IntroductionThis study investigated the pathological characteristics and risk factors of early cardiovascular disease (CVD) associated with rheumatoid arthritis (RA) using a collagen-induced arthritis (CIA) rat model.MethodsA total of 120 SPF-grade male SD rats were used. Following CIA induction, echocardiography, histopathology, molecular biology, and lipid profile analysis were employed to dynamically monitor cardiac function, structural changes, and lipid profiles across disease stages (D0-D112) .ResultsSequential progression of cardiac dysfunction: Echocardiography revealed a significant decrease in the mitral valve E/A ratio (MVE/A) starting from D84 (P<0.05), indicating diastolic impairment preceding systolic dysfunction.Myocardial structural abnormalities: The heart-to-body weight ratio (HW/BW) in CIA rats was significantly higher than that in the control group starting from day 84 (*P < 0.01), indicating cardiac hypertrophy. Masson staining revealed progressive myocardial fibrosis with increasing collagen deposition from D56. Abnormal lipid profiles and biomarkers: LDL-C significantly increased from D84 to D112 (*P<0.01), while OX-LDL rose from D98 to D112 (P<0.05); B-type natriuretic peptide (BNP) significantly increased at D112 (*P<0.01), indicating heart failure risk. Negative atherosclerosis findings: No plaque formation was detected in the Oil Red O staining of the aorta and coronary arteries. While macroscopic atherosclerotic plaques were not apparent, microvascular endothelial dysfunction may play a role in the early stages of cardiovascular disease (CVD) .DiscussionCardiovascular lesions in CIA rats exhibit sequential progression: diastolic dysfunction and myocardial fibrosis emerge first (from D56), followed by systolic dysfunction (from D98), accompanied by lipid metabolism disorders driven by LDL-C and OX-LDL. This model provides an experimental basis for studying the mechanisms of RA-associated cardiac lesions and early intervention.

BACKGROUND:Autoimmune diseases such as primary Sjögren's syndrome and type 1 diabetes are frequently complicated by hepatic injury, yet therapies that simultaneously target inflammation and parenchymal damage remain limited. Mitochondrial dysfunction with excessive reactive oxygen species (ROS) production drives a self-amplifying pathogenic loop by activating the cGAS-STING innate immune pathway. We previously observed that a Chinese herbal formula preserved mitochondrial ultrastructure in autoimmune NOD mice, and computational screening identified trifolirhizin-a natural pterocarpan flavonoid-as the candidate active constituent mediating this protection. Here, we investigated the hepatoprotective effects and underlying mechanisms of trifolirhizin in autoimmune-associated liver injury. METHODS:Female NOD mice received trifolirhizin (5, 10, or 20 mg/kg/day) for four weeks, with C57BL/6J mice as healthy controls. Hepatic histopathology, inflammatory cytokines, mitochondrial ultrastructure (TEM), mitochondrial membrane potential (ΔΨm), and ROS levels were evaluated. Integrated transcriptomic and metabolomic profiling was performed to unbiasedly characterize protective mechanisms. In vitro, H2O2-induced oxidative stress was established in HepG2 cells. Cells were treated with trifolirhizin (15-25 µM) and assessed for antioxidant enzyme activities, ΔΨm, ROS production, glycolytic and mitochondrial respiration (Seahorse analysis), and cGAS-STING pathway protein expression. Pharmacological rescue experiments using the cGAS agonist cGAMP were conducted to test pathway dependency. RESULTS:Trifolirhizin dose-dependently alleviated hepatic pathological damage and reduced pro-inflammatory cytokine levels in NOD mice. Multi-omics profiling revealed that oxidative stress responses, the mitochondrial electron transport chain, and glutathione metabolism were the most significantly restored pathways. Trifolirhizin preserved mitochondrial ultrastructure, restored ΔΨm, and attenuated ROS accumulation both in vivo and in vitro. Functionally, Seahorse analysis demonstrated that trifolirhizin rescued overall cellular bioenergetics, restoring both glycolytic capacity and mitochondrial respiratory parameters (basal respiration, ATP production, maximal respiration, and spare respiratory capacity). Mechanistically, trifolirhizin suppressed the cGAS-STING-TBK1-IRF3 axis, as evidenced by reduced expression of cGAS, p-STING, ZBP1, p-TBK1, and p-IRF3. Importantly, the cGAS agonist cGAMP abrogated the protective effects of trifolirhizin, confirming that the cGAS-STING pathway is functionally required for its action downstream of mitochondrial protection. CONCLUSION:Trifolirhizin attenuates liver injury in the nod mouse by preserving mitochondrial integrity, maintaining cellular energy metabolism, and thereby suppressing the ROS/cGAS-STING inflammatory cascade. These findings position trifolirhizin as a promising mitochondria-targeted therapeutic candidate for pSS-related hepatic complications and provide a mechanistic framework for discovering active compounds from mitochondrially active herbal formulations.

BackgroundBone destruction constitutes the primary cause of disability in rheumatoid arthritis (RA). Herbal medicines feature unique multi-target advantages, rendering them promising therapeutic candidates for attenuating RA-associated bone damage.ObjectiveThis study aimed to investigate the therapeutic efficacy and underlying mechanisms of astilbin, a core bioactive flavonoid extracted from Tufuling (Smilax glabra), against bone destruction in RA.MethodsA CIA mouse model was established via tail vein injection of type II collagen. Micro-CT, HE staining and TRAP staining were applied to evaluate the inhibitory and therapeutic effects of astilbin on RA bone destruction. Network pharmacology and bioinformatics analyses were performed to screen the potential targets and signaling pathways of astilbin for RA treatment. Mendelian randomization analysis was further conducted to genetically validate the correlation between candidate genes and RA. Molecular docking was utilized to calculate binding energies between astilbin and core pathogenic targets of RA. Immunofluorescence, elisa, WB and qPCR were adopted to verify the key targets and anti-inflammatory activity of astilbin in ameliorating RA bone erosion.ResultsIn vivo animal experiments demonstrated that astilbin alleviated RA bone destruction, suppressed synovial hyperplasia, inhibited osteoclastogenesis, and downregulated the expression of pro-inflammatory cytokines. Network pharmacology identified MAPK3, MAPK1, PTPN11, HSP90AA1, STAT1 and SRC as the core therapeutic targets of astilbin against RA. KEGG enrichment analysis revealed that the anti-RA effects of astilbin were tightly associated with the MAPK signaling pathways and so on. Mendelian randomization analysis further verified a strong genetic correlation between the apoptotic protein MAPK3 and RA. Molecular docking results exhibited favorable binding affinity between astilbin and key pathogenic targets of RA.ConclusionAstilbin may exert multiple pharmacological effects including anti-inflammation, inhibition of osteoclast activation, improvement of bone microarchitecture and alleviation of bone destruction in RA via regulating the MAPK signaling pathway, and it exhibits favorable safety in vivo.

Background Patients with rheumatoid arthritis (RA) face a significantly increased risk of cardiovascular disease (CVD). This study aimed to evaluate the combined predictive value of systemic autoimmune inflammatory burden and chronic glucose-lipid metabolic disorder on long-term CVD outcomes in RA patients and to elucidate the dynamic trajectories of these factors during follow-up and their prognostic implications. Methods This prospective longitudinal cohort study included 4,902 RA patients without baseline CVD. Baseline and follow-up exposure matrices (G1-G4 groups) were constructed using the triglyceride-glucose (TyG) index and DAS28-ESR score. Multistage nested Cox proportional hazard regression models were employed to assess the independent prognostic value of combined exposure and dynamic trajectories on incident CVD. Restricted cubic splines (RCS) quantified nonlinear dose-response relationships, and the Delta method analysis evaluated additive interaction synergistic effects. Results During a median 6-year follow-up, 355 incident CVD events occurred (7.24%). In the fully adjusted multifactorial model (Model 3), the baseline dual-high immune-metabolic exposure group (G4) showed significantly elevated incident CVD risk compared to the dual-low control group (G1) (HR 9.46, 95% CI 3.90-22.96, P < 0.001). Additive interaction analysis confirmed a significant synergistic effect (relative excess risk due to interaction [RERI] of 3.55; 95% CI, 0.46–6.64), with 38% of CVD events in the dual-high group attributable to this additive interaction. RCS analysis demonstrated significant nonlinear associations between both continuous variables and CVD risk ( P < 0.05). Dynamic trajectory analysis revealed that sustained dual-high exposure (G4→G4) during follow-up was associated with a progressive increase in CVD risk (HR 6.95, 95% CI 2.06–23.41, P < 0.001), whereas the inflammation-controlled but metabolic-high-risk group (G2→G3) demonstrated residual cardiovascular risk (HR 1.24, 95% CI 0.28–5.48). Conclusions Baseline dual-high immune-metabolic status and adverse longitudinal trajectories are independently associated with incident CVD events in RA patients, with significant synergistic amplification effects. These findings underscore the clinical urgency to transition from a single anti-inflammatory paradigm toward combined dual-track immune-metabolic targeted intervention strategies to optimize the prevention and control of cardiovascular comorbidity in RA.

Deep learning-based computed tomography (CT) image prediction models often suffer from poor local feature perception, severe class imbalance, and a scarcity of high-quality labeled data. Existing fine-tuning methods are sample-inefficient and prone to overfitting. To address these issues, this study proposes a Qwen3-VL vision-language model based on adaptive semi-supervised learning. A novel data augmentation strategy for minority classes is introduced, utilizing diffusion models to learn the distribution of minority-class data and generate new samples. Perceptual similarity and generation quality are evaluated to ensure visual fidelity, while two-level feature selection is performed based on local density to increase the number of high-quality samples in the feature space. A fine-tuning method based on log-sum regularization is proposed, which decomposes pre-trained weights into direction and magnitude components, guiding the magnitude along specific directions to enhance the perception of fine-grained features. The multi-view prediction problem is transformed into a mass function using evidence theory, quantifying uncertainty and generating high-confidence pseudo-labels to improve prediction accuracy and generalization performance. Experiments are conducted on 1 980 CT samples of interstitial lung disease related to rheumatoid arthritis from Guang’anmen Hospital, China Academy of Chinese Medical Sciences, using three-fold cross-validation. The proposed model achieves accuracy, recall, and F1-score of 89.85

Although standard therapies for acute gouty arthritis, such as nonsteroidal anti-inflammatory drugs, colchicine, and glucocorticoids demonstrate efficacy, their clinical application is limited by potential adverse reactions, which remains an unresolved issue. Qing Zhu Granules is a traditional Chinese medicine (TCM) compound preparation used for the treatment of primary acute gouty arthritis with dampness-heat obstruction syndrome. This multicenter, randomized, double-blind, placebo-controlled phase 3 clinical trial conducted in China aimed to evaluate the efficacy and safety of Qing Zhu Granules. Patients who met the Western medical diagnostic criteria for gout, met the TCM syndrome differentiation criteria for dampness-heat obstruction syndrome, had an acute attack duration ≤48 h, and a visual analog scale (VAS) score of joint pain ≥ 40 mm in the current attack were included. Participants were randomly assigned in a 1:1 ratio to the Qing Zhu Granules group or the placebo group, with an oral dose of 6 g, administered 3 times a day, for a treatment course of 3 days. During the treatment period, diclofenac sodium enteric-coated tablets could be used as rescue medication in case of intolerable pain. The primary endpoint was the change in joint pain VAS score (0–100 mm) from baseline at 72 h after treatment. The secondary endpoints included changes in joint pain VAS score from baseline at 24 and 48 h after treatment, changes in the total score and each individual item score of the TCM syndrome rating scale from baseline, changes in C-reactive protein levels from baseline at 72 h after treatment, total dose and frequency of rescue medication within 72 h of treatment, and the interval between the first use of rescue medication and the first use of the study drug after treatment initiation.Clinical trial registrationhttps://clinicaltrials.gov/, identifier NCT06068478.

To assess the effectiveness and safety of Biqi Capsules in the treatment of rheumatoid arthritis (RA). This multicenter, prospective cohort study was conducted across more than 100 centers in China. Data on RA patients were collected from the CERTAIN database between January 2019 and March 2024. Patients were categorized into an exposed group and a control group. The control group was treated with conventional Western medicine, and the exposed group was combined with Biqi Capsules (0.3 g/capsule, 4 capsules per dose, orally, 2–3 times/d) on the basis of conventional treatment. Propensity score matching (PSM) was applied to balance baseline characteristics. The main outcomes was the Disease Activity Score-28 (DAS28-ESR), and secondary outcomes included Health Assessment Questionnaire (HAQ), Visual Analogue Scale (VAS) for pain, tender joint count (TJC), swollen joint count (SJC), Patient Global Assessment (PGA), and Evaluator Global Assessment (EGA) scores, as well as erythrocyte sedimentation rate (ESR), and other laboratory test results as safety indicators. A total of 2,267 patient records were analyzed, with 711 in the exposed group and 1,556 in the control group. After PSM, 710 patients were included in each group, with comparable baseline demographic characteristics (P>0.05). Following matching, pre-treatment HAQ and TJC were similar between groups (P>0.05), while significant differences were observed in DAS28-ESR, EGA, PGA, VAS, SJC, TJC, and ESR (P<0.01). Post-treatment analysis showed that all indices improved significantly in both groups (P<0.01). Furthermore, post-treatment levels of EGA, PGA, VAS, SJC, and TJC were statistically significant between the two groups (P<0.01). The reduction in DAS28-ESR was significantly greater in the exposed group than in the control group (P<0.01). Statistically greater improvements were also found in EGA, PGA, SJC, TJC, and ESR, indicating superior clinical improvement in the exposed group (P<0.01). The incidence of abnormal γ-glutamyl transferase and creatinine levels were higher in the control group than in the exposed group (P<0.01 or P<0.05), while no significant differences were observed in other safety indicators between the two groups (P>0.05). Biqi Capsules combined with conventional treatment of Western medicine effectively reduce RA disease activity, lower inflammation levels, relieve clinical symptoms, and do not increase the incidence of adverse events. (Registration No. NCT05219214)

Objective:Fibromyalgia syndrome(FMS)is a chronic pain condition characterized by central sensitivity to pain,and it is universally ac-knowledged as a recalcitrant disease.A single-blind randomized controlled trial was conducted to assess the effectiveness and safety of the Roujin formula in treating FMS patients with liver depression and spleen deficiency syndrome,aiming to provide more scientific and effective treatment options. Methods:Forty-eight eligible participants were enrolled and randomly assigned to either the Roujin formula group(n=24)or the pla-cebo group(n=24).The Roujin formula group received 150mLofthe Roujin formula twice daily,whereas the placebo group was given a tenth of the Roujin formula dosage,twice daily.The treatment lasted for 8 weeks,with a follow-up extending to 12 weeks.The primary outcome was the improvement in the pain Visual Analogue Scale(VAS)score,whereas secondary outcomes included enhancements in the Pittsburgh Sleep Quality Index(PSQI),Beck Depression Inventory-Ⅱ(BDI-Ⅱ),Revised Fibromyalgia Impact Questionnaire(FIQR),and 36-item Short-Form Health Survey(SF-36)scores.These measures were assessed at baseline and after 4,8,and 12 weeks.The Pa-tients' Global Impression of Change(PGIC)was collected at week 12.Safety assessments were based on routine blood tests,urine tests,and liver and kidney function evaluations. Results:The improvement in the pain VAS score was significantly greater in the Roujin formula group than that in the placebo group at the 4-,8-,and 12-week follow-ups(p＜0.05).At the 8-week treatment and the 12-week follow-up,improvements in PSQI and FIQR scores were also superior in the Roujin formula group compared with the placebo group(p＜0.05).There were no differences between the 2 groups in the improvement of BDI-Ⅱ scores,SF-36 physical component summary,and mental component summary scores at any observation time points.At the 12-week follow-up,PGIC ratings were significantly better in the Roujin formula group(p＜0.05).There were 4 adverse events,all of which occurred in the Roujin formula group,including 3 cases of diarrhea and 1 case of stomach pain;no serious adverse events were reported during the study. Conclusion:The Roujin formula can effectively enhance the overall condition of FMS patients,relieve pain,improve sleep quality,and elevate physical and mental well-being.Only mild gastrointestinal reactions were observed.The Roujin formula may be a viable candi-date for clinical implementation.

Objective Qingre Huoxue Decoction (QRHXD) is a traditional Chinese herbal prescription widely used in clinical practice with significant therapeutic effects on RA; however, its mechanism of action remains unclear. This study aimed to investigate the efficacy and underlying mechanisms of QRHXD in treating RA through clinical research, multiomics approaches, and animal experiments.Methods We conducted a 24-week clinical study in which QRHXD was the primary treatment, collecting serum samples from patients before and after treatment for integrated proteomic and metabolomic analysis to identify potential therapeutic targets. Bioinformatics analysis of differentially expressed proteins (DEPs) and differential metabolites (DMs) was performed using hierarchical clustering, volcano plots, heat maps, Gene Ontology (GO), and Kyoto Encyclopaedia of Genes and Genomes (KEGG) analysis. To validate the identified therapeutic targets, we constructed a collagen-induced arthritis (CIA) mouse model.Results Clinical research has shown that QRHXD can improve clinical symptoms and relevant indicators in RA patients, including the disease activity score-28 (DAS28), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), tender joint count (TJC), swollen joint count (SJC), visual analogue scale (VAS), patient-reported outcome (PRO), and health assessment questionnaire (HAQ). Proteomics and metabolomics analysis identified 83 DEPs and 54 DMs, including 46 upregulated and 37 downregulated proteins, as well as 11 upregulated and 43 downregulated metabolites. KEGG enrichment analysis revealed that DEPs are primarily associated with fatty acid degradation, ferroptosis, glycerolipid metabolism, and related pathways. The identified DMs are primarily associated with the AMPK signalling pathway, FoxO signalling pathway, glycolysis/gluconeogenesis, MTOR signalling pathway, and so on. GO enrichment analysis indicated that the DEPs were mainly associated with apoptotic mitochondrial changes, protein modification processes, fatty-acyl-CoA binding, and so on. Integrated proteomics and metabolomics analyses revealed a significant increase in fructose-1,6-biphosphatase 1 (FBP1) levels and a reduction in AMP-activated protein kinase (AMPK) levels in patients with RA. QRHXD inhibited FBP1 and activated AMPK signalling. Animal experiments validated the findings from proteomics and metabolomics analyses, demonstrating that QRHXD could also delay bone destruction and reduce inflammatory factor levels in CIA mice.Conclusion QRHXD may reduce the disease activity of RA, attenuate the inflammatory response, and delay bone destruction by inhibiting FBP1 and activating the AMPK signalling pathway.

IntroductionRheumatic immune diseases are a type of immune-inflammatory disease that affects muscles, bones, joints, and surrounding soft tissues. They have a long course and a high disability rate, seriously affecting the quality of life of patients. Traditional Chinese medicine plays an important role in the diagnosis and treatment of rheumatic immune diseases. The unique theoretical system and rich treatment methods of traditional Chinese medicine are preserved in ancient Chinese medical books.MethodsThis study takes the content related to rheumatism in ancient traditional Chinese medicine books as the research object, integrates ontology theory and technology into the knowledge graph, and realizes the reconstruction of traditional Chinese medicine information knowledge. It provides a basic data structure for data mining and knowledge discovery.ResultsThis study is the first rheumatism-specific knowledge graph constructed based on ancient traditional Chinese medicine books. It has explored the construction method of a knowledge graph from ancient books by combining automatic labeling of mainstream large language models with manual review. Considering the knowledge characteristics of ancient traditional Chinese medicine books, where existing word segmentation technology struggles to accurately reproduce the original meaning, a new type of entity extraction method is proposed.DiscussionThis provides an important foundation for improving the clinical diagnosis and treatment level of traditional Chinese medicine in treating rheumatism, further exploring the knowledge representation and application of traditional Chinese medicine in rheumatism treatment, and it has potential for future expansion and improvement.

Introduction: Ankylosing spondylitis (AS) is a systemic inflammatory disorder that predominantly involves the axial skeleton, often leading to irreversible structural damage and disability. Although several therapeutic measurements are available, limitations in efficacy and long-term outcomes remain significant. Therefore, identifying novel biomarkers and therapeutic targets is of critical importance for optimizing clinical management and prognostic evaluation in AS patients. Objectives: This study aims to elucidate the immune features and discover potential biomarkers for AS by the integration of deep plasma proteomics and deep learning strategies. Methods: The deep quantitative proteomics was applied to analyze the plasma samples from 104 participants of AS patients with active and stable stages, along with healthy controls. The immune and functional features of AS patients in different stages were assessed. By integrating random forest (RF) with orthogonal partial least squares discriminant analysis (OPLS-DA), a machine learning model-based score matrix was constructed to identify biomarkers. ELISA experiments were performed on an independent cohort of 79 participants to confirm the potential biomarkers for AS. Results: Patients with AS exhibit significant dysregulation in the distributions and characteristics of immune cells. Several key proteins involved in integrin signaling pathway were significantly differentially expressed in patients with AS, highlighting the pathway’s role in the pathogenesis of AS. Four proteins including SAA1, FERMT3, ILK, and TLN1, were identified as potential biomarkers for AS and further verified by ELISA experiments. Conclusions: By integrating the machine learning-based method with deep proteomics analysis, we explored the pathological mechanism and identified biomarkers for AS. Our study provides insights into the distinct protein expression patterns and pathogenesis of AS and may contribute to diagnosis, long-term monitoring, and therapy for this disease.

Daidzin, as one of isoflavone glycosides, has been reported to have multiple activities with few absorbed into body. However, the metabolic behavior of daidzin by intestinal flora has not been researched, that this defect severely constrains its applications. In this study, daidzin and its metabolites were qualitatively and quantitatively analyzed by HPLC and ultra-high performance liquid chromatography coupled to high-resolution mass spectrometry (UHPLC-HRMS) in the fermentation system for daidzin and fecal bacteria. Meanwhile, the alterations of intestinal flora with daidzin were detected by 16S rRNA sequencing technology. Based on the results of intestinal flora, the daidzin and its metabolites transformed by the screened probiotics were quantified and qualified, which the results would corroborate the transformation of daidzin and fecal bacteria. Eventually, daidzin was decreased from 0.30158mg/mL at 0h to 0.01176mg/mL at 48h, daidzein, as the aglycone of daidzin, was increased from 0.02963mg/mL at 0h to 0.04682mg/mL at 48h, suggesting the presence of other metabolites. Next, 31 metabolites including the products of ketone removal, Retro-Diels-Alder (RDA) fragmentation, hydroxylation, methylation, C ring cracking and sulfation were identified. The results of 16S rRNA sequencing showed that the intestinal flora, especially Bifidobacterium, was dramatically altered after incubation with daidzin (p<0.05). Hereby, the fermentation systems of five probiotics (Lactobacillus 3044, Bifidobacterium adolescentis 1.2190, Bifidobacterium longum 25033, Lactobacillus plantarum F1 and Lactobacillus plantarum B2) and daidzin were approved, and these results showed that most metabolites of daidzin were able to be identified with the identical transformation reactions. The study revealed the rationality of daidzin biotransformation at the new perspective, and constructs a new model for fecal metabolites of compounds. These results will also broaden the continued research on daidzin.

Interstitial lung disease (ILD) is a common and severe comorbidity of rheumatoid arthritis (RA), yet reliable diagnostic biomarkers remain lacking. Alveolar type II (ATII) cells are widely recognized to play a key role in the pathogenesis of ILD. This study first aimed to screen and validate potential autoantigens involved in RA-ILD using ATII cells. Sera from multiple patient groups were subjected to immunoprecipitation with ATII cells and analyzed for candidate autoantigens related to RA-ILD through proteomic methods. Antibody concentrations in the sera were subsequently measured using protein chips and ELISA. Expression levels of target antigens in the lung tissues of collagen-induced arthritis-bleomycin (CIA-BLM) mice were evaluated via immunohistochemistry, while their expression in ATII-BLM cells was assessed using indirect immunofluorescence. The diagnostic value of these antibodies was further examined by ROC curve analysis. Preliminary studies also explored the cellular mechanisms involved. We identified exosome component 4 (EXOSC4) as a potential autoantigen in RA-ILD, with significantly higher levels of EXOSC4 antibodies found in the sera of RA-ILD patients. Moreover, EXOSC4 expression was elevated in the lung tissues of CIA-BLM mice and in ATII-BLM cells. Clinical assessments showed that the area under the curve (AUC) for EXOSC4 antibody in diagnosing RA-ILD was 0.809, increasing to 0.890 (95

Background The recurrent nature and prolonged course of ankylosing spondylitis (AS) impose substantial psychological disorders on patients. The aim of this study was to assess psychological disorders and analyze the overall risk of psychological disorders as well as the factors associated with depression, anxiety, and stress in ankylosing spondylitis. Methods Patients diagnosed with AS were selected from the China Rheumatoid Arthritis Registry of Patients with Chinese Medicine (CERTAIN) database for data analysis. General demographic characteristics and disease-related features of the patients were collected. The study analyzed clinical differences between patients with and without psychological disorders. Specific clinical characteristics of depression, anxiety, and stress were statistically analyzed. Clinical factors associated with overall psychological status and specific psychological disorders (depression, anxiety and stress) were analyzed by multivariate logistic regression. Results In our study cohort, 26.72% of AS patients were identified with psychological disorders, with 17.5% experiencing depression, 21.1% suffering from anxiety, and 7.9% reporting stress. We also observed significant overlaps among depression, anxiety, and stress in AS patients, with 53.47% experiencing multiple psychological disorders. Disease activity, health index, fatigue levels, and PGA were identified as significant factors associated with psychological disorders. Age, health index, fatigue levels, and PGA were the main influencing factors for depression; disease activity and PGA for anxiety; and disease activity, ASAS-HI, and fatigue for stress. Conclusions The study reveals a significant prevalence of psychological disorders among individuals with AS, which correlates closely with disease activity, health index, fatigue levels, and PGA. These findings highlight the imperative for assessment of psychological conditions into the comprehensive management approach for AS patients.

OBJECTIVES:Quality of life (QoL) in patients with Sjögren's disease (SjD) is a critical area of research that demands attention due to the impact of SjD on patients' lives. This study utilised bibliometric methods, aiming to comprehensively explore the research content and hotspots in the field of QoL in patients with SjD. METHODS:The literature data source for this study was the Web of Science Core Collection. CiteSpace and VOSviewer were used to analyse publications in relation to authors, countries, institutions, journals, references, and keywords. RESULTS:The study focused on literature that addressed QoL in SjD patients, involving a total of 922 authors and 336 articles published across 151 journals. The study revealed that the number of publications in this field has remained relatively low, exhibiting a stable yet gradual upward trend, with no evidence of explosive growth. Key journals in this field include the Journal of Annals of the Rheumatic Diseases, Rheumatology (Oxford), Clinical and Experimental Rheumatology, and the Journal of Arthritis & Rheumatology. Asghar Bowman Simon J is the most prolific author in the field (21 publications), and England and the University Hospitals Birmingham NHS Foundation Trust and University of Groningen have the most publications. The most high-frequency keywords are "Sjögren's syndrome", "quality of life," "fatigue", "xerostomia", "depression", "sexual dysfunction" and "xerophthalmia". CONCLUSIONS:This study represents a bibliometric analysis focusing on QoL in patients with SjD. It underscores the need for more extensive and systematic research in this area, emphasising the importance of a multidisciplinary approach. Despite advancements in medical research for SjD, there is a crucial need to focus on QoL to enhance patient satisfaction and overall well-being. The findings advocate for more personalised treatment plans and a better understanding of the psychosocial needs of patients with SjD to improve their quality of life.

Objective:To explore the mechanisms of Lushi Runzao decoction (LSRZT) in Treating Sjögren's Syndrome (SS) through gut flora, short-chain fatty acid (SCFAs) and metabolomics. Methods:Non Obese Diabetes (NOD) /LtJ mice were used as the model group, LSRZT and hydroxychloroquine (HCQ) were administered to the treatment group. Fecal samples were collected 4 weeks after the intervention. The microbiota, SCFAs and metabolites were analyzed using 16S ribosomal Ribonucleic Acid, Gas chromatography mass spectrometry analysis and Ultra High Performance Liquid Chromatography-Quadrupole Time-of-Flight Mass Spectrometry. Results:LSRZT had obvious anti-inflammatory effect and can effectively improve the functional injury of submandibular gland; It improves the imbalance of gut microbiota and the related metabolic levels of SCFAs and bile acids, and regulates the levels of inflammatory factors and the contents of bile acids and caproic acid by regulating the abundance of Erysipelatoclostridiaceae, Gammaproteobacteria and Ruminococcaceae. Conclusion:LSRZT can reduce the level of inflammation and improve the imbalance of gut microbiota and metabolism. It provides a scientific basis for the clinical treatment of SS by LSRZT.

ObjectiveWe developed a consensus-based core outcome set (COS) for Traditional Chinese Medicine clinical trials in rheumatoid arthritis (COS-TCM-RA) that to addresses heterogeneity in outcome measurement and reporting across studies.MethodsWe performed a comprehensive systematic review to establish a repository of clinical outcome set for TCM interventions in RA management. Then, a semi-structured interview was conducted to identify additional important outcomes from the patient’s perspective. This was followed by an online three-round Delphi survey conducted with professionals to prioritize and refine clinically relevant outcomes from a previously developed longlist. Core entries were finalized based on three Delphi surveys and one expert consensus meeting.ResultsThe systematic review screened 2,959 records and included 69 eligible studies. From these, a comprehensive list of reported outcomes was extracted and standardized, which after standardization, yielded a final list of 52 unique outcomes for the preliminary consensus process. After semi-structured interviews, three Delphi survey rounds and one consensus meeting, the most important outcomes were determined for COS of Traditional Chinese Medicine for RA (COS-TCM-RA), including physician assessment of global status, Clinical laboratory tests, radiographic assessment, Signs and symptoms, quality of life and security incident.ConclusionThis study developed the first COS-TCM-RA, comprising 11 indicators across five domains: overall disease evaluation, physical and chemical indicators, quality of life, TCM syndromes, and adverse events. By integrating internationally recognized RA assessment tools with patient-reported outcomes and TCM-specific measures, the COS-TCM-RA provides a standardized, multi-dimensional framework to enhance trial quality, improve comparability, and support the integration and internationalization of TCM in evidence-based medicine.

Background and Aims:Biomarkers are essential tools in the diagnosis and management of various diseases. Rheumatoid arthritis (RA) is a systemic inflammatory disorder that frequently results in damage to joints and organs. Here, we examined potential biomarkers and therapeutic agents for RA patients. Methods:Three microarray datasets and clinical data for synovial tissue were sourced from the publicly available Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) in RA versus osteoarthritis (OA) patients were identified, followed by functional enrichment analysis, gene set enrichment analysis (GSEA), and protein-protein interaction (PPI) network analysis to explore DEG-associated pathways and identify hub genes. Furthermore, serum levels of relevant antibodies were measured using enzyme-linked immunosorbent assay (ELISA). Additionally, potential therapeutic compounds for RA were predicted using the Connectivity Map (CMap) database, and molecular docking was conducted to assess their binding affinities with target proteins. Results:A total of 409 DEGs were identified, with Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and GSEA analyses highlighting enrichment in cytokine activity, cytokine-receptor interactions, and the primary immunodeficiency pathway. Five key modules and hub genes were found using Cytoscape, and expression levels of CD40LG, ITGAX, and PTPRC were validated with another GEO data set. ELISA confirmed elevated serum CD40LG antibody levels in RA patients, suggesting its potential as a biomarker, especially in those with interstitial lung disease (ILD) or bone destruction. Connectivity map analysis identified small molecules that may reverse DEGs, and molecular docking showed emetine, oligomycin, cromoglicic acid, sulfinpyrazone, buspirone, and chlorogenic acid had favorable binding energies. Conclusion:CD40LG is a potential biomarker for RA, especially in patients with ILD or bone damage. Emetine, oligomycin, cromoglicic acid, sulfinpyrazone, buspirone, and chlorogenic acid are potential therapeutic agents for RA treatments.