ANNALS OF THE RHEUMATIC DISEASES风湿病年鉴
ANNALS OF THE RHEUMATIC DISEASES(英文缩写 ANN RHEUM DIS),ISSN 0003-4967,eISSN 1468-2060,中文译名:风湿病年鉴 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 28.003 | Q1 |
| 2022 | 27.400 | Q1 |
| 2023 | 20.300 | Q1 |
| 2024 | 20.600 | Q1 |
| 2025 | 24.000 | Q1 |
ANNALS OF THE RHEUMATIC DISEASES 最新收录文献
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1. Immune reset in rheumatic autoimmune disease: from a tantalising metaphor to a measurable therapeutic state.
PMID:日期:2026-10-01Immune reset is increasingly invoked to describe the possibility that a one-off intervention is able to produce durable treatment-free control of rheumatic autoimmune diseases. However, the term remains imprecise and is often conflated with lymphodepletion or immune reconstitution. We argue that immune reset should denote a persistently normalised therapeutic state rather than an inferred consequence of profound immunodepletion. A credible immune reset claim should require sustained off-therapy clinical control beyond the expected pharmacodynamic window, stabilisation or improvement of the involved organs, and demonstrable reconfiguration of disease-relevant immune circuits in blood and accessible tissue. Importantly, restoration of immune competence, including protective immunoglobulins, vaccine responsiveness, and host defence against infection, is an essential part of immune reset. Naïve B-cell repopulation, serological improvement, repertoire rejuvenation, or transient clinical remission alone are insufficient to document immune reset because pathogenic compartments, irreversible organ damage, and acquired immune deficiency may persist. Until validated prospectively, the concept of immune reset should remain a hypothetical construct or perhaps a clinical aspiration rather than a therapeutic reality across treatment modalities and autoimmune disease entities.
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2. DNA methylation signatures distinguish gout from asymptomatic hyperuricaemia and converge with genetic risk at immune-metabolic loci.
2. DNA甲基化特征区分痛风与无症状高尿酸血症并在免疫代谢位点与遗传风险趋同PMID:日期:2026-09-29Why only a minority of hyperuricaemic individuals develop gout remains unclear, and epigenetic differences between these states are poorly characterised. We aimed to define DNA methylation signatures distinguishing gout from asymptomatic hyperuricaemia and evaluate their utility for molecular stratification. We conducted a 2-stage case-control epigenetic study of gout (n = 124), asymptomatic hyperuricaemia (n = 121), and normouricaemic controls (n = 124). Peripheral-blood DNA methylation was profiled by genome-wide targeted bisulphite sequencing in a discovery cohort (n = 83), integrating differentially methylated regions (DMRs) and cytosines (DMCs) with genome-wide association study loci and transcription-factor binding sites (TFBSs). Candidate signatures were then tested by targeted amplicon methylation sequencing in an independent cohort (n = 286), and least absolute shrinkage and selection operator logistic regression constructed methylation-only and epigenetic-clinical classifiers. DMRs were identified across all 3 pairwise comparisons of gout, hyperuricaemia, and normouricaemic controls, mapping to 84 genes that overlapped gout/serum urate risk loci-including HLA-DRB1, TAP2, and GNAS-and were enriched at TFBSs, with ZNF571 linked to IL27 and SAA2. One hundred thirteen DMCs were validated and used to build classifiers: a methylation-only model distinguished gout from normouricaemic controls (test-set area under the curve 0.96) and outperformed clinical variables in gout vs nongout controls (0.91 vs 0.78; DeLong P = 0.032), while integrating methylation with clinical variables improved the most challenging distinction-gout vs asymptomatic hyperuricaemia-from 0.67 to 0.87 (DeLong P = 0.018). Peripheral-blood DNA methylation captures reproducible, stage-specific differences across gout, hyperuricaemia, and normouricaemic states converging with immune-metabolic genetic risk. These signatures support methylation-based molecular stratification, although prospective validation is needed before clinical deployment.
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3. HOXD13 links positional identity to primary cilia-dependent signalling in synovial fibroblasts.
3. HOXD13将位置身份与滑膜成纤维细胞中初级纤毛依赖性信号传导相联系PMID:日期:2026-09-23Homeobox (HOX) transcription factors establish positional identity along the embryonic body axis, yet their functional roles in adult tissues remain poorly understood. Synovial fibroblasts (SFs) and synovial tissue from rheumatoid arthritis (RA), osteoarthritis (OA), and noninflammatory donors were analysed using transcriptomic, epigenetic, and functional approaches. HOXD10, HOXD11, and HOXD13 were silenced in primary SFs, followed by RNA sequencing, gene set enrichment analysis, and assessment of proliferation, cell-cycle progression, and DNA damage responses. Primary cilia were assessed by immunofluorescence in SFs, and cilia-dependent Hedgehog signalling was evaluated using a GLI luciferase reporter assay. HOXD10, HOXD11, and HOXD13 were selectively expressed in SFs from distal joints. We identify epigenetic mechanisms that maintain the anatomically restricted expression of these genes in adult SFs. Silencing of 5' HOXDs induces transcriptional changes in SFs that mirror joint-specific differences observed in RA. Notably, HOXD13 emerges as a key regulator of primary cilia function, influencing cell-cycle control and DNA damage responses, and genome stability. Consistent with these findings, we uncover joint-specific differences in primary cilia morphology, cell-cycle regulation, and DNA damage repair capacity in SFs. Our results identify a previously unrecognised role for HOXD13 in linking embryonic positional identity to adult stromal cell function through primary cilia-dependent pathways. We propose that HOXD13-mediated regulation of primary cilia contributes to joint-specific SF phenotypes, providing a mechanistic framework linking positional identity to anatomically distinct fibroblast states. These findings suggest that developmental patterning genes can shape site-specific inflammatory responses.
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4. Predictive molecular signatures for successful tapering of canakinumab in systemic juvenile idiopathic arthritis.
PMID:日期:2026-09-22Canakinumab induces clinical remission in a substantial proportion of patients with systemic juvenile idiopathic arthritis (sJIA), although not all achieve a complete response. However, tapering and withdrawal frequently lead to disease flares. This study aimed to identify serum and transcriptomic biomarkers that predict successful or unsuccessful tapering of canakinumab in sJIA. Seventy-nine patients with sJIA in remission on canakinumab enrolled in a randomised withdrawal study were analysed; 71 had samples available for gene expression profiling. Serum biomarkers were quantified using Luminex assays. Whole-blood RNA was assessed by RNA sequencing (RNA-Seq) and a targeted 67-gene NanoString panel informed by exploratory analyses. Differential expression, hierarchical clustering, and enrichment analyses were performed. Biomarkers and gene signatures were compared between patients who later successfully withdrew canakinumab and those who experienced unsuccessful tapering. Lower serum levels of sCD163, CXCL9, interleukin (IL)-1RA, and IL-18 were associated with successful tapering. RNA-Seq showed marked differences between active and inactive sJIA and revealed that future nonresponders exhibited lower expression of type I IFN-induced and higher expression of erythopoiesis-related genes. NanoString profiling identified 9 genes (ATF6, BCL6, FAS, IL1B, MAPK1, PPARG, SLC25A37, TNFAIP3, and UBE2D1) overexpressed in patients with unsuccessful tapering, reflecting persistent inflammation and cellular stress. A composite score of these genes discriminated successful from unsuccessful discontinuation (area under curve, AUC, 0.71). Serum inflammatory markers and targeted gene expression signatures identify patients with sJIA at higher risk of flare during canakinumab tapering. Combined molecular biomarker profiling may enable individualised tapering strategies and support precision medicine approaches for Still's disease.
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5. Estimating 2-year risk of first relapse in ANCA-associated vasculitis: derivation of a risk-prediction model based on participants in the PEXIVAS trial.
PMID:日期:2026-09-22Individuals with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) differ in their risk of relapse. Estimation of an individual's risk may inform decision-making around monitoring and treatment. We performed a post hoc analysis of participants with AAV with an estimated glomerular filtration rate (eGFR) <50 mL/min/1.73 m or diffuse alveolar haemorrhage enrolled in a trial assessing the effects of plasma exchange and a reduced glucocorticoid dosing regimen who achieved disease remission. We estimated the risk of first relapse within 2 years of remission. We first identified candidate predictors from the literature. Candidate predictors measured in our data set and associated with relapse within 2 years of remission underwent further selection using least absolute shrinkage and selection operator regression and time-to-event analysis. Model stability was assessed with variable inclusion, multiple shrinkage methods, and VanderWeele's E. Model discrimination was assessed using concordance statistics, and calibration using the slope. We included data from 649 trial participants, of whom 100 experienced a relapse within 2 years of remission. The final risk estimation model included sex, use of oral cyclophosphamide or rituximab as induction agent, ANCA subtype, nonhaemorrhagic respiratory involvement or mucous membrane/eye involvement at presentation, and eGFR at remission. The optimism-corrected Harrell's area under the receiver-operator curve 0.709 (95% CI 0.707-0.710). The calibration slope was 0.99 (95% CI 0.65-1.34). Our model estimates the risk of first relapse for individuals with AAV within 2 years after achieving disease remission. This may inform monitoring and treatment decisions. The model will benefit from future external validation.
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7. MRI and ultrasound predictors of progression to inflammatory arthritis in anti-CCP-positive individuals with musculoskeletal symptoms without clinical synovitis: a prospective cohort study.
PMID:日期:2026-09-18This study aims to evaluate the prevalence of magnetic resonance imaging (MRI) and ultrasound features in anti-cyclic citrullinated peptide (anti-CCP) positive individuals with musculoskeletal symptoms without clinical synovitis (CCP+ at-risk), and compare their prognostic value for progression to inflammatory arthritis (IA). Overall, 130 CCP+ at-risk underwent baseline contrast-enhanced 3 T MRI of the dominant/most symptomatic hand and both feet. Images were scored for synovitis, tenosynovitis, osteitis, and erosions using Rheumatoid Arthritis Magnetic Resonance Imaging Score (RAMRIS) by a rheumatologist and a radiologist. Ultrasound used a 36-joint and 18-tendon protocol for the assessment of synovitis, tenosynovitis, and bone erosions. Associations between imaging findings, clinical variables, and progression to IA were assessed using Cox models with prespecified MRI (binary and continuous score) and ultrasound (individual lesions and overall positivity) parameterisations. At baseline, ≥1 RAMRIS abnormality was present in all CCP+ at-risk individuals (including ultrasound-negative individuals), while ultrasound abnormalities were detected in 25.4%. Over a median follow-up of 36.5 months, 48 (36.9%) progressed to IA. Hand tenosynovitis was the only MRI feature consistently associated with progression across binary and continuous analyses. Ultrasound-detected bone erosions were the most consistently predictive ultrasound feature. A composite of MRI tenosynovitis and ultrasound-detected erosions showed an additional increase in risk, highest in individuals with both features (hazard ratio 5.83). In this cohort of CCP+ at-risk undergoing contemporaneous ultrasound and MRI, MRI-detected hand tenosynovitis and ultrasound bone erosions independently predicted progression to IA. Their combination identified those at the highest risk, supporting complementary roles for both modalities. The feasibility and cost-effectiveness of combined hand MRI and extensive ultrasound require evaluation.
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9. Conceptual framework for the definition of disease modification in systemic sclerosis and potential implications for drug development and clinical study design.
PMID:日期:2026-09-14Systemic sclerosis (SSc) is a multifaceted systemic autoimmune disease, characterised by the interplay of vascular alterations, immune dysregulation, and fibrosis. The molecular changes and the clinical presentation of SSc are highly heterogeneous and vary considerably between individual patients. This heterogeneity has hampered efforts to reach a unified and pragmatic definition of disease modification in SSc. Using a consensus approach among SSc experts, the authors seek to identify current challenges in defining SSc disease modification. The definition of disease modification in SSc requires a nuanced approach that considers molecular, mechanistic, and clinical aspects. Disease-modifying treatments in SSc should target core pathways or cells rather than regulatory mechanisms. Disease-modifying treatments should show sustained effects on disease activity and prevent progression of damage across organs, manifestations, disease stages, and disease endotypes. The complex and variable nature of SSc needs to be reflected in preclinical drug development efforts and clinical trial designs to demonstrate disease-modifying effects of drug candidates for SSc. We herein provide a first framework for the definition of disease modification of vascular, inflammatory, and fibrotic domains in SSc. Advances in our understanding of the cellular and molecular mechanisms driving the progression of SSc will enable further refinement of the definition of disease modification and guide optimal preclinical modelling and innovative clinical trial design in future efforts.
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10. Sequential disease activity assessment for predicting future treatment trajectories in patients with rheumatoid arthritis treated with JAK inhibitors: a group-based trajectory and landmark analysis.
10. 用于预测用JAK抑制剂治疗的类风湿性关节炎患者未来治疗轨迹的序贯疾病活动性评估：基于组的轨迹和里程碑分析PMID:日期:2026-09-10This study aimed to identify disease activity trajectories in patients with rheumatoid arthritis (RA) treated with Janus kinase (JAK) inhibitors and to determine whether early disease activity improved prediction of long-term treatment trajectories. We analysed 843 patients treated with JAK inhibitors from a multicentre registry. Group-based trajectory modelling was used to identify distinct Clinical Disease Activity Index (CDAI) trajectories over 52 weeks. Landmark analyses at weeks 4 and 12 were performed using multivariate logistic regression with multiple imputations. Model performance was evaluated using the area under the receiver operating characteristic curve, Brier score, and bootstrap-based internal validation. Four distinct trajectory groups were identified: rapid responders (64.9%), partial responders with persistent residual disease activity (18.1%), responders with high baseline disease activity (12.7%), and persistent nonresponders (4.3%). Week-52 remission rates ranged from 0.0% to 47.7% across the groups. Incorporating the CDAI at landmark time points substantially improved the prediction of a favourable trajectory, whereas the CDAI slope provided minimal additional predictive value. Brier scores improved markedly after incorporating week-12 CDAI, with minimal further improvement after CDAI slope inclusion. Bootstrap validation demonstrated minimal optimism and good calibration. The optimal CDAI thresholds for predicting a favourable trajectory were 12.0 and 9.3 at weeks 4 and 12, respectively. Early disease activity dynamically refined the prediction of future treatment trajectories in patients with RA treated with JAK inhibitors. The absolute CDAI at landmark time points was more informative than change-based metrics, supporting sequential disease activity assessment for time-anchored treatment decision-making.