Objective Although both osteoarthritis (OA) and rheumatoid arthritis (RA) can necessitate total knee arthroplasty (TKA), their mechanisms and radiographic patterns of joint space narrowing (JSN) differ. Deep learning (DL) enables compartment-specific measurement of minimum joint space width (mJSW). This study compared JSN patterns between patients with RA and OA undergoing TKA and evaluated the associations between mJSW and RA disease activity. Methods In this retrospective study, 409 patients with RA undergoing TKA (2000-2021) were age- and sex-matched with OA patients. A validated DL model quantified medial and lateral mJSW from anteroposterior knee radiographs at 2 timepoints: early (> 2 years before TKA) and late (≤ 2 years before TKA). The rate of JSN was calculated in 302 patients with paired radiographs. Mixed-effects models adjusted for BMI and alignment. RA disease activity, serology, and medications were recorded. Results RA demonstrated narrower lateral mJSW than OA at the late timepoint (5.6 vs 7.0 mm; P < 0.001), with comparable medial values. RA exhibited uniform bicompartmental JSN, whereas OA showed medial narrowing. RA had a faster mean lateral ΔmJSW (0.11 mm/year; P = 0.01), whereas OA had a faster mean medial ΔmJSW (0.21 mm/year; P < 0.001). Longer RA duration and higher inflammatory markers were negatively associated with lateral mJSW. Seronegative patients showed faster lateral ΔmJSW in the surgical knee than seropositive patients (0.12 vs 0.06 mm/year; P = 0.03). Conclusion Patients with RA demonstrated diffuse, symmetric cartilage loss that contrasted with medial- predominant narrowing in patients with OA. Automated DL-based measurement enables scalable, compartment- specific assessment of joint degeneration patterns.

This article highlights Mayo Clinic's pioneering efforts to integrate artificial intelligence (AI) and machine learning into rheumatology, focusing on genomics, imaging, pathology, and clinical data science to improve diagnosis, treatment and operational efficiency. Key innovations include transformer-based models for genomic analysis, autonomous ultrasound devices, multimodal imaging solutions, and generative AI tools for clinical documentation and patient education, all aimed at bridging the gap between research and routine clinical care. The article emphasizes the need for rigorous validation, explainable AI, electronic health records integration, clinician training, and global collaboration to ensure safe and effective adoption of AI-powered tools in clinical practice.

OBJECTIVES:To compare the efficacy and safety of belimumab and anifrolumab in adult patients with SLE. METHODS:We conducted a systematic review and network meta-analysis (NMA) of randomized controlled trials (RCTs) in SLE. We included RCTs comparing belimumab or anifrolumab plus standard of care versus placebo plus standard of care. Outcomes included SRI-4, BICLA, selected BILAG organ-domain responses, and safety endpoints; belimumab BICLA data were derived from post hoc analyses. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated. Risk of bias was assessed with RoB 2; certainty in network estimates was evaluated using the GRADE approach as applied in the CINeMA framework. RESULTS:Eleven trials (n = 8607) were included (4 anifrolumab; 7 belimumab, including 2 safety-only trials). Both biologics were associated with higher odds of achieving an SRI-4 response than placebo: anifrolumab OR 1.78 (95% CI 1.41-2.24); belimumab OR 1.62 (95% CI 1.38-1.90), with no significant difference between active treatments. For BICLA, anifrolumab was superior to belimumab (OR 1.56, 95% CI 1.10-2.21). Mucocutaneous and musculoskeletal responses favored both biologics versus placebo, whereas renal and cardiovascular/respiratory effects were not statistically significantly different. In safety analyses, SAEs and serious infections were similar between biologics, whereas herpes zoster was higher with anifrolumab versus belimumab (OR 4.74, 95% CI 2.00-11.21). CONCLUSION:In this NMA, anifrolumab and belimumab achieved similar SRI-4 responses. Anifrolumab showed a higher BICLA response than belimumab, but this finding should be interpreted cautiously given reliance on indirect evidence and moderate certainty. Clinically, these data support individualized biologic selection, weighing potential benefit on BICLA against the consistently higher herpes zoster risk with anifrolumab.

INTRODUCTION/OBJECTIVES:We aimed to investigate associations between menopausal characteristics, including age at menopause and cause (natural vs. artificial), with long-term outcomes in women with rheumatoid arthritis (RA), incident Alzheimer's disease and related dementias (ADRD), RA severity, and overall mortality. We hypothesized that atypical menopausal characteristics increase ADRD risk and disease severity. METHODS:Women with incident RA in 1980-2014 who were ≥50 years of age at RA incidence were included. Menopause cause and age at menopause (categorized as <45, 45-54, ≥55 years) were abstracted from medical records. Associations between menopausal characteristics and ADRD, extra-articular manifestations (ExRA), erosions, cardiovascular events, and mortality were evaluated using Cox models. Associations with clinic visits for flares and remissions were assessed using mixed-effects models. Data were collected using the Rochester Epidemiology Project medical records-linkage system. RESULTS:Both early/premature and late menopause were associated with nonsignificant near two-fold increases in ADRD risk. In addition, early/premature (HR 2.40; 95% CI 1.15-5.01) and late menopause (HR 2.17; 95% CI 1.01-4.66) significantly increased severe ExRA risk. Menopausal characteristics were not associated with presence of erosions or mortality. Artificial menopause was associated with fewer cardiovascular events and fewer visits for RA remission. Early/premature menopause was associated with fewer remission visits (OR 0.50; 95% CI 0.29-0.87). CONCLUSION:Women with early/premature and late menopause had nonsignificant, increased risk of incident ADRD. Menopausal characteristics had significant associations with RA severity and cardiovascular events, and may be relevant contextual factors in long-term risk assessment for women with RA.

INTRODUCTION:Hematuria is a hallmark clinical manifestation of IgA nephropathy (IgAN) and largely reflects underlying glomerular inflammation. Despite this, current guidelines prioritize proteinuria and estimated glomerular filtration rate for risk assessment, and the association between urinary findings and underlying histologic lesions remains incompletely characterized. METHODS:Here, we conducted a multicenter retrospective cohort study of patients with biopsy-proven IgAN (July 2015-July 2025) with concurrent urinalysis. Associations between hemoglobinuria (dipstick), hematuria (microscopy), proteinuria and individual Oxford Classification MEST-C components, and composite inflammatory lesions (M1, E1, and/or C1/C2; and E1 and/or C1/C2) were evaluated using unadjusted cohort-specific logistic regression models. Pooled odds ratios (ORs) were estimated using random-effects meta-analysis. RESULTS:Among 441 patients, hemoglobinuria was associated with M1 lesions (pooled OR 1.77, 95% CI 1.25-2.51), E1 lesions (1.75, 1.44-2.11), and crescentic lesions (1.57, 1.20-2.07). Hematuria was also associated with M1 lesions (1.24, 1.14-1.35), E1 lesions (1.22, 1.13-1.31), and C1/C2 lesions (1.18, 1.09-1.28). For the composite outcome (M1, E1, and/or C1/C2), pooled ORs were 2.28 (1.76-2.97) for hemoglobinuria, 1.36 (1.22-1.51) for hematuria, and 1.20 (1.04-1.38) for proteinuria. Hemoglobinuria and hematuria were not associated with chronic lesions, whereas proteinuria was consistently associated with T1/T2 lesions (1.35, 1.20-1.52). CONCLUSIONS:Dipstick hemoglobinuria is associated with histologic markers of active disease in IgAN and may provide clinically relevant information to complement current assessment of disease activity in IgAN.

The underlying immunopathogenesis of inflammatory arthritis (IA) immune-related adverse event (irAE) remains obscure. Unlike rheumatoid arthritis (RA), where autoantibodies and B cell dysfunction are central features, the contribution of humoral immunity to IA-irAE is unclear. Here, we performed immunophenotyping of peripheral blood from patients with IA-irAE and compared them with patients with seronegative RA, immune checkpoint inhibition-treated patients without irAE, and healthy controls. IA-irAE was marked with increased cytotoxic gene expression and metabolic activation in T cells and reduced CXCR3 and CCR6 expression in CD4+ T cells. Contrary to seronegative RA, patients with IA-irAE displayed no substantial elevation in autoantibody levels or atypical CD11c+CD21- B cells. IA-irAE was further characterized by elevated levels of interleukin-6 (IL-6), IL-12, and type I interferon, which correlated with the T cell activation phenotypes. Together, our findings define IA-irAE as a disease with certain immunological features distinctive from RA, representing a potentially T cell-driven, autoantibody-independent autoimmunity. These results offer insights into immune tolerance breakdown and therapeutic targeting in irAEs.

Introduction:The aim of this study was to evaluate the prognostic value of the Mayo Clinic Chronicity Score (MCCS) compared with the National Institutes of Health (NIH) Chronicity Index (NIH-CI) in lupus nephritis (LN). Methods:We conducted a retrospective cohort study of 307 patients with biopsy-proven LN evaluated at Mayo Clinic (1992-2023). Chronic histologic injury was graded using the NIH-CI and MCCS. Outcomes were proteinuria remission < 500 mg/d (PR500), complete renal response (CRR), end-stage kidney disease (ESKD), and all-cause mortality. Sex-stratified, age-adjusted Cox models were used. Prognostic performance was evaluated using change in Harrell's C-index (ΔC over a clinical model) and decision-curve analysis was used to assess clinical utility for 5-year ESKD. Subgroup analyses were used to test for effect modification by baseline estimated glomerular filtration rate (eGFR) (< 60 vs. ≥ 60 ml/min per 1.73 m2) and histologic class (proliferative vs. nonproliferative). Results:Higher NIH-CI and MCCS scores were associated with lower likelihood of PR500 and CRR (hazard ratio [HR]: 0.75 for both) and greater risk of ESKD (HR: 1.40 for NIH-CI; 1.33 for MCCS). Adding either score to a clinical model improved discrimination for PR500 (C-index: 0.65 to 0.71), CRR (0.64 to 0.71), and ESKD (0.81 to 0.85), but not mortality (ΔC = 0.00). Decision-curve analysis showed similar net benefits for NIH-CI and MCCS. Interstitial fibrosis (IF) and tubular atrophy (TA) (IF/TA) were the only components independently predictive of renal outcomes. Our findings support applicability of both scores in nonproliferative LN and in patients with reduced baseline kidney function. Conclusion:The MCCS and NIH-CI provide comparable and additive prognostic information in LN. MCCS captured the chronic lesions most strongly associated with renal outcomes, with IF/TA as the principal determinant of prognosis.

Early and accurate diagnosis of Sjogren's syndrome (SjD) remains a significant challenge due to the disease's heterogeneous clinical presentation and the high dimensionality of transcriptomic data. Meta-heuristic optimizers are attractive for navigating such landscapes, yet existing algorithms tend either to over-explore or to converge prematurely. To address this, we propose DSMAL, a Differential-Evolution & Slime-Mould Algorithm with adaptive Refresh Local Search, as the first hybrid optimization framework tailored to SjD diagnostics. DSMAL partitions the population into two co-evolving sub-swarms: a Differential-Evolution (DE) cohort that drives broad exploration through differential mutation, and a Slime-Mould (SMA) cohort that intensifies exploitation via adaptive position updates. A novel Refresh Local Search (RLS) operator periodically re-diversifies both cohorts, mitigating stagnation without sacrificing convergence speed. For SjD diagnostics, DSMAL is integrated with an XGBoost classifier, forming the DSMAL-XGBoost model, which is trained and validated using gene expression profiles derived from three GEO datasets (GSE23117, GSE40611, and GSE84844). DSMAL optimizes XGBoost hyperparameters in a cross-validation loop to identify the most predictive feature set and classifier configuration. The final model is evaluated using an independent external test set (GSE7451) and demonstrates superior diagnostic performance, achieving 96.6% F1-score, 96.4% recall, 95.0% precision, and 97.6% AUC. Benchmark testing on the IEEE CEC 2021 suite further validates DSMAL's theoretical strengths, outperforming ten state-of-the-art optimizers in both accuracy and computational efficiency. These findings underscore the potential of DSMAL-XGBoost as a robust tool for transcriptomic-based SjD diagnosis, with broader implications for complex autoimmune disease modeling.

OBJECTIVE:We aim to identify risk factors to enable stratification of patients' susceptibility to inflammatory arthritis immune-related adverse events (IA-irAEs). This retrospective study mainly examines whether preexisting osteoarthritis (OA) increases the likelihood of de novo IA-irAEs. METHODS:The prevalence of OA among immune checkpoint inhibitor (ICI)-treated patients who developed IA-irAE, those who developed other types of irAEs but not IA (non-IA irAEs), and those who did not develop any irAEs (non-irAEs) were compared. Electronic medical records were reviewed to extract demographic, clinical, and laboratory data. Group comparisons and logistic regression analyses were performed. RESULTS:A total of 181 de novo IA-irAE patients, 140 non-IA irAE patients, and 170 non-irAE patients were included. The prevalence of OA was significantly higher in the IA-irAE group (69%) than in the non-IA irAE group (48%) and the non-irAE group (48%) (both P < 0.001). The IA-irAE group demonstrated a higher frequency of multisite OA, with more predominant hand involvement (62%) than the non-IA irAE with OA group (13%) and the non-irAE with OA group (13%) (both P < 0.001). A family history of autoimmune disease (AID) (odds ratio [OR] 2.03, 95% confidence interval [CI] 1.02-4.05), preexisting OA (OR 2.88, 95% CI 1.85-4.52), and melanoma (OR 2.63, 95% CI 1.56-4.47) were identified as risk factors for the development of IA-irAE. CONCLUSION:OA was more prevalent among ICI-treated patients developing IA-irAE than those who were not. Hand OA was the most common OA pattern in IA-irAE patients. Preexisting OA, melanoma, and a family history of AID were associated with IA-irAE.

BACKGROUND/OBJECTIVE:Dietary, supplement, and activity exposures have only been studied in spondyloarthritis (SpA) with retrospective studies. We aimed to determine the association of diet, supplements, and physical activity with incident SpA. PATIENTS AND METHODS:We performed a case-control study in the Mayo Clinic Biobank from 2009 through 2015, matching criteria-confirmed incident SpA cases to controls 1:5 on age, sex, recruitment year, and location. Questionnaires assessed 16 dietary, 29 supplement, and leisure-time/work activity exposures. Logistic regression models calculated adjusted odds ratios (aOR) with 95% CIs of SpA for each exposure, adjusting for covariates. Sensitivity analyses were conducted within HLA-B27-positive patients, and those with baseline questionnaires completed 5+ years before index. RESULTS:We identified 73 cases of incident SpA matched with 365 controls (mean age: 60, 70% females). No dietary or activity exposures were associated with SpA overall. However, among HLA-B27-positive individuals, non-diet soft drink consumption was associated with increased risk of SpA (aOR: 4.82, 95% CI: 1.29-18.1), whereas caffeinated coffee was associated with decreased risk (aOR: 0.20, 95% CI: 0.04-0.89). Zinc was associated with increased risk of SpA (aOR: 4.16, 95% CI: 1.19-14.6), as were B vitamins in the HLA-B27-positive subgroup (aOR: 4.21, 95% CI: 1.04-17.1). In the 5-year sensitivity analysis, low leisure-time physical activity plus high work physical activity was associated with increased risk of SpA (relative excess risk due to interaction: 0.50, 95% CI: 0.03-0.98). CONCLUSIONS:Due to small sample size and multiple comparisons, the risk factors we identified (non-diet soft drinks, B vitamins, and zinc) should be considered hypothesis-generating and warrant further investigation.

Objective The purpose of this study was to determine the cumulative incidence of diagnosis switching, drug-free remission, and initiation of a biologic or targeted synthetic disease-modifying antirheumatic drug (b/tsDMARD) in individuals with seronegative rheumatoid arthritis (RA).Methods Adult residents of Olmsted County, Minnesota, with incident seronegative (rheumatoid factor negative/anti-cyclic citrullinated peptide antibody negative) RA meeting the 1987 and/or 2010 American College of Rheumatology classification criteria were included. Data were collected from January 1, 2005, to December 31, 2023, through manual chart review. Drug-free remission was defined as a period of at least six months where the individual was no longer taking treatment for RA and did not have evidence of active inflammatory arthritis upon evaluation by a rheumatologist. We calculated the 10-year cumulative incidence of a change in diagnosis, adjusting for the competing risk of death, and of drug-free remission and initiation of a b/tsDMARD, adjusting for the competing risks of death or change in diagnosis.Results A total of 176 individuals with seronegative RA (68% women) were included. The 10-year cumulative incidence of a change in diagnosis was 12.8% (95% confidence interval [CI] 8.7%-18.9%). The most common change in diagnosis was to spondyloarthritis (4%). The 10-year cumulative incidence of drug-free remission and initiation of a b/tsDMARD was 26.6% (95% CI 20.7%-34.2%) and 19.9% (95% CI 14.7%-26.9%), respectively. Over a median follow-up of 11.8 years, 49 individuals entered drug-free remission.Conclusion After initial diagnosis of seronegative RA, about 13% of individuals had a change in diagnosis and a quarter experienced drug-free remission within 10 years.

Objective The objective of this study was to investigate the association between dual seropositive, single seropositive, and seronegative rheumatoid arthritis (RA) with radiographic erosions, disease flares, and death. Methods We performed a retrospective, population‐based study of residents in Southern Minnesota with incident RA who fulfilled criteria for RA in 2003 to 2019. Radiographic erosions and flares were evaluated within one year of incident RA. All‐cause mortality was obtained from medical records and death certificates. Cox models adjusted for age, sex, smoking status, year of incident RA, and comorbidities were used. Results The study included 1,373 patients with RA. At RA incidence, 37% were dual seropositive, 13% seropositive for anti–cyclic citrullinated protein (anti‐CCP) only, 12% seropositive for rheumatoid factor (RF) only, and 38% seronegative. The highest proportion of radiographic erosions before or within one year of RA incidence was in the dual seropositive (31%) and lowest in those seropositive for anti‐CCP only (13%). Flares occurred in 69% of the dual seropositive and 51% of the seropositive for anti‐CCP only within the first year of RA incidence. Those seropositive for RF only had over a two‐fold increase in mortality rates compared with the seronegatives (adjusted hazard ratio [aHR] 2.18, 95% confidence interval [CI] 1.47–3.24). In contrast, the dual seropositives had only a >50% increase in mortality rates (aHR 1.66, 95% CI 1.21–2.28), and those seropositive only for anti‐CCP had a >30% increase in mortality rates (aHR 1.32, 95% CI 0.83–2.11). Conclusion Patients with RA seropositive for RF only have an increase in mortality rates compared with patients who are dual seronegative. RF positivity could be an indicator of inflammation that requires pharmacologic treatment to decrease mortality rates.

OBJECTIVE:Epidemiologic estimates for age of systemic lupus erythematosus (SLE) diagnosis are limited, particularly for men and racial and ethnic subpopulations in the United States. Leveraging the Centers for Disease Control and Prevention (CDC) National Lupus Registry network of population-based SLE registries, meta-analyses were performed estimating age-specific incidence of SLE by sex, race, and ethnicity. METHODS:The CDC network of SLE registries includes five state-based registries, plus a sixth Indian Health Service registry. Incidence periods spanned calendar years 2002-2018. Registries provided age-specific incidence of SLE, fulfilling the American College of Rheumatology (ACR) SLE classification criteria, per 100,000 person-years, stratified by sex, race, and ethnicity for the meta-analyses. RESULTS:Incidence rates among women were highest for those aged 30-39 (12.7, 95%CI: 9.5-16.8), while rates among men were highest for those aged 60-69 (2.1, 95%CI: 1.3-3.4). Black women aged 20-39 had the highest SLE incidence rates (23.6, 95%CI: 20.7-26.8). Among women diagnosed with SLE before age 20, incidence was highest among Asian (6.5, 95%CI: 2.8-15.2) individuals. Among women diagnosed with SLE after age 60, incidence was highest among American Indian/Alaska Native (9.4, 95%CI: 3.4-15.4) individuals. Weighted percentages show 10.0% of those with SLE were diagnosed before age 20, while 15.1% were diagnosed after age 60. The largest proportion of individuals with SLE, 22.1%, were diagnosed between 30-39 years. CONCLUSIONS:This study provides comprehensive sex- and race-specific estimates of age at SLE diagnosis. The substantial later in life SLE incidence among men and disease burden in pediatric and older populations should raise awareness in considering SLE in the differential diagnosis in previously underrecognized groups.

Objective We aimed to identify the strongest individual gene-respiratory interactions for rheumatoid arthritis (RA) risk. Methods This case-control study used the Mayo Clinic (MC) and Mass General Brigham (MGB) biobanks for discovery and validation, respectively. We matched criteria-confirmed incident RA cases to four non-RA controls on age, sex, and duration electronic health record (EHR) history. Genetic exposures included known RA risk alleles. We identified respiratory diseases by codes and defined “respiratory burden” as the total number of respiratory codes divided by EHR duration before index date of RA. Using logistic regression models adjusting for potential confounders, we estimated odds ratios (OR) with 95% confidence intervals (CI) for the interactions between genetic and respiratory exposures for RA risk. Results We identified 1,125 incident RA cases and 4,495 non-RA controls (mean age 64 years, 70% female in MC; 54 years, 76% female in MGB). In MC, both interstitial lung disease (OR 1.55, 95% CI 1.00-2.40) and overall respiratory burden (OR 1.67, 95% CI 1.30-2.15) were associated with incident RA. Four novel gene-respiratory interactions validated in MGB including CD83/RNF182 (rs12530098)-acute pharyngitis for seronegative RA (OR 4.06 [95% CI 1.61-10.3] MC; 3.68 [95% CI 1.42-9.56] MGB) and JARID2 (rs113532504)-asthma for seropositive RA (OR 2.66 [95% CI 1.30-5.44] MC; 1.93 [95% CI 1.20-3.08] MGB). The CD83/RNF182-acute pharyngitis interaction exhibited the strongest dose-response association (OR 8.54 [95% CI 1.59-45.9] for highest respiratory burden). Conclusion This study identified novel respiratory risk factors and gene-respiratory endotypes for RA, which may be useful for RA prevention, diagnosis, and treatment.

Rheumatoid arthritis (RA) is associated with a wide spectrum of comorbidities that substantially influence quality of life and long-term outcomes. These include extra-articular manifestations, cardiovascular disease, cerebrovascular accidents, dementia, malignancy, infection, mental health disorders and osteoporosis. Patterns of comorbidity in RA have evolved over the past three decades, with declining prevalence of some complications alongside persistently high or increasing burdens of interstitial lung disease, anxiety and depression. Shifts in the comorbidity landscape probably reflect advances in RA management, including the expanded use of biologic and targeted synthetic disease-modifying antirheumatic drugs (DMARDs) and a widespread adoption of treat-to-target strategies. Consideration of comorbidity-specific epidemiology, the potential effect of DMARDs on comorbidity risk and opportunities to address both RA and comorbid disease are increasingly relevant in clinical care. Preventive strategies, including selected enhanced screening approaches such as those for cervical cancer, interstitial lung disease, cardiovascular disease and osteoporosis, form an important component of comprehensive RA management. Awareness of the changing comorbidity landscape could support more integrated and individualized care for people with RA.

PV252 / #394 Poster Topic:AS24 - SLE-Treatment We aimed to examine glucocorticoid (GC) use over 4 decades in a population-based incident cohort of patients with SLE. Residents of Olmsted County, MN, with incident SLE meeting the 2019 EULAR/ACR SLE classification criteria between 1976-2018 were included. Index date was defined as the date of criteria fulfillment. GC use (oral daily prednisone equivalents) was abstracted from the index date until death or last follow-up through 12/31/2023. Cumulative daily dose of GCs in the first year after SLE incidence was calculated. Logistic regression models of any GC use in the first year and linear regression models of log cumulative GC dose in the first year adjusted for age and sex were used to examine time trends. The study included 198 patients with SLE (mean age 44.4 [SD 17.8] years; 166 [84%] female) who were subdivided into 4 decades (1976-1988, 1989-1998, 1999-2008 and 2009-2018) for analysis (Table). Patients in the most recent decade were somewhat older at diagnosis, and the population became more diverse over time. DMARD use in the first year after SLE incidence became more common over time, and the proportion of patients initiating GC increased over time (age and sex-adjusted p=0.045) while the proportion of patients using pulse GC in the first year remained stable over time. The starting dose of oral GCs decreased over the first 3 decades but increased again in the most recent decade (p=0.040). Cumulative GC use in the first year decreased over time (age and sex-adjusted p=0.005). This association persisted after additional adjustment for DMARD use. Most of the decline in cumulative GC use occurred in the 2000s with very little improvement subsequently. Table. Demographic and clinical characteristics of the incident cohort of patients with systemic lupus erythematosus in 1976-2018. GC dosage at initiation had declined over time, but increased in the most recent decade, along with increases in the proportion of patients initiating GCs despite increased use of DMARDs. Cumulative GC use in the first year of SLE declined in the 2000s and has remained stable subsequently. These trends are mostly encouraging, but there is still room for more GC-sparing efforts in this population.

Objectives To examine associations between multimorbidity, the social determinants of health (SDoHs) and rheumatoid arthritis (RA) flare and remission.Methods All patients aged ≥18 years in Olmsted County, Minnesota, with incident RA in 1999–2014 were identified. Using a list of 55 chronic medical conditions, multimorbidity was defined as the presence of ≥2 conditions and substantial multimorbidity as ≥5 conditions. The Area Deprivation Index and Social Vulnerability Index (SVI) were used as proxies for adverse SDoH burden. Flare and remission were defined using Outcome Measures in Rheumatoid Arthritis Clinical Trials definitions. Mixed effects models were used to assess associations between flare/remission and multimorbidity, adverse SDoH burden and other patient characteristics.Results This study included 659 patients with incident RA. Multimorbidity and substantial multimorbidity predicted 29% (OR:1.29, 95% CI:1.04 to 1.59) and 26% (OR:1.26, 95% CI:1.03 to 1.53) higher odds of flare, respectively. Both were associated with 34% (OR:0.66, 95% CI:0.49 to 0.90) and 33% (OR:0.67, 95% CI:0.51 to 0.90) lower odds of remission, respectively. SVI predicted 8% lower odds of remission for every 0.1 increase above 0.3 (OR:0.92, 95% CI:0.85 to 0.99). Flare was also associated with female sex, smoking, younger age and shorter disease duration, but not seropositivity. Remission was also associated with male sex, never smoking, older age and longer disease duration, but not seropositivity.Conclusions Multimorbidity predicts higher odds of RA flare and lower odds of remission. Adverse SDoH burden predicts lower odds of remission. These findings have the potential to inform disease prognostication and clinician interventions.