OBJECTIVE:To develop and validate a predictive model for predicting psychological complications of Sjögren's syndrome (SS) in combination with tongue and pulse characteristics. METHODS:This cross-sectional study was based on a prospective cohort study including SS patients recruited from 30 major tertiary hospitals in China. Nomograms were developed based on the clinical characteristics, tongue and pulse manifestations, and laboratory tests of these patients, and univariate and multivariate logistic regression analyses were used to screen for various correlates of anxiety and depression, and the column charts were evaluated using the area under the curve (AUC), calibration curves, and decision curve analysis. RESULTS:A total of 444 patients were included, comprising 424 females (95.5%) and 20 males (4.5%), with a mean age of (46 ± 13) years. The prevalence of anxiety and depression was 45.5% (n = 202) and 42.1% (n = 187), respectively. Peeled tongue was associated with higher rates of both anxiety and depression among SS patients [odds ratio (OR) for anxiety = 0.44, 95% CI (0.26, 0.74), P = 0.002; OR for depression = 0.44, 95% CI (0.27, 0.73), P = 0.002]. Regarding pulse diagnostics, a thready pulse was linked to increased anxiety [OR= 1.99, 95% CI(1.11, 3.60), P = 0.022], while a slippery pulse correlated with depression [OR = 0.32, 95% CI(0.14, 0.74), P = 0.007]. Nomograms developed from these findings demonstrated good predictive performance, with AUC values of 0.767 for anxiety and 0.741 for depression in both training and validation cohorts. CONCLUSIONS:Integrating Traditional Chinese Medicine diagnostics with conventional clinical assessments provides a robust predictive model for psychological comorbidities in SS. The innovative approach enhances personalized management, offering a pathway for targeted interventions to treat anxiety and depression effectively in affected patients.

Sjögren’s disease (SD) is an autoimmune disorder characterized by dysregulated interferon (IFN) signaling, but the causal genes and regulatory mechanisms remain unclear. We integrated transcriptomic, epigenomic, and genetic data using summary data-based Mendelian randomization (SMR) and colocalization analyses. A meta-analysis of three datasets (N = 124) identified 331 differentially expressed IFN-associated genes enriched in immune cells. SMR analysis of blood and minor salivary gland (MSG) expression quantitative trait locus (eQTL)/DNA methylation QTL (mQTL) data with the SD genome-wide association study (GWAS) identified five causal genes: SH2B3, LGALS9, CD40, GRB2, and DTX3L. DNA methylation at specific CpG sites regulated the expression of SH2B3 and LGALS9. Colocalization revealed that these genes interact with inflammatory cytokines, including C-C motif chemokine 19 (CCL19), interleukin-2 receptor subunit beta (IL-2Rβ), IL-10, and CCL4. Enzyme-linked immunosorbent assay (ELISA) validation in 16 patients with SD confirmed elevated serum levels. This study elucidates the epigenetic regulation of IFN-associated genes in SD pathogenesis and identifies potential therapeutic targets.

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.

This study aimed to investigate the mechanism of ophiopogonin D (OD) in treating primary Sjögren's syndrome (pSS) through integrated analysis of gut microbiota and metabolomics. Non-obese diabetic/LtJ mice, a well-established pSS model, were used as the model group and treated with OD or hydroxychloroquine. Fecal and tissue samples were collected starting 4 weeks after administration. Basic pathological examination, 16S rRNA sequencing, and ultra-high-performance liquid chromatography-mass spectrometry were employed to assess changes in tissue function, inflammation levels, gut microbiota, and metabolite profiles across all groups. The results showed that OD reduced the expression levels of inflammatory factors, regulated immune balance, and ameliorated functional damage of the submandibular gland. It also modulated the abundance of Rikenella, Mycoplasmataceae, Mycoplasmatales, and Erysipelotrichales, thereby affecting glycerophospholipid metabolism and improving the disease phenotype in pSS mice. In conclusion, OD may treat pSS by lowering inflammation, restoring salivary gland function, and correcting gut microbiota and metabolic imbalances.

The accurate prediction of epitopes associated with Systemic Lupus Erythematosus (SLE) plays a vital role in advancing our understanding of autoimmune pathogenesis and in designing effective immunotherapeutics. Traditional bioinformatics methods often struggle to capture the intricate sequence patterns and high-dimensional signals characteristic of epitope data. Deep learning presents a compelling alternative, with its ability to perform automatic feature learning and model complex dependencies inherent in biological sequences. This study proposes a hybrid deep learning architecture that synergistically integrates handcrafted biochemical features with data-driven deep sequence modeling to improve the identification of SLE-associated epitopes. The framework comprises six interconnected components: (1) handcrafted feature extraction encoding biochemical and physicochemical attributes; (2) an embedding layer for dense sequence representation; (3) a Convolutional Neural Network (CNN) branch that captures local patterns from handcrafted features; (4) a Long Short-Term Memory branch for learning temporal dependencies in sequence data; (5) a scaled dot-product attention-based fusion module that integrates complementary information from both branches; and (6) a Multi-Layer Perceptron for final classification. Model evaluation employed metrics such as Accuracy, Precision, Recall, F1-score, and the area under the receiver operating characteristic curve (ROCAUC). The hybrid model outperformed both baseline machine learning algorithms and ablated versions of itself. It achieved a ROCAUC of 0.9506 and an F1-score of 0.8333 on the SLE epitope prediction task. Notably, ablation studies revealed that the CNN component had the most substantial influence on performance, while the custom fusion mechanism yielded better integration of features than conventional strategies. These findings underscore the model’s robustness and capacity to generalize across complex epitope prediction tasks. This work presents an interpretable, biologically informed deep learning approach for predicting SLE-associated epitopes. By merging domain-specific handcrafted features with dynamic deep learning representations, the model not only enhances predictive accuracy but also provides meaningful biological insights. The framework holds promise for broader applications in immunoinformatics and autoimmune disease research.

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

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.

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.

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.

Background:There are currently no effective pharmacological treatments for Sjögren's disease (SjD). Our study aims to identify potential therapeutic targets for the condition using druggable genome-wide Mendelian randomization (MR). Methods:Druggable genome data were obtained from the Drug-Gene Interaction Database (DGIdb) and the study by Finan et al. We then integrated these druggable genes with blood-derived cis-eQTL, cis-mQTL, and cis-pQTL datasets, each analyzed separately in two-sample MR analyses using SjD GWAS summary statistics as the outcome, applying a genome-wide MR approach focused on druggable targets. Bayesian colocalization was applied to validate shared causal genetic variants. Protein levels of prioritized genes were validated in clinical serum samples from SjD patients and controls using ELISA. Phenome-wide MR (Phe-MR) analysis was conducted across 1359 phenotypes from the UK Biobank to evaluate potential pleiotropic effects and safety profiles of the identified targets, assessed side effects and alternative indications of identified targets. Results:Fourteen druggable genes were identified, with eight (PLAT, SIRPB1, LAIR2, NEU1, SLC22A16, RAD52, PSPH, and CDH23) demonstrating consistent causal relationships with SjD. ELISA validation supported differential protein expression for these targets. Key findings include the protective role of NEU1 and PSPH in systemic immune regulation, the pathogenic impact of PLAT, SIRPB1, BRD2, and LAIR2 on inflammation, and the potential involvement of SLC22A16 and RAD52 in metabolic stress and immune activation. Existing pharmacological compounds targeting these genes, including Aminocaproic acid, Resveratrol, Levocarnitine, Imatinib, and Zinc chloride were identified as potential therapeutic candidates. No significant adverse effects were detected through Phe-MR analysis. Conclusion:Our research indicated PLAT, SIRPB1, LAIR2, NEU1, SLC22A16, RAD52, PSPH, and CDH23 may serve as promising targets for SjD, while the effectiveness of Aminocaproic acid, Resveratrol, Levocarnitine, Imatinib, and Zinc chloride for SjD requires further validation.

BackgroundHyperuricemia (HUA) is a metabolic disorder characterized by elevated serum uric acid levels resulting from dysfunction in purine metabolism and/or inadequate uric acid excretion. It is an independent risk factor for many chronic diseases and is associated with a poor long-term prognosis. Existing uric acid-lowering drugs often lead to numerous adverse reactions, resulting in poor patient compliance and limited clinical application. Therefore, this study aims to investigate the effect of Kuiyuan Chewing Tablet (KYCT) on serum uric acid (SUA) levels in patients with HUA, and to seek a safe alternative therapy for reducing uric acid.Methods and analysisThis study is a multicenter, randomized, double-blind, parallel-controlled trial. HUA patients who meet the inclusion criteria will be randomly assigned in a 1:1 ratio to either (1) the control group (placebo of KYCT, specifications: 0.3g per tablet, 1.2g per dose, twice a day, taken with warm water 30 minutes after meals) or (2) the experimental group (KYCT, specifications: 0.3g per tablet, 1.2g per dose, twice a day, taken with warm water 30 minutes after meals). Both groups will receive dietary control, comorbidity prevention, and health education during the intervention period. The primary outcome will be the proportion of subjects with SUA levels <420 umol/L. Secondary outcomes will include the proportion of subjects with SUA levels <360 umol/L, the percentage change in SUA levels from baseline to each visit, the maximum percentage change in SUA levels from baseline to the third month, the number of gout attacks, changes in body measurements (weight, waist circumference, hip circumference, BMI), blood pressure, blood lipids, fasting blood glucose levels, and the proportion of subjects reporting gout attacks (cumulative up to each visit). Each group of patients will be assessed at baseline, as well as at the 4th, 8th, and 12th weeks.DiscussionThis study aims to evaluate the effects of a 12-week treatment with KYCT on patients with HUA. We hypothesize that compared to placebo, KYCT would significantly improve SUA levels without provoking significant adverse reactions. These findings potentially pave the way for a safe and effective alternative therapy for HUA.

Sjogren’s syndrome (SS) is a chronic inflammatory and difficult-to-treat autoimmune disease. Timosaponin AIII (TAIII), a plant-derived steroidal saponin, effectively inhibits cell proliferation, induces apoptosis, and exhibits anti-inflammatory properties. This study explored the mechanisms of action of TAIII in SS treatment by studying gut microbiota and short-chain fatty acids (SCFAs) using fecal metabolomics. The model group used non-obese diabetic (NOD) mice. The treatment group was classified into TAIII and hydroxychloroquine groups. The gut microbiota, SCFAs, and metabolites were analyzed using 16S rRNA sequencing, gas chromatography–mass spectrometry analysis, and liquid chromatography–mass spectrometry, respectively. TAIII effectively alleviated dry mouth in NOD mice, slowed the progression of salivary gland tissue injury, reduced inflammatory factor expression, and increased the levels of aquaporins 1 and 5. TAIII regulated SCFA content and tryptophan metabolism by altering the abundance of the Rikenellaceae_RC9_gut_group, thereby reducing the inflammatory response. TAIII can improve imbalances in the gut microbiota and the metabolic levels of related SCFAs and tryptophan, thereby reducing the level of inflammation. The significant differences observed in the abundance of the Rikenellaceae_RC9_gut_group between the treatment and control groups indicated the potential relationship between bacteria and metabolites in SS.

BACKGROUND:Rheumatoid arthritis (RA) is characterized by synovial inflammation and bone erosion driven by osteoblast-osteoclast imbalance. Qingre Huoxue decoction (QRHXD), a traditional Chinese medicine, alleviates RA symptoms, yet its mechanism in mitigating bone erosion remains unclear. METHODS:Network pharmacology identified active compounds and targets of QRHXD. Collagen-induced arthritis (CIA) rats were treated with QRHXD or Methotrexate. Arthritis severity (HE staining), bone microstructure (X-ray micro-CT), osteoblast/osteoclast markers (RT-qPCR, TRAP staining), and ATF4 expression (Western blot, immunofluorescence staining) were assessed. Primary osteoblasts from CIA rats were treated with QRHXD or its active compound to validate ATF4 modulation. RESULTS:QRHXD reduced joint swelling, arthritis scores, and bone loss in CIA rats, restoring trabecular parameters (Tb.N, Tb.Th, BV/TV) and suppressing bone resorption markers (TRAP, CTX-1, RANKL). Moreover, the number of osteoclast was significantly reduced. Protein interaction analysis highlighted ATF4 as a core regulator of bone remodeling and potentially regulated by the active compound Quercetin in QRHXD. Both QRHXD and Quercetin inhibited ATF4 hyperactivation in CIA osteoblasts, rebalancing RUNX2 and RANKL expression, with Quercetin showing greater efficacy. Molecular docking further exhibited strong binding affinity between Quercetin and the ATF4-regulating transcription factors RAD21, CBFB and HDAC2. CONCLUSION:QRHXD attenuates bone erosion in RA by inhibiting ATF4 hyperactivation via Quercetin, restoring osteoblast-osteoclast crosstalk.

BackgroundPlant active substances are extensively utilized in treating rheumatoid arthritis (RA). Despite numerous experimental and clinical studies on plant active substances their efficacy remains largely unsubstantiated. The widespread use of these extracts as therapeutic measures for RA is problematic due to the lack of compelling evidence.ObjectiveOur research aims to assess the impact of plant active substances on RA by conducting a network meta-analysis.MethodsWe systematically searched four electronic databases—PubMed, EMBASE, the Cochrane Central Register of Controlled Trials, and Web of Science—from their inception to August 2024. The main focus was on assessing primary outcomes, including the Visual Analogue Scale (VAS), inflammatory markers, Swollen Joint Count (SJC), Tender Joint Count (TJC), and Disease Activity Score on 28 joints (DAS28). We performed data analysis using StataMP 15.1 software and ranked the therapeutic effects based on the Surface Under the Cumulative Ranking Curve (SUCRA) probability values.ResultsBased on screening procedures, 18 eligible studies were incorporated into the analysis. These studies encompassed a total of 1,674 RA patients and investigated 10 different plant active substance therapies. Specifically, 10 studies included VAS indicators, 17 studies included inflammatory marker indicators, 14 studies included DAS28 indicators, 13 studies included SJC indicators, and 13 studies included TJC indicators. Based on SUCRA values, quercetin appeared to be the most effective treatment for decreasing serum VAS levels (67.3%). Furthermore, curcumin emerged as the most promising option for reducing inflammatory marker levels (72.3%), SJC (75.6%), and TJC (76.2%). Lastly, with respect to DAS28, resveratrol emerged as the optimal choice (74.3%).ConclusionAccording to the network meta-analysis (NMA), curcumin exhibited superior efficacy compared to placebo in decreasing SJC and TJC. Additionally, curcumin demonstrated greater effectiveness in reducing inflammatory markers. Quercetin was more effective in reducing VAS, and resveratrol was more effective in reducing DAS28. Patients with RA may benefit from these findings. Insightful information from this study is helpful for RA patients to consider using plant active substance therapies. For their efficacy and safety to be confirmed, more proof is needed.

ETHNOPHARMACOLOGICAL RELEVANCE:Qingrehuoxue (QRHX) granules, composed of 12 Chinese herbs, have been used for over 40 years to treat rheumatoid arthritis (RA) in China and show potential in protecting bone health. However, high-quality evidence on their effects is limited. AIM OF THE STUDY:To assess the effects of QRHX granules on bone marrow edema (BME) in active RA patients. MATERIALS AND METHODS:This multicenter, randomized, double-blind, placebo-controlled trial enrolled RA patients from 13 hospitals in China. Participants were randomly assigned in a 1:1 ratio to receive either QRHX granules (10 g, twice daily) plus methotrexate (MTX) or a placebo plus MTX for 24 weeks. The primary outcome was the change in MRI-assessed BME score at week 24. Secondary outcomes included changes in bone erosion scores, Disease Activity Score in 28 joints, and safety outcomes. RESULTS:A total of 204 patients (mean age, 48.77 years; SD, 11.96) were randomized to either the QRHX or placebo group. At week 24, the QRHX group showed a significantly greater reduction in BME scores compared to the placebo group (adjusted between-group difference, -2.50; 95 % CI, -4.76 to -0.25; P = 0.030). QRHX also significantly reduced bone erosion progression (adjusted between-group difference, -2.90; 95 % CI, -5.49 to -0.31; P = 0.030). Adverse events were rare and similar across both groups, with no deaths or life-threatening events. CONCLUSION:QRHX granules, combined with MTX, significantly reduced MRI-detected BME and slowed bone erosion in active RA, suggesting potential as a complementary treatment for bone protection in RA.

BACKGROUND:Sjögren's syndrome (SS) is a complicated autoimmune disorder, encompassing multifaceted pathogenesis of inflammatory response, immune dysregulation and metabolic abnormalities. Shaoteng Decoction (STD) is a type of traditional Chinese medicine preparation that has been shown to effectively improve inflammatory damage and immune dysfunction in patients with SS. Nevertheless, the exact mechanism has not been unspecified. PURPOSE:This work aims to determine the mechanism of STD treatment on SS, identifying potential therapeutic targets and their relationships. METHODS:Non-obese diabetic mice served as a disease model. This study analyzes potential signaling pathways of STD treatment for SS through network pharmacology, and assesses the role of STD in reducing inflammatory damage using pathological staining, ELISA, and immunohistochemistry. Additionally, the study apply gut microbiota, metabolomics, and proteomics analyses to identify the key microbiota, metabolites and proteins, aiming to find potential action targets of STD. We use Western blotting and immunohistochemistry to verify the authenticity of the relevant targets and study the interactions among gut microbiota, metabolites, and proteins. RESULTS:Proteobacteria is the important intestinal bacteria, Bile Acid Biosynthesis is the main metabolic pathway, IfI30, Ndufv3, and Ndufs6 are the crucial differential expressed proteins. Moreover, there is a strong correlation among the three. STD treats SS by reducing the abundance of Proteobacteria, increasing Bile Acid Biosynthesis, decreasing IfI30 expression, and increasing the expression of Ndufv3 and Ndufs6. CONCLUSION:STD inhibits inflammatory responses, improves immune dysregulation and energy metabolism abnormalities, and prevents the progression of SS through regulating the gut microbiota, enhancing Bile Acid Biosynthesis, and modulating proteins expression levels.

To evaluate the dynamic changes of glucocorticoid (GC) dose and the feasibility of GC discontinuation in rheumatoid arthritis (RA) patients under the background of Chinese medicine (CM). This multicenter retrospective cohort study included 1,196 RA patients enrolled in the China Rheumatoid Arthritis Registry of Patients with Chinese Medicine (CERTAIN) from September 1, 2019 to December 4, 2023, who initiated GC therapy. Participants were divided into the Western medicine (WM) and integrative medicine (IM, combination of CM and WM) groups based on medication regimen. Follow-up was performed at least every 3 months to assess dynamic changes in GC dose. Changes in GC dose were analyzed by generalized estimator equation, the probability of GC discontinuation was assessed using Kaplan-Meier curve, and predictors of GC discontinuation were analyzed by Cox regression. Patients with <12 months of follow-up were excluded for the sensitivity analysis. Among 1,196 patients (85.4