1%] had COVID-19;3 [2.4%] had herpes zoster) and malignancies (myeloproliferative neoplasm) affected 1 pt (0.8%);no pts had cardiac disorders. There were no cases of deep vein thrombosis or pulmonary embolism in either subgroup.ConclusionIn this interim analysis of FILOSOPHY, no unexpected safety signals emerged at up to 6 months. Although infections and cardiac disorders affected a numerically greater proportion of pts aged ≥65 years or with ≥1 CV risk vs those aged <65 years with no CV risk, longer follow-up on a broader cohort is necessary to further characterize the safety of FIL in different groups of pts with RA.Reference[1]Winthrop K, et al. Ann Rheum Dis 2022;81:184–92Table 1.Baseline characteristics and CV risk factorsBaseline demographics/CV risk factorsAll FIL-treated pts (N=480)≥65 years or with ≥1 CV risk factor (n=354)<65 years and no CV risk factor (n=126)*Female sex, n (%)351 (73.1)252 (71.2)99 (78.6)Age, years, mean (SD)57.6 (11.5)60.4 (10.8)49.6 (9.6)Rheumatoid factor positive, n (%)†228 (47.5)167 (47.2)61 (48.4)Anti-citrullinated protein antibody positive, n (%)‡243 (50.6)176 (49.7)67 (53. 2)Body mass index, kg/m2, mean (SD)27.6 (5.7) n=43728.0 (5.4) n=33126.3 (6.4) n=106RA disease duration, years, mean (SD)10.4 (9.4) n=47810.5 (9.5) n=35310.0 (8.8) n=125Tender joint count 28, mean (SD)8.6 (6.9) n=4578.7 (7.1) n=3408.3 (6.3) n=117Swollen joint count 28, mean (SD)5.6 (5.2) n=4525.7 (5.4) n=3365.4 (4.4) n=116Former smoker, n (%)§86 (17.9)86 (24.3)0Current smoker, n (%)§81 (16.9)81 (22.9)0Non-smoker, n (%)§203 (42.3)130 (36.7)73 (57.9)Family history of myocardial infarction, n (%)41 (8.5)41 (11.6)0Medical history of: n (%) CV disease33 (6.9)33 (9.3)0 Diabetes35 (7.3)35 (9.9)0 Dyslipidemia49 (10.2)49 (13.8)0 Hypertension155 (32.3)155 (43.8)0 Ischemic CNS  vascular disorders11 (2.3)11 (3.1)0 Peripheral vascular disease17 (3.5)17 (4.8)0*Includes 53 pts with missing smoking status data who were aged <65 years with no other CV risk factors.†Missing/unknown in 154 pts;‡Missing in 153 pts;§Smoking status data missing in 110 pts (22.9%).AcknowledgementsWe thank the physicia s and patients who participated in this study. The study was funded by Galapagos NV, Mechelen, Belgium. Publication coordination was provided by Fabien Debailleul, PhD, of Galapagos NV. Medical writing support was provided by Debbie Sherwood, BSc, CMPP (Aspire Scientific, Bollington, UK), and funded by Galapagos NV.Disclosure of InterestsPatrick Verschueren Speakers bureau: AbbVie, Eli Lilly, Galapagos, Roularta, Consultant of: Celltrion, Eli Lilly, Galapagos, Gilead, Nordic Pharma, Sidekick Health, Grant/research support from: Galapagos, Pfizer, Jérôme Avouac Speakers bureau: AbbVie, AstraZeneca, BMS, Eli Lilly, Galapagos, MSD, Novartis, Pfizer, Sandoz, Sanofi, Consultant of: AbbVie, Fresenius Kabi, Galapagos, Sanofi, Grant/research support from: BMS, Fresenius Kabi, Novartis, Pfizer, Karen Bevers Grant/research support from: Galapagos, Susana Romero-Yuste Speakers bureau: AbbVie, Biogen, BMS, Lilly, Pfizer, Consultant of: Sanofi, Lilly, Grant/research support from: Lilly, MSD, Roberto Caporali Speakers bureau: AbbVie, Amgen, BMS, Celltrion, Eli Lilly, Galapagos, Janssen, MSD, Novartis, Pfizer, Sandoz, UCB, Consultant of: AbbVie, Amgen, BMS, Celltrion, Eli Lilly, Fresenius Kabi, Galapagos, Janssen, MSD, Novartis, Pfizer, Roche, Sandoz, UCB, Thomas Debray Consultant of: Biogen, Galapagos, Gilead, Francesco De Leonardis Employee of: Galapagos, James Galloway Speakers bureau: AbbVie, Biogen, Eli Lilly, Galapagos, Gilead, Janssen, Novartis, Pfizer, Roche, UCB, Consultant of: AbbVie, Eli Lilly, Galapagos, Gilead, Janssen, Novartis, Pfizer, Grant/research support from: AstraZeneca, Celgene, Gilead, Janssen, Medicago, Novavax, Pfizer, Monia Zignani Shareholder of: Galapagos, Employee of: Galapagos, Gerd Rüdiger Burmester Speakers bureau: AbbVie, Amgen, BMS, Chugai, Galapagos, Lilly, Pfizer, Sanofi, Consultant of: AbbVie, Amgen, BMS, Galapagos, Lilly, Pfizer, Sanofi.

COMPARATIVE DISEASE BURDEN IN PATIENTS WITH RHEUMATOID ARTHRITIS, PSORIATIC ARTHRITIS OR ANKYLOSING SPONDYLITIS: DATA FROM COVAD PATIENT-REPORTED E-SURVEY

BackgroundRheumatoid arthritis (RA) and spondyloarthritis, including either Psoriatic Arthritis (PsA) and Ankylosing Spondylitis (AS), are some of the most diagnosed autoimmune rheumatic diseases (AIRDs) in rheumatologists' routine clinical practice [1]. Understanding patients' health and functional status is crucial to provide personalized management strategies to optimize disease control and enhance the quality of life.ObjectivesWe aimed to compare disease burden in patients with RA, PsA or AS by assessing Patient-Reported Outcome Measurement Information System (PROMIS) Physical Health, Global Mental Health, Physical Function and Fatigue 4a together with VAS Pain.MethodsData were obtained in the international COVID vaccination in autoimmune rheumatic diseases study second e-survey (COVAD study). Demographics, AIRD diagnosis, disease activity, PROMIS Global Physical health, PROMIS Global Mental Health, PROMIS Physical Function SF10 and PROMIS Fatigue 4a score were extracted from the COVAD study database. For this study, we only included patients with self-reported RA or spondyloarthritis (either PsA or AS) undergoing active treatment with conventional synthetic disease-modifying drugs (DMARDs) and/or biologic DMARDs, who answered all the survey questions. Active disease was defined as the patient's perception of their disease as active in the four weeks before their first COVID-19 vaccine shot. Analysis of Variance with Bartlett's and Tukey's test was used to compare continuous variables between groups.ResultsFrom January to June 2022, n.1907 patients with RA, female 87.62% (1671/1907), with mean age (±SD) 50.95 ±13.67, n.311 patients with PsA, female 67.20% (209/311), with a mean age of 50.42 ±12.70, and n.336 patients with AS, male 51.31% (209/311), with a mean age of 43.13 ±12.75 years, responded to the COVAD e-survey.In those with active disease, neither physical health, global mental health, physical function, fatigue, nor pain were different among groups (Table 1, Figure 1). Patients with inactive AS had higher mean global physical health scores than RA patients (13.13 ±2.93 VS RA 12.48 ±2.90, p=0.01, Table 1). Those with inactive RA or PsA showed more severe fatigue (PsA 10.58 ±2.22, RA 10.45 ±4.08 VS 9.4 ±4.13, p =0.01 for both). Patients with inactive RA also reported poorer physical function and more residual pain than those with AS (37.79 ±8.86 VS 41.13 ±7.79, p<0.001;3.87 ±2.45 VS 3.34 ±2.39, p=0.01, respectively). Similarly, residual pain was perceived as higher in patients with inactive PsA than those with AS (4.04 ±2.50 VS 3.34 ±2.39, p=0.01)ConclusionDisease burden is roughly comparable in patients with active RA, PsA or AS. Patients with inactive RA and PsA suffer higher disease burden than those with inactive AS.Reference[1]Mease PJ, Liu M, Rebello S, Kang H, Yi E, Park Y, Greenberg JD. Comparative Disease Burden in Patients with Rheumatoid Arthritis, Psoriatic Arthritis, or Axial Spondyloarthritis: Data from Two Corrona Registries. Rheumatol Ther. 2019 Dec;6(4):529-542.Table 1.Patient-Reported Outcome Measures between groups.Inactive diseaseAS (n.185)PsA (n.179)RA (n.1167)MeanSDMeanSDMeanSDPROMIS Global Physical Health13.13*2.9512.433.2712.482.90p=0.01, VS RAPROMIS Global Mental Health13.313.3612.973.3312.843.17PROMIS Fatigue 4a9.44.1310.58*4.2210.45*4.08p=0.01, bothPROMIS Physical Function SF10 Score41.137.3939.279.0137.79*8.86p<0.001, VS ASVAS Pain3.342.394.04*2.503.87*2.45p=0.01, bothActive DiseaseAS (n.35)PsA (n.38)RA (n.189)MeanSDMeanSDMeanSDPROMIS Global Physical Health11.053.1910.102.7611.243.41PROMIS Global Mental Health11.313.2610.843.6311.893.30PROMIS Fatigue 4a12.944.8712.844.4211.754.68PROMIS Physical Function SF10 Score35.829.6233.528.7634.909.80VAS Pain4.682.775.02.544.682.61Figure 1.Violin plots showing kernel densities, quartiles and median for Patient-Reported Outcome Measures for patients with RA, PsA and AS, stratified by disease activity status.[Figure omitted. See PDF]Acknowledgements:NIL.Disclosure of InterestsVincenzo Venerito: None declared, Marc Fornaro: None declared, Florenzo Iannone: None declared, Lorenzo Cavagna: None declared, Masataka Kuwana: None declared, Vishwesh Agarwal: None declared, Naveen Ravichandran: None declared, Jessica Day Grant/research support from: JD has received research funding from CSL Limited., Mrudula Joshi: None declared, Sreoshy Saha: None declared, Syahrul Sazliyana Shaharir: None declared, Wanruchada Katchamart: None declared, Phonpen Akarawatcharangura Goo: None declared, Lisa Traboco: None declared, Yi-Ming Chen: None declared, Parikshit Sen: None declared, James B. Lilleker Speakers bureau: JBL has received speaker honoraria/participated in advisory boards for Sanofi Genzyme, Roche, and Biogen. None is related to this manuscript., Consultant of: JBL has received speaker honoraria/participated in advisory boards for Sanofi Genzyme, Roche, and Biogen. None is related to this manuscript., Arvind Nune: None declared, John Pauling: None declared, Chris Wincup: None declared, Ai Lyn Tan Speakers bureau: ALT has received honoraria for advisory boards and speaking for Abbvie, Gilead, Janssen, Lilly, Novartis, Pfizer, and UCB., Nelly Ziade Speakers bureau: NZ has received speaker fees, advisory board fees, and research grants from Pfizer, Roche, Abbvie, Eli Lilly, NewBridge, Sanofi-Aventis, Boehringer Ingelheim, Janssen, and Pierre Fabre;none are related to this manuscript, Grant/research support from: NZ has received speaker fees, advisory board fees, and research grants from Pfizer, Roche, Abbvie, Eli Lilly, NewBridge, Sanofi-Aventis, Boehringer Ingelheim, Janssen, and Pierre Fabre;none are related to this manuscript, Marcin Milchert: None declared, Abraham Edgar Gracia-Ramos: None declared, Carlo Vinicio Caballero: None declared, COVAD Study: None declared, Vikas Agarwal: None declared, Rohit Aggarwal Speakers bureau: RA has a consultancy relationship with and/or has received research funding from the following companies: Bristol Myers-Squibb, Pfizer, Genentech, Octapharma, CSL Behring, Mallinckrodt, AstraZeneca, Corbus, Kezar, Abbvie, Janssen, Alexion, Argenx, Q32, EMD-Serono, Boehringer Ingelheim, and Roivant., Grant/research support from: RA has a consultancy relationship with and/or has received research funding from the following companies: Bristol Myers-Squibb, Pfizer, Genentech, Octapharma, CSL Behring, Mallinckrodt, AstraZeneca, Corbus, Kezar, Abbvie, Janssen, Alexion, Argenx, Q32, EMD-Serono, Boehringer Ingelheim, and Roivant., Latika Gupta: None declared.

PLACEBO-CONTROLLED EFFICACY AND SAFETY OF UPADACITINIB THROUGH ONE YEAR IN PATIENTS WITH NON-RADIOGRAPHIC AXIAL SPONDYLOARTHRITIS

BackgroundUpadacitinib (UPA), a Janus kinase inhibitor, was effective and well tolerated in patients (pts) with non-radiographic axial spondyloarthritis (nr-axSpA) through 14 weeks (wks) of treatment.[1]ObjectivesThis analysis assessed the efficacy and safety of UPA vs placebo (PBO) through 1 year.MethodsThe SELECT-AXIS 2 nr-axSpA study included a 52-wk randomized, double-blind, PBO-controlled period. Enrolled adults had a clinical diagnosis of active nr-axSpA fulfilling the 2009 ASAS classification criteria, objective signs of inflammation based on MRI sacroiliitis and/or elevated C-reactive protein, and an inadequate response to NSAIDs. One-third of pts had an inadequate response to biologic DMARDs. Pts were randomized 1:1 to UPA 15 mg once daily or PBO. Concomitant medications, including NSAIDs, had to be kept stable through wk 52. The study protocol outlined that pts who did not achieve ASAS20 at any two consecutive study visits between wks 24 to 52 should receive rescue therapy with NSAIDs, corticosteroids, conventional synthetic/biologic DMARDs, or analgesics. Cochran-Mantel-Haenszel (CMH) test with non-responder imputation incorporating multiple imputation (NRI-MI) was used to handle missing data and intercurrent events for binary efficacy endpoints. Mixed-effect model repeated measures (MMRM) was used to assess continuous efficacy endpoints. NRI was used for binary endpoints after rescue and as observed analysis excluding data after rescue for continuous endpoints. Treatment-emergent adverse events (TEAEs) are reported through wk 52.ResultsOf the 314 pts randomized, 259 (82%;UPA, n=130;PBO, n=129) completed wk 52 on study drug. More pts achieved an ASAS40 response with UPA vs PBO from wks 14 to 52 with a 20% treatment difference at wk 52 (63% vs 43%;nominal P <.001;Figure 1). The proportion of pts achieving ASDAS inactive disease with UPA remained higher than PBO at wk 52 (33% vs 11%;nominal P <.0001;Figure 1). Consistent improvements and maintenance of efficacy were also seen across other disease activity measures. Between wks 24 and 52, fewer pts on UPA (9%) than PBO (17%) received rescue therapy. A similar proportion of pts in each treatment group had a TEAE (Table 1). Infections were the most common TEAE;the rates of serious infections and herpes zoster were higher with UPA vs PBO, although no new serious infections were reported from wks 14 to 52. COVID-19 events were balanced between treatment groups. No opportunistic infections, malignancy excluding non-melanoma skin cancer, adjudicated major adverse cardiovascular events, inflammatory bowel disease, or deaths were reported. Two pts (1.3%) on PBO had adjudicated venous thromboembolic events.ConclusionUPA showed consistent improvement and maintenance of efficacy vs PBO through 1 year across multiple disease activity measures. No new safety risks were identified with longer-term UPA exposure. These results continue to support the benefit of UPA in pts with active nr-axSpA.Reference[1]Deodhar A, et al. Lancet. 2022;400(10349):369–379.Table 1.Safety through week 52Event, n (%)PBO (n = 157)UPA 15 mg QD (n = 156)Any AE103 (66%)107 (69%)Serious AE6 (3.8%)6 (3.8%)AE leading to D/C4 (2.5%)6 (3.8%)COVID-19-related AE22 (14%)24 (15%)Deaths00Infection60 (38%)68 (44%) Serious infection1 (0.6%)2 (1.3%) Herpes zoster1 (0.6%)5 (3.2%)Malignancy other than NMSC00NMSC1 (0.6%)0Hepatic disorder7 (4.5%)6 (3.8%)Neutropenia1 (0.6%)8 (5.1%)MACE (adjudicated)00VTE (adjudicated)2 (1.3%)a0Uveitisb3 (1.9%)2 (1.3%)Inflammatory bowel disease00aBoth patients had non-serious events of deep vein thrombosis in the lower limb with risk factors including obesity and prior deep vein thrombosis in one patient and concomitant COVID-19 infection in the other patient.bThree events of uveitis occurred in each treatment group (among n = 3 patients in the PBO group and n = 2 patients in the UPA group);two events in the PBO group and one in the UPA group occurred in patients with a history of uveitis.AcknowledgementsAbbVie funded this study and participated in the study design, res arch, analysis, data collection, interpretation of data, review, and approval of the . All authors had access to relevant data and participated in the drafting, review, and approval of this publication. No honoraria or payments were made for authorship. Medical writing support was provided by Julia Zolotarjova, MSc, MWC, of AbbVie.Disclosure of InterestsFilip van den Bosch Speakers bureau: AbbVie, Amgen, Galapagos, Janssen, Lilly, Merck, MoonLake, Novartis, Pfizer, and UCB., Consultant of: AbbVie, Amgen, Galapagos, Janssen, Lilly, Merck, MoonLake, Novartis, Pfizer, and UCB., Atul Deodhar Consultant of: AbbVie, Amgen, Aurinia, BMS, Celgene, GSK, Janssen, Lilly, MoonLake, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie, Bristol Myers Squibb, Celgene, GSK, Lilly, Novartis, Pfizer, and UCB, Denis Poddubnyy Speakers bureau: AbbVie, Biocad, BMS, Galapagos, Gilead, GlaxoSmithKline, Janssen, Lilly, MSD, Medscape, MoonLake, Novartis, Peervoice, Pfizer, Roche, Samsung Bioepis, and UCB, Consultant of: AbbVie, Biocad, BMS, Galapagos, Gilead, GlaxoSmithKline, Janssen, Lilly, MSD, Medscape, MoonLake, Novartis, Peervoice, Pfizer, Roche, Samsung Bioepis, and UCB, Grant/research support from: AbbVie, Lilly, MSD, Novartis, and Pfizer., Walter P Maksymowych Consultant of: AbbVie, BMS, Celgene, Galapagos, Gilead, Janssen, Lilly, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie, Novartis, Pfizer, and UCB, Employee of: Chief Medical Officer of CARE Arthritis Limited, Désirée van der Heijde Consultant of: AbbVie, Bayer, BMS, Cyxone, Eisai, Galapagos, Gilead, GSK, Janssen, Lilly, Novartis, Pfizer, and UCB, Employee of: Director of Imaging Rheumatology BV, Tae-Hwan Kim Speakers bureau: AbbVie, Celltrion, Kirin, Lilly, and Novartis., Mitsumasa Kishimoto Consultant of: AbbVie, Amgen, Asahi-Kasei Pharma, Astellas, Ayumi Pharma, BMS, Chugai, Daiichi Sankyo, Eisai, Gilead, Janssen, Lilly, Novartis, Ono Pharma, Pfizer, Tanabe-Mitsubishi, and UCB., Xenofon Baraliakos Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, and UCB, Consultant of: AbbVie, BMS, Chugai, MSD, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie and Novartis, Yuanyuan Duan Shareholder of: AbbVie, Employee of: AbbVie, Kristin D'Silva Shareholder of: AbbVie, Employee of: AbbVie, Peter Wung Shareholder of: AbbVie, Employee of: AbbVie, In-Ho Song Shareholder of: AbbVie, Employee of: AbbVie.

BIOLOGIC TREATMENT SUSPENSION AND ASSOCIATED FACTORS IN PATIENTS WITH RHEUMATIC DISEASES DURING THE COVID-19 PANDEMIC: DATA FROM MEXICAN ADVERSE REGISTRY (BIOBADAMEX)

BackgroundThe COVID-19 pandemic triggered serious challenges in the treatment of chronic diseases due to the lack of access to medical attention. Patients with rheumatic diseases (RD) must have adequate treatment compliance in order to reach and maintain remission or low activity of their diseases. Treatment suspension because of non-medical reasons might lead to disease activation and organ damage.ObjectivesIdentify the frequency of biologic treatment (bDMARD) suspension in patients with RD during the COVID-19 pandemic and determine the associated factors for suspension.MethodsIn this study we included all patients registered in the Mexican Biologics Adverse Events Registry (BIOBADAMEX), that started bDMARD before March 2019 and suspended treatment during the COVID-19 pandemic. We used descriptive statistic to analyze baseline characteristics and main treatment suspension causes. We used Chi[2] and Kruskal Wallis tests to analyze differences between groups.ResultsA total of 832 patients patients registered in BIOBADAMEX were included in this study, 143 (17%) suspended bDMARD during the COVID-19 pandemic. The main causes of suspension were inefficacy in 54 (38%) patients, followed by other motives in 49 (34%) patients from which 7 (5%) was loss of medical coverage. Adverse events and loss of patients to follow up were the motive in 16 (11%) and 15 (11%) patients respectively.When we compared the group that suspended bDMARD with the non-suspenders (Table 1), we found statistical differences in patient gender, with 125 (87%) female patients that suspended bDMARD, with a median age of 52 (42-60) years, and a treatment duration of 3.8 years.ConclusionIn our study we found that 17% of patients with RD suspended bDMARD treatment during the COVID-19 pandemic and that non-medical motives such as lack of patients follow up and loss of medical coverage due to unemployment were important motives. These results are related to the effect of the pandemic on other chronic diseases.Table 1.Patients baseline characteristicsPatients that did not suspended bDMARD during pandemic (n = 689)Patients that suspended bDMARD during pandemic (n = 143)pFemale gender, n(%)549 (79.7)125 (87.4)0.02Age, median (IQR)55 (45 – 63)52 (42 – 60)0.04Body mass index, median (IQR)26.4 (23 – 30.4)27.23 (24.2 – 30.46)0.13Social security, n(%)589 (85.5)128 (89.5)0.2Diagnosis0.7- Rheumatoid arthritis444 (64.4)97 (67.8)- Juvenil idiopathic athritis29 (4.2)2 (1.4)- Ankyosing sponylitis93 (13.5)19 (13.3)- Psoriasic arthritis43 (6.2)6 (4.2)- Systemic lupus erithematosus32 (4.6)9 (6.3)- Others48 (6.9)10 (6.9)Disease duration, median (IQR)11 (7 – 19.5)12 (6 - 18)0.95Comorbidities, n(%)305 (44.3)73 (51)0.08Previos biologic, n(%)249 (36.1)60 (42)0.1Treatment at pandemic iniciation, n(%)0.8 - Etanercept a34 (4.9)5 (3.5)- Infliximab a24 (3.5)5 (3.5)- Adalimumab130 (18.9)22 (15.4)- Rituximab a61 (8.9)25 (17.5)- Abatacept76 (11)20 (14)- Tocilizumab82 (11.9)18 (12.6)- Certolizumab92 (13.4)28 (19.6)- Rituximab b7 (1)0- Golimumab36 (5.2)5 (3.5)- Tofacitinib14 (2)1 (0.7)- Infliximab b4 (0.5)2 (1.4)- Etanercept b31 (4.5)6 (4.2)- Baricitinib12 (1.7)1 (0.7)- Belimumab5 (0.7)1 (0.7)- Secukinumb8 (1.2)3 (2.1)Steroids use, n(%):254 (36.9)57 (39.9)0.2Steroids dose (mg), median (IQR)6 (5 – 10)6 (5 – 10)0.47DMARD use, n(%):538 (78.1)118 (82.5)0.1Treatment duration, median (IQR)5.06 (4.04 – 5.78)3.82 (3.35 – 4.95)0.001Suspension motive, n(%)NA- Inefficacy-54 (37.8)- Adverse event-16 (11.2)- Pregnancy-2 (1.4)- Loss of patient-15 (10.5)- Remission-7 (4.9)- Others-49 (34.2)Adverse events, n(%):102 (14.8)24 (16.8)0.3- Severe, n(%)13 (1.9)5 (3.5)0.4a original, b biosimilarREFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsVijaya Rivera Teran: None declared, Daniel Xavier Xibille Friedmann: None declared, David Vega-Morales: None declared, Sandra Sicsik: None declared, Angel Castillo Ortiz: None declared, Fedra Irazoque-Palazuelos: None declared, Dafhne Miranda: None declared, Iris Jazmin Colunga-Pedraza: None declared, Julio Cesar Casasola: None declared, Omar Elo Muñoz-Monroy: None declared, Sandra Carrilo: None declared, Angélica Peña: None declared, Sergio Duran Barragan: None declared, Luis Francisco Valdés Corona: None declared, Estefanía Torres Valdéz: None declared, Azucena Ramos: None declared, Aleni Paz: None declared, ERICK ADRIAN ZAMORA-TEHOZOL: None declared, Deshire Alpizar-Rodriguez Employee of: Scientific Advisor in GSK México.

ANTI-TNF TREATMENT MODIFIES PAIN MODULATION DESCENDING PATHWAYS. A PROSPECTIVE, 6 MONTHS STUDY IN ACTIVE CHRONIC INFLAMMATORY RHEUMATISM PATIENTS' NAÏVE OF BDMARD

BackgroundIn rheumatoid arthritis (RA) and spondyloarthritis (Spa), persistent pain remains challenging. In active disease, diffuse noxious inhibitory controls (assessed through conditioned pain modulation (CPM)) are impaired [1]. Little is known regarding impairment of pain pathways in patients under bMDARD.ObjectivesThe main objective of the RAPID (Rheumatism Pain Inhibitory Descending pathways) study, was to assess descending pain modulation (through CPM paradigm) in patients with active RA or Spa, after introduction of first bDMARD with anti-TNF.MethodsWe included 50 RA and 50 Spa patients with active disease, naïve of bDMARD. We assessed clinical disease variables for patients, together with responses to various psychological questionnaires. All participants underwent QST with the determination of heat and cold pain thresholds (HPT-CPT) on dominant forearm and CPM. CPM paradigm require a conditioning stimulus, here applied to the non-dominant foot (cold circulating bath at 8°C during 1min). Descending pain control was assessed as the change in HPT (in °C) following the conditioning stimulus: the higher the CPM effect, the more efficient the inhibitory control. Patients were followed at 3 and 6 months after TNF inhibitor initiation. At both follow-up visits, clinical monitoring of the rheumatism and repeated thermal QST and CPM.ResultsOne hundred patients were included, 59 women, mean age 45.8 (± 14.6) and mean disease duration 7.93 (± 7.96) years. Due to COVID surge 87 patients initiated an anti-TNF, 74 patients completed the follow-up. At 6 months, 40 patients achieved a good therapeutic response (good EULAR response or ASDAS major improvement), 19 patients had a moderate therapeutic response (moderate EULAR response or clinically important improvement) and 15 patients had no therapeutic response. At the end of follow-up, 51 patients were in remission or low disease activity and 47 patients had a pain intensity <4/10. Thermal pain thresholds did not significantly change during follow-up. Mean HPT was at beaseline 42.35°C (+/- 3.68) and at 6 months 42.17°C (+/- 3.67). Mean CPT was at baseline 13.11°C (+/- 10.04) and at 6 months 12.86°C (+/- 9.45). Conditioned pain modulation was significantly changed during follow-up. Mean CPM effect was at baseline 0.25°C (±2.57), 2.64°C (±2.12) at 3 months and 2.96°C (±2.50) at 6 months. At the end of the 6 months follow-up, mean CPM effect was significantly higher in patients with residual mean pain intensity <4/10 compared to patients with persisting pain ≥ 4/10: 3,25°C (± 2,68) vs 2,47 (± 2,11) (p=0.04).ConclusionAfter TNF inhibitor initiation in active RA or SpA, impaired diffuse noxious inhibitory controls are significantly improved. Apart from their articular efficacy, TNF inhibitor have an action on the central nervous system and pain modulation pathways. In patients with persisting pain under bDMARD, diffuse noxious inhibitory controls are not as efficient as patient without residual pain.Reference[1]Trouvin AP, Simunek A, Coste J, Medkour T, Carvès S, Bouhassira D, Perrot S. Mechanisms of chronic pain in inflammatory rheumatism: the role of descending modulation. Pain. 2022 Aug 3. doi: 10.1097/j.pain.0000000000002745.Figure 1.Acknowledgements:NIL.Disclosure of InterestsNone Declared.

AVASCULAR NECROSIS OF THE FEMORAL HEAD – NOT TO BE OVERLOOKED SEQUELA AFTER COVID 19 INFECTION

BackgroundCOVID 19 infection could lead to different sequelae in survivors, known as post-COVID or long COVID 19 syndromes. Some of them are thought to be due to the thrombophylic changes observed in COVID 19 infection, but some are thought to be caused by the administrated (especially high dose) corticosteroid treatment. Avascular necrosis of the femoral head (AVNFH) is a multifactorial disease which leads to compromised vascular supply, ischemia and finally necrosis of the femoral head. As corticosteroids usage and thrombophylic states are among the main known risk factors for the development AVNFH [1], it could be presumed that the frequency of this disease will increase with the COVID 19 pandemic. The exact corticosteroid dose needed for the development of AVNFH is not clear, but it has been stated that a higher daily dose and a larger total cumulative dose increase substantially the risk for the development of osteonecrosis [2].ObjectivesTo describe in detail the characteristics of AVNFH diagnosed in patients after COVID 19 infection.MethodsThe study was done in a tertiary university rheumatological clinic. Data was extracted from the records of patients who have been referred to the clinic because of hip pain between June and December 2022. Inclusion criteria were: - a new onset of uni-or bilateral hip pain that started after a documented COVID 19 infection;and an MRI scan of the hip joints showing osteonecrosis of one or both femoral heads. Exclusion criteria were the presence of hip pain prior to the COVID 19 infection, anamnesis of traumatic injuries of the hips or pelvis, personal history of hypercoagulable states.ResultsNine patients (4 women and 5 men) with an average age 59.1 years (range 38-72) were included in the study. Four patients had been diagnosed with bilateral and five – with unilateral AVNFH, thus 13 hip joints were analysed in total (8 left and 5 right sided). The mean time lap between the COVID 19 infection and the start of the hip pain was 26.2 weeks (range 10-48 weeks). All patients had limited and painful movement in their symptomatic hip(s), especially internal rotation and four of the patients had also elevated CRP levels (mean 11.7 mg/L). The stage of the AVNFH was evaluated according to the Ficat-Arlet classification (0-IV stage). In four hips the AVNFH was stage I, five hips were classified as stage II and the remaining four joints - as stage III. All symptomatic hip joints exhibited effusion/synovitis on both ultrasound examination and the corresponding MRI scan. It should be noted that the presence of hip effusion was found to be related with a worse prognosis in AVNFH [1]. In three patients the amount of the effusion required arthrocentesis and fluid aspiration. The analysis of the joint fluid was consistent with a degenerative disease (i.e., low WBC count with predominant lymphocytes and no crystals). All patients included in our study had received corticosteroids during their COVID19 infection, while 6 of the patients had also been hospitalized due to more severe disease. According to the patients' documentation, the mean cumulative dose of the received corticosteroids was 936.2 mg prednisolone equivalent per patient (range 187-2272 mg).ConclusionAVNFH must not be overlooked in a new onset hip pain after COVID 19 infection. Our results show that corticosteroids administrated during the infection and the presence of hip joint effusion on ultrasound are especially suggestive for the development of osteonecrosis, as they were registered in all of our patients. The presence of these two factors necessitates patient referral for an MRI scan of the hips, in order that AVNFH be detected timely.References[1]Petek D, Hannouche D, Suva D. Osteonecrosis of the femoral head: pathophysiology and current concepts of treatment. EFORT Open Rev. 2019 Mar 15;4(3):85-97.[2]Kerachian MA, Séguin C, Harvey EJ. Glucocorticoids in osteonecrosis of the femoral head: a new understanding of the mechanisms of action. J Steroid Biochem Mol Biol. 2009 Apr;114(3-5):121-8.Acknowledgements:NIL.Disclosur of InterestsPLAMEN TODOROV Speakers bureau: speaker at national level for AbbVie, Novartis and UCB, Lily Mekenyan: None declared, Anastas Batalov Speakers bureau: Speaker at national level for AbbVie, Novartis, Pfizer, Stada, Elly Lilly.

COVID-19–RELATED ADVERSE EVENTS IN THE PHASE 3 POETYK TRIALS OF THE ALLOSTERIC TYROSINE KINASE 2 INHIBITOR, DEUCRAVACITINIB, IN PATIENTS WITH MODERATE TO SEVERE PLAQUE PSORIASIS

BackgroundDeucravacitinib is a first-in-class, oral, selective, allosteric tyrosine kinase 2 (TYK2) inhibitor approved in multiple countries for the treatment of adults with plaque psoriasis. Deucravacitinib suppresses signaling of cytokines involved in the pathogenesis of immune-mediated diseases including psoriasis, psoriatic arthritis, and systemic lupus erythematosus. Deucravacitinib was efficacious compared with placebo in phase 2 trials in psoriatic arthritis and systemic lupus erythematosus.[1,2] In two phase 3 trials in patients with moderate to severe plaque psoriasis (POETYK PSO-1 [NCT03624127], PSO-2 [NCT03611751]), deucravacitinib showed superior efficacy versus placebo and apremilast.[3,4] Upon completion of either psoriasis trial, patients could enroll in the POETYK long-term extension (LTE) trial (NCT04036435).ObjectivesTo evaluate the incidence rate and severity of adverse events (AEs) due to COVID-19 with deucravacitinib treatment in the POETYK PSO-1 and POETYK PSO-2 trials and open-label POETYK LTE trial.MethodsIn PSO-1 (N=666) and PSO-2 (N=1020), adult patients with moderate to severe plaque psoriasis were randomized 2:1:1 to deucravacitinib 6 mg once daily, placebo, or apremilast 30 mg twice daily. At Week 16, placebo patients in both trials switched to deucravacitinib. Based on their Week 24 PASI response, apremilast patients continued with apremilast or switched to placebo or deucravacitinib. In PSO-1, patients randomized to deucravacitinib continued treatment for 52 weeks;in PSO-2, some patients randomized to deucravacitinib had a randomized treatment withdrawal period. At Week 52, patients could enroll in the open-label LTE and receive deucravacitinib. Incidence rates and severity of COVID-19–related AEs in the POETYK trials (n=1364;2076.7 person-years [PY] of follow-up) were compared with the Janssen/Johnson & Johnson COVID-19 vaccine trial placebo group (n=19,544;3096.1 PY of follow-up). This reference population was selected due to the study design and timing of the trial, which occurred when variants were in circulation.ResultsAs of October 1, 2021, 1519 patients received ≥1 dose of deucravacitinib over a 2-year follow-up period;1364 patients met criteria for this analysis, with deucravacitinib exposure since the pandemic onset (estimated to be January 1, 2020). In total, 153 deucravacitinib patients reported a COVID-19–related AE, for an overall exposure-adjusted incidence rate (EAIR) of 7.4/100 PY (95% CI, 6.2–8.6). Serious COVID-19–related AEs occurred in 43 patients (EAIR, 2.1/100 PY;95% CI, 1.5–2.8), including 30 with COVID-19 and 13 with COVID-19 pneumonia;this rate was within the margins of those for moderate to severe COVID-19 reported in the reference population (EAIR, 16.5/100 PY;95% CI, 15.0–17.9). Deaths due to COVID-19 occurred in 6 patients (EAIR, 0.3/100 PY;95% CI, 0.1–0.6), with the COVID-19–related mortality rate being consistent with the reference population (EAIR, 0.23/100 PY;95% CI, 0.1–0.5). Treatment was discontinued due to COVID-19 or COVID-19 pneumonia in 7 patients, including the 6 patients who died due to COVID-19.ConclusionCOVID-19 was among the most frequently reported AEs during the 2-year period of the pooled PSO-1, PSO-2, and LTE trials due to the temporal overlap of the pandemic with the trials. However, COVID-19 infection and death rates did not differ from the reference population;most infections were not serious and did not lead to treatment discontinuation. Based on this analysis, deucravacitinib did not appear to increase the risk of COVID-19 nor its progression to severe outcomes.References[1]Mease PJ, et al. Ann Rheum Dis. 2022;81:815-822.[2]Morand E, et al. Arthritis Rheumatol. 2022;Nov 11 (Epub ahead of print).[3]Armstrong A, et al. J Am Acad Dermatol. 2022;S0190-9622(22)02256-3.[4]Strober B, et al. J Am Acad Dermatol. 2022;S0190-9622(22)02643-3.AcknowledgementsThese clinical trials were sponsored by Bristol Myers Squibb.Disclosure of InterestsDiamant Thaçi Speakers bureau: AbbVie, Almirall, Amgen, Biogen Idec, Boeh inger Ingelheim, Bristol Myers Squibb, Eli Lilly, Galapagos, Galderma, Janssen-Cilag, Leo Pharma, Novartis, Pfizer, Regeneron, Roche, Sandoz-Hexal, Sanofi, Target Solution, and UCB, Consultant of: AbbVie, Almirall, Amgen, Biogen Idec, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, Galapagos, Galderma, Janssen-Cilag, Leo Pharma, Novartis, Pfizer, Regeneron, Roche, Sandoz-Hexal, Sanofi, Target Solution, and UCB, Grant/research support from: AbbVie, Almirall, Amgen, Biogen Idec, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, Galapagos, Galderma, Janssen-Cilag, Leo Pharma, Novartis, Pfizer, Regeneron, Roche, Sandoz-Hexal, Sanofi, Target Solution, and UCB, Kenneth B Gordon Consultant of: Amgen, Almirall, Dermira, Leo Pharma, Pfizer, and Sun Pharma, Grant/research support from: Amgen, Almirall, Dermira, Leo Pharma, Pfizer, and Sun Pharma, AbbVie, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Janssen, Novartis, and UCB, Melinda Gooderham Speakers bureau: Glenmark, Actelion, AbbVie, Galderma, Leo Pharma, Pfizer, and Regeneron, Amgen, Boehringer Ingelheim, Celgene, Eli Lilly, Janssen, Novartis, Sanofi Genzyme, and Valeant, Consultant of: Amgen, Boehringer Ingelheim, Celgene, Eli Lilly, Janssen, Novartis, Sanofi Genzyme, and Valeant, Andrew Alexis Speakers bureau: Pfizer, Regeneron, and Sanofi Genzyme, Consultant of: AbbVie, Allergan, Almirall, Amgen, Arcutis, AstraZeneca, Bausch Health, Beiersdorf, Bristol Myers Squibb, Dermavant, Galderma, Janssen, Leo Pharma, L'Oreal, Pfizer, Sanofi-Regeneron, Sol-Gel, UCB, Valeant, VisualDx, and Vyne, Grant/research support from: Almirall, Amgen, Arcutis, Bristol Myers Squibb, Cara, Galderma, Leo Pharma, Menlo, Novartis, and Valeant (Bausch Health), Varsha Lalchandani Shareholder of: Bristol Myers Squibb, Employee of: Bristol Myers Squibb, Julie Scotto Shareholder of: Bristol Myers Squibb, Employee of: Bristol Myers Squibb, Lauren Hippeli Shareholder of: Bristol Myers Squibb, Employee of: Bristol Myers Squibb, Matthew J Colombo Shareholder of: Bristol Myers Squibb, Employee of: Bristol Myers Squibb, Subhashis Banerjee Shareholder of: Bristol Myers Squibb, Employee of: Bristol Myers Squibb, Tamara Lezhava Shareholder of: Bristol Myers Squibb, Employee of: Bristol Myers Squibb, Mark Lebwohl Consultant of: Aditum Bio, Almirall, AltruBio, AnaptysBio, Arcutis, Arena, Aristea, Arrive Technologies, Avotres, BiomX, Boehringer Ingelheim, Brickell Biotech, Bristol Myers Squibb, Cara, Castle Biosciences, CorEvitas' (Corrona) Psoriasis Registry, Dermavant, Dr. Reddy's Laboratories, Evelo Biosciences, Evommune, Forte Biosciences, Helsinn Therapeutics, Hexima, Leo Pharma, Meiji Seika Pharma, Mindera, Pfizer, Seanergy, and Verrica, Grant/research support from: AbbVie, Amgen, Arcutis, Avotres, Boehringer Ingelheim, Dermavant, Eli Lilly, Incyte, Janssen, Ortho Dermatologics, Regeneron, and UCB.