INTRODUCTION:Rheumatoid Arthritis (RA) is a chronic autoimmune disease characterized by persistent synovial inflammation and progressive joint destruction. Emerging evidence suggests that metabolic reprogramming plays a pivotal role in rheumatoid Arthritis (RA) pathogenesis. However, existing studies have focused predominantly on isolated pathways. This study aimed to systematically investigate the molecular interplay between metabolic reprogramming and immune dysregulation in RA. METHODS:Twelve metabolism-related gene sets from MSigDB were analyzed across two bulk RNA-seq datasets (GSE93272: 232 RA/43 controls; GSE110169: 84 RA/77 controls). Based on bulk RNA-seq datasets related to RA, feature genes were selected using machine-learning algorithms, and an ensemble-learning model for RA diagnosis was developed. Subsequent analyses included Gene Set Enrichment Analysis (GSEA), immune cell infiltration profiling, drug-target prediction, and gene-disease network construction to further explore the potential functions of the feature genes. Additionally, a single-cell RNA sequencing (scRNA-seq) dataset containing a single RA patient (GSE159117) was used to identify key cell populations and investigate the interactions between cell populations. Finally, six candidate genes were validated by qPCR (RA n=5; control n=6). RESULTS:Three high-performance diagnostic models were developed by combining the LASSO regression and XGBoost algorithms. The ensemble model (AUCs of 0.960-0.970 in training and 0.819 in external validation) integrating the 3 individual models outperformed the individual model, and 13 feature genes were identified via the ensemble model. Functional enrichment revealed significant associations with metabolic and immune pathways. Immune infiltration profiling revealed notably elevated T-cell subsets in RA patients, with multiple feature genes strongly correlated with T-cell activation. Single-cell analysis confirmed T cells as key mediators, with IRF7 regulating TXN and related genes. qPCR validated significant dysregulation of AKR1C3, ARG1, TXN, and C1QB in RA patients compared with controls (p<0.05). DISCUSSION:These findings suggest that metabolic reprogramming is not merely a consequence but may be a driver of immune dysfunction in RA. The strong association between metabolic gene signatures and T cell activity raises the possibility that targeting metabolic pathways could modulate immune responses in RA. Further studies are needed to explore the causal relationships and therapeutic potential of these interactions in clinical settings. CONCLUSION:Our study provides a comprehensive characterization of metabolic-immune crosstalk in RA, identifying novel diagnostic biomarkers and therapeutic targets. Our findings advance the understanding of RA pathogenesis and may facilitate the development of precision medicine approaches.

Background: Adult‐onset Still’s disease (AOSD) is a rare systemic inflammatory disorder of unknown etiology and pathogenesis. Some patients fail to respond to conventional glucocorticoids and immunosuppressant therapies, a condition known as refractory AOSD. The prognosis for patients with refractory AOSD is typically poor, significantly impacting their quality of life and overall health. This study retrospectively analyzes the predictive factors for refractory AOSD to provide new strategies and insights for clinical diagnosis and treatment. Methods: Overall, 105 AOSD patients hospitalized between January 2008 and October 2024 were selected, 41 of whom were classified as refractory. Multivariate logistic regression analysis was conducted to identify risk factors for refractory AOSD, and receiver operating characteristic (ROC) curves were used to evaluate the predictive power of these indicators. Results: Patients with refractory AOSD were more likely to develop splenomegaly and MAS. Additionally, the neutrophil‐to‐lymphocyte ratio (NLR), lactate dehydrogenase, serum ferritin (SF) levels, and AOSD system score were higher in refractory cases than in nonrefractory cases, while lymphocyte count and platelet (PLT) count were lower in the refractory AOSD group ( p < 0.05). Multivariate logistic regression analysis identified PLT, NLR, and AOSD system scores as independent risk factors for predicting refractory AOSD. ROC curve analysis revealed that the area under the curve for PLT, NLR, and AOSD system scores were 0.659, 0.661, and 0.660, respectively. The optimal cutoff values for PLT, NLR, and AOSD system score in predicting refractory AOSD were 314.5 × 10 9 /L, 10.555, and 5.5, respectively, with sensitivities of 80.5%, 53.7%, and 75.6% and specificities of 46.9%, 75.0%, and 50.0%, respectively. Conclusion: PLT < 314.5 × 10 9 /L, NLR > 10.555, or an AOSD system score of > 5.5 before treatment may serve as independent risk factors for predicting refractory AOSD, providing clinicians with an early warning to identify disease progression.

To investigate the clinical characteristics, associated factors, and outcomes of posterior reversible encephalopathy syndrome (PRES) in patients with systemic lupus erythematosus (SLE). This retrospective case–control study, conducted from 2009 to 2022, included 32 patients with SLE who developed PRES and 50 matched controls with neuropsychiatric SLE (NPSLE). Controls were matched for age, sex, and disease duration. Clinical characteristics, laboratory indices, neuroimaging findings, and treatment approaches were systematically evaluated. Multivariate logistic regression was performed to identify factors associated with PRES in patients with SLE. In addition, survival outcomes were compared according to different glucocorticoid (GC) dosing regimens. Patients with SLE who developed PRES had significantly longer hospitalizations and a higher frequency of hypertension compared with NPSLE controls (P < 0.05). Laboratory findings showed elevated white blood cell (WBC) and neutrophil (NE) counts, as well as increased levels of creatinine (Cr), blood urea nitrogen (BUN), and C-reactive protein (CRP); in contrast, serum albumin (Alb) and magnesium levels were markedly lower before the onset of neurological symptoms in the PRES group (all p < 0.05). PRES patients also demonstrated higher rates of nephritis and hypomagnesemia compared with NPSLE controls without PRES (p < 0.05). At the time of neurological symptom onset, seizures, visual impairment, and vomiting were more common in the PRES group, whereas acute confusional state were less frequent (p < 0.05). Neuroimaging revealed that patients with PRES more often exhibited lesions involving the parietal, occipital, frontal, and temporal lobes (p < 0.05). Multivariate logistic regression analysis identified several factors associated with an increased risk of PRES in patients with SLE: hypertension (OR 38.419, 95

Objective The objective of this study was to explore the associations of body mass index (BMI), fat mass index (FMI), skeletal mass index (SMI) and secondary osteoporosis (OP) in patients with rheumatoid arthritis (RA). Methods The bone mineral density (BMD) at sites of the femur neck (Neck), total hip (Hip) and lumbar vertebrae 1–4 (L1-4) was measured by dual-energy X-ray absorptiometry. The skeletal muscle index, body fat percentage and mineral content were measured by biological electrical impedance for calculating BMI, FMI and SMI. Results A total of 433 patient with RA and 158 healthy controls were enrolled. The BMDs at each site of the RA patients were lower compared with those of the healthy controls (p < 0.0001), and the prevalence of OP (36.1%, 160/443) and sarcopenia (65.2%, 288/443) in the RA patients were higher than those in the controls (12.7%, 20/158, p < 0.0001; 9.0%, 14/156, p < 0.0001). Significant differences in the BMD, FMI, SMI, mineral content, body fat percentage and skeletal muscle mass were found among the RA patients in the different BMI groups (p < 0.05). In RA patients with BMI < 18.5 kg/m 2 , the prevalence of OP in the RA patients with sarcopenia was similar to that in those without sarcopenia (44.4% vs. 66. 7%, χ 2 = 0. 574, p = 0.449). In the RA patients with a normal BMI or who were overweight or obese, prevalence of OP in the RA patients with sarcopenia was significantly higher than that in the RA patients without sarcopenia (42.8% vs. 21.7%, χ 2 = 10.951, p = 0.001; 61.1% vs. 13.0%, χ 2 = 26.270, p < 0.0001). In the RA patients without sarcopenia, the prevalence of OP in the RA patients in the different BMI groups was different (p = 0.039). In the RA patients with sarcopenia, there was no significant difference in the prevalence of OP among the RA patients in the different BMI groups (p = 0. 128). The linear correlation analysis showed that the SMI in RA patients was positively correlated with the BMD of each site measured and BMI and FMI (p < 0.0001). However, there was a negative linear correlation between SMI and disease duration (p = 0.048). The logistic regression analysis found that SMI (OR = 0.569, p = 0.002, 95% CI 0.399–0.810), BMI (OR = 0.884, p = 0.01, 95% CI 0.805–0.971) and gender (1 = female, 2 = male) (OR = 0.097, p < 0.0001, 95% CI 0.040–0.236) were protective factors for OP in RA, while age (OR = 1.098, p < 0.0001, 95% CI 1.071–1.125) was the risk factor. Conclusion BMI and SMI are associated with the occurrence of OP in RA patients, and both SMI and BMI are important protective factors for OP secondary to RA.

RNA-binding proteins (RBPs), which are key effectors of gene expression, play critical roles in inflammation and immune regulation. However, the potential biological function of RBPs in ankylosing spondylitis (AS) remains unclear. We identified differentially expressed genes (DEGs) in peripheral blood mononuclear cells (PBMCs) of five patients with AS and three healthy persons by RNA-seq, obtained differentially expressed RBPs by overlapping DEGs and RBPs summary table. RIOK3 was selected as a target RBP and knocked down in mouse bone marrow mesenchymal stem cells (mBMSCs), and transcriptomic studies of siRIOK3 mBMSCs were performed again using RNA-seq. Results showed that RIOK3 knockdown inhibited the expression of genes related to osteogenic differentiation, ribosome function, and β-interferon pathways in mBMSCs. In vitro experiments have shown that RIOK3 knockdown reduced the osteogenic differentiation ability of mBMSCs. Collectively, RIOK3 may affect the differentiation of mBMSCs and participate in the pathogenesis of AS, especially pathological bone formation.

目的 探讨肌少症对女性类风湿关节炎(RA)患者发生骨质疏松(OP)的影响.方法 纳入女性RA患者(RA组)402 例和健康女性(对照组)98 例.根据BMI将RA组患者分为消瘦组(BMI＜18.5 kg/m2,62 例)、正常组(18.5 kg/m2≤BMI＜24.0 kg/m2,221 例)及超重/肥胖组(BMI≥24.0 kg/m2,119 例),再根据是否合并肌少症将RA组患者分为肌少症组(247 例)和非肌少症组(155 例),根据是否合并OP将RA组患者分为OP组(158 例)和非OP组(244 例).采用直接节段多频率生物电阻断法测定四肢和躯干骨骼肌质量,计算骨骼肌质量指数(SMI);采用双能X线骨密度吸收仪测定腰椎和髋部骨密度(BMD),收集所有受试者的一般临床资料、疾病活动性指标、实验室检查指标、关节功能分期、X线分期及Sharp评分并分组进行比较.采用多元logistic回归分析评估女性RA患者发生OP的影响因素.结果 RA组患者除L1外各部位BMD及SMI均低于对照组,除L1外各部位OP及肌少症患者比例均高于对照组(P＜0.001).消瘦组、正常组及超重/肥胖组患者SMI依次升高,而肌少症发生率依次降低(P＜0.001).肌少症组患者除L1 外各部位BMD均低于非肌少症组,除L1外各部位OP患者比例均高于非肌少症组(P＜0.001).OP组患者年龄、病程、HAQ评分、Sharp评分均高于非OP组,晨僵时间低于非OP组;两组患者关节功能及X线分期构成比比较差异均有统计学意义(P＜0.05).OP组患者各部位骨骼肌质量及SMI均低于非OP组,肌少症患者比例高于非OP组(P＜0.001).多元logistic回归分析结果显示,年龄和Sharp评分是女性RA患者发生OP的危险因素,BMI和SMI是其保护因素(P＜0.05).结论 女性RA患者肌少症和OP的发生率显著增高,肌少症与女性RA患者发生OP的关系密切.

To explore the synergistic effect of vitamin D deficiency and sarcopenia on vertebral osteoporostic fracture (VF) in patients with rheumatoid arthritis (RA). A total of 188 patients with RA and 158 control subjects were enrolled. Bone mineral density (BMD) at the total hip, neck of femur, lumbar vertebra 1–4, and skeletal muscle mass was measured by dual energy X-ray absorptiometry (DXA) and biological electrical impedance, respectively. Serum 25(OH)D was tested by electrochemiluminescence. The prevalence of VF and osteoporosis (OP) were compared between RA and controls. The synergism of sarcopenia and vitamin D deficiency on VF in patients with RA was tested by χ2 test and logistic regression. The prevalence of OP at all measured sites and VF in RA patients were all higher than those in controls (P < 0.0001). The incidence of VF in RA either with sarcopenia or with vitamin D deficiency was higher than for those without sarcopenia or without vitamin D deficiency (χ2 = 5.069, P = 0.027, χ2 = 8.822, P = 0.001). Age, disease duration, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), DAS28, health assessment questionnaire (HAQ), Sharp score, and body mass index (BMI) were significantly different between RA with sarcopenia or not (P < 0.05). Logistic regression analysis found that age (OR = 1.095, 95%, CI: 1.044–1.150, P < 0.0001) was a significant risk factor for VF in patients with RA, while high skeletal muscle mass (SMI) (OR = 0.513, 95% CI: 0.327–0.804, P = 0.004) was a protective factor for VF in RA patients. VF, sarcopenia, and vitamin D deficiency are common in patients with RA. Sarcopenia and vitamin D deficiency may be risk factors for the incidence of VF in RA patients. • RA patients had a higher incidence of OP and VF, also a high prevalence of sarcopenia and vitamin D deficiency. • Vitamin D deficiency and sarcopenia may might have a synergistic effect on VF in RA. • Aging and sarcopenia are risk factors for VF in RA patients, and sarcopenia were associated with disease activity and structural damage.

Purpose:Non-steroidal anti-inflammatory drugs (NSAIDs) have generally been viewed as first-line therapy for axial spondyloarthritis (axSpA). Imrecoxib is a selective COX-2 inhibitor developed independently in China. At present, only one single-center RCT trial has shown that imrecoxib is equally effective as celecoxib in treating axSpA. Based on real-world data, our study aims to explore the efficiency of imrecoxib and TNF inhibitor (TNFi) combined with imrecoxib in treating axSpA. Patients and Methods:A total of 163 patients with axSpA who had more than two follow-up records in 6 months and treated with imrecoxib/celecoxib/TNFi combined with imrecoxib/TNFi combined with celecoxib from the First Affiliated Hospital of Anhui Medical University SpA Real World Database (AHSpA) were selected for analysis of our study. The linear mixed model was used to compare efficacy indexes before and after treatment and between different groups, adjust baseline measurement value and follow-up time. The Kaplan-Meier survival analysis was used to identify the differences in cumulative clinical remission rates between groups with different treatment at the follow-up period. Results:Results showed that after treatment ASDAScrp was slightly improved in imrecoxib group and celecoxib group within 6 months (p < 0.05). CRP, ESR, BASDAI, ASDAScrp, BASFI, occiput to wall distance and finger floor distance all significantly improved in TNFi combined with imrecoxib group and TNFi combined with celecoxib group within 6 months (all p < 0.05). According to the Kaplan-Meier survival curve and Log rank test analysis, the clinical remission rate was not significantly different between different treatment during 24-month follow-up (all p > 0.05). Conclusion:ASDAScrp improved slightly within 6 months after treatment with imrecoxib, and TNFi combined with imrecoxib significantly improved multiple effect indexes in axSpA patients. The efficacy of imrecoxib and celecoxib in the treatment of axSpA is equivalent. Also, they have the same efficacy after being combined with TNFi.

目的 探讨类风湿关节炎(RA)合并2型糖尿病(T2DM)的危险因素.方法 根据是否合并T2DM,将782例RA患者分为合并T2DM组(70例)和未合并T2DM组(712例),比较两组患者的临床资料.采用趋势χ2检验比较不同年龄段、不同病程RA患者T2DM的发病率,RA患者合并T2DM的危险因素分析采用二分类logistic回归分析.结果 RA患者合并T2DM的患病率为8.95％,且随年龄和病程增长患病率逐渐增高(P<0.05).合并T2DM组患者较不合并T2DM组年龄、合并原发性高血压和使用糖皮质激素(GC)患者比例、GC日剂量、Sharp评分更高,病程和使用GC疗程更长(P<0.05).二分类logistic回归分析结果显示,年龄(OR=1.028,P=0.017,95％CI 1.005～1.051)、使用GC(OR=1.911,P=0.023,95％CI 1.095～3.336)及合并原发性高血压(OR=1.985,P=0.014,95％CI 1.151～3.423)是RA合并T2DM的危险因素.结论 8.95％的RA患者合并T2DM,且随年龄和病程增长患病率逐渐增高,高龄、使用GC及合并原发性高血压为RA患者合并T2DM的危险因素.

To investigate the rate of subclinical inflammation in patients with axial spondyloarthritis (axSpA) with nonsteroidal anti-inflammatory drug (NSAID)/anti-tumor necrosis factor (TNF)-α drug-induced clinical remission and to explore factors influencing clinical and imaging remission. One hundred twenty-five patients with axSpA followed up for at least 6 months were enrolled in this prospective study and randomly divided into two groups. Ninety patients were treated with anti-tumor necrosis factor (TNF)-α or anti-TNF-α combined with nonsteroidal anti-inflammatory drugs (NSAIDs) (anti-TNF-α treatment group), and thirty-five patients were treated with only NSAIDs (non anti-TNF-α treatment group). The improvements in the clinical remission rate, imaging remission rate, and disease parameters before and after the different treatments were compared. Risk factors for clinical and imaging remission were analyzed by multivariate logistic regression analysis. The clinical and imaging remission rate was increased after treatment especially in the anti-TNF-α group (P < 0.001). The remission rate of imaging in the group with clinical remission was higher than that in the group with clinical non-remission (P < 0.05). After treatment, the remission rates of imaging in the clinical remission and non-remission group were significantly higher than those before treatment (P < 0.0001). The results of multivariate logistic regression analysis showed that higher CRP was a risk factor for failure of clinical remission in axSpA (OR = 2.034, 95% CI:1.595 ~ 2.617, P < 0.001), while higher ASDAScrp was a risk factor for failure of imaging remission (OR = 1.306, 95% CI:1.026 ~ 1.688, P < 0.05). Anti-TNF-α treatment was a protective factor for both clinical (OR = 0.234, 95% CI:0.091 ~ 0.605, P < 0.05) and imaging remission (OR = 0.511, 95% CI:0.286 ~ 0.914, P < 0.05). Even after regular treatment, some clinical remission patients continued to have evidence of subclinical inflammation. Higher CRP and ASDAScrp are risk factors for clinical and imaging non-remission in axSpA respectively, Continuous NSAID treatment (more than 1 year) can effectively improve clinical and MRI inflammation in patients, but anti-TNF-α treatment is more beneficial for clinical and imaging remission.

This study investigated the effect of poor balance and sarcopenia on vertebral spinal osteoporotic fracture (VOPF) in female rheumatoid arthritic (RA) patients. A total of 195 female RA and 126 normal subjects were enrolled, and the correlations between sarcopenia, poor balance and VOPF were analyzed. Furthermore, we explored the relationships between sarcopenia or poor balance with disease related indexes of female RA. Binary logistic regression analyses were performed to identify potential risk factors for VOPF in female RA. We found that female RA had an increased risk of sarcopenia, poor balance (Berg balance scale, BBS ≤ 40) and VOPF than controls ( P < 0.0001). Female RA with VOPF were more likely to have poor balance and sarcopenia than those without VOPF ( P < 0.0001–0.05). Meanwhile, female RA with sarcopenia and poor balance often had higher disease activity, more serious joint damage and worse joint function ( P < 0.05) compared with those without sarcopenia and poor balance. Binary logistic regression analysis (LR backwald) revealed that age (OR = 1.112, 95% CI 1.065–1.160, P < 0.0001), OP (OR = 10.137, 95% CI 4.224–24.330, P < 0.0001) and GCs usage (OR = 3.532, 95% CI 1.427–8.741, P = 0.006) were risk factors, while SMI (OR = 0.386, 95% CI 0.243–0.614, P < 0.0001) and BBS (OR = 0.952, 95% CI 0.929–0.976, P < 0.0001) were protective factors for VOPF in female RA. Hence, sarcopenia and poor balance are associated with a higher risk for VOPF and are closely related to disease activity and joint structure damage of female RA.

[This corrects the article DOI: 10.2147/IJGM.S349435.].

目的 探讨肌少症对女性类风湿关节炎(RA)患者脊柱骨质疏松性骨折(OPF)发生的影响.方法 纳入399例女性RA患者(RA组)和98例年龄等相匹配的健康女性(对照组).根据是否合并脊柱OPF,将RA患者分为OPF组82例和非OPF组317例;根据是否合并肌少症,将RA患者分为肌少症组246例和无肌少症组153例;根据是否合并骨质疏松(OP),将RA患者分为OP组156例和非OP组243例.比较各组患者的临床资料,采用多元logistic回归分析评估女性RA患者发生脊柱OPF的影响因素.结果 RA组患者各部位骨密度(BMD)、骨骼肌质量指数(SMI)均低于对照组,OP、脊柱OPF及肌少症的发生率均高于对照组(P＜0.001).肌少症组年龄、病程、健康状况问卷(HAQ)评分、Sharp评分、绝经患者比例及OP的发生率均高于无肌少症组,BMI及各部位BMD均低于无肌少症组(P＜0.05).OP组绝经患者比例高于无OP组(P＜0.001).OPF组患者各部位骨骼肌质量、SMI及晨僵时间均低于无OPF组,年龄、病程、HAQ评分、使用糖皮质激素(GC)及绝经患者比例均高于无OPF组(P＜0.05).多元logistic回归分析结果显示,年龄、使用GC为女性RA患者发生脊柱OPF的危险因素,SMI为其保护因素(P＜0.05).结论 女性RA患者脊柱OPF和肌少症的发生率明显增高,较高的SMI为女性RA患者发生脊柱OPF的保护因素.

OBJECTIVES:This study aimed to investigate the synergistic effect of sarcopenia and poor balance on osteoporotic vertebral fracture (VOPF) in Chinese patients with rheumatoid arthritis (RA).METHODS:A total of 238 RA patients and 158 normal subjects were enrolled in the case-control study. Poor balance capability (Berg balance scale (BBS) score < 40) and sarcopenia (skeletal muscle mass index (SMI) <7.0 (male)/5.7 (female)) between RA patients and normal subjects were compared. Associations of poor balance capability or sarcopenia with disease activity, structural damage, and joint function in different groups were also investigated.RESULTS:The incidence of sarcopenia in RA was 58.4%, significantly higher than that in controls (P<0.0001). Moreover, the percentages of low balance capacity (BBS<40) in RA were 43.7%, which was higher than that in controls (P<0.0001). The prevalence of VOPF in the case group was 19.3%, which was higher than that in the controls (P<0.0001). In the RA group, compared to RA patients without VOPF, RA patients with VOPF had higher percentages of poor balance and sarcopenia (P<0.05). Compared with RA patients without sarcopenia or good balance, RA patients with sarcopenia or poor balance had a higher incidence of VOPF, higher disease activity, severer structural damage, and worse joint function (P<0.05). The incidence of VOPF in patients combined with good balance and non-sarcopenia (4.8%) was significantly lower than that in patients combined with poor balance and sarcopenia (38.2%) (P<0.0001). Logistic regression indicated that higher SMI and higher BBS scores were protective factors for VOPF in RA patients, while age was a risk factor for VOPF in RA patients (P<0.0001).CONCLUSION:Sarcopenia and poor balance are popular in Chinese patients with RA, and they are associated with disease activity and structural damage. There is a synergistic effect of sarcopenia and poor balance on VOPF in RA. Key Points • Sarcopenia and balance capability were popular (about a half) in patients with RA. • Sarcopenia and poor balance had a synergistic effect on VOPF in RA.

目的 调查安徽医科大学第一附属医院风湿免疫科门诊患者胃肠道危险因素的流行病学特征.方法 通过问卷调查936例我院风湿免疫科门诊患者胃肠道危险因素的发生情况,分别比较不同病种间各胃肠道危险因素发生率的差异.结果 936例患者中,类风湿关节炎(RA)268例(28.6％,RA组),系统性红斑狼疮(SLE)205例(21.9％,SLE组),其他弥漫性结缔组织病(CTD)159例(17.0％),脊柱关节炎(SpA)122例(13.0％),骨关节炎(OA)101例(10.8％,OA组),痛风39例(4.2％),其他疾病42例(4.5％).936例患者中各胃肠道危险因素的发生情况:年龄≥60岁205例(21.9％),有消化性溃疡史99例(10.6％),曾使用抗凝药物9例(1.0％),曾使用非甾体抗炎药(NSAIDs)387例(41.3％),曾使用糖皮质激素(GC)527例(56.3％),曾使用低剂量阿司匹林(ASA)109例(11.6％),曾感染幽门螺杆菌4例(0.4％),吸烟51例(5.4％),酗酒10例(1.1％).其中,低风险54例(5.8％);中风险795例(84.9％),其中存在1项胃肠道危险因素466例(49.8％),存在2项胃肠道危险因素329例(35.1％);高风险(存在至少3项胃肠道危险因素)87例(9.3％).936例患者中曾使用抗凝药物、NSAIDs、GC或低剂量ASA任何1项644例(68.8％),曾使用其中两项及以上191例(20.4％),其中使用NSAIDs和GC联合治疗87例(9.3％),而未曾使用上述4种药物仅101例(10.8％).RA组年龄≥60岁、曾使用NSAIDs、NSAIDs联合GC患者比例高于SLE组(P<0.001),曾使用抗凝药物、GC、低剂量ASA患者比例低于SLE组(P<0.01).RA组使用GC、NSAIDs联合GC患者比例均高于OA组(P<0.001).SpA组使用NSAIDs、吸烟及酗酒患者比例均高于RA组、OA组(P<0.05).结论 94.2％的风湿免疫科门诊患者存在中度以上胃肠道风险,单项胃肠道危险因素发生率最高者为GC使用(超过50％),其次为NSAIDs使用(约40％),不同风湿免疫性疾病患者的胃肠道危险构成比存在明显差异.

This work aims to analyze and construct a novel competing endogenous RNA (ceRNA) network in ankylosing spondylitis (AS) with bone bridge formation, lncRNA. Using RNA sequencing and bioinformatics, we analyzed expression profiles of long noncoding RNAs (lncRNAs), microRNAs (miRNAs), and mRNAs in whole blood cells from 5 AS patients and 3 healthy individuals. Next, we verified the expression levels of candidate lncRNAs in 97 samples using the ΔΔCt value of real-time quantitative polymerase chain reaction (qRT-PCR). We used multivariate logistic regression analysis to screen lncRNAs and clinical indicators for use in the prediction model. Both SPSS 24.0 and R software were used for data analysis and prediction model construction. The results showed that compared with the normal controls, 205 long noncoding RNAs (lncRNAs), 961 microRNAs (miRNAs), and 200 mRNAs (DEmRNAs) were differentially expressed in the AS patients. We identified lncRNA 122K13.12 and lncRNA 326C3.7 among 205 lncRNAs differentially expressed between AS patients and healthy humans. Then, we noted that 30 miRNAs and five mRNAs formed a ceRNA network together with these two lncRNAs. These ceRNA networks might regulate the tumor necrosis factor (TNF) signaling pathway in AS development. In addition, the expression level of lncRNA 122K13.12 and lncRNA 326C3.7 correlated with various structural damage indicators in AS. Specifically, the lncRNA 326C3.7 expression level was an independent risk factor in bone bridge formation [area under the ROC curve (AUC) = 0.739 (0.609–0.870) and p = 0.003], and the best Youden Index was 0.405 (sensitivity = 0.800 and specificity = 0.605). Moreover, we constructed a lncRNA-based nomogram that could effectively predict bone bridge formation [AUC = 0.870 (0.780–0.959) and p < 0.001, and the best Youden Index was 0.637 (sensitivity = 0.900 and specificity = 0.737)]. In conclusion, we uncovered a unique ceRNA signaling network in AS with bone bridge formation and identified novel biomarkers and prediction models with the potential for clinical applications.

Patients with rheumatoid arthritis (RA) had higher incidences of sarcopenia, falls, osteoporosis, and vertebral osteoporotic fractures (VOPF). Sarcopenia was associated with longer disease duration, higher disease activity, and more severe RA. The interactive effect of sarcopenia and falls was associated with a higher risk of VOPF in patients with RA. Whether sarcopenia and falls are a risk factor for vertebral fracture in RA patients has not been demonstrated. This study aimed to explore the incidence of vertebral osteoporotic fracture (VOPF) and its relationship with sarcopenia and falls in RA patients. A total of 474 RA patients and 156 controls were enrolled in this study. Anteroposterior and lateral X-ray examinations of the vertebral column (T4-L4) were used for the semiquantitative assessment of VOPF. Bone mineral density was measured by dual-energy X-ray absorptiometry. Skeletal muscle mass was measured by direct segmental multifrequency bioelectrical impedance analysis (DSM-BIA method). RA patients had an increased risk of sarcopenia (62.4% vs 9.0%, x2 = 47.478, P < 0.001), falls (30.2% vs 3.2%), osteoporosis (OP) (33.5% vs 12.8%, x2 = 134.276, P < 0.001), and VOPF (20.3% vs 3.8%, x2 = 47.478, P < 0.001) than controls. Patients with sarcopenia were more likely to have VOPF than RA without sarcopenia (24.0% vs 14.0%, x2 = 6.802, P = 0.009). RA with sarcopenia and prior falls had the highest incidences of VOPF (36.7%). Older age (OR = 1.056, P < 0.001, 95% CI 1.030–1.083), falls (OR = 2.043, P = 0.003, 95% CI 1.238–3.371), OP (OR = 1.819, P = 0.034, 95% CI 1.046–3.163), and usage of glucocorticoids (GCs) (OR = 1.862, P = 0.022, 95% CI 1.093–3.172) were risk factors for VOPF in RA patients, while a higher skeletal muscle index (SMI) was a protective factor (OR = 0.754, P = 0.038, 95% CI 0.578–0.984) for VOPF in RA patients. The interactive effect of sarcopenia and falls is associated with a higher risk of VOPF in patients with RA.

The authors regrets that the original published version of this article contained errors.

目的 探讨肌少症、骨量减少/骨质疏松在类风湿关节炎(rheumatoid arthritis,RA)患者合并脊柱骨质疏松性骨折发生中的临床意义.方法 选择2017年1月至2018年12月我院383例RA患者和158名健康者,记录RA临床、实验室指标.摄脊柱(T5-L5)X线正侧位片并采用半定量法判断有无脊柱骨折发生,以生物电阻抗法测四肢骨骼肌质量,双能X线骨密度吸收仪测定髋部和腰椎骨密度(bone mineral density,BMD).383例RA患者根据其骨骼肌质量指数(skeletal muscle mass index,SMI)和BMD分为4组:无肌少症且无骨量减少/骨质疏松组64例,有肌少症无骨量减少/骨质疏松组44例,无肌少症有骨量减少/骨质疏松组86例,有肌少症且有骨量减少/骨质疏松组189例,分析肌少症、骨量减少/骨质疏松在RA患者合并脊柱骨质疏松性骨折发生的意义.结果 RA组脊柱骨折发生率显著高于对照组(21.1％vs 3.8％,χ2=24.954,P<0.001),RA组较对照组骨量减少/骨质疏松和肌少症发生率均明显增高(71.8％vs 41.8％,χ2=43.287;60.8％vs 9.0％,χ2=120.093,P均<0.001),且4组RA间脊柱骨折发生率有明显差别(4.7％、11.4％、17.4％和30.7％,χ2=23.947,P<0.001).非参数检验显示4组RA间关节压痛、压痛指数、血沉、DAS28、糖皮质激素日剂量和疗程、HAQ及sharp评分均有明显差异(P均<0.05).多元Logistic回归结果 显示:年龄(OR=1.073,P<0.001,95％CI:1.041～1.107)和糖皮质激素的使用(OR=3.221,P=0.001,95％CI:1.663～6.242)是RA患者发生脊柱骨折的危险因素,而腰椎BMD(OR=0.093,P=0.009,95％CI:0.015～0.555)和SMI(OR=0.716,P=0.032,95％CI:0.527～0.973)是RA患者发生脊柱骨折的保护因素.结论 RA患者肌少症、骨量减少/骨质疏松和脊柱骨质疏松性骨折发生率均明显增高,肌少症、骨量减少/骨质疏松与RA患者的脊柱骨质疏松性骨折的发生密切相关.

中轴型脊柱关节炎(axSpA)是一组以中轴关节及其周围组织慢性进展性炎症为特征的疾病,在疾病后期可引起脊柱或受累关节强直畸形,常导致终身残疾.2012年国际工作组提出的axSpA治疗目标和推荐意见[1]及其2017年修订版[2]均认为axSpA达标治疗的目标为肌肉、骨骼和关节外表现的临床缓解或疾病停止活动,推荐采用C反应蛋白(CRP)及强直性脊柱炎疾病活动性评分(ASDAS)对患者进行评估,此外,磁共振(MRI)检查结果也是评价axSpA治疗效果的重要因素.本文对近年来axSpA达标治疗及MRI检查在其中应用价值的研究进展作一综述.