脊柱关节炎中的促炎细胞因子:一项病例对照研究。

IF 3.9 3区 医学 Q2 IMMUNOLOGY Expert Review of Clinical Immunology Pub Date : 2024-06-01 Epub Date: 2024-01-17 DOI:10.1080/1744666X.2024.2304080
Maroua Slouma, Lobna Kharrat, Aymen Tezegdenti, Rim Dhahri, Ezzeddine Ghazouani, Imen Gharsallah
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引用次数: 0

摘要

研究目的我们旨在确定促炎细胞因子在区分脊柱关节炎患者与健康人方面的鉴别价值,并评估这些细胞因子与脊柱关节炎特征之间的关联:我们进行了一项病例对照研究,包括 144 名年龄和性别匹配的受试者:72 名脊柱关节炎患者(G1)和 72 名对照组(G2)。使用 ASDAS-CRP 和 BASDAI 评估疾病活动性。用 BASRI 评估结构性损伤。白细胞介素(IL)IL-1、IL-6、IL-8、IL-17、IL-23和肿瘤坏死因子α(TNFα)的水平进行了测定:每组包括 57 名男性。结果:每组包括 57 名男性,平均年龄为 44.84 ± 13.42 岁。除IL-8外,患者体内所有细胞因子水平均明显高于对照组(IL-1:p = 0.05;IL-6:p = 0.021;TNFα:p = 0.039;IL-17和IL-23:p = 0.029)和BASRI(p = 0.002)。多变量分析显示,结构性损伤与男性(p = 0.017)、病程长(p = 0.038)和疾病活动性高(p = 0.044)有关。疾病活动与病程长(p = 0.012)和 IL-6 水平升高(p = 0.05)有关:我们的研究表明,IL-17最能区分脊柱关节炎患者和对照组,这表明IL-17可能有助于脊柱关节炎的诊断。
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Pro-inflammatory cytokines in spondyloarthritis: a case-control study.

Objectives: We aimed to determine the discriminative values of pro-inflammatory cytokines to distinguish spondyloarthritis patients from healthy subjects and to assess the association between these cytokines and spondyloarthritis characteristics.

Methods: We conducted a case-control study, including 144 subjects matched for age and sex: 72 spondyloarthritis patients(G1) and 72 controls (G2). The disease activity was assessed using ASDAS-CRP and BASDAI. Structural damage was assessed using BASRI. The levels of interleukin (IL) IL-1, IL-6, IL-8, IL-17, IL-23, and tumor necrosis factor α(TNFα) were measured.

Results: Each group included 57 men. The mean age was 44.84 ± 13.42 years. Except for IL-8, all cytokine levels were significantly higher in patients compared to controls (IL-1: p = 0.05, IL-6: p = 0.021, TNFα: p = 0.039, IL-17 and IL-23: p < 0.001). Cutoff values of IL-17 and IL-23 distinguishing patients in G1 from those in G2 were 17.6 and 7.96 pg/mL, respectively. TNFα level correlated to BASDAI (p = 0.029) and BASRI (p = 0.002). Multivariate analysis showed that structural damage was associated with the male gender (p = 0.017), longer disease duration (p = 0.038), and high disease activity (p = 0.044). Disease activity was associated with longer disease duration (p = 0.012) and increased IL-6 levels (p = 0.05).

Conclusion: Our study showed that IL-17 was the ablest to distinguish between spondyloarthritis patients and controls, suggesting that IL-17 may be helpful for the diagnosis of spondyloarthritis.

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来源期刊
CiteScore
7.60
自引率
2.30%
发文量
221
审稿时长
6-12 weeks
期刊介绍: Expert Review of Clinical Immunology (ISSN 1744-666X) provides expert analysis and commentary regarding the performance of new therapeutic and diagnostic modalities in clinical immunology. Members of the International Editorial Advisory Panel of Expert Review of Clinical Immunology are the forefront of their area of expertise. This panel works with our dedicated editorial team to identify the most important and topical review themes and the corresponding expert(s) most appropriate to provide commentary and analysis. All articles are subject to rigorous peer-review, and the finished reviews provide an essential contribution to decision-making in clinical immunology. Articles focus on the following key areas: • Therapeutic overviews of specific immunologic disorders highlighting optimal therapy and prospects for new medicines • Performance and benefits of newly approved therapeutic agents • New diagnostic approaches • Screening and patient stratification • Pharmacoeconomic studies • New therapeutic indications for existing therapies • Adverse effects, occurrence and reduction • Prospects for medicines in late-stage trials approaching regulatory approval • Novel treatment strategies • Epidemiological studies • Commentary and comparison of treatment guidelines Topics include infection and immunity, inflammation, host defense mechanisms, congenital and acquired immunodeficiencies, anaphylaxis and allergy, systemic immune diseases, organ-specific inflammatory diseases, transplantation immunology, endocrinology and diabetes, cancer immunology, neuroimmunology and hematological diseases.
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