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To synthesise current evidence on artificial intelligence (AI) in rheumatology with a specific focus on AI-induced technostress, job insecurity and professional identity, and to propose a pragmatic framework for an 'AI-augmented' rheumatologist. A narrative review was conducted using focused searches for articles published between January 2015 and March 2026. Search terms combined AI- and rheumatology-related concepts with terms related to technostress, burnout and professional identity. Reference lists of key rheumatology AI reviews and empirical studies were screened for additional publications. Eligible works included empirical studies, reviews and conceptual papers on AI in rheumatology or AI-related technostress and psychological or professional consequences for physicians. Current AI applications in rheumatology span imaging, risk prediction, data integration and large language model (LLM)-based tools, but routine use remains low despite largely positive expectations among rheumatologists and patients. Evidence from mixed-specialty cohorts indicates that AI-related self-esteem threat is a central driver of job insecurity and may contribute to burnout. Rheumatology's reliance on longitudinal pattern recognition, uncertainty management and relationship-centred care makes perceived threats to expertise particularly salient, although similar dynamics likely affect other specialties. Building on this evidence, a four-pillar framework for an 'AI-augmented' rheumatologist is proposed: clear role boundaries between humans and AI, rheumatology-specific AI literacy, clinician- and teamled implementation and governance, and routine monitoring of technostress and well-being. AI can meaningfully support rheumatology care and, when well-designed and implemented, may even reduce certain forms of technostress by offloading administrative and repetitive tasks. At the same time, AI-related technostress, perceived self-esteem threat and job insecurity can undermine professional identity and wellbeing if introduced without attention to role boundaries, governance and multiprofessional collaboration. The proposed framework aims to help rheumatologists and institutions integrate AI in ways that preserve core professional values and clinician well-being.
Background and Objectives: Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease in which persistent synovial inflammation and joint damage are influenced not only by immune dysregulation but also by environmental, genetic, and epigenetic factors. Vitamin D is a secosteroid hormone and has emerged as a key immunomodulatory hormone, with reported effects on innate and adaptive immune responses, with potential relevance to RA clinical activity and treatment. This narrative review synthesizes mechanistic and clinical evidence enlightening vitamin D's immunomodulatory role in RA pathogenesis and management. Methods: A comprehensive literature search was carried out on PubMed and MEDLINE databases using Medical Subject Headings (MeSH) terms: "Vitamin D", "Cholecalciferol", "Arthritis, Rheumatoid", "Seasons", "Epigenomics", "DNA Methylation", and "Therapy". The narrative review highlights evidence published mainly in the last 5 years on the link between vitamin D and RA, focusing on epigenetic interactions, circannual rhythms, and therapeutic implications. Results: Emerging data suggest that vitamin D-related epigenetic mechanisms (e.g., DNA methylation, histone acetylation, and microRNA regulation) and genetic polymorphisms have been associated with disease susceptibility and treatment outcomes. Latitude and seasonal fluctuations in serum 25-hydroxyvitamin D levels correlate with variations in RA disease activity, although results remain heterogeneous across studies. Overall, the available evidence supports an association between vitamin D deficiency and greater RA disease activity, while its adequate supplementation has been associated with improvements in inflammatory markers and selected clinical outcomes, especially when tailored to baseline status and individual risk factors, such as limited dietary intake and sunlight exposure. Conclusions: Current evidence emphasizes the need for further studies using standardized methods and larger, geographically diverse cohorts to define how best to leverage seasonal vitamin D variations in RA management, considering also the range of concomitant epigenetic modifiers that may influence the effects of vitamin D on the management of RA patients.
Glucocorticoid (GC) bridging therapy is recommended in patients with rheumatoid arthritis commencing a disease-modifying anti-rheumatic drug (DMARD). It is not clear whether GC therapy is better administered intramuscularly or orally and at what dose level. The aim of the LEADER trial is to identify the most effective and safest way of using steroids in patients with uncontrolled RA who are starting a DMARD. A multicentre, randomised, open-label, four-arm, parallel-group clinical trial with an internal pilot phase, economic evaluation and qualitative study of acceptability. Participants will be randomised to one of four arms: arm A, 30 mg oral prednisolone tapering over 6 weeks; arm B, 15 mg oral prednisolone tapering over 4 weeks; arm C, Intramuscularly 120 mg methylprednisolone; and arm D, Intramuscularly 80 mg methylprednisolone. Participants will be assessed at baseline (pre-GC intervention), 4, 12 and 24 weeks. The primary outcome measure is the mean DAS(CRP)-28 over 12 weeks. The primary comparison will be according to route of administration (oral vs intramuscular GC treatment) with secondary comparisons within route of administration to provide evidence of dose effectiveness. Toxicity will be measured using the Glucocorticoid Toxicity Index, a clinical outcome assessment and early morning cortisol level. LEADER will be conducted in ~30 sites delivering NHS care, recruiting a sample size of 448. Economic evaluation will compare cost-effectiveness within a trial and over a lifetime horizon from the English National Health Service perspective. The LEADER trial received MHRA and Leicester Central Research Ethics Committee ethics approval (REC reference: 24/EM/0277, IRAS 1010280), opened to recruitment on Protocol Version 4.0 and is currently recruiting on Protocol Version 5.0. Participants will provide written informed consent in accordance with the Declaration of Helsinki and applicable regulatory requirements. Trial results will be disseminated via presentations at national and international meetings, published in open-access journals and to patients. ISRCTN32090559.
To explore the clinical features, diagnosis, treatment and prognosis of arterial involvement in paediatric Behçet's disease (BD) for clinical reference. A retrospective cohort study analysed 76 paediatric BD patients (January 2013 - May 2024). Nineteen with arterial involvement were the experimental group, and 57 without vascular involvement were the control group. The experimental group mainly involved medium-sized (15/19, 78.95%), large-sized (13/19, 68.42%) or both (9/19, 47.37%) arteries, most commonly abdominal aorta (8/19, 42.11%), pulmonary artery (7/19, 36.84%) and femoral artery (7/19, 36.84%). Notably, we found a high prevalence of coronary artery involvement, exclusively manifesting as left main coronary artery dilation. Lesions were mainly wall thickening (9/19, 47.37%), lumen dilation (8/19, 42.11%) and stenosis (7/19, 36.84%). Compared with the control group, it had later onset age (11.0 vs. 7.0 years), shorter disease duration (6.0 vs. 24.0 months), and higher incidences of fever, multi-organ involvement (neurological, renal, cardiac), and elevated inflammatory markers including C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). It also had more intensive treatment and surgery but had significantly higher rates of cerebrovascular accidents (15.79% vs. 0%), cardiac complications (31.58% vs. 0%), and mortality (10.53% vs. 0%). Paediatric BD with arterial involvement is a severe phenotype with a poor prognosis, characterized by intense inflammation and multi-organ damage. This underscores the critical need for early identification, aggressive treatment, and close monitoring to improve long-term outcomes.
Inclusion body myositis (IBM) is the most common idiopathic inflammatory myopathy after age 50, causing progressive weakness of quadriceps and finger flexors. With no effective disease-modifying therapies, accessible non-pharmacological strategies are needed. Exercise is safe, may slow disease progression and improve strength. However, most studies focus on lower limb strengthening, despite hand strength being vital to independence. Our study analysed the acceptability, tolerability and efficacy of an at-home TheraPutty® hand exercise intervention on grip strength and function in adults with IBM. In this 12-week, single-arm pilot study, thirteen participants underwent baseline, 6-week, and 12-week assessments of grip/pinch strength (hand-held dynamometry), dexterity (Nine-Hole Peg Test, Box and Block Test), and function (IBM Functional Rating Scale, Duruöz Hand Index). Use of intention-to-treat and per-protocol approaches assessed the effect of adherence on strength outcomes. Adherence (≥75% sessions), acceptability, and tolerability were assessed through weekly diaries and an end-of-study questionnaire. Nine participants (69%) achieved ≥75% adherence. Intention-to-treat analysis showed no significant changes in grip or pinch strength, although Box and Block performance improved significantly bilaterally. In the per-protocol analysis, significant improvements were observed in non-dominant 2-point and bilateral 3-point pinch strength. Fatigue, pain, and difficulty using even the lowest resistance TheraPutty® limited adherence. Overall, participants rated the programme as moderately acceptable (mean 3.5/5) and tolerable (3.4/5). A home-based TheraPutty® programme is feasible and generally acceptable in IBM, with potential signals of benefit among adherent participants. Future larger, longer-term studies should refine treatment protocols to reduce fatigue and optimise efficacy.
Myocarditis is a heterogeneous inflammatory syndrome with aetiologies ranging from viral infection and drug hypersensitivity to systemic autoimmune/autoinflammatory disease and immune checkpoint inhibitor (ICI) therapy. In response to these triggers, the innate immune response and inflammasome activation can amplify myocardial injury via IL-1, providing a mechanistic rationale for IL-1 pathway inhibition as a targeted therapeutic strategy. This review synthesizes preclinical and clinical evidence for IL-1 blockade in myocarditis and related inflammatory cardiac syndromes. The immune system plays a central role in the pathogenesis of myocarditis, both in idiopathic/viral cases and in systemic autoimmune and autoinflammatory diseases (SAAD). Interleukin-1 (IL-1) has emerged as a key mediator linking inflammation to myocardial dysfunction, supported by experimental and translational evidence implicating activation of the NLRP3 inflammasome. Clinically, the randomized trial of anakinra in acute myocarditis (ARAMIS) did not improve outcomes in a largely low-risk cohort, but accumulating case reports and small series suggest potential benefit in fulminant/hyperinflammatory myocarditis and chronic active refractory myocarditis. In contrast, IL‑1 inhibitors have robust randomized and real-world evidence in recurrent pericarditis, supporting a myo‑pericardial inflammatory continuum and validating IL‑1 pathway engagement as an actionable target in selected inflammatory cardiac phenotypes. Together, these findings support the evolving concept of cardioimmunology. Current management of myocarditis remains largely supportive, with limited disease-modifying options. Anti-IL-1 therapies, particularly anakinra, have shown promising efficacy in selected severe and refractory cases, with a favourable safety profile. However, evidence is mainly derived from case reports and small series, and robust randomized data are lacking. Key clinical questions remain unresolved, including patient selection, timing of initiation, and treatment duration. Future studies should focus on identifying inflammatory endotypes and evaluating targeted immunomodulatory strategies, including in emerging settings such as ICI-associated myocarditis in which IL‑1 blockade remains investigational.
Newborn screening (NBS) for inborn errors of immunity increasingly uses T-cell receptor excision circles (TREC) and, in some programs, Kappa-deleting recombination excision circles (KREC) to detect early T- and B-cell lymphopenia. While TREC-based screening is well established, the significance and management of isolated low KREC remain unclear. To evaluate the implications of two different regional post-screening algorithms for isolated low KREC and to characterize the clinical course, immunological profile, and follow-up of term newborns with transient B-cell lymphopenia. We performed a retrospective multicenter study of term newborns with isolated low KREC identified through NBS, confirmed B-cell lymphopenia, and subsequent normalization during follow-up. KREC levels, B-cell counts, and serum immunoglobulins were assessed longitudinally by RT-PCR and flow cytometry. Eighteen newborns were enrolled. At the first evaluation (V1; mean age 13.5 days), all had marked peripheral B-cell lymphopenia (CD19+ ≤ 2%; mean 54 cells/μL), although repeat dried blood spot (DBS) testing already showed KREC values above the diagnostic cutoff in 78%. By the second visit (V2; mean age 50 days), B-cell percentages and absolute counts normalized in all infants, with emerging IgA and IgM production, and normal KREC on whole blood. No infectious or immunological complications were recorded over 39.5 person-years of follow-up (mean 2.3 ± 1.7 years). Isolated low KREC at birth may identify newborns with transient B-cell lymphopenia that resolves during early infancy. Repeat KREC testing on a second DBS before referral may represent a pragmatic triage step to reduce unnecessary immunological evaluations, while preserving early assessment for newborns with persistent abnormalities. Prospective studies are needed to refine post-screening strategies.
This study aimed to investigate the mechanism and therapeutic potential of targeting the extracellular signal-regulated kinase 1/2 (ERK1/2) signalling pathway in myositis-associated interstitial lung disease, focusing on its role in neutrophil extracellular traps (NETs)-mediated pro-inflammatory and pro-fibrotic processes. Lung tissue samples were collected from patients with idiopathic inflammatory myopathy-associated ILD (IIM-ILD) and from mice with experimental autoimmune myositis (EAM) and a myositis-associated interstitial lung disease model (MAILD). Multiple experimental techniques, including immunohistochemistry, western blotting, immunofluorescence and transcriptome sequencing were employed to analyse ERK1/2 activation, NETs infiltration and the expression of epithelial-mesenchymal transition (EMT)-related markers. The ERK1/2 inhibitor U0126 was applied both in vivo and in vitro for interventional validation. The ERK1/2 signalling pathway was activated in the lung tissues of IIM-ILD patients and in the EAM and MAILD mouse models. Substantial NETs infiltration was observed in the lung tissues of EAM and MAILD mice. NETs induced EMT and the release of pro-inflammatory factors by activating ERK1/2. Inhibiting NETs formation attenuated ERK1/2 phosphorylation and the downstream fibrotic process. Administration of the ERK1/2 inhibitor U0126 not only effectively alleviated NETs-induced EMT and inflammatory responses but also significantly reduced pulmonary inflammation infiltration and NETs formation in the MAILD model. NETs-mediated pro-inflammatory and pro-fibrotic processes contribute to the progression of myositis-associated interstitial lung disease by activating the ERK1/2 signalling pathway. Targeting ERK1/2 effectively inhibits this pathogenic cascade, providing a novel strategy for clinical treatment.
Anti-topoisomerase I antibody (ATA) is typically associated with diffuse cutaneous systemic sclerosis (dcSSc). However, subset of limited cutaneous SSc (lcSSc) patients also present with ATA positivity. Emerging data suggest that ATA-positive lcSSc may represent a distinct or intermediate clinical phenotype. This study aimed to compare the demographic, clinical, and treatment features of early ATA-positive lcSSc patients with those of ACA-positive lcSSc and ATA-positive dcSSc patients. Patients were recruited from the multicentre Turkish SOLAR cohort (Systemic sclerOsis Longitudinal Assessment Registry). Among 295 SSc patients screened, 172 were included: 74 ACA-positive lcSSc, 55 ATA-positive lcSSc, and 43 ATA-positive dcSSc. Demographic, clinical, and treatment-related variables were analysed and compared across groups. ATA-positive lcSSc patients were younger at the onset of Raynaud's phenomenon (RP) (p=0.042), the first non-RP symptom (p=0.016), and at diagnosis (p=0.018) compared with ACA-positive lcSSc patients. Interstitial lung disease (ILD) was significantly more frequent in ATA-positive lcSSc (74.5%) than ACA-positive lcSSc (8.1%, p<0.001) and was comparable to ATA-positive dcSSc. Modified Rodnan skin scores were highest in ATA-positive dcSSc but were also significantly elevated in ATA-positive lcSSc (p<0.001). Pitting scars were more frequent in dcSSc. Among patients with ILD, ATA-positive lcSSc and ATA-positive dcSSc showed similar HRCT patterns. ATA-positive lcSSc patients were more frequently treated with glucocorticoids and mycophenolate mofetil than ACA-positive lcSSc, whereas cyclophosphamide was highest in dcSSc. ATA-positive lcSSc patients exhibit a clinically distinct phenotype characterized by a substantial risk of internal organ involvement, despite having less extensive skin disease. Their overlap with dcSSc and divergence from ACA-positive lcSSc highlight the importance of incorporating both skin involvement and serologic subtyping into the early management and risk stratification of SSc.
Psychological distress influences pain and disease severity perception among patients affected by psoriatic arthritis (PsA). Alexithymia, a personal trait characterised by the difficulty in recognising and articulating emotions, has been observed in other rheumatic diseases, but its role in PsA remains underrecognised. We investigated the prevalence of alexithymia in PsA and its association with disease activity, psychological burden, and treatment complexity. A cross-sectional observational study was conducted across three Italian rheumatology centers, enrolling PsA patients on stable biological therapy. Toronto Alexithymia Scale (TAS-20), Pain Catastrophising Scale (PCS), Beck's Depression Inventory (BDI), Widespread Pain Index (WPI), Symptom Severity Scale (SSS), alongside Disease Activity Index for PsA (DAPSA), Bath Axial Spondyloarthritis Disease Activity Index (BASDAI), and Axial Spondyloarthritis Disease Activity Index-C Reactive Protein (ASDAS-CRP) were assessed at last follow-up. Associations with alexithymia were explored by univariate analyses, Spearman correlation, and multivariable logistic regression. Among 207 PsA patients, 63 (30.4%) were classified as alexithymic (TAS≥61). Patients with alexithymia exhibited significantly higher pain-VAS, patient and physician global assessment, tender joint count, PCS, WPI+SSS, and BDI scores, as well as elevated DAPSA, BASDAI, ASDAS-CRP, while inflammatory markers and swollen joint count were similar between groups. Alexithymic patients underwent multiple biological therapy lines and reported increased conventional synthetic DMARDs and non-steroidal anti-inflammatory drug usage. A strong correlation emerged between TAS-20 and PCS, alongside female sex, concomitant fibromyalgia and higher DAPSA were independent predictors of alexithymia in multivariable model. Alexithymia is present in PsA and is linked to increased pain perception, disease activity and treatment burden.
Physical activity is central to spondyloarthritis (SpA) management, yet many patients avoid movement due to fear of pain and negative beliefs about exercise. The relationships between fear-avoidance beliefs, disease activity, pain catastrophising, and quality of life remain unclear. This study aimed to assess the prevalence and determinants of fear-avoidance beliefs related to physical activity in patients with axial spondyloarthritis (axSpA) and psoriatic arthritis (PsA), and to identify associated clinical, demographic, and psychological factors. This monocentric observational study enrolled 159 consecutive patients (70 axSpA, 89 PsA) attending the Rheumatology Unit of Campus Bio-Medico University Hospital. Physical activity avoidance beliefs were assessed with the FABQ-PA (scores ≥15 = high avoidance). Disease activity, quality of life, pain catastrophising, and anxiety/depression were recorded. Group comparisons, Spearman correlations, and uni-/multivariable logistic regression were performed. High physical activity avoidance was observed in 31.4% of the cohort (32.9% axSpA, 30.3% PsA). In axSpA, FABQ-PA ≥15 was associated with higher disease activity, greater PC and poorer SF-36 scores. In multivariable models, BASDAI remained significantly associated with high avoidance, with magnification retaining a weaker independent association, whereas SF-36 and other psychometric variables lost significance. In PsA, FABQ-PA was not associated with BASDAI or DAPSA. High avoidance was independently linked to female sex, higher level of helplessness and rumination, and lower SF-36, PhCS, and MCS scores, even after adjusting for disease activity. Physical activity avoidance in SpA reflects distinct but overlapping pathways. In axSpA, avoidance is predominantly associated with inflammatory disease activity, whereas in PsA it is more closely associated with psychological and quality-of-life-related factors.
To comprehensively evaluate the effects of baricitinib on bone structure and bone-related biomarkers in patients with rheumatoid arthritis (RA) using high-resolution peripheral quantitative computed tomography (HR-pQCT). RA patients initiating baricitinib were enrolled in this prospective study. Bone structure in the second and third metacarpal heads was assessed using HR-pQCT at baseline and after 6 and 12 months. Synovitis, tenosynovitis, and osteitis were evaluated using ultrasound and MRI. Serum cytokines, chemokines, and bone-related biomarkers were analysed through a multiplex bead assay. Fourteen patients with RA who initiated baricitinib were included in the analysis. No new bone erosions were detected during the 12-month period, and several pre-existing erosions showed partial repair. HR-pQCT revealed favourable trends in trabecular bone parameters, including increases in volumetric bone mineral density and trabecular thickness. Serum osteoprotegerin (OPG) significantly increased, while osteopontin (OPN) and interleukin-23 (IL-23) decreased, indicating suppression of the IL-23/Th17/RANKL axis and enhancement of bone preservation pathways. In addition, baricitinib modulated inflammatory mediators, including increased Eotaxin and decreased MCP-3. These changes were accompanied by improvements in synovitis, osteitis, and tenosynovitis assessed by multiple imaging modalities. Baricitinib treatment inhibited the progression of bone erosions and also induced partial repair in some lesions, accompanied by improvements in periarticular bone microarchitecture. These favourable effects on bone structure were paralleled by beneficial modulation of bone-related and inflammatory biomarkers. Collectively, these findings indicate that baricitinib contributes to the prevention of joint destruction primarily through structural preservation, supported by parallel molecular mechanisms.
Interleukin-2 (IL-2) plays anti-inflammatory and immunoregulatory roles and has been implicated in the pathogenesis of rheumatoid arthritis (RA). However, the relationship between its circulating serum levels and specific clinical features of the disease remains unclear. In this study, we aimed to investigate the association between serum IL-2 concentrations and a wide range of RA-related characteristics, including cardiovascular comorbidities. 216 RA patients underwent assessments of disease characteristics and activity indices. Lipid profile was obtained, insulin resistance indices were calculated, and metabolic syndrome criteria were applied. Carotid ultrasound examinations were performed to assess arterial stiffness, intima-media thickness, and the presence of carotid plaques. Cardiovascular risk was estimated using the SCORE2 tool. Serum IL-2 levels were measured using the Simoa (Single Molecule Array) technique. Finally, a multivariable linear regression analysis was conducted to explore the associations between disease characteristics and IL-2 levels. After multivariable adjustment, IL-2 was independently and positively associated with disease activity. Patients positive for rheumatoid factor and anti-citrullinated protein antibodies also exhibited significantly higher IL-2 levels than seronegative individuals. Furthermore, IL-2 showed a positive relationship with pancreatic beta-cell function. Notably, circulating IL-2 concentrations were significantly associated with increased cardiovascular risk as estimated by the SCORE2 algorithm. Circulating IL-2 levels are independently and positively associated with both disease activity and cardiovascular risk in patients with RA. These findings further emphasise the pivotal role of IL-2 in the pathophysiology of RA and its associated cardiovascular comorbidities, highlighting IL-2 as a potential biomarker and therapeutic target in this population.
Relapsing polychondritis (RP) is a rare, multisystem inflammatory disease characterized by heterogeneous clinical manifestations and a substantial impact on patients' daily functioning and well-being. Health-related quality of life (HR-QoL) in RP remains insufficiently characterized, and no disease-specific measurement tool is available so far. This study aimed to develop and validate the RP-QoL, a multilingual, patient-reported outcome instrument specifically designed to assess HR-QoL in individuals with RP. The RP-QoL was developed within the European Reference Network ReCONNET using a structured four-step approach: (1) identification of relevant HR-QoL domains through systematic literature review, an international patient survey and expert consensus; (2) item generation; (3) pilot testing including cognitive debriefing; and (4) comprehensive psychometric validation. Validation analyses included assessment of internal consistency, structural validity, construct validity, convergent validity with the SF-36, and criterion-related validity. Domain identification incorporated input from 274 patients across 22 countries, leading to a 31-item pilot questionnaire with a 28-day recall period and 5-point response scale. Cognitive debriefing confirmed clarity, relevance, and feasibility. Validation in 239 patients from 19 countries (median age 55 years; 80% female) demonstrated excellent internal consistency (Cronbach's α = 0.96). Exploratory factor analysis supported near-unidimensionality, with the first factor explaining 46.6% of variance. RP-QoL scores correlated strongly with disease impact (p = -0.62, P < 0.0001) and SF-36 physical (p = 0.65) and mental (p = 0.55, P < 0.0001) components (both P < 0.0001, P < 0.0001). Discriminative ability was high (AUC = 0.87). The RP-QoL is the first validated, disease-specific HR-QoL instrument for RP, with robust psychometric performance and applicability in both clinical practice and research.
Gastrointestinal (GI) bleeding is a serious complication of immunoglobulin A vasculitis (IgAV), but reliable predictors are still lacking. This study aimed to identify clinical risk factors and develop a prediction model for IgAV-related GI bleeding in a large patient cohort. In this retrospective study, 968 patients with IgAV from the Affiliated Hospital of Southwest Medical University (2019-2024) were divided into GI bleeding (n=484) and non-bleeding (n=484) groups. We analysed seasonal onset patterns and used multivariate logistic regression with ROC curve validation to identify predictors. This retrospective study revealed that summer-onset disease was associated with a significantly higher risk of GI bleeding compared to other seasons (OR=1.67, 95% CI:1.15-2.45; p=0.007), representing a 13.8% absolute risk increase (p<0.001). The neutrophil-to-albumin ratio (NAR) was the strongest biochemical predictor (OR=1.79; 95% CI:1.33-2.47; AUC=0.723). High systemic immune-inflammation index levels also increased risk (OR=2.91, 95% CI:1.67-5.08), while mean platelet volume (MPV) was protective (OR=0.78, 95% CI:0.68-0.90). A combined model including seasonality, NAR, and MPV showed superior predictive performance (AUC=0.742, 95% CI:0.711-0.772). Summer onset, elevated NAR, and decreased MPV help identify IgAV patients at high risk of GI bleeding. A model combining these factors allows effective risk stratification and supports targeted monitoring in clinical practice, particularly for summer-admitted patients with high neutrophil-to-albumin ratios.
Baseline kidney biopsy is the gold standard for diagnosing lupus nephritis (LN). However, in certain cases, biopsy may not be feasible due to medical, technical, or patient-related factors, leading to a clinical diagnosis of LN. This study compares outcomes between biopsy-confirmed and clinically diagnosed LN to inform clinical decision-making in scenarios where a kidney biopsy is not feasible. This retrospective study included patients with SLE enrolled between 2000 and 2024 who developed incident LN in an inception cohort at a tertiary centre. Inclusion began in 2000 to reflect treatment changes following the introduction of mycophenolate mofetil. Outcomes included: (1) complete proteinuria recovery (CPR) at 6 months and one year, and (2) a sustained ≥30% eGFR decline, end-stage kidney disease (ESKD), or death (composite outcome). Time-to-event outcomes were assessed using Kaplan-Meier curves and Cox proportional hazards regression. Among 127 patients with incident LN, 84 (66.1%) had biopsy-confirmed and 43 (33.9%) clinically diagnosed LN. Clinically diagnosed patients were younger, with lower baseline proteinuria and disease activity. CPR at 6 months and one year, as well as the composite outcome, did not differ significantly between groups. Individual events, including ≥30% eGFR decline, ESKD, and death, were also not statistically different. Renal outcomes were not statistically different between biopsy-confirmed and clinically diagnosed LN when managed with standard treatment in a tertiary care setting. These findings offer reassurance in cases where biopsy is not feasible; however, biopsy remains the diagnostic gold standard and should be pursued whenever possible.
To compare overweight and obesity prevalence in Swiss patients with psoriatic arthritis (PsA) against the general Swiss population from 2007-2022, evaluate temporal trends, and assess socioeconomic correlates (age, sex, education). We performed a repeated cross-sectional analysis of adults with PsA in the Swiss Clinical Quality Management in Rheumatic Diseases (SCQM) registry who had BMI recorded in 2007, 2012, 2017, or 2022 (patients could contribute to more than one index year). Age-, sex-, and education-stratified BMI distributions were compared with Swiss Health Survey data using χ² goodness-of-fit tests. Within PsA, clinical and socioeconomic variables were compared across BMI categories using Fisher's exact or Kruskal-Wallis tests; pairwise changes over time were assessed with one-sided Wilcoxon rank-sum tests. Among 1,150 PsA patients in 2022, 37.6% were overweight and 28.2% obese, versus 30.9% and 12.1% in the Swiss population. In cross-sectional comparisons, obesity was associated with more frequent elevated C-reactive protein (55.8% vs. 37.0%), higher patient global assessment (mean [SD] 3.2 [2.4] vs. 2.8 [2.2]) and physician global assessment (2.5 [2.0] vs. 2.1 [1.8]), and lower EQ-5D-3L health state (0.7 [0.2] vs. 0.8 [0.2]). Obesity prevalence rose from 19.4% in 2007 to 28.2% in 2022, a trend driven by men. Obesity prevalence varied across educational strata but did not follow a monotonic social gradient; within each stratum obesity was markedly more common in PsA than in the Swiss general population. Overweight and obesity affect nearly two-thirds of Swiss PsA patients and have increased since 2007. Cross-sectional associations between obesity, higher inflammatory burden and poorer patient-reported health state, together with the widening gap versus the general population, support integrating structured, multidisciplinary weight-management programmes into PsA treat-to-target care, particularly for men.
Chronic eosinophilic pneumonia is a rare inflammatory lung disease that typically responds to systemic glucocorticoids but is frequently complicated by relapses and treatment-related toxicity. In recent years, monoclonal antibodies targeting the interleukin-5 (IL-5) pathway have emerged as effective glucocorticoid-sparing therapies in relapsing or glucocorticoid-dependent chronic eosinophilic pneumonia. Alongside these advances, a substantial proportion of patients develops progressive fibrotic changes over time, challenging the traditional view of chronic eosinophilic pneumonia as a fully reversible condition. This narrative review summarises current clinical evidence on the use of anti-IL-5/IL-5 receptor subunit α biologicals in chronic eosinophilic pneumonia, examines the emerging phenotype of fibrotic chronic eosinophilic pneumonia, and discusses the mechanistic links between eosinophilic inflammation and pulmonary fibrosis. We also review experimental and clinical data implicating eosinophils, type 2 cytokines, epithelial alarmins and extracellular traps in fibroblast activation and extracellular matrix deposition, providing a biological rationale for a continuum from inflammation to irreversible lung remodelling. Available data on the use of IL-5-targeted therapies in fibrotic disease are limited, and no prospective studies have specifically addressed this patient population. Conversely, antifibrotic agents such as nintedanib have demonstrated efficacy in progressive fibrosing interstitial lung diseases but have been rarely studied in eosinophilic lung disorders. We propose a phenotype-adapted therapeutic framework in which sustained control of eosinophilic inflammation aims to prevent fibrotic progression in early disease, while antifibrotic therapy may be considered in patients with established or progressive fibrosis. Fibrotic chronic eosinophilic pneumonia thus represents a clinical entity at the crossroads between inflammation and fibrosis, requiring individualised management strategies and dedicated future studies.
Colchicine is an ancient drug that remains a cornerstone in the management of crystal-induced inflammatory diseases, particularly gout and calcium pyrophosphate crystal disease (CPPD). Its clinical use is supported by well-established pharmacological and mechanistic evidences, mainly derived from experimental studies. Colchicine interferes with microtubule-dependent cellular functions, inhibits neutrophil activation, and modulates NLRP3 inflammasome signalling, resulting in reduced interleukin-1β production. In addition, colchicine exerts pleiotropic anti-inflammatory effects that extend beyond crystal synovitis, including modulation of platelet-leukocyte interactions and vascular inflammation. Owing to its narrow therapeutic index, low-dose regimens and careful attention to drug-drug interactions are essential. This narrative review summarises the pharmacology, mechanisms of action, and clinical applications of colchicine in rheumatic disorders, particularly gout and CPPD, and its expanding use in cardiovascular diseases, dermatology, and other inflammatory disorders.
The potential impact of NET (neuroendocrine tumor)-related disease burden on musculoskeletal health remains inconclusive. To assess the musculoskeletal status, its prognostic relevance and association with tumor aggressiveness in NET patients. This cross-sectional study included 41 patients with grade (G) 1, 2, or 3 gastroenteropancreatic (GEP) and lung NETs. Among them, 38 were selected for comparison with 47 healthy controls matched for age, sex and body mass index (BMI). The musculoskeletal health was assessed by dual-energy X-ray absorptiometry (DXA) scan. Within the NET group (median age=72 years old, 46% women), degraded TBS (trabecular bone score) was found in 71% of patients, with osteopenia affecting up to 59% at the femoral neck. The prevalence of hypovitaminosis D was 68%, whereas of low RSMI (relative skeletal muscle index) suggestive of sarcopenia 37%. Patients with advanced-stage NETs showed significantly lower L1-L4 BMD (bone mineral density), L1-L4 T-score, L1-L4 Z-score, 25-hydroxyvitamin D [25(OH)D] levels and BMI than those with earlier-stage disease. G2 NETs were associated with worse L1-L4 BMD, L1-L4 T-score, total hip T-score and diaphysis BMD than G1 NETs. In multivariate analysis, higher 25(OH)D levels and BMI were independently associated with longer progression-free survival (PFS), whereas higher Ki-67 was associated with shorter PFS. Correlation analyses showed inverse associations between Ki-67 and total hip T-score (rho = -0.314, p=0.048) and diaphysis BMD (rho = -0.354, p=0.025); age at NET diagnosis correlated with poorer bone parameters, whereas higher BMI was associated with better bone indices and RSMI. Compared with healthy controls, NET patients had significantly lower TBS, regardless of BMD, T-score or Z-score. NET patients showed a substantial burden of musculoskeletal impairment, with trabecular microarchitecture deterioration detectable despite BMD versus healthy controls. Advanced disease stage, higher grade and systemic treatment were associated with poorer bone health. Increased vitamin D levels and BMI were independently associated with longer PFS, supporting a potential relationship between nutritional-metabolic status and oncological outcomes. Low muscle mass was also frequent, although not significantly associated with tumor aggressiveness. These exploratory findings highlight the need for structured musculoskeletal assessment in NET patients and require validation in larger prospective studies.