The co-occurrence of axial spondyloarthritis (SpA) and rheumatoid arthritis (RA) is rarely reported and poses significant diagnostic and therapeutic challenges due to their distinct pathophysiological mechanisms. While tumor necrosis factor (TNF) inhibitors are effective for both conditions, optimal strategies for patients with inadequate response remain unclear. We report a 65-year-old male with a long-standing history of HLA-B27-positive ankylosing spondylitis (AS) with radiographic bamboo spine who subsequently developed seropositive RA. After 15 years of successful treatment with adalimumab, the patient developed peroneal tendonitis suggestive of active enthesitis, prompting a switch to bimekizumab, an IL-17A/F inhibitor. Although the tendonitis improved, the patient experienced a severe flare of peripheral polyarthritis within one year. Switching to a Janus kinase (JAK) inhibitor led to rapid improvement of both RA-related arthritis and AS manifestations. Our literature review identified a limited number of reported SpA-RA overlap cases treated with biologics or JAK inhibitors (n = 6). Together with our case, all patients had a history of treatment with TNF inhibitors. Among them, three achieved successful therapeutic responses, whereas the remaining four experienced primary or secondary treatment failure, respectively. Our case, together with one prior report, suggests that IL-17 inhibitors may be effective for SpA-related manifestations but insufficient for controlling RA-associated synovitis, even in cases of SpA-RA overlap. Although the number of reported cases remains limited, this case-based review suggests the different patterns of therapeutic response consistent with known differences in inflammatory pathways in SpA-RA overlap and underscores the importance of individualized therapeutic strategies integrating clinical phenotype and treatment response.

Idiopathic inflammatory myopathies (IIM) have historically been considered to cause painless muscle weakness. However, recent studies suggest that pain can be an important symptom for patients with IIM. This study aims to examine the discussions related to myositis and pain on Reddit to understand its frequency and impact. Reddit posts from Academic Torrents were searched for myositis-related terms using the Pushshift archive. A two-step cleaning process was used, including a large language model-based classification, to retain posts describing suspected or confirmed IIM. Posts were analyzed for pain descriptors and anatomical regions. A semantic network of the top 500 pain posts was built to map connections between descriptors, body regions and experiences. The dataset included 1,529 IIM-related Reddit posts written by 968 unique authors. Pain-related terms were present in 63.0% of the posts. Pain was described using qualifiers reflecting chronicity and severity, including "chronic", "constant" and "severe" pain. Muscle was the most frequently mentioned body region (18.5%) in pain-related posts. Semantic network analysis showed nine distinct communities, showing that pain-related discussions were closely integrated with core disease concepts such as myositis, muscle involvement, and weakness. Additional clusters reflected dermatomyositis-related skin features, sensory and neuropathic pain experiences, and comorbid autoimmune conditions. Pain is a common topic among people discussing myositis on Reddit. Results suggest pain as a prevalent symptom and highlight the need for more research to understand the pain to help provide more effective strategies for management.

Elastographic data regarding thyroid involvement in systemic sclerosis (SSc) are limited. This study aimed to evaluate thyroid parenchymal stiffness in patients with SSc using two-dimensional shear wave elastography (2D-SWE) and to investigate its relationship with clinical parameters. This single-center, cross-sectional case-control study included 36 SSc patients and 36 age- and gender-matched healthy controls. All participants underwent thyroid ultrasonography and 2D-SWE. Thyroid volume was calculated using the ellipsoid formula, and elasticity values were recorded in kilopascals (kPa). Clinical characteristics, laboratory parameters, and disease severity indices were recorded, and correlation analyses were performed. Thyroid volume and isthmus thickness were similar between groups (all p > 0.05; d = 0.10-0.35). Right, left, and total thyroid elasticity values were significantly higher in SSc patients than in controls before and after smoking adjustment (all unadjusted p ≤ 0.001; all adjusted p ≤ 0.007; d = 0.83, 0.79, and 0.90, respectively). Right lobe elasticity correlated weakly with erythrocyte sedimentation rate (r = 0.355; p = 0.034), while left and total thyroid elasticity correlated moderately with ejection fraction (r = 0.423; p = 0.010 and r = 0.390; p = 0.019, respectively). No significant associations were found with disease duration, modified Rodnan skin score, EUSTAR Activity Index, Medsger Disease Severity Score, autoantibody status, or major organ involvement. In SSc, thyroid parenchymal stiffness increases without volume change. This suggests that the fibrotic process may be reflected in the thyroid tissue at a subclinical level. Thyroid elastography may be a potential method for evaluating organ-specific fibrotic changes in SSc; further large-scale and prospective studies are needed to clarify its clinical significance.

Rheumatic diseases (RDs) are chronic immune-mediated disorders associated with disproportionately increased cardiovascular morbidity and mortality. Accelerated atherogenesis in these diseases is driven by persistent systemic inflammation, autoantibody-mediated endothelial injury, oxidative stress, and dysregulated lipid metabolism, resulting in premature vascular remodeling manifested by increased carotid intima-media thickness, arterial stiffness, impaired flow-mediated dilation, and coronary artery calcification. This review synthesizes evidence regarding subclinical atherosclerosis and cardiometabolic risk across common RDs. In rheumatoid arthritis and systemic lupus erythematosus, vascular alterations correlate with inflammatory burden, disease duration, autoantibody profiles, renal involvement, and glucocorticoid exposure. Emerging biomarkers-including apolipoprotein B48, FIB-4 index, asymmetric dimethylarginine, and adhesion molecules-provide incremental prognostic value beyond traditional lipid parameters. Advanced imaging modalities, such as ^18F-sodium fluoride PET/CT and vascular elastography, enhance early detection of arterial calcification and stiffness. Growing evidence in primary Sjögren syndrome, Behçet disease, systemic sclerosis, and ankylosing spondylitis similarly confirms increased subclinical atherosclerosis and endothelial dysfunction. Importantly, tight disease control and targeted immunomodulatory therapies-including methotrexate, biologic agents, antimalarials, and cytokine-directed treatments-are associated with improved vascular and metabolic profiles and attenuation of disease progression. Subclinical atherosclerosis represents a critical interface between autoimmunity and cardiovascular disease in RDs. Early vascular assessment integrated with disease-specific and metabolic risk stratification is essential to implement precision-based cardiovascular prevention in this high-risk population.

Interleukin-23 inhibitors (IL-23i) are effective in psoriatic arthritis (PsA) in randomized trials; however, real-world data from Latin America remain limited. We described baseline characteristics and treatment line at IL-23i initiation, physician-reported reasons for selecting IL-23 inhibition, and pragmatic effectiveness and persistence at 6 and 12months in Argentina. Multicenter, observational, retrospective cohort study across seven Argentine sites. Adults with rheumatologist-diagnosed PsA initiating IL-23i (guselkumab or risankizumab) in routine care were included. Baseline demographics, disease duration, domains, key activity measures, prior advanced therapy lines, and physician-reported rationale were abstracted from records. Patients were assessed at ~ 6 and 12months. Primary outcome was physician-recorded minimal disease activity (MDA); persistence was remaining on IL-23i. Analyses were descriptive, with no inferential/predictive analyses due to sample size. Fifty-five patients were included (48% female; age 56 ± 11years). Mean PsA duration before IL-23i was 7.7 ± 5.8years and psoriasis duration 19 ± 11years. IL-23i was initiated as the 1st, 2nd, or ≥ 3rd advanced line in 26%, 34%, and 39%, respectively; prior TNF inhibitor exposure was 75% and IL-17 inhibitor exposure 25%. Domain involvement was frequent (peripheral 95%, skin 91%, nails 44%, enthesitis 43%, dactylitis 13%, axial 17%). Physicians selected IL-23i mainly for safety (73.9%) and expected skin efficacy (69.6%). MDA was achieved by 70% at 6months (90% persistence) and 75% at 12months (80% persistence). In Argentine routine care, IL-23 inhibition achieved high MDA rates with substantial 12-month persistence in complex, treatment-experienced PsA, supporting its pragmatic use in daily practice.

Gout is traditionally monitored through serum urate levels (SUA). However, the inflammatory component of the disease may not fully parallel short-term urate fluctuations. We aimed to evaluate longitudinal within-patient dynamics of systemic inflammatory activation and to determine whether inflammation persists beyond clinically apparent flares and may not always reflect contemporaneous SUA.Patients with gout were assessed across three successive outpatient clinic visits. Systemic immune-inflammation index (SII), calculated from the values of the complete blood count, and SUA were measured at each visit. Gout flares, as documented in medical records, were analyzed in relation to inflammatory indices, SUA, and visit order using models adjusted for age and sex.Median SII was significantly higher in patients with gout compared with controls (544.5 vs. 383.9, p < 0.001). Non-flare visits were associated with lower SII values compared with flare visits (β = -203.7, SE = 52.6, p < 0.001), independent of age, sex, visit order, and SUA levels. Notably, visit-specific SUA was not independently associated with SII, and no interaction was observed between flare status and SUA. Elevated inflammatory activity was detectable across visits and was not fully explained by acute flare episodes.Systemic inflammatory activity in gout may persist beyond clinically apparent flares and may not always be fully captured by serum urate levels alone. These findings suggest that inflammatory activity and urate levels do not always align in routine clinical practice, highlighting the potential value of complementary inflammatory assessment.

VEXAS syndrome is characterized by high glucocorticoid (GC) requirements and frequent relapses during tapering, yet dose-response relationships remain poorly defined. We conducted a pilot study to assess the feasibility of granular longitudinal treatment-line reconstruction and to explore GC dose-response patterns associated with disease activity and flare risk. In this retrospective single-center study, we reconstructed detailed treatment trajectories of patients with VEXAS syndrome. Disease courses were segmented into treatment-line periods defined by any therapeutic modification, including GC dose changes. For each period, GC dose, concomitant therapies, and clinical activity were recorded. Associations between GC dose and disease activity were analyzed using multivariable models adjusting for concomitant treatments. Twelve patients were included, representing 315 treatment-line periods over a mean follow-up of 45months. Mean annual GC exposure was 3.27 ± 2.26g per patient. Higher GC dose (continuous variable) was independently associated with lower odds of clinical activity (aOR 0.91 per mg increase [95% CI 0.88-0.94], p < 0.001). Exploratory threshold analyses suggested increased flare risk below approximately 15mg/day (or 0.2mg/kg/day), with a lower-risk plateau above 20mg/day. The increased flare risk below 15mg/day remained significant after adjustment for concomitant therapies (HR 0.24 [95% CI 0.11-0.54], p = 0.001). Organ-specific analyses suggested heterogeneous glucocorticoid sensitivity, with higher doses appearing required for lung involvement and lower doses appearing sufficient for fever, skin, and joint manifestations. This pilot study demonstrates the feasibility of detailed treatment-line reconstruction in VEXAS syndrome and identifies GC dose-response trends. These preliminary findings provide planning parameters for a future adequately powered study aimed at validating dose thresholds and refining tapering strategies in VEXAS.

Lupus panniculitis (LEP) is a rare form of cutaneous lupus (CLE) characterised by progressive, often disfiguring course and poor response to treatment. Type I interferon inhibition through anifrolumab (ANF) is effective in CLE but limited data are available for its use in LEP. To address this issue, we screened patients with CLE and/or systemic lupus erythematosus (SLE) for biopsy-proven diagnoses of LEP and treatment with ANF. Besides demographics, general clinical features, concomitant treatments before and after ANF and safety signals, we measured disease activity and damage with the SLE disease activity index 2000 (SLEDAI-2K), the CLE Disease Area and Severity Index activity (CLASI-A) and damage scores and the SLE International collaborating clinics/American College of Rheumatology damage index. The same data were retrieved, when available, from existing cases extracted from systematic literature review. Sixteen cases were identified, including 3/421 newly described patients, with two receiving ANF as first-line immunosuppressant and one as an early treatment devoid of oral corticosteroids. All patients had a good response to treatment and most of them could taper or discontinue corticosteroids. CLASI-A scores were markedly reduced after ANF treatment [11.5 (7-29)] to 0 (0-2); p = 0.005]. The time to response was within five months in most cases. No significant adverse events were reported. Taken together, our data suggest that ANF might be effective in LEP and used as a first-line treatment to prevent LEP-related damage accrual.

Despite improvement in treatment, rheumatoid arthritis (RA) management remains inconsistent. To evaluate the worldwide disparities in the use of biological and targeted molecules (advanced) RA therapies, focusing on differences across continents and socioeconomic strata, and to identify factors associated with their utilisation. Cross-sectional analysis of the international COVAD-2 cohort, including demographics, socioeconomic factors, disease characteristics, patient-reported outcomes, and treatments. Primary outcomes assessed treatment distribution by continent, secondary outcomes evaluated distribution by Human Development Index (HDI), with predictors analysed using multivariable logistic regression. At the time of analysis, COVAD2 included 10,739 participants; 2007 had RA, 1997 with geographical data included in this study (mean age 50.9years, 88.1% women). Most patients came from Europe (39.4%) and Asia (24.8%); 61.3% and 23.7% were from very high- and high-HDI countries, respectively. Overall, 29.6% of patients used advanced therapies, with the highest rate in Europe (44.0%), followed by North America and Oceania (33.9%), South America (31.1%), Asia (11.7%), and Africa (5.3%) (p < 0.001). Usage correlated strongly with HDI: 2.7% in low-HDI to 38.8% in very-high-HDI countries (Compared to very-high income, Odds Ratio for high 0.561 (95% CI 0.403;0.782), for medium 0.288 (95% CI 0.153;0.539), and for low income 0.275 (95% CI 0.034;2.199); p < 0.001). Regions with limited access relied more on glucocorticoids. Disparities across continents and HDI categories remained after adjusting for confounders(demographic characteristics, disease activity, comorbidities, and patient-reported outcomes. Marked continent- and HDI-based inequities in biologic and targeted DMARD use persist globally, demanding coordinated action from the rheumatology community to ensure equitable RA care across resource settings.

Sacroiliac joint (SIJ) anatomical variants are common on MRI and may complicate interpretation by mimicking inflammatory sacroiliitis; however, their relationship with inflammatory back pain (IBP)-like symptom patterns is not well defined in patients without axial spondyloarthritis (axSpA). To characterize inflammatory back pain (IBP)-like symptom patterns and accompanying MRI findings that may mimic sacroiliitis in patients with chronic low back pain (CLBP) and sacroiliac joint (SIJ) anatomical variants who did not fulfill classification criteria for axial spondyloarthritis (axSpA). In this cross-sectional study, consecutive patients younger than 45 years at the time of SIJ MRI/clinical evaluation, with chronic low back pain lasting at least 3 months, who underwent SIJ MRI between September 2023 and September 2025 were retrospectively screened for predefined SIJ anatomical variants and lumbosacral transitional anomalies. Patients with lumbosacral transitional anomalies were excluded at the screening stage. Those with at least one SIJ anatomical variant were invited for a standardized clinical assessment in which IBP features were captured using a single questionnaire covering the Calin, Rudwaleit (Berlin), and ASAS IBP criteria. All participants were systematically assessed against the ASAS classification criteria for axial spondyloarthritis (axSpA), and those who fulfilled these criteria were excluded from the final analysis. SIJ MRIs were read independently by two radiologists blinded to clinical data; agreement for variant detection was almost perfect (κ = 0.90). Bone marrow edema (BME) was evaluated according to the ASAS/OMERACT definition of MRI findings highly suggestive of active sacroiliitis, and structural changes were also recorded. Of 260 screened patients with CLBP, SIJ anatomical variants were identified in 108/260 (41.5%). After exclusions (n = 20), 88 patients were included in the final analysis; 75/88 (85.2%) were female, with a median age of 36 years (Q1-Q3: 28-39) and a median symptom duration of 3.0 years (Q1-Q3: 1.6-9.8). IBP positivity varied by criteria set: 51.1% (Calin), 34.1% (Berlin), and 27.3% (ASAS). Variants were predominantly bilateral (76/88, 86.4%). Among 98 recorded variant findings, accessory joint (n = 27) and iliosacral complex (n = 25) were the most frequent. ASAS/OMERACT-positive BME was present in 10/88 patients (11.4%); structural lesions included sclerosis in 22/88 (25.0%), erosions in 7/88 (8.0%), and fat metaplasia in 5/88 (5.7%). HLA-B27 positivity was observed in 4/69 tested patients (5.8%), and median CRP was 3.2mg/L (Q1-Q3: 1.0-7.0). In a non-axSpA, variant-positive cohort, IBP-like symptom patterns were common, whereas ASAS/OMERACT-positive BME was infrequent. SIJ variants may therefore complicate clinical judgment because of symptom overlap in young patients within the typical age range for axSpA onset. Although infrequent, imaging features that mimic inflammatory disease highlight the need for careful clinical correlation to avoid misclassification as axSpA.