脂联素、内脂素、抵抗素在系统性红斑狼疮患者血清中的变化及临床意义

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目的探讨系统性红斑狼疮(SLE)患者血清脂联素、内脂素、抵抗素表达水平,及其在SLE、狼疮肾炎和SLE合并骨坏死中的作用及临床意义。方法选取2015年9月至2016年2月就诊于山东大学附属省立医院风湿免疫科SLE患者58例(SLE组),其中SLE合并骨坏死患者12例(SLE合并骨坏死组)、SLE未合并骨坏死患者46例(SLE未合并骨坏死组);狼疮肾炎患者23例(狼疮肾炎组)、SLE无肾损伤患者35例(SLE无肾损伤组)。同期选取该院查体中心健康人43例(健康对照组)。采用酶联免疫吸附法检测SLE组和健康对照组血清脂联素、内脂素、抵抗素表达水平,分析其与狼疮肾炎、SLE合并骨坏死的关系,及其与临床及实验室指标抗双链DNA抗体、抗核小体抗体、补体3、补体4、血沉、C反应蛋白、SLE疾病活动度评分(SLEDAI)、血清白蛋白、血清肌酐及24 h尿蛋白的相关性。结果 SLE组血清脂联素、内脂素、抵抗素水平较健康对照组明显升高(P<0.001);狼疮肾炎组脂联素和抵抗素水平明显高于SLE无肾损伤组(P<0.001,P=0.033);脂联素、内脂素、抵抗素在SLE合并骨坏死组和SLE未合并骨坏死组表达差异无统计学意义(P=0.117;P=0.058;P=0.674);内脂素表达水平与血沉呈相关性(rs=0.281,P=0.046);多元线性回归分析显示,体质量指数(BM I)和血沉均为影响内脂素表达水平的重要因素(P=0.010,0.020);BMI是影响抵抗素表达水平的重要因素(P=0.046)。结论血清脂联素、内脂素、抵抗素的高表达可能与SLE相关,且脂联素和抵抗素水平升高与SLE肾损害具有相关性,其确切作用机制尚需进一步研究。 Objective To investigate the expression of adiponectin, visfatin and resistin in patients with systemic lupus erythematosus (SLE) and their roles in SLE, lupus nephritis and SLE combined with osteonecrosis. Methods From September 2015 to February 2016, 58 patients (SLE group) with rheumatoid arthritis (SLE) who were admitted to the Provincial Hospital of Shandong University were enrolled. Among them, 12 were SLE patients with osteonecrosis (SLE group) and SLE patients were not combined 46 cases of osteonecrosis (SLE without osteonecrosis), 23 cases of lupus nephritis (lupus nephritis), 35 cases of SLE without renal injury (SLE without renal injury). In the same period, 43 healthy people from the physical examination center were selected (healthy control group). The levels of serum adiponectin, visfatin and resistin in SLE group and healthy control group were detected by enzyme-linked immunosorbent assay (ELISA), and their relationship with lupus nephritis and SLE with osteonecrosis and their relationship with clinical and laboratory markers Chain DNA antibody, antinucleosome antibody, complement 3, complement 4, ESR, C reactive protein, SLE disease activity score (SLEDAI), serum albumin, serum creatinine and 24 h urinary protein. Results Serum levels of adiponectin, visfatin and resistin in SLE group were significantly higher than those in healthy control group (P <0.001). The levels of adiponectin and resistin in lupus nephritis group were significantly higher than those in SLE group without renal injury (P <0.001) , P = 0.033). There was no significant difference in the expression of adiponectin, visfatin and resistin in SLE with osteonecrosis and without SLE (P = 0.117; P = 0.058; P = 0.674) The level of lipoprotein was correlated with erythrocyte sedimentation rate (rs = 0.281, P = 0.046). Multiple linear regression analysis showed that body mass index (BMI) and erythrocyte sedimentation rate (ESR) were both important factors affecting the expression of visfatin (P = 0.010, 0.020). BMI was an important factor affecting resistin expression (P = 0.046). Conclusions The high expression of serum adiponectin, visfatin and resistin may be related to SLE, and the increase of adiponectin and resistin is correlated with renal damage of SLE. The exact mechanism remains to be further studied.
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