Visfatin levels and intima-media thicknesses in rheumatic diseases
Visfatin levels and intima-media thicknesses in rheumatic diseases
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DOI：
10.1007/s10067-010-1649-2
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发表时间：
2011-06-01
影响因子：
3.4
通讯作者：
Isik, Ahmet
中科院分区：
文献类型：
--
作者：
Ozgen, Metin;Koca, Suleyman Serdar;Isik, Ahmet
慢性炎症风湿性疾病导致动脉粥样硬化患病率增加。然而，这种早期且加速的动脉粥样硬化不能仅用传统的心血管危险因素来解释。慢性炎症条件下细胞粘附分子和促炎细胞因子的永久过度表达可能参与加速动脉粥样硬化。 Visfatin 是一种新型脂肪细胞因子，具有潜在的胰岛素样作用和促炎作用。因此，本研究的目的是确定类风湿性关节炎（RA）、系统性红斑狼疮（SLE）、系统性硬化症（SSc）和Beh双匕首病（BD）患者的血清内脂素水平及其与颈总动脉内膜中层厚度（IMT）的关系，IMT是动脉粥样硬化的预测因子。该研究涉及 29 名 RA、26 名 SLE、25 名 SSc、30 名 BD 患者和 29 名健康对照 (HC)。采用酶联免疫吸附测定法和胰岛素抵抗稳态模型评估（HOMA-IR）指标分析血清TNF-α、IL-6、visfatin水平，并测定IMT。 RA 组的血清内脂素水平高于所有其他组。此外，活动性 BD 亚组的内脂素水平高于非活动性 BD 亚组。在研究组中，内脂素水平与 HOMA-IR 指数和 IMT 不相关。尽管内脂素血清浓度与某些风湿性疾病中的胰岛素抵抗和颈动脉粥样硬化无关，但其在 RA 和活动性 BD 组中较高，但在 SLE 和 SSc 组中则不然。 Visfatin 水平可能与 Th1/Th2 平衡有关。需要进一步的研究来更精确地阐明内脂素的促炎活性。
Chronic inflammatory rheumatic diseases lead to increased prevalence of atherosclerosis. However, this early and accelerated atherosclerosis cannot be explained by traditional cardiovascular risk factors alone. The permanent overexpression of cellular adhesion molecules and pro-inflammatory cytokines in chronic inflammatory conditions may participate in accelerated atherosclerosis. Visfatin, a novel adipocytokine, has a potential insulin-like action and pro-inflammatory effects. Therefore, the aim of the study was to determine serum visfatin level and its association with common carotid intima-media thickness (IMT), which is a predictor of atherosclerosis, in patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), systemic sclerosis (SSc), and Beh double dagger et's disease (BD). The study involved 29 RA, 26 SLE, 25 SSc, 30 BD patients, and 29 healthy controls (HC). Serum levels of TNF-alpha, IL-6, and visfatin were analyzed using enzyme-linked immunosorbent assay method and homeostasis model assessment for insulin resistance (HOMA-IR) indexes, and IMTs were determined. Serum visfatin level was higher in the RA group than all the other groups. In addition, visfatin level was higher in the active BD subgroup than the inactive BD subgroup. In the study groups, visfatin levels were not correlated with HOMA-IR indexes and IMTs. Whereas visfatin serum concentration was not associated with insulin resistance and carotid atherosclerosis in selected rheumatic diseases, it was higher in the RA and active BD groups, but not in the SLE and SSc groups. Visfatin levels may be associated with Th1/Th2 balance. Further studies are needed for more precise elucidation of the pro-inflammatory activities of visfatin.