CD38 is highly expressed on various immune cells, including long-lived plasma cells, making it a potential therapeutic target in autoimmune diseases. This phase Ib/IIa study aimed to explore the safety, pharmacokinetics, pharmacodynamics, and preliminary efficacy of CM313, an anti-CD38 antibody, in patients with systemic lupus erythematosus (SLE). Eligible patients were sequentially enrolled in four ascending dose groups (2, 4, 8, and 16 mg/kg) and randomized 4:1 to receive CM313 or placebo intravenously at days 1, 29, 36, 43, and 50. The primary endpoint was safety, and efficacy was exploratorily investigated. Between October 14, 2022, and March 7, 2024, 40 patients were enrolled, including 8 patients in each CM313 dose group and the pooled placebo group. Adverse events occurred in 90.6% and 62.5% of participants receiving CM313 and placebo, all of which were mild or moderate. Upper respiratory tract infection (87.5%/62.5% vs. 12.5%), urinary tract infection (12.5%/25.0% vs. 0), and herpes zoster (25.0%/0 vs. 0) were more frequent in CM313 8 and 16 mg/kg groups than the placebo group. The CM313 groups had greater reductions in anti-ds-DNA antibodies, immunoglobulin G (IgG), IgA, IgM, IgE, and greater increases in complement C3 and C4 compared with placebo. Systemic Lupus Erythematosus Responder Index-4 response rates were 33.3%, 40.0%, 62.5%, 71.4%, and 37.5% in CM313 2, 4, 8, 16 mg/kg, and placebo groups at day 57, respectively. CM313 showed a manageable safety profile in SLE patients at 2–16 mg/kg and encouraging clinical efficacy at 8 and 16 mg/kg. The results support further investigation of CM313 for treating SLE patients (ClinicalTrials.gov ID: NCT05465707).

Extrafollicular age-associated B cells (ABCs) excessively expand and produce autoantibodies in systemic lupus erythematosus (SLE), and the regulatory mechanism remains elusive. We found that the m6A demethylase fat mass and obesity-associated protein (FTO) was highly expressed in ABCs from patients with SLE, which was positively associated with renal immune damage. FTO overexpression in murine and human B cells facilitated ABC expansion and exacerbated SLE in lupus-prone mice, whereas FTO ablation ameliorated ABC-driven autoimmunity. FTO expression was up-regulated upon activation of the toll-like receptor 7-myeloid differentiation primary response protein 88 (TLR7-MyD88) signaling pathway. FTO, in turn, promoted TLR7-driven ABC differentiation by targeting ATPase H+ transporting V1 subunit G1 (ATP6V1G1), a subunit of the vacuolar H+-ATPase (V-ATPase), in an m6A-dependent manner. Mechanistically, FTO deficiency impaired lysosomal autophagy by reducing ATP6V1G1-mediated V-ATPase activity. The accumulation of damaged mitochondria led to mitochondrial dysfunction in human and murine B cells, characterized by reduced oxidative phosphorylation and elevated reactive oxygen species. This dysfunction limited cell proliferation and blocked ABC differentiation by dampening cellular responsiveness to interleukin-12. Thus, TLR7-FTO-ATP6V1G1 signaling metabolically shapes extrafollicular ABCs in SLE, providing a potential therapeutic target.

OBJECTIVE:To investigate the role of growth differentiation factor 15 (GDF-15) in ankylosing spondylitis (AS). METHODS:A proteoglycan-induced arthritis mouse model was established to mimic the pathologic changes of AS. Expression of GDF-15 in serum and the edge of the vertebral cartilage plate and the spinal entheseal sites in the model group was detected by enzyme-linked immunosorbent assay and immunohistochemistry. Then primary fibroblasts from the ligaments of patients with femoral neck fracture (healthy controls [HC]) and patients with AS were extracted. Western blotting, alkaline phosphatase (ALP) staining and activity assay, and alizarin red staining were used to detect the osteogenic ability of primary fibroblasts. RESULTS:Expression of GDF-15 was up-regulated in serum and the edge of the vertebral cartilage plate and the spinal entheseal sites in the model group. In vitro, our results showed that GDF-15 promoted the osteogenic differentiation of HC and AS fibroblasts. Furthermore, our results showed that in AS fibroblasts, GDF-15 elevated the expression of osteogenic marker genes (SP7, RUNX2, and COL1) as well as p-glycogen synthase kinase 3β and β-catenin, which are involved in the Wnt/β-catenin signaling pathway. This effect of GDF-15 in AS fibroblasts could be reversed by the inhibitor of the Wnt/β-catenin signaling pathway, DKK-1, suggesting that GDF-15 promoted the osteogenic differentiation of AS fibroblasts via the Wnt/β-catenin signaling pathway. Furthermore, knockdown of GDF-15 also suppressed osteogenic differentiation and inhibited Wnt/β-catenin signaling in AS fibroblasts. CONCLUSION:This study revealed aberrant up-regulation of GDF-15 in an AS mouse model and osteogenic effect of GDF-15 in AS fibroblasts via the Wnt/β-catenin signaling pathway, which may be one of the mechanisms and therapeutic targets of new bone formation in AS.

This investigation aimed to evaluate the efficacy and safety of belimumab and telitacicept in active systemic lupus erythematosus (SLE) and to explore potential predictors within a treat-to-target paradigm. 101 individuals were retrospectively enrolled at Guangdong Provincial People’s Hospital between January 2021 and December 2023, receiving either belimumab (n = 50) or telitacicept (n = 51) in conjunction with standard therapy for more than 24 weeks. Key clinical endpoints were evaluated, with lupus low disease activity state (LLDAS) as the primary outcome. Multivariate analysis was employed to investigate factors associated with failure to attain LLDAS. Baseline characteristics were balanced in both groups after propensity score-based inverse probability of treatment weighting. At 24 weeks, the rates of attainment of LLDAS were 54.86

Anti-melanoma differentiation-associated protein 5 antibody-positive dermatomyositis (anti-MDA5-positvie DM) is a subtype of dermatomyositis with a poor prognosis, characterized by rapidly progressive interstitial lung disease (RP-ILD). The study aims to investigate the significance of serum cytokines profiles and peripheral lymphocytes in predicting prognoses of anti-MDA5-positvie DM with RP-ILD. Furthermore, it seeks to analyze longitudinal data of lymphocytes during hospitalization to identify distinct trajectories and cluster patients accordingly. A total of 168 patients with anti-MDA5-positive DM were enrolled in this retrospective study from two cohorts. Univariate and multivariate Cox regression analyses were conducted to determine the predictors of 6-month all-cause mortality and RP-ILD. Group-based trajectory modeling (GBTM) was employed to model the trajectories of longitudinal peripheral lymphocytes. In the multivariate Cox regression analysis, IL-6 ≥ 13.41pg/mL, lymphocytes < 0.5 × 109 /L, lymphocytes from 0.5 to 1.0 × 109 /L, older age, and elevated LDH were identified as independent predictors of 6-month all-cause mortality. Furthermore, IL-6 ≥ 13.41pg/mL, lymphocytes < 0.5 × 109 /L, and lymphocytes from 0.5 to 1.0 × 109 /L were found to be independent predictors of RP-ILD. Additionally, three trajectory groups of lymphocytes within the first week after admission were established based on GBTM. These groups included: Group 1, with low-level of lymphocytes that declined; Group 2, with medium-level of lymphocytes that slightly rose; and Group 3, with high-level of lymphocytes that rose. Notably, group 1 showed the highest mortality (90.7

To evaluate the safety of secukinumab (SEC) in the treatment of patients with axial spondyloarthritis (axSpA) and concurrent hepatitis B virus (HBV) infection or latent tuberculosis infection (LTBI). This is a retrospective cohort study. Adult axSpA patients with HBV infection or LTBI receiving SEC treatment for at least 3 months from March 2020 to July 2022 in Guangdong Provincial People’s Hospital were included. Patients were screened for HBV infection and LTBI before SEC treatment. During follow-up, reactivation of HBV infection and LTBI was monitored. Relevant data were collected and analyzed. A total of 43 axSpA patients with HBV infection or LTBI were included, of whom 37 were with HBV infection, 6 were with LTBI. Six out of thirty-seven (16.2

Axial spondyloarthritis (Ax-SpA) is a chronic inflammatory disease that predominantly affects the axial joints and is most common in young men. However, the precise immune cell subset involved in Ax-SpA remains unclear. Our study characterized the periphery immune landscape of Ax-SpA patients before and after anti-TNF alpha treatment using single-cell transcriptomics and proteomics sequencing and elucidated the effects of anti-TNF alpha treatment at the single-cell level. First, we found that peripheral granulocytes and monocytes significantly increased in Ax-SpA patients. Second, we identified a more functional subtype of regulatory T cells, which was present in synovial fluid and increased in patients after treatment. Third, we identified a cluster of inflammatory monocyte subset with stronger inflammatory and chemotactic characteristics. A potential interaction between classical monocytes and granulocytes via the CXCL8/2-CXCR1/2 signaling pathway was observed, which decreased after treatment. Together, these results defined the complex expression profiles and advanced our understanding of the immune atlas in Ax-SpA patients before and after anti-TNF alpha treatment.

BackgroundAnkylosing spondylitis (AS) is a disabling chronic inflammatory disease. Mechanisms of ferroptosis in AS remain unclear. Using bioinformatics analysis, we aimed to identify key molecules involved in ferroptosis, provide potential therapeutic targets for AS, and further explore mechanisms of ferroptosis in AS.MethodsGSE25101 was downloaded from the Gene Expression Omnibus and intersected with a ferroptosis gene dataset. The ferroptosis‐relate differentially‐expressed genes were further subjected to functional enrichment analysis, protein interaction network analysis, and gene‐miRNA interaction network analysis, from which potential key ferroptosis genes in the pathogenesis of ankylosing spondylitis were screened.ResultsA total of 20 differentially expressed genes were screened, most of which are involved in phosphoinositide 3 kinase‐Akt or mitogen‐activated protein kinase (MAPK) signaling pathways or the endoplasmic reticulum stress response. The following target genes were identified through protein‐protein interaction network analysis and screening of key modules constructed from genes associated with PI3K‐Akt and MAPK signaling pathways: TP53, PTEN, TLR4, HSPB1, DDIT3, and XBP1. In addition, PI3K‐Akt and MAPK signaling were associated with oxidative stress, which may play a role in AS pathological ossification related to ferroptosis. Only hsa‐miR‐205‐5p was found to target at least two genes by gene‐miRNA interaction network analysis.ConclusionsFuture therapeutic drug development may intervene by modulating MAPK or PI3K‐Akt signaling pathways rather than directly affecting the interleukin 17 pathway. hsa‐miR‐205‐5p may be a potential novel biomarker for AS.

Axial spondyloarthritis (Ax-SpA) is a chronic inflammatory disease that predominantly affects the axial joints and is most common in young men. However, the precise immune cell subset involved in Ax-SpA remains unclear. Our study characterized the periphery immune landscape of Ax-SpA patients before and after anti-TNFα treatment using single-cell transcriptomics and proteomics sequencing and elucidated the effects of anti-TNFα treatment at the single-cell level. First, we found that peripheral granulocytes and monocytes significantly increased in Ax-SpA patients. Second, we identified a more functional subtype of regulatory T cells, which was present in synovial fluid and increased in patients after treatment. Third, we identified a cluster of inflammatory monocyte subset with stronger inflammatory and chemotactic characteristics. A potential interaction between classical monocytes and granulocytes via the CXCL8/2-CXCR1/2 signaling pathway was observed, which decreased after treatment. Together, these results defined the complex expression profiles and advanced our understanding of the immune atlas in Ax-SpA patients before and after anti-TNFα treatment.

Ankylosing spondylitis (AS) is a chronic inflammatory disease characterized by abnormal bone metabolism, with few effective treatments available. Danshensu [3-(3,4-dihydroxy-phenyl) lactic acid) is a bioactive compound from traditional Chinese medicine with a variety of pharmacologic effects. In the present study, we investigated the pharmacologic effect and molecular mechanism of Danshensu in AS. Potential targets of Danshensu were identified in four drugs-genes databases; and potential pharmacologic target genes in AS were identified in three diseases-genes databases. Differentially expressed genes related to AS were obtained from the Gene Expression Omnibus database. Overlapping targets of Danshensu and AS were determined and a disease–active ingredient–target interaction network was constructed with Cytoscape software. Enrichment analyses of the common targets were performed using Bioconductor. To test the validity of the constructed network, an in vitro model was established by treating osteoblasts from newborn rats with low concentrations of tumor necrosis factor (TNF)-α. Then, the in vitro model and AS fibroblasts were treated with Danshensu (1–10 μM). Osteogenesis was evaluated by alkaline phosphatase staining and activity assay, alizarin red staining, quantitative PCR, and western blotting. We identified 2944 AS-related genes and 406 Danshensu targets, including 47 that were common to both datasets. The main signaling pathways associated with the targets were the c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) pathways. A low concentration of TNF-α (0.01 ng/ml) promoted the differentiation of osteoblasts; this was inhibited by Danshensu, which had the same effect on AS fibroblasts but had the opposite effect on normal osteoblasts. Danshensu also decreased the phosphorylation of JNK and ERK in AS fibroblasts. There results provide evidence that Danshensu exerts an anti-osteogenic effect via suppression of JNK and ERK signaling, highlighting its therapeutic potential for the treatment of AS.

The objective of this study was to explore the association between transformation growth factor beta 1 (TGF- β 1) gene polymorphisms and different types of arthritis. PubMed, Medline, Web of Science, Cochrane Library, Biosis and four Chinese databases: China Biology Medicine, China National Knowledge Infrastructure, Wanfang and CQVIP, were searched. Studies that analyzed the association of the TGF- β 1 polymorphisms with different types of arthritis were included. OR, 95% confidence interval and P value were calculated in three models including allele, dominant and recessive models, using D + L method. The Newcastle–Ottawa Scale was used to assess the quality of the included studies. TGF- β 1 869T > C polymorphism was significantly associated with rheumatoid arthritis (RA) in allele and recessive models, but not in dominant model (allele model T vs. C: OR = 1.30, 95% CI = 1.13–1.49, P < 0.001; recessive model CC vs. TT + TC: OR = 0.57, 95% CI = 0.43–0.76, P < 0.001; dominant model TT vs. TC + CC: OR = 1.20, 95% CI = 0.99–1.45, P = 0.063). Additionally, allele and recessive models showed that TGF- β 1 -509C > T was significantly correlated with RA susceptibility, while dominant model revealed nonsignificant correlation (allele model: C vs. T: OR = 1.51; 95% CI = 1.00–2.28; P = 0.049; recessive model: TT vs. CC + TC: OR = 0.52, 95% CI = 0.37–0.72, P = 0.000; dominant model: CC vs. TT + TC: OR = 1.48; 95% CI = 0.79–2.76; P = 0.223). However, no significant association was found between TGF- β 1 polymorphisms and ankylosing spondylitis (AS) or osteoarthritis (OA) risk. This study demonstrated that 869T > C, -509 C > T polymorphisms of TGF- β 1 gene were associated with increased susceptibility of RA, while polymorphisms of TGF- β 1 gene were not associated with OA and AS. These findings suggest that studying TGF- β 1 genotype may be useful in the prevention and management of RA. However, more studies are needed to evaluate the association of TGF- β 1 gene polymorphisms with the susceptibility of OA and AS.

Objective:The current evidence suggests that tumor necrosis factor-inhibitor (TNFi) treatment can be used to achieve clinical remission or low disease activity in patients with ankylosing spondylitis (AS). After achieving remission / low disease activity, however, the follow-up treatment options are unclear. The purpose of this review is to conduct an extensive and systematic literature review of the studies conducted from September 2014 to July 2020 to assess the feasibility and effectiveness of tapering of biological agents.Methods:After searching for the related papers and abstracts and applying inclusion/exclusion criteria, a structured extraction process was used to include the studies into this study.Results:A total of 13/93 studies were included into the analysis of the tapering of biological agents in AS patients, in which 7/13 adopted the dose reduction regimen, 3/13 adopted the extended interval between doses regimen, and 5/13 did not provide or formulate the detailed reduction regimen. We summarized the feasibility of TNFi tapering schemes in the published studies and summarized the tapering rules. Only one study showed that reduced TNFi levels worsened the quality of life and resulted in a relapse within 12 months.Conclusion:More research is needed to understand the long-term effects of these strategies on efficacy, safety, and cost in the treatment of AS.

系统性红斑狼疮(systemic lupus erythematosus,SLE)是一种育龄期,尤其是20～40岁女性高发的疾病.此年龄段患者多有怀孕生子的需求,但SLE患者合并妊娠时不但疾病本身可能反复或加重,不良妊娠风险亦显著增加,因此做好SLE患者妊娠期综合管理极其重要.本文主要阐述SLE与妊娠的相互影响及妊娠期SLE患者的综合管理,以期指导临床更好地认识该问题,从而改善SLE患者的妊娠结局.

o n b e t w e e n T G F b e t a 1 polymorphisms and different

Purpose: Pulmonary fibrosis (PF) is a severe lung disease causing significant morbidity and mortality. PF pathogenesis is attributed to the fibroblast-to-myofibroblast transition (FMT) driven by the most potent pro-fibrogenic factor TGF-beta 1 activating the Smad3-dependent TGF-beta 1 canonical pathway. Iguratimod (IGU) is a novel anti-rheumatic drug that suppresses the secretion of inflammatory factors, but is also able to modulate the differentiation of multiple cells. Therefore, the aim of this work was to investigate the effect of IGU on FMT. Materials/methods: PF mouse model was induced in C57BL/6 male mice by bleomycin. The effect of IGU was assessed through the evaluation of lung morphology by H&E and through the collagen accumulation in the lung by Masson staining. Primary human lung fibroblasts (pHLFs) were also used to evaluate the effect of IGU in vitro on TGF-beta 1-stimulated cells, and proliferation, migration and invasion were measured, together with genes and proteins involved in FMT. Results: IGU attenuated bleomycin-induced PF in mice and improved the pathological changes in their lungs. In addition, IGU significantly inhibited proliferation, migration and invasion in TGF-beta 1-stimulated pHLFs without causing apoptosis. Moreover, IGU significantly reduced TGF-beta 1-induced increase of collagen I and III mRNA expression, thus reducing lung function impairment, and alpha-SMA, Smad2 and Smad3 phosphorylation, fibronectin expression and F-actin microfilament formation, thus attenuating FMT through the inhibition of the Smad3 pathway. Conclusions: Our results collectively revealed the beneficial effect of IGU on the inhibition of FMT, thus suggesting that it might act as an effective anti-fibrotic agent in preventing the progression of PF.

Iguratimod (IGU) is a novel small molecule anti-rheumatic drug with the effect of non-steroidal anti-inflammatory drug and disease-modifying anti-rheumatic drug. IGU has various mechanisms of action, including inhibition of prostaglandin E2, tumor necrosis factor-α (TNF-α), interleukin-17 (IL-17) production, inhibition of macrophage migration inhibitory factor (MIF)-induced proinflammatory effects, inhibition of osteoclastogenesis, and promotion of osteoblastic differentiation. Ankylosing spondylitis (AS) is the major subtype of spondyloarthritis that affects the axial skeleton, causing inflammatory back pain, which can lead to impairments in structure and function and a decrease in quality of life. Theories on pathogenesis of AS include misfolding of human leukocyte antigen-B27 during its assembly leading to endoplasmic reticulum stress and unfolded protein response (UPR). Activation of UPR genes results in release of TNF-α and IL-17, which have been shown to be important in the development of AS. In addition, current evidence suggests the importance of cyclooxygenase-2/prostaglandin E2 pathway and MIF in the pathogenesis of AS. Current drugs for the treatment of AS are limited and exploration of effective drugs is needed. IGU may be effective for the treatment of AS given that its mechanisms of action are closely related to the pathogenesis of AS. In fact, several small-scale clinical trials have shown the efficacy of IGU for the treatment of AS. This article reviews the molecular mechanisms of IGU that are related to the pathogenesis of AS and clinical trials of IGU for the treatment of AS, providing a reference for future clinical application of IGU for AS.

Objective. Ankylosing spondylitis (AS) is a chronic inflammatory disease that affects the axial skeleton, leading to joint disability. Our study aims at investigating the change of oxidative and antioxidative stress linked biomarkers in AS. Methods. This systematic review and meta-analysis was performed following the Preferred Reporting Items of Systematic Reviews and Meta-Analyses (PRISMA) statement. PubMed, Web of Science, and Cochrane Library databases till May 2020 were searched. Only articles published in English were included. Two reviewers screened relevant studies, extracted data, and assessed the quality of included studies using the Newcastle-Ottawa scale independently. Either random or fixed effect model was adopted base on the heterogeneity testing by I2 statistic. Standardized mean difference (SMD) and 95% confidence intervals (CI) of oxidative and antioxidative markers were calculated. p value <0.05 was considered statistically significant. Results. A total of 22 studies including 931 AS patients and 917 healthy controls met the selection criteria. Significantly increased levels of all oxidative stress markers except myeloperoxidase, and significantly decreased levels of total antioxidant status (SMD=−1.19, 95% CI -2.35 to -0.03, p=0.044) and paraoxonase 1(SMD=−1.01, 95% CI -1.78 to -0.24, p=0.010) in serum were observed in AS patients when compared with healthy controls. However, there were no significant differences of all oxidative and anti-oxidative stress biomarkers in erythrocytes. Additionally, the levels of malondialdehyde (SMD=0.51, 95% CI 0.21 to 0.81, p=0.001) and advanced oxidation protein products (SMD=0.95, 95% CI 0.58 to 1.31, p<0.001) in serum were significantly higher in active patients when compared with inactive AS patients. Conclusion. This meta-analysis demonstrated an overall increase of oxidative markers and decrease of antioxidative markers in AS, suggesting that oxidative stress may play an important role in the pathogenesis of AS.

强直性脊柱炎(AS)是一种以骶髂关节和脊柱中轴关节病为主要病变的慢性进行性炎症性疾病.骨外组织异常钙化、骨赘形成是AS发展的根源,异位骨形成、骨量减少、骨质疏松目前被认为是AS的共同特征,其中关键的异位骨形成机制尚未明确.细胞核因子KB受体活化因子(RANK)/细胞核因子KB受体活化因子配体(RANKL)/骨保护素(OPG)通路、骨形态发生蛋白(BMPs)介导通路、Wnt信号通路及白细胞介素(IL)-23/IL-17轴是目前研究较多的影响AS骨代谢的通路,也有少数文献报道机械载荷(ML)介导信号通路影响AS骨形成.应用骨代谢标志物,包括骨形成标志物和骨吸收标志物在AS患者异常改变,以及双能X线(DXA),定量计算机断层扫描法(QCT)、MRI、骨小梁评分(TBS)等影像学检查可协助了解AS骨代谢情况,为目前有效的治疗方法提供随访的量化指标.该文从AS骨代谢通路、AS骨代谢标志物、AS骨代谢在影像学中表现等方面对AS骨代谢的研究进展进行综述.

Aim Inflammatory joint diseases (IJDs) are chronic arthritis, but frequently present with co-morbidities of other organs and systems, which is known as extra-articular manifestations (EAMs). It is still unclear which clinical characteristics or bio-markers can predict the development of EAMs. The aim of this study was to estimate the proportion of EAMs in southern Chinese patients with IJDs and to explore the risk factors. Methods This was a retrospective cohort study of a total 1135 IJDs patients, including 788 rheumatoid arthritis (RA) patients, 307 ankylosing spondylitis (AS) patients and 40 psoriatic arthritis (PsA) patients. Demographic data, disease characteristics, laboratory blood tests, medical imaging, and the presence of EAMs were recorded. Results We found 459 (40.44%) patients presented with EAMs: 30.84% had cardiovascular involvement, 7.67% had pulmonary involvement, 5.29% had osteoporosis/low bone mineral density, 2.29% had ocular, 0.79% had gastrointestinal and 0.26% had renal involvements. Multivariate logistic regression showed older age (odds ratio [OR] 1.06, P < .001) and higher anti-cyclic citrullinated peptide antibody (anti-CCP) levels (OR 1.003, P = .019) were independent risks of EAMs in RA patients. In the AS group, older age (OR 1.07, P < .001) and higher disease activity (OR 3.24-7.42, both P < .05), were independent risks of EAMs. In the PsA group, longer disease duration (OR 1.01, P = .036) and higher disease activity (OR 1.15, P = .004) were univariate associated factors. Conclusion These results suggested the high prevalence of EAMs, and it is important to regularly screen for EAMs, as they influence treatment decisions and impact on patients' quality of life.

炎症性关节病是一组以慢性关节炎为特征的疾病,主要包括类风湿关节炎、强直性脊柱炎和银屑病关节炎.本篇综述回顾了近年来炎症关节病合并心血管损害的相关文献,发现炎症关节病患者合并心血管疾病的风险较普通人群升高,可能与高度炎症反应和长病程有关;心血管损害表现形式多样,可累及血管、心脏瓣膜、心包和心脏电传导系统,且临床症状隐匿,显著增加了患者的死亡风险.这提示我们应提高对炎性关节病合并心血管损害的重视,对炎症关节病患者进行心血管疾病筛查,积极早期诊断及治疗,以期改善患者的预后.