Pain is a frequent symptom in people with inflammatory arthritis (IA), which has substantial impact on their quality of life. Analyses of electronic health record data indicate that UK pain care in people with IA often involves prescribing long-term opioids and gabapentinoids, despite absent trial evidence for efficacy. Patient survey data suggest that non-pharmacological pain care with supportive trial evidence is underused. A UK-specific guideline on pain management for people with IA is required to address this. This comprehensive life-course guideline is the first British Society for Rheumatology Guideline to specifically address pain in people with IA. It provides evidence-based recommendations on how pain can be best managed in people with IA. It was developed using the methods outlined in the British Society for Rheumatology's 'Creating Clinical Guidelines' protocol by a multidisciplinary Guideline Working Group, comprising healthcare professionals with expertise in paediatric and adult rheumatology and people with lived experience. By undertaking and considering the evidence from several systematic literature and umbrella reviews, 23 recommendations were developed. These address how pain should be assessed in people with IA alongside the role of the following treatments in IA pain management: DMARDs, glucocorticoids, analgesics, neuromodulators, exercise and physical activity, psychological interventions, ergonomic and orthotic interventions (excluding orthoses for foot pain), education, weight management and diet, addressing sleep problems, fatigue management, digital technologies and medical devices, complementary therapies, and support from others. An audit tool is provided to support the Guideline's implementation, and key recommendations made for future research.
Cardiovascular disease (CVD) accounts for approximately 40% of deaths among patients with rheumatoid arthritis (RA), yet the burden of heart failure (HF) within this population remains poorly characterized. Using the KURAMA cohort, we aimed to quantify the prevalence of HF among RA outpatients and develop a practical HF screening tool that uses variables readily available to rheumatologists in routine clinical practice. A cross-sectional study of 542 outpatients with RA was conducted. Their HF status was determined using a prespecified multistep algorithm that integrated clinical history, loop diuretic use, N-terminal pro-B-type natriuretic peptide (NT-proBNP), echocardiography, and careful differentiation from interstitial lung disease (ILD). Adaptive LASSO regression was applied to identify independent factors associated with HF and construct a detection score using non-cardiac variables. Heart failure was detected in 26.5% of patients with RA. Older age, lower haemoglobin (Hb) levels, higher serum creatinine (CRE) levels, and higher Simplified Disease Activity Index (SDAI) were identified as independent non-cardiac factors associated with HF. A 4-factor HF detection score was constructed based on adjusted odds ratios. The area under the receiver operating characteristic curve (AUC) for the discrete score based on variables routinely available in rheumatology clinics was 0.793, comparable to that of NT-proBNP ≥ 125 pg/mL alone (AUC = 0.814). HF affects over one in four RA outpatients. A simple 4-factor score may serve as a practical first-line triage tool to identify patients who warrant further cardiac evaluation and cardiology referral.
To compare the effects of two physiotherapist-guided, personalized, stepwise-adapted exercise interventions-a home-based program (HomeEX) and an immersive virtual reality (IVR) exergaming program (JiaFitXR)-on physical fitness, functional capacity and physical activity in adolescents with Juvenile Idiopathic Arthritis (JIA). This randomized controlled trial included 50 adolescents aged 13-18 years with JIA, randomly assigned (1:1) to HomeEX or JiaFitXR. Both programs targeted balance, strength, endurance and agility, delivered twice weekly for 8 weeks under physiotherapist supervision. Functional capacity (6-Min Walk Test, Sit-to-Stand, Step-Up/Step-Down tests) and physical fitness (FitnessGram components, muscle strength, EMG activation, grip force) were assessed pre- and post-intervention by blinded physiotherapists. Analyses were performed using paired and independent t-tests and repeated-measures ANOVA, following the intention-to-treat principle. Both physiotherapist-guided interventions significantly improved physical fitness, functional capacity and daily activity (P < 0.05). Greater gains in 1-Min Sit-to-Stand, Step-Up and Step-Down tests, as well as in lower-extremity endurance and neuromuscular activation, were observed in the JiaFitXR group (P < 0.05). The HomeEX group showed superior improvements in flexibility and upper-extremity strength (P < 0.05). Step counts increased similarly in both the groups, while perceived exertion remained stable throughout the program. Both physiotherapist-guided exercise approaches effectively enhanced physical and functional outcomes in adolescents with JIA. The IVR-based intervention provided additional benefits in lower-extremity endurance and engagement, supporting its potential as an innovative and motivating adjunct to paediatric rheumatology rehabilitation. ClinicalTrials.gov; NCT06176846.
The role of C-reactive protein (CRP) in Psoriatic Arthritis (PsA) as a diagnostic and prognostic marker is debated. We compared clinical and epidemiological features, as well as long-term outcomes, between patients with "elevated" (>0.5 mg/dL) and patients with "normal" (≤0.5 mg/dL) CRP at diagnosis. In this real-world study, we analyzed data from 609 PsA patients categorized by their CRP at diagnosis. Demographics, clinical characteristics, comorbidities, and long-term outcomes were compared. The statistically significant variables in the univariate analyses were used to build two multivariable logistic regression models: i. assessing associations between CRP and features at PsA diagnosis, ii. examining its link with long-term outcomes (including "difficult to manage" and "persistent disease") and characteristics throughout the disease course. Of 609 patients, 132 (21.7%) displayed normal and 477 (78.3%) elevated CRP values at diagnosis. By univariate analysis, elevated CRP was associated with longer disease follow-up, BMI > 25 Kg/m2, enthesitis (at diagnosis and disease course), hypertension, hyperuricemia, new bone formation and "persistent disease". By multivariable analyses, elevated CRP at diagnosis was independently linked with BMI >25 Kg/m2 (OR 1.69, 95% CI 1.05-2.72), enthesitis (OR 2.04, 95% CI 1.24-3.38), hypertension (OR 2.07, 95% CI 1.04-4.11), new bone formation (OR 2.57, 95% CI 1.33-4.94), and "persistent disease" (OR 4.36, 95% CI 2.22-8.59). Overall PsA characteristics are comparable, irrespective of the CRP-levels at diagnosis, apart from new bone formation, enthesitis, "persistent disease" and increased cardiometabolic burden which were independently associated with elevated CRP-levels at PsA diagnosis.
Chemokine CXCL10 plays an important role in PsA, an inflammatory arthritis associated with psoriasis. CXCL10 is post-translationally regulated by dipeptidyl peptidase-4 (DPPIV). The objectives of this study were to measure levels of DPPIV, CXCL10 and DPPIV enzyme activity (EA) in patients with PsA, psoriasis without arthritis (PsC), OA and healthy controls (HC), and in PsA patients before and after MTX treatment initiation. Serum samples were acquired from 80 PsA, 80 PsC, 40 HC and 40 patients before and after 24 weeks of MTX treatment. SF and matched serum were collected from 14 PsA and 14 sex-matched OA patients. Levels of DPPIV and CXCL10 were quantified using ELISA, DPPIV EA was measured using a luminescent protease assay. Patients with PsA had higher DPPIV levels than PsC, whereas HC had the highest level compared with both. Significant increase in DPPIV levels was observed in PsA patients after MTX treatment, whereas CXCL10 levels decreased significantly. DPPIV levels were negatively correlated with CXCL10 levels after MTX treatment (r = -0.27, P = 0.02). DPPIV levels were significantly higher in SF of PsA compared with OA patients. Higher DPPIV levels were detected in SF compared with serum samples of PsA patients. CXCL10 concentration in SF displayed similar patterns to DPPIV. Our exploratory findings suggest that DPPIV SF levels may be an important indicator of joint inflammation in PsA patients. In PsA patients, DPPIV may be associated with MTX response. CXCL10 may be regulated post translationally by DPPIV.
Current guidelines recommend influenza and pneumococcal vaccination in the majority of patients with rheumatic diseases. This study aimed to summarize the coverage of influenza and pneumococcal vaccines among these patients. A literature search was conducted in PubMed, Embase, Web of Science and Scopus for eligible studies. Vaccination rate was presented as a percentage with 95% CI. Clinical characteristics of the vaccinated patients were shown as the mean difference or odds ratio with 95% CI. Sensitivity analyses, subgroup analyses and meta-regression were performed to identify sources of heterogeneity. A total of 51 studies were identified. The pooled vaccination rates of influenza vaccine in patients with RA, SLE, SpA and PsA were 50%, 42%, 43% and 53%, respectively. The corresponding rates of pneumococcal vaccination in patients were 37%, 30%, 39% and 41%, respectively. Compared with unvaccinated RA patients, vaccinated RA patients were associated with older age and an increased prevalence of comorbidities. Geographical location and use of DMARDs were two significant factors affecting the heterogeneity of the study results. A larger proportion of patients received vaccine education from rheumatologists rather than general practitioners, and the two major reasons for not receiving vaccination were 'lack of awareness' and 'not offered by doctors'. Influenza and pneumococcal vaccine coverage was still suboptimal in patients with rheumatic diseases. Enhancing vaccine education from physicians and improving awareness of patients may become two important approaches to improve vaccination rates.
To evaluate the relationship between IFN-related gene (IRG) expression and disease activity, organ involvement and serological subgroups in JDM and to assess its potential as a biomarker for disease monitoring and treatment response. Patients with JDM enrolled in a single-centre cohort were assessed using standardized clinical measures, including physician's global assessment (PGA), Childhood Myositis Assessment Scale (CMAS), Manual Muscle Testing (MMT8) and modified skin disease activity score. Associations between IRG expression and clinical features were analysed using correlation analyses and mixed-effects models. Longitudinal trajectories of disease activity were explored using latent class mixed models. Seventy-four patients contributed 158 samples. Expression of type-I IRGs (IFI27, IFI44L, IFIT1, RSAD2, SIGLEC1) and CXCL10 was significantly higher in active disease and correlated with muscle and skin disease activity. IRG expression inversely correlated with CMAS and MMT8 and positively with mDAS. Distinct organ-specific associations were identified: CXCL9 expression was associated with interstitial lung disease, while IL-18 was associated with calcinosis, cutaneous ulceration and gastrointestinal involvement. Higher IRG expression was observed in patients with anti-MDA5 and anti-NXP2 autoantibodies. Longitudinal analyses demonstrated that IRG expression paralleled disease activity trajectories and decreased in patients achieving inactive disease, including those treated with baricitinib. IFN pathway activation is closely associated with disease activity and organ involvement in JDM. IRG expression reflects dynamic changes in disease status and may serve as a clinically useful biomarker for monitoring disease activity, stratifying patients by organ involvement and supporting response assessment to targeted therapies.
Identifying which patients with psoriasis (PsO) may develop psoriatic arthritis (PsA) is a research priority. We have previously shown that elafin along with IL-36g are excellent cutaneous biomarkers for PsO. The protease inhibitor elafin and its target protease, neutrophil elastase (NE), can be detected in both serum and epidermal samples. Our aims were to assess if known PsO biomarkers are expressed differentially in patients affected by plaque PsO with and without PsA. Protein expression of NE and elafin were analysed in matched epidermal samples and serum of PsO, PsA patients and healthy controls. Findings were validated in independent PsA and arthritis cohorts. The ratio between NE and elafin differed significantly between PsO and PsA patients. Expression of elafin was reduced in PsA samples as compared to plaque PsO patients. The ratio of NE to secretory leukocyte protease inhibitor was also increased in PsA as compared to PsO patients with no PsA, healthy controls and other arthritis patients. PsA patients show a reduced NE inhibitor expression in both the skin and blood compartment compared to those with plaque PsO only. This may suggest differences in the ability to regulated neutrophil activity in PsA patients.
To determine disease-specific associations of serum vascular cell adhesion molecule-1 (VCAM-1) and associated mortality in systemic sclerosis (SSc). Participants were identified from the Australian Scleroderma Cohort Study. Data were linked with the National Death Index for cause-specific mortality. VCAM-1 was measured using a magnetic Luminex assay. Participant characteristics and information on organ specific manifestations were extracted until February 2024. Participants were stratified into VCAM-1 quartiles. Of 388 participants, 87.1% were female and 76.8% had limited cutaneous disease. Median age at diagnosis was 45.7 years (IQR 36.4-56.7).Participants with upper quartile VCAM-1 (Q4) had increased mortality compared to others (HR 2.17, 1.54-3.04; p < 0.001). Despite the significant increased mortality in Q4, there were no statistically significant differences in sex, age, disease duration, disease subtype, autoantibody profile or forced vital capacity across the VCAM-1 quartiles.Q4 were more likely to have pulmonary arterial hypertension (PAH; p = 0.028), SSc-attributable myocardial disease (p = 0.009) and digital ulcers (p = 0.003). In cause-specific mortality analysis, Q4 were more likely to have PAH (HR 3.08;1.68-5.65, p < 0.001), SSc-attributable myocardial disease (HR 2.85;1.51-5.38, p = 0.001) and all-cause cardiovascular disease (HR 2.50;1.60-3.89, p < 0.001) listed as a cause or contributor to death. Q4 VCAM-1 level was not associated with interstitial lung disease presence, severity or cause-specific mortality. The increased mortality in participants with SSc and Q4 VCAM-1 levels is attributable to increased frequency of vascular disease manifestations. Q4 participants do not have a disproportionate frequency of other established risk factors for increased mortality, suggesting an independent role for VCAM-1 in disease pathophysiology.
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.
We examined whether annual gout flare frequency, as a marker of cumulative inflammatory burden, predicts long-term major adverse cardiovascular events (MACEs). Using the TriNetX Global Collaborative Network, we identified adults with a first EHR-recorded treated gout flare in 2017. Using a 12-month landmark exposure window, patients were classified as low (≤3), moderate (4-6) or high (≥7) flares/year. Modified MACE (myocardial infarction, stroke, heart failure) was followed from the landmark. Groups were compared using 1:1 propensity score matching. A sensitivity analysis applied a stricter flare definition (gout diagnosis with colchicine, corticosteroid or intra-articular injection within 0-3 days; NSAIDs excluded). Among 44 705 patients, matching produced balanced cohorts (high vs low, 13 179 pairs; moderate vs low, 9700 pairs). A graded dose-response was observed: at 7 years, MACE risk was higher in the high (RR 1.45; 95% CI 1.37-1.53) and moderate (RR 1.24; 1.15-1.33) groups vs low. Heart failure risk was elevated in both the groups (HR 1.27 [high]; 1.17 [moderate]); stroke and myocardial infarction were elevated only in the high group (7-year HR 1.28 each), with stroke significant from 3 years. Findings were consistent under the stricter sensitivity definition (7-year MACE HR 1.19 [high] and 1.12 [moderate]). Annual gout flare frequency is a graded marker of sustained cardiovascular risk. Heart failure risk rises with both moderate and high burden, whereas atherothrombotic events emerge predominantly with high-flare frequency, suggesting they require greater cumulative inflammatory exposure.
To assess whether fluctuations in immunoglobulin G anti-double stranded DNA (IgG anti-dsDNA) antibodies and C3 levels predict flares and sustained activity in patients with prolonged serologically active clinically quiescent (SACQ) systemic lupus erythematosus (SLE), and to explore additional risk factors for flare. SLE patient data from the University College London Hospital Lupus cohort were collected (2020-2025). Prolonged SACQ was defined as ≥6 months of elevated IgG anti-dsDNA and/or low C3 without clinical activity (BILAG-2004 index D/E in all domains). Associations between biomarker changes and outcomes, adjusted for main confounders, were tested longitudinally with generalized estimating equations (GEE). Sixty patients (531 visits) were included. Over a mean 3.3-year follow-up, 38 patients (63.3%) experienced ≥1 flare. Baseline characteristics were comparable between patients with and without flares, except for longer follow-up duration (P = 0.005) and a higher prevalence of anti-Ro positivity (P = 0.018) among those who developed flares. In GEE-models, higher IgG anti-dsDNA and lower C3 levels independently predicted flares and sustained activity at the subsequent visit, including moderate-to-severe cases. Most SACQ patients developed clinical flares. Changes in IgG anti-dsDNA and C3 levels emerged as strong predictors of flare in prolonged SACQ patients in a visit-by-visit analysis, supporting close clinical monitoring and highlighting the value of serological trends despite the presence of prolonged clinical quiescence and sustained biomarker abnormalities.
ANCA-associated vasculitides (AAVs) are rare diseases characterized by small-vessel necrotizing vasculitis, multiorgan involvement and positivity for ANCAs. The main phenotypes are granulomatosis with polyangiitis, microscopic polyangiitis and eosinophilic granulomatosis with polyangiitis, representing distinct yet partially overlapping entities in terms of pathogenesis, clinical expression and therapeutic management. Patients with AAV face a substantial cardiovascular (CV) and thrombotic risk, with higher rates of myocardial infarction, ischaemic stroke and venous thromboembolism than the general population. The excess CV burden reflects a complex, time-dependent interplay between disease-related inflammation, traditional CV risk factors and treatment-related toxicity, with inflammatory activity emerging as a key driver of early CV events. Across the disease course, this evolving risk profile requires multidisciplinary management to limit CV damage accrual and related mortality. This review integrates evidence on pathogenesis, clinical manifestations and management of CV disease in AAV, highlighting its time-dependent trajectory and key unmet needs.
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Smoking has been consistently associated with a paradoxically lower risk of Sjögren's disease (SjD). We used genetic approaches to investigate whether this association reflects a causal effect of smoking or shared genetic architecture, and to identify shared loci that may help explain this paradox and inform disease biology. We applied an integrated cross-trait genetic framework using genome-wide association data for smoking initiation and SjD. Conventional Mendelian randomization (MR) was used as an initial test of association, followed by genome-wide causal modelling (CAUSE and latent causal variable analysis) to distinguish directional causality from shared genetic architecture. Shared loci were identified using cross-trait pleiotropy analysis, refined through colocalization, and further explored using proteome-informed mediation analyses. Conventional MR showed an inverse association between genetic liability to smoking initiation and SjD risk (OR 0.53, 95% CI 0.34-0.84). However, genome-wide modelling did not support a causal effect and instead suggested the association was driven by shared genetic influences. Cross-trait pleiotropy analysis identified 1536 variants across 11 loci, with colocalization supporting shared causal variants at five regions (3q13.32, 2q22.3, 8p21.2, 14q24.3 and 5q34). These loci implicated pathways related to neuroimmune signalling, epithelial organization and interferon regulation. Proteome-informed analyses identified no circulating proteins that robustly mediated the smoking-SjD relationship. The inverse smoking-SjD association likely reflects shared genetic liability rather than a protective causal effect. These findings highlight biological pathways relevant to SjD pathogenesis and emphasize the importance of cautious interpretation of MR estimates when traits share genetic architecture.
This study aimed to characterize the clinical phenotypes of adult-onset Still's disease-related lung disease (AOSD-LD) in a Chinese cohort, and to evaluate the associations of lung disease and distinct radiographic patterns with macrophage activation syndrome (MAS) and disease relapse. In this cohort of 209 patients with AOSD, individuals were retrospectively stratified into AOSD-LD and non-lung disease groups based on radiographic findings. Clinical features associated with AOSD-LD were characterized. Multivariable Cox regression and subgroup analyses were performed to evaluate the impact of AOSD-LD on MAS and disease relapse. AOSD-LD was further categorized into acute exudative, interstitial, and suspected pulmonary hypertension (PH) patterns to assess pattern-specific outcomes. Lung involvement was identified in 49 (23.4%) patients, yet 69.4% were asymptomatic. Pleuritis emerged as the strongest independent risk factors of AOSD-LD (P<0.0001). AOSD-LD was independently associated with both MAS (HR = 2.62, 95% CI: 1.38-4.96, P=0.0041) and disease relapse (HR = 2.66, 95% CI: 1.50-4.71, P=0.0012) in multivariable COX analysis. Radiographically, the acute exudative pattern was most prevalent, followed by interstitial and suspected PH patterns. Prognostic stratification revealed the acute exudative pattern was strongly associated with early MAS development (P=0.0315), whereas the interstitial pattern was associated with a chronic, refractory course (P=0.0059). AOSD-LD defines a severe disease phenotype and serves as a critical independent predictor for life-threatening MAS and chronic relapse. Differentiating radiographic patterns offers valuable prognostic insights, underscoring the necessity for chest CT screening and phenotype-guided management strategies in AOSD.
Although B cell activating factor (BAFF) serum levels are reported to correlate with the extent of skin fibrosis and markers of systemic inflammation in SSc, their relationship with BAFF-receptor (BAFF-R) expression levels and their potential as biomarker for active disease is not investigated so far. This study was undertaken to investigate BAFF/BAFF-R dynamics in SSc and how they relate to autoantibody subtype and disease activity. Peripheral blood mononuclear cells of 69 SSc patients (ACA+: n = 37; ATA+: n = 32) and 10 age- and sex-matched controls were stained for BAFF-R followed by flow cytometry analyses. Serum BAFF and autoantibody levels were measured by ELISA. BAFF levels were significantly elevated in SSc patients compared with the controls. This was more pronounced in clinically active than clinically stable patients, and in ATA+ compared with the controls and ACA+ SSc patients. Concurrently, BAFF-R expression was reduced on total and on several B cell subsets. BAFF-R expression correlated inversely to serum BAFF levels. In addition, BAFF levels correlated with ESR and CRP in ATA+ SSc patients. Of note, we observed a moderate correlation between BAFF and ATA-IgG, but not between BAFF and ACA-IgG. Our study indicates that elevated BAFF levels, coupled with a reduction in BAFF-R expression, are significant characteristics in ATA+ SSc and of clinically active patients regardless of autoantibody status. Furthermore, BAFF levels show correlations with markers of systemic inflammation and autoantibody levels, specifically in ATA+ SSc. These findings might indicate distinct regulation of B cell responses in ATA+ and ACA+ SSc, particularly emphasizing their relevance in the context of clinically active SSc.
Data regarding progression from oligoarticular to polyarticular psoriatic arthritis (PsA) are sparse. Using FOREMOST, we identify progression predictors and evaluate apremilast's treatment effect in early PsA. FOREMOST (NCT03747939) randomized N = 308 patients with early (mean duration, 9.9 months) PsA and limited joint involvement (>1 to ≤4 swollen and >1 to ≤4 tender joints; not confirmed by imaging) to apremilast or placebo for 24 weeks, followed by open-label apremilast through week 48. Multivariable logistic regression modelled predictors of progression from oligoarticular (≤4 active [swollen and/or tender] joints) to polyarticular (>4 active joints) PsA at week 16 and the effect of apremilast. Disease progression, disease activity, clinical signs/symptoms and tolerability were summarized through week 48 for N = 291 patients receiving ≥1 apremilast dose (from randomization or switched from placebo). Most (268/308 [87.0%]) patients had oligoarticular PsA at baseline; 25.1% (59/235) progressed to polyarticular PsA by week 16 (data as observed). Apremilast reduced odds of progression vs placebo by 58% (odds ratio [OR; 95% CI]: 0.42 [0.22, 0.77]). In placebo-treated patients, being female, being csDMARD-naïve, and having dactylitis significantly increased odds of progression (OR: 3.35 [1.20, 9.34], 3.42 [1.18, 9.93], and 9.26 [1.32, 65.09], respectively). Apremilast treatment for up to 48 weeks maintained low rates of disease progression and improvements in disease activity/clinical signs and symptoms, with no new safety signals. Initiating apremilast treatment during the early, oligoarticular phase of PsA reduced disease activity and delayed progression to polyarticular disease, with benefits maintained with up to 48 weeks of treatment. ClinicalTrials.gov; NCT03747939.
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