BACKGROUND:Rheumatological extraintestinal manifestations (EIMs) represent the most frequent complications of inflammatory bowel disease (IBD). Despite their clinical relevance, they remain heterogeneously defined and inconsistently assessed in both clinical practice and clinical trials. This narrative review aimed to summarize current evidence on the diagnostic assessment of IBD-associated rheumatological EIMs and to identify unmet needs for clinical evaluation and trial design. METHODS:A literature search was performed to identify studies evaluating the diagnosis and assessment of IBD-associated rheumatological EIMs. Data were extracted on diagnostic definitions, classification systems, outcome measures, and the use of patient-reported outcomes (PROs) across observational studies and randomized controlled trials. RESULTS:Substantial heterogeneity was observed in the diagnostic assessment of IBD-associated rheumatological EIMs, with inconsistent use of classification criteria and frequent reliance on nonstandardized clinical evaluation. No PRO instruments specifically developed or validated for IBD-associated rheumatological EIMs were identified. In randomized controlled trials, rheumatological EIMs were variably reported, with heterogeneous endpoints and limited structured assessment, particularly in phase 3 IBD trials. CONCLUSIONS:Evidence from this review reflects considerable methodological variability in the assessment of rheumatological EIMs in IBD. Standardized definitions, harmonized outcome measures, and the development of EIM-specific PROs are needed to support consistent endpoint selection and improve the evaluation of rheumatological outcomes in future clinical trials.

OBJECTIVES:Psoriatic arthritis (PsA) arises in roughly 20-30% of individuals with psoriasis (PsO); notably, >80% of PsA cases are preceded by PsO after a clinically silent interval of immunogenetic priming and subclinical synovio-entheseal inflammation. Identification of this at-risk and subclinical window is hindered by absent staging criteria, validated biomarkers, and standardised surveillance, limiting opportunities for early intervention to prevent irreversible joint damage. METHODS:We conducted a structured narrative review of PubMed (through June 2025) targeting studies on: 1. immunogenetic and molecular drivers of PsO-to-PsA transition, 2. temporal staging frameworks and risk-stratification algorithms, 3. screening instruments and polygenic risk models, 4. imaging modalities for occult inflammation, and 5. pharmacologic and lifestyle interventions aimed at disease interception. RESULTS:Long-term factors (PsO severity, nail disease, family history, obesity) and short-term indicators (arthralgia, imaging-detected enthesitis or synovitis) help stratify PsA risk. Advanced ultrasound and MRI can reveal subclinical inflammation in asymptomatic PsO, though predictive validity remains to be confirmed. Observational data hint at a possible delay in PsA onset with early bDMARD exposure, but randomised prevention trials are lacking. Lifestyle interventions appear promising yet remain untested. CONCLUSIONS:Framing PsA as a staged continuum supports a precision-medicine model that integrates genetic profiling, validated screening, advanced imaging, and targeted intervention. Prospective, biomarker-driven trials and integrated dermatology-rheumatology pathways are needed to validate predictive algorithms and establish effective prevention and early-treatment strategies.

Background: In psoriatic arthritis (PsA), clinical tenderness and ultrasound (US) capture distinct yet related aspects of entheseal disease activity. However, their longitudinal relationship after initiation of biologic disease-modifying antirheumatic drugs (bDMARDs), and the clinical significance of early discordance during follow-up remain unclear. Methods: In this retrospective observational cohort study based on routinely collected medical records, patients with CASPAR-defined PsA and clinically and ultrasonographically active enthesitis at baseline (Clin+/US+) who initiated bDMARD therapy underwent paired, same-day, blinded clinical and US assessments at approximately 6 and 12 months. Agreement between clinical and US findings was quantified using Cohen's kappa. Discordant states (Clin-/US+ and Clin+/US-) were prespecified, and predictors of Clin-/US+ status at 6 months were analyzed using models that accounted for within-patient clustering. Results: Thirty-nine patients contributed 82 entheses and were treated with either tumour necrosis factor inhibitors (53.8%) or interleukin-17 inhibitors (46.2%). At 6 months, agreement between clinical and US assessments was fair (κ = 0.286; 95% confidence interval [CI], 0.080 to 0.492), with 23.2% of entheses classified as Clin-/US+ and 52.4% as concordantly inactive. At 12 months, agreement improved to substantial-to-almost-perfect levels (κ = 0.779; 95% CI, 0.595 to 0.963), with only 1.2% of entheses remaining Clin-/US+ and 80.5% achieving concordant remission. NSAID exposure was the only significant predictor of Clin-/US+ status at 6 months in univariable analysis (odds ratio [OR], 3.82; 95% CI, 1.27 to 11.47; p = 0.017) and remained associated after multivariable adjustment (OR, 6.16; 95% CI, 1.14 to 33.2; p = 0.03). Conclusions: In PsA patients starting bDMARD therapy, clinical and US assessments of enthesitis showed partial discordance at 6 months, followed by greater convergence at 12 months. These findings suggest that clinical and imaging abnormalities may resolve asynchronously during follow-up and should therefore be interpreted in an integrated, time-aware manner. Residual US abnormalities in the setting of clinical improvement should be interpreted cautiously and within the broader clinical context.

Metabolic syndrome (MetS) has been increasingly recognised as a relevant comorbidity in systemic autoimmune diseases; however, data on its prevalence and clinical associations in systemic sclerosis (SSc) remain limited and heterogeneous. This study aimed to evaluate the prevalence of MetS in a large Italian SSc cohort and to explore its clinical, functional, and vascular associations. A cross-sectional multicenter study enrolled 613 SSc patients from 11 tertiary Rheumatology centres across Italy, fulfilling ACR/EULAR 2013 criteria. MetS was defined according to the International Harmonised 2009 Joint Interim Statement criteria. Clinical, laboratory, functional, and imaging data were collected. Comparisons were performed between MetS+ve and MetS-ve patients. Logistic regression analysis was performed to identify factors associated with MetS. Among 570 patients with complete data, MetS was identified in 8.4

OBJECTIVES: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. METHODS: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. RESULTS: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. CONCLUSIONS:Alexithymia is present in PsA and is linked to increased pain perception, disease activity and treatment burden.

OBJECTIVE:To describe clinical phenotype, selected imaging findings and remission trajectories in adults with acute parvovirus B19-associated inflammatory musculoskeletal disease referred for rheumatological assessment. METHODS:This was a non-interventional multicentre observational study in GIRRCS rheumatology units. Adults with new-onset inflammatory musculoskeletal manifestations, positive anti-parvovirus B19 IgM and symptom onset within 4 weeks were enrolled. Clinical, laboratory and clinically indicated imaging data were collected. Time to first documented clinical remission was defined as the interval from symptom onset to the first rheumatologist-confirmed assessment showing resolution of inflammatory musculoskeletal manifestations. Patients requiring disease-modifying escalation were analysed separately. RESULTS:Twenty-four adults were enrolled; 18 were women (75.0%) and mean age was 44.4 ± 14.8 years. Clinical involvement was polyarticular in 14 patients (58.3%) and oligoarticular in 10 (41.7%); enthesitis occurred in 4 (16.7%) and dactylitis was absent. Inflammatory markers were modestly elevated, and most patients with complete autoantibody data were seronegative. Imaging was performed selectively and documented inflammatory abnormalities in clinically indicated examinations. Follow-up data were available for 21 patients, of whom 20 (95.2%) achieved clinical remission without DMARD escalation; median documented remission timing was 21 days (IQR 10-60; range 7-135). One patient required biologic escalation for persistent inflammatory disease. Exploratory regression analyses did not identify robust associations with documented remission timing. CONCLUSION:Acute parvovirus B19-associated inflammatory musculoskeletal disease may mimic inflammatory rheumatic disease in adults referred for rheumatological assessment. Most patients achieved remission without disease-modifying escalation, although remission timing varied and one patient required biologic therapy for persistent inflammatory disease.

ObjectivesTo evaluate the therapeutic management of patients with active adult-onset Still’s disease (AOSD) in a multicentre real-world setting and to provide and compare current real-world treatment strategies with existing recent international recommendations.MethodsFrom January 2022 to December 2023, 173 consecutive patients with active AOSD attending centres participating in the Gruppo Italiano di Ricerca in Reumatologia Clinica e Sperimentale (GIRRCS) AOSD research study group were prospectively enrolled. Demographic, clinical, and laboratory data were collected, and therapeutic strategies prescribed by the treating physicians were systematically recorded. Factors associated with the administration of biologic disease-modifying antirheumatic drugs (bDMARDs), including IL-1 and IL-6 inhibitors, were analysed.ResultsGlucocorticoids were administered in 97.7% of patients. Conventional synthetic DMARDs were prescribed in 58.8% of cases, mainly methotrexate and cyclosporin A. Overall, 43.3% of patients received bDMARDs, predominantly IL-1 and IL-6 inhibitors. Specifically, 33.5% were treated with IL-1 inhibitors, 5.8% with IL-6 inhibitors, and 4.0% with tumour necrosis factor inhibitors. After three months of treatment, 86.7% of patients achieved clinical inactive disease as assessed by the treating physician. Comparing recorded treatment strategies with international recommendations, no compliance was found regarding the use of glucocorticoids, which are recommended to be markedly limited or avoided, and early administration of bDMARDs, which were administered within 3 months in a minority of patients.ConclusionsThis multicentre real-world study outlines current therapeutic approaches for patients with active AOSD and highlights a gap between international treatment recommendations and clinical practice, underscoring the need for further studies to optimize patient management.

Enteropathic spondyloarthritis is a common, under-recognised musculoskeletal manifestation of inflammatory bowel disease and a potentially preventable contributor to long-term disability. Epidemiological, imaging, and biomarker data support a continuum from at-risk states (ie, high-risk inflammatory bowel disease phenotypes with early extraintestinal manifestations and non-specific pain), through subclinical MRI-defined or ultrasound-defined sacroiliac and entheseal inflammation, to early clinical enteropathic spondyloarthritis with overt synovitis, enthesitis, and inflammatory back pain, often after prolonged diagnostically ambiguous symptoms. This transition unfolds within a gut-derived inflammatory milieu shaped by type-3 immunity, dysbiosis, epithelial barrier dysfunction, gut-homing and tissue-resident lymphocyte circuits, and polygenic susceptibility, with only partial synchrony between intestinal and musculoskeletal trajectories. Clinically, these mechanisms yield phase-specific signatures in which faecal calprotectin, C-reactive protein, and HLA-B27 act as probabilistic modifiers, and power Doppler ultrasound and sacroiliac or spinal MRI enable recognition of inflammation before irreversible structural change. In this Review, we synthesise mechanistic and clinical evidence across the at-risk-to-early articular continuum (this term refers to individuals at-risk of enteropathic spondyloarthritis, individuals with subclinical musculoskeletal disease, and patients with early clinical articular disease). We propose a precision, dual-compartment strategy addressing both gut and joint involvement, integrating structured musculoskeletal screening, probability-guided imaging, and timely use of therapies with proven gut-joint efficacy into inflammatory bowel disease care, aiming to prevent diagnostic delay, limit structural damage, and reframe enteropathic spondyloarthritis as an interceptable, treat-to-target phenotype along the gut-joint axis.

Luisa Costa,1,* Francesco Caso,1,2,* Francesco Maione,2 Roberto Giacomelli,3,4 Piero Ruscitti51Department of Clinical Medicine and Surgery, University of Naples Federico II, Naples, Italy; 2Immunopharmalab, Department of Pharmacy, School of Medicine and Surgery, University of Naples Federico II, Naples, Italy; 3Clinical Unit of Immunorheumatology, Fondazione Policlinico Universitario Campus Bio-Medico, Rome, Italy; 4Research Unit of Immunorheumatology, Department of Medicine and Surgery, Campus Bio-Medico University of Rome, Rome, Italy; 5Rheumatology Unit, Department of Biotechnological and Applied Clinical Sciences, University of L’Aquila, L’Aquila, Italy*These authors contributed equally to this workCorrespondence: Francesco Caso, Department of Clinical Medicine and Surgery, University of Naples Federico II, Naples, Italy, Email francesco.caso@unina.it; francescocaso1@yahoo.itAbstract: Janus kinase (JAK) inhibition is an established therapeutic strategy in rheumatoid arthritis, but heterogeneous treatment responses, persistent safety concerns, and the need for more precise therapeutic positioning continue to stimulate the development of additional JAK-directed compounds. This structured narrative review evaluates the pharmacological rationale, clinical efficacy, structural and imaging outcomes, safety evidence, and developmental maturity of emerging, regionally approved, and investigational agents. Peficitinib has the most mature evidence base, including Phase 3 efficacy, radiographic protection, long-term extension data, and pooled safety analyses. Ivarmacitinib has phase 3 and exploratory MRI data, whereas the phase 3 trial of TLL-018 has reached primary completion, with sponsor-reported topline findings available but complete results not yet published. CPL409116/CPL’ 116 remains supported by limited Phase 2 evidence. Decernotinib represents an informative historical proof-of-concept programme. Overall, no emerging agent has yet demonstrated a reproducible advantage over established JAK inhibitors in sustained remission, structural preservation, difficult-to-treat disease, or overall benefit–risk balance. Future development should prioritise active comparators, prespecified structural outcomes, prolonged safety assessment, and prospectively validated treatment-specific biomarkers.Keywords: rheumatoid arthritis, Janus kinase inhibitors, targeted synthetic disease-modifying antirheumatic drugs, emerging therapies, JAK

Dactylitis (from the Greek word dactylos, meaning "digit") is a medical condition commonly known as "sausage digit", referring to the diffuse swelling of a finger or toe. Dactylitis is most commonly associated with the spectrum of spondyloarthritis, particularly psoriatic arthritis (PsA), and more rarely with other inflammatory conditions such as sarcoidosis and gout. In PsA, dactylitis is associated with increased disease severity and radiographic progression, and its recognition may facilitate early diagnosis and timely treatment. In sarcoid disease, dactylitis is clinically relevant, reflecting granulomatous inflammation and potentially indicating multisystem involvement. Although most commonly linked to inflammatory disorders, it may also manifest in a variety of other conditions, such as trauma, congenital deformities, infectious diseases, and neoplastic processes, all of which can present with a clinically indistinguishable phenotype. This review provides a comprehensive, up-to-date overview of dactylitis, beginning with the origin of the term and its earliest historical and scientific references, and concluding with the latest insights into aetiopathogenesis, classification, anatomy, imaging, and therapeutic strategies. Through the integration of clinical knowledge with new developments in imaging, the paper explores how the study of dactylitis can extend beyond PsA.

Breast cancer radiotherapy and autoimmune myositis intersect in a clinically complex setting in which paraneoplastic disease, pre-existing inflammatory myopathy, and radiation-related muscle injury may overlap. Dermatomyositis is the idiopathic inflammatory myopathy most strongly associated with malignancy, and breast cancer is one of the solid tumours most frequently reported in cancer-associated myositis, particularly in anti-TIF1γ- and anti-NXP2-positive subsets. A structured narrative review of PubMed and Scopus was performed from database inception to March 2026. Evidence was synthesised qualitatively owing to limited and heterogeneous literature. Muscle symptoms during breast cancer treatment may reflect autoimmune, paraneoplastic, radiation-induced, fibrosis-related, or recall myositis. MRI is the most informative modality for pattern-based assessment, with FDG PET-CT and ultrasound providing complementary value in selected cases. Although direct disease-specific evidence is sparse and derives largely from retrospective series, mixed connective tissue disease cohorts, radiobiological studies, and case reports, radiotherapy does not appear to represent an automatic contraindication when disease activity, multidisciplinary evaluation, and conformal planning are taken into account. Breast cancer radiotherapy in patients with autoimmune or cancer-associated myositis requires structured differential diagnosis rather than categorical avoidance. Diagnostic assessment should integrate timing, field distribution, imaging, serology, systemic features, and treatment sequence. Further studies should refine risk stratification, muscle-specific dose constraints, and biomarkers distinguishing radiation-related from autoimmune or paraneoplastic myositis.

OBJECTIVE:Here we investigate the status of the adiponectin-PEPITEM pathway in early, treatment naive rheumatoid arthritis (RA) and psoriatic arthritis (PsA) and the therapeutic efficacy of PEPITEM administration in preclinical models. METHODS:Peripheral blood was isolated from patients with clinical suspect arthralgia and suspected inflammatory arthritis and analyzed by flow cytometry or Western blot. Effect of PEPITEM treatment on inflammatory arthritis was assessed in mice by histology, single-cell RNA sequencing, flow cytometry, or multiplex analysis. RESULTS:Patients newly diagnosed with RA and PsA had significantly reduced expression of adiponectin receptor 2 and its downstream signaling adapter protein APPL-1 on their peripheral-blood mononuclear cells, resulting in diminished response to adiponectin and local synovial concentrations of PEPITEM. Building on these observations, treatment with PEPITEM in three distinct inflammatory arthritis animal models significantly reduced arthritis severity, joint swelling, leukocyte infiltration, and expression of several pro-inflammatory mediators (eg, JE [CCL2], RANTES, interleukin-16) in the synovium. Mechanistically, PEPITEM treatment suppressed the cyclooxygenase 2 and NF-κB signaling pathways. Moreover, PEPITEM altered the composition of leukocyte subsets recruited into the joint. CONCLUSION:Collectively, these findings underscore the importance of understanding the dysregulation of the adiponectin-PEPITEM pathway in different immune-mediated inflammatory diseases (IMIDs), such as RA and PsA. The observed differences in expression and downstream signaling through adiponectin receptors suggest potential targets for therapeutic intervention to restore the balance of this regulatory pathway to mitigate chronic inflammation and disease progression in these patients, paving the way for its clinical use as an alternative and/or combination therapy for early IMIDs.

Background The use of heterogeneous empirical definitions to assess disease activity in adult-onset Still's disease limits evidence on the efficacy of immunosuppressive agents. Thus, we aimed to specifically develop and validate definitions of clinical criteria for the assessment of disease activity in adult-onset Still's disease. Methods We used data from the GIRRCS (Gruppo Italiano Di Ricerca in Reumatologia Clinica e Sperimentale) adult-onset Still's disease cohort to develop and validate clinical criteria for disease activity. From Jan 1, 2022, to Dec 31, 2023, consecutive patients attending the Italian rheumatological centres involved in the GIRRCS adult-onset Still's disease were included if they were aged ≥18 years and fulfilled the Yamaguchi criteria for diagnosis of adult-onset Still's disease. Patients' clinical characteristics were assessed at baseline and 3 months and 6 months. Additionally, we used baseline data from the CONSIDER (Canakinumab for treatment of adult-onset Still's disease to achieve reduction of arthritic manifestation) trial to externally validate the criteria (recruitment June 21, 2012, to May 5, 2018). The item reduction was based on correlations between clinical characteristics and disease activity as scored by physicians, principal component analysis, and a longitudinal linear mixed model with disease activity as the dependent variable. Performance of the developed criteria was evaluated using area under the receiver operating characteristic curves (AUROCs), separately for development and validation data. People with lived experience of adult-onset Still's disease were involved in study design and implementation. Findings 187 patients from GIRRCS (130 [70%] in the development cohort and 57 [30%] in the preliminary validation cohort; 94 [50%] female and 93 [50%] male; mean age 40·8 years [SD 17·3]) and 41 patients from the CONSIDER trial (28 [68%] female and 13 [32%] male; mean age 43·0 years [13·1]) were evaluated. Fever, skin rash, arthritis, patient global assessment of at least 2 cm, and C-reactive protein (CRP) greater than 10 mg/L were selected as the criteria for disease activity assessment. Active adult-onset Still's disease was defined as fever and one of the following criteria: skin rash, arthritis, patient global assessment of at least 2 cm, CRP greater than 10 mg/L; or as no fever but at least three of the other criteria (AUROC of 0·93 in development cohort, 0·85 in the preliminary validation cohort, and 0·88 in the external validation cohort). Patients with no fever and no more than one of the aforementioned criteria were considered to have low disease activity (AUROC of 0·86 at 3 months and 0·94 at 6 months in the preliminary validation cohort). Clinically inactive disease was defined as the absence of all five criteria. Interpretation Disease activity criteria in adult-onset Still's disease were developed to support the attainment of clinically inactive disease as the main treatment target in patient management. Funding None.

ObjectivesThis study aims to explore the application of machine learning techniques in assessing macrophage activation syndrome (MAS) in Still’s disease.MethodsA multicenter, observational, prospective study was conducted, including patients with Still’s disease enrolled in the Gruppo Italiano di Ricerca in Reumatologia Clinica e Sperimentale (GIRRCS) AOSD Study Group and the AutoInflammatory Disease Alliance (AIDA) Network Still’s Disease Registry.ResultsA total of 737 patients (age: 35.5 ± 17.8, male sex: 44.7%) with Still’s disease were assessed; 11.4% were affected by MAS, and 3% had a poor prognosis. First, random forest imputation was applied to the original dataset. Subsequently, a machine-learning-driven assessment was developed to explore MAS occurrence. Collectively, regression models, an exploration decision tree, and a random forest were applied, suggesting the importance of ferritin, age, C-reactive protein (CRP), and systemic score. A logistic regression model accounting for data leakage concerns was then generated using these variables, and missing values were imputed using random forest imputation. This analysis supported the role of the selected variables, which were further combined across different clinical scenarios to estimate the probability of MAS. The highest risk of MAS was estimated for patients simultaneously characterized by age ≥ 45 years, ferritin ≥ 4,178.10 ng/mL, CRP ≥ 27.15 mg/L, and a systemic score ≥ 7, corresponding to a 34.7% probability of MAS, as well as for those characterized by ferritin ≥ 4,178.10 ng/mL, CRP ≥ 27.15 mg/L, and systemic score ≥ 7, corresponding to a 33.5% probability of MAS.ConclusionsA machine-learning-driven prediction of MAS was explored in Still’s disease, highlighting the importance of age of onset, hyperferritinaemia, increased CRP, and multiorgan involvement. A combination of these features may suggest a clinician-friendly algorithm for stratifying the probability of MAS during Still’s disease.

INTRODUCTION:Psoriatic arthritis (PsA) is an immune-mediated inflammatory disease in which the IL-23/Th17/IL-17 axis contributes to musculoskeletal and extra-musculoskeletal inflammation. Ocular manifestations, particularly dry eye disease (DED), uveitis, and less frequently episcleritis and scleritis, are increasingly recognized across psoriatic disease, although their pathobiology and relationship to systemic inflammatory pathways remain incompletely defined. AREAS COVERED:This narrative review examines evidence linking IL-17 to ocular disease in psoriatic disease, with emphasis on ocular surface inflammation. We summarize ocular involvement in PsA, review mechanistic and translational data across skin, enthesis, synovium, and the lacrimal-ocular surface unit, and appraise clinical data on IL-17-pathway inhibitors, including their established musculoskeletal and cutaneous efficacy and less consistent ocular effects. EXPERT OPINION:IL-17 may contribute to ocular surface inflammation in PsA, but this remains largely inferential because direct PsA-specific ocular data are scarce. IL-17A inhibitors are effective in musculoskeletal and cutaneous disease, yet ocular benefit cannot be assumed from systemic efficacy. Current evidence suggests limited impact on established DED and less consistent uveitis protection than monoclonal TNF inhibition. Prospective studies with adjudicated ocular endpoints and tear/conjunctival profiling are needed to define whether IL-17-responsive ocular phenotypes exist in PsA.

INTRODUCTION:Still's disease is a systemic inflammatory disorder characterized by a complex cytokine network involving interleukin (IL)-1, IL‑6, IL‑18 and interferon (IFN)-γ. Although IL‑1 and IL‑6 inhibitors represent the cornerstone of current targeted therapy, a subset of patients remains refractory or develops treatment-related limitations. Janus kinase inhibitors (JAKis) have emerged as a promising therapeutic strategy. AREAS COVERED:We reviewed the possible role of JAKis in the management of Still's disease, with a focus on their mechanistic rationale, clinical evidence, and potential positioning within current therapeutic strategies. A narrative review was conducted through a comprehensive search of MedLine via PubMed accordingly. EXPERT OPINION:Preliminary evidence, mainly derived from small observational studies, suggests that JAKis may improve systemic and articular manifestations and allow glucocorticoid sparing. In addition, agents such as ruxolitinib may have a role in macrophage activation syndrome through inhibition of IFN‑γ-dependent pathways. However, incomplete modulation of IL‑1-driven and inflammasome-dependent mechanisms may represent a potential limitation in specific disease phenotypes. JAKis represent a promising addition to the therapeutic armamentarium of Still's disease, particularly in refractory cases. Further prospective studies are needed to define the role of JAKis within the treatment algorithm of Still's disease.

To assess the contribution of Systemic sclerosis (SSc)-specific features on type II diabetes mellitus (T2D) in a large cohort of Italian SSc patients. A total of 613 SSc patients from 11 tertiary Rheumatology Units across Italy were included. All patients underwent full history taking, clinical examination, and relevant laboratory and radiological evaluations. Demographic, socioeconomic, and disease-specific factors were compared between SSc patients with and without T2D. The prevalence of T2D in the study cohort was 7.6