首页> 外文期刊>The Egyptian Rheumatologist >Clinical significance of serum TNFα and -308 G/A promoter polymorphism and serum Il-6 and -174 G/C promoter polymorphism in systemic lupus erythematosus patients
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Clinical significance of serum TNFα and -308 G/A promoter polymorphism and serum Il-6 and -174 G/C promoter polymorphism in systemic lupus erythematosus patients

机译:系统性红斑狼疮患者血清TNFα和-308 G / A启动子多态性及血清IL-6和-174 G / C启动子多态性的临床意义

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Introduction Systemic lupus erythematosus (SLE) is a disorder of immune regulation where cytokine imbalance and genetic factors are implicated in its pathogenesis. Aim of the work To evaluate the clinical significance of serum levels of tumor necrosis factor alpha (TNFα) and its -308 G/A promoter polymorphism as well as the IL-6 and -174 promoter polymorphism in SLE patients and find any association to the clinical and laboratory features as well as to the disease activity and severity. Patients and methods We studied 37 female SLE patients and age and gender matched healthy control. Demographic, clinical and serological data were evaluated and the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) and the Systemic Lupus International Collaboration Clinics/ACR Damage Index (SLICC) were assessed. Serum TNF-α and IL-6 levels were measured using enzyme-linked immunosorbent assay (ELISA) and DNA genotyped for TNF-α promoter (-308 G/A) and IL-6 promoter (-174 G/C) by polymerase-chain reaction-restriction fragment-length polymorphism (PCR-RFLP) analysis. Results Serum TNF-α and IL-6 levels were significantly higher in the SLE patients compared to control. Regarding IL-6, there was a statistically significant difference between the levels in the three groups according to the promoter polymorphisms. Patients with constitutional symptoms showed higher level of IL-6 while the TNF-α level was significantly lower in those with pulmonary manifestations. There was a tendency to a higher TNF-α and IL-6 level in those with neuropsychiatric manifestations. Conclusion Serum TNF-α, -308 G/A promoter polymorphism, IL-6 and -174 G/C were higher in SLE patients than in healthy controls. To confirm our results we propose that larger scale, multicenter studies with longer evaluation periods are needed.
机译:简介系统性红斑狼疮(SLE)是一种免疫调节疾病,其中细胞因子失衡和遗传因素参与其发病机理。该研究的目的是评估SLE患者血清中肿瘤坏死因子α(TNFα)及其-308 G / A启动子多态性以及IL-6和-174启动子多态性的临床意义,并与之相关联。临床和实验室特征以及疾病活动和严重程度。患者和方法我们研究了37位女性SLE患者以及年龄和性别匹配的健康对照。评估了人口统计学,临床和血清学数据,并评估了系统性红斑狼疮疾病活动指数(SLEDAI)和系统性红斑狼疮国际协作诊所/ ACR损伤指数(SLICC)。使用酶联免疫吸附测定(ELISA)测量血清TNF-α和IL-6的水平,并通过聚合酶-法对TNF-α启动子(-308 G / A)和IL-6启动子(-174 G / C)进行基因分型。链反应-限制性片段长度多态性(PCR-RFLP)分析。结果SLE患者的血清TNF-α和IL-6水平明显高于对照组。关于IL-6,根据启动子多态性,三组水平之间在统计学上有显着差异。有体质症状的患者表现出较高的IL-6水平,而具有肺部表现的患者的TNF-α水平则显着降低。具有神经精神病学表现的患者有升高TNF-α和IL-6水平的趋势。结论SLE患者血清TNF-α,-308 G / A启动子多态性,IL-6和-174 G / C高于健康人。为了证实我们的结果,我们建议需要更长的评估周期的大规模,多中心研究。

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