ACR Open Rheumatology最新文献

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease. The complex relationships between race and ethnicity and social determinants of health (SDOH) in influencing SLE and its course are increasingly appreciated. Multiple SDOH have been strongly associated with lupus incidence and outcomes and contribute to health disparities in lupus. Measures of socioeconomic status, including economic instability, poverty, unemployment, and food insecurity, as well as features of the neighborhood and built environment, including lack of safe and affordable housing, crime, stress, racial segregation, and discrimination, are associated with race and ethnicity in the US and are risk factors for poor outcomes in lupus. In this scientific statement, we aimed to summarize current evidence on the role of SDOH in relation to racial and ethnic disparities in SLE and SLE outcomes, primarily as experienced in the U.S. Lupus Foundation of America's Health Disparities Advisory Panel, comprising 10 health disparity experts, including academic researchers and patients, who met 12 times over the course of 18 months in assembling and reviewing the data for this study. Sources included articles published from 2011 to 2023 in PubMed, Centers for Disease Control and Prevention data, and bibliographies and recommendations. Search terms included lupus, race, ethnicity, and SDOH domains. Data were extracted and synthesized into this scientific statement. Poorer neighborhoods correlate with increased damage, reduced care, and stress-induced lupus flares. Large disparities in health care affordability, accessibility, and acceptability exist in the US, varying by region, insurance status, and racial and minority groups. Preliminary interventions targeted social support, depression, and shared-decision-making, but more research and intervention implementation and evaluation are needed. Disparities in lupus across racial and ethnic groups in the US are driven by SDOH, some of which are more easily remediable than others. A multidimensional and multidisciplinary approach involving various stakeholder groups is needed to address these complex challenges, address these diminish disparities, and improve outcomes.

Objective: To investigate the clinical outcomes of patients with rheumatoid arthritis (RA) with COVID-19.

Methods: This retrospective study consisted of 361 patients with RA+ and 45,954 patients with RA- (March 2020 to August 2022) who tested positive for SARS-CoV-2 by polymerase-chain-reaction in the Montefiore Health System, which serves a large low-income, minority-predominant population in the Bronx and was an epicenter of the initial pandemic and subsequent surges. Primary outcomes were hospitalization, critical illness, and all-cause mortality associated with SARS-CoV-2 infection. Comparisons were made with and without adjustment for covariates, as well as with 1083 matched controls of patients with RA- and COVID-19.

Results: Patients with RA+ and COVID-19 were older (62.2 ± 23.5 vs. 45.5 ± 26.3; P < 0.001), were more likely females (83.1% vs. 55.8%; P < 0.001), were Black (35.5% vs. 30.3%; P < 0.05), and had higher rates of comorbidities (P < 0.05), hospitalization (52.4% vs. 32.5%; P < 0.005), critical illness (10.5% vs. 6.9%; P < 0.05), and mortality (11.1% vs. 6.2%; P < 0.01) compared with patients with RA- and COVID-19. Patients with RA+ with COVID-19 had higher odds of critical illness (adjusted odds ratio [aOR] = 1.46, 95% confidence interval [CI]: 1.09-1.93; P = 0.008) but no differences in hospitalization (aOR = 1.18 [95% CI: 0.93-1.49]; P = 0.16) and mortality (aOR = 1.34 [95% CI: 0.92-1.89]; P = 0.10) after adjusting for covariates. Odds ratio analysis identified age, hospitalization status, female sex, chronic kidney disease, chronic obstructive pulmonary disease, and Black race to be significant risk factors for COVID-19-related mortality. Pre-COVID-19 steroid and biologic therapy to treat RA were not significantly associated with worse outcomes (P > 0.05). Outcomes were not different between patients with RA+ and propensity-matched RA- controls (P > 0.05).

Conclusion: Our findings suggest that risk factors for adverse COVID-19 outcomes were not attributed to RA per se but rather age and preexisting medical conditions of patients with RA.

Objective: Understanding how medical cannabis (MC) use is integrated into medical practice for rheumatic disease management is essential. We characterized rationale for MC use, patient-physician interactions around MC, and MC use patterns among people with rheumatic conditions in the US and Canada.

Methods: We surveyed 3406 participants with rheumatic conditions in the US and Canada, with 1727 completing the survey (50.7% response rate). We assessed disclosure of MC use to health care providers, MC authorization by health care providers, and MC use patterns and investigated factors associated with MC disclosure to health care providers in the US versus Canada.

Results: Overall, 54.9% of US respondents and 78.0% of Canadians reported past or current MC use, typically because of inadequate symptom relief from other medications. Compared to those in Canada, fewer US participants obtained MC licenses, disclosed MC use to their health care providers, or asked advice on how to use MC (all P values <0.001). Overall, 47.4% of Canadian versus 28.2% of US participants rated their medical professionals as their most trusted information source. MC legality in state of residence was associated with 2.49 greater odds of disclosing MC use to health care providers (95% confidence interval: 1.49-4.16, P < 0.001) in the US, whereas there were no factors associated with MC disclosure in Canada. Our study is limited by our convenience sampling strategy and cross-sectional design.

Conclusion: Despite widespread availability, MC is poorly integrated into rheumatic disease care, with most patients self-directing use with minimal or no clinical oversight. Concerted efforts to integrate MC into education and clinical policy is critical.

Objective: To investigate whether digital activity fluorescence optical imaging (FOI) patterns of inflammation can identify distinct rheumatoid arthritis (RA) phenotypes.

Methods: The hands of newly diagnosed patients with RA were evaluated by clinical examination, musculoskeletal ultrasound, and FOI. Inflammation on FOI was defined when capillary leakage and/or fluorophore perfusion was present. The FOI composite image was quantified into a digital disease activity (DACT) score, using novel computerized algorithms. Unsupervised clustering on FOI inflammatory patterns was used to identify subgroups of patients relative to anticyclic citrullinated peptides (ACPA) and/or rheumatoid factor (RF).

Results: Of 1326 examined hand joints in 39 patients with RA (72% female; 56% ever-smokers; 54% RF positive and 69% ACPA positive), 400 (30%) showed inflammation by FOI, and 95% (37 of 39) of patients had DACT-FOI scores greater than 1. Unsupervised analysis on FOI patterns revealed two patient clusters, cluster 1 (n = 29) and cluster 2 (n = 10). The proportion of seropositive patients was significantly higher in cluster 1 versus cluster 2 (90%, 26 of 29 vs. 30%, 3 of 10; P < 0.01), whereas C-reactive-protein levels (minimum-maximum) were significantly higher in cluster 2 (20 mg/l [1-102]) versus cluster 1 (2 mg/l [0-119]; P = 0.01). A wider variety and proportion of inflamed joints emerged for patients with RA in cluster 2 versus cluster 1, in which inflammation was more concentrated around the wrists and the right metacarpophalangeal 2 (MCP2), bilateral MCP3, and, to a lesser degree, left MCP2 and proximal interphalangeal joint and tendon regions. Cluster 1 displayed lower mean (±SD) DACT scores compared with cluster 2 (3.6 ± 2.1 vs. 5.4 ± 2.1; P = 0.03).

Conclusion: FOI-based digital quantification of hand joint inflammation revealed two distinct RA subpopulations with and without ACPA and RF related autoantibodies.

Objective: To determine if the efficacy of biologics differ based on magnetic resonance imaging (MRI) and C-reactive protein (CRP) findings.

Methods: We compared four subgroups (MRI+/CRP+, MRI+/CRP-, MRI-/CRP+, MRI-/CRP-) from randomized controlled trials (RCTs). A comprehensive database search was performed to include axial spondylarthritis (axSpA; both radiographic axSpA [r-axSpA] and nonradiographic axSpA [nr-axSpA]) RCTs with treatment efficacy reported by different MRI and CRP subgroups. Study-specific disease activity scores (at 12-16 weeks) were pooled using a random-effects model and compared between the four subgroups.

Results: Five trials (all nr-axSpA) were included: three with tumor necrosis factor inhibitors (TNFi, N = 729) and two with interleukin-17 inhibitors (IL-17i, N = 794). TNFi and IL-17i showed efficacy based on the Assessment of Spondyloarthritis International Society 40 (ASAS40) and Bath Ankylosing Spondylitis Disease Activity Index 50 (BASDAI50) in all MRI and CRP subgroups, except the CRP-/MRI- subgroup, which had a single study with only 39 patients. There was no statistically significant difference between the four subgroups in terms of patients achieving ASAS40 (P = 0.60, I² = 0%) or BASDAI50 (P = 0.27, I² = 23.9%). The number needed to treat was three for the CRP+/MRI+ and CRP+/MRI- subgroups and six for the CRP-/MRI+ and CRP-/MRI- subgroups. All trials had a low risk of bias. Between-study heterogeneity was low to moderate. Sensitivity analyses comparing TNFi or IL-17i versus placebo similarly showed no difference between subgroups in terms of ASAS40 (TNFi, P = 0.57; IL-17i, P = 0.28) and BASDAI50 (TNFi, P = 0.37; IL-17i, P = 0.18).

Conclusion: In this systematic review, there was no statistically significant difference between the four subgroups in terms of efficacy based on ASAS40 or BASDAI50.

Objective: To evaluate gene expression in blood of patients with psoriatic arthritis (PsA) versus healthy controls and identify changes associated with guselkumab treatment.

Methods: Whole blood transcriptome profiling via paired-end RNA sequencing was conducted using samples from DISCOVER-1 and DISCOVER-2 at baseline (n = 673) and at weeks 4 and 24 from a representative subgroup that received placebo or guselkumab (n = 227 [longitudinal PsA cohort]). Baseline samples were compared with demographically matched healthy controls (n = 21). Guselkumab-mediated changes in gene expression were assessed in participants from the longitudinal PsA cohort who did versus did not achieve at least 20% improvement in American College of Rheumatology response criteria (ACR20) or at least 75% improvement in Psoriasis Area and Severity Index (PASI75). Differential gene expression was analyzed using edgeR.

Results: At baseline, 355 upregulated and 314 downregulated genes (PsA-associated genes) were identified in patients with PsA versus healthy controls. Upregulated genes were related to neutrophil, mononuclear cell, and CD11b+ gene sets. No cell type-specific gene sets were identified among downregulated genes. Most PsA-associated genes were modulated by guselkumab treatment. At week 24, genes downregulated by guselkumab were enriched with neutrophil, monocyte, eosinophil, and macrophage gene sets; genes upregulated by guselkumab were enriched with B cell, T cell, and natural killer cell gene sets. Reductions in expression of upregulated PsA-associated gene sets were more pronounced in ACR20 and PASI75 responders than in nonresponders.

Conclusion: These findings suggest a dysregulation of immune cell profiles in blood from patients in the baseline PsA cohort that approached levels in healthy controls after guselkumab treatment.

Objective: In a study of physical and cognitive functioning among predominantly Black individuals with systemic lupus erythematosus (SLE), we compared remotely administered physical and cognitive performance assessments to those collected in person.

Methods: A subset of participants who completed an in-person visit in our parent study from 2021 to 2022 (n = 30) were recruited to complete a second, remote visit within 28 days. Physical performance (measured by a modified Short Physical Performance Battery [SPPB]; range 0-12; subscale ranges 0-4; higher = better performance) and cognitive performance (episodic and working memory adjusted t-scores, measured using NIH Toolbox) were measured at both visits. Mean scores were compared using paired t-tests; intraclass correlation coefficients (ICCs) were obtained from two-way mixed effects models. Linear and logistic models were used to estimate stratified associations between performance measures and related outcomes.

Results: Participants were primarily female (93.3%) and Black (93.3%). In-person versus remote overall SPPB (8.76 vs. 9.43) and chair stand (1.43 vs. 1.90) scores were statistically significantly lower. t-Scores for episodic memory (47.27 vs. 49.53) and working memory (45.37 vs. 47.90) were lower for in-person versus remote visits. The ICC for overall SPPB indicated good agreement (0.76), whereas the ICCs for episodic (0.49) and working memory (0.57) indicated poor-moderate agreement. Associations between assessments of performance with related outcomes were similar and did not statistically significantly differ by modality of visit.

Conclusion: To possibly expand and diversify pools of participants in studies of physical and cognitive performance in SLE, remote administration of assessments should be considered for future research.