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2型糖尿病合并慢性阻塞性肺疾病患者血清瘦素水平的变化及其临床意义
作者:黄国兰1  杨卫红1  浦柳美2 
单位:1. 上海交通大学医学院附属第九人民医院奉城分院 内分泌科, 上海 201411;
2. 上海交通大学医学院 附属第六人民医院南院 呼吸内科, 上海 201499
关键词:2型糖尿病 慢性阻塞性肺疾病 瘦素 IL-6 
分类号:R587.1;R563.3
出版年·卷·期(页码):2017·36·第五期(721-725)
摘要:

目的:探讨2型糖尿病合并慢性阻塞性肺疾病患者血清瘦素水平的变化及其临床意义。方法:收集110例患者信息,受试对象严格按入选标准入组,分为健康对照组10例、单纯慢性阻塞性肺疾病急性发病期(AECOPD)组、单纯COPD稳定期组、单纯2型糖尿病(T2DM)组、AECOPD期合并T2DM组,COPD合并T2DM组,每组各20例;采用酶联免疫测定法(ELISA)检测各组血清瘦素和IL-6的含量。结果:患者血清中瘦素水平比较:COPD稳定期组低于其它各组(P<0.05);AECOPD低于T2DM+AECOPD组(P<0.05),高于对照组(P<0.05),与T2DM组差异无统计学意义(P>0.05);T2DM+COPD组与对照组差异无统计学意义(P>0.05),高于COPD组(P<0.05);T2DM+AECOPD组高于对照组(P<0.01)、AECOPD组(P<0.05)及T2DM组(P<0.05);T2DM组高于对照组(P<0.05)。患者血清中IL-6水平比较:各组均高于对照组(P<0.05);COPD组与T2DM差异无统计学意义(P>0.05),低于其它各组(P<0.05);AECOPD组低于T2DM+AECOPD组(P<0.05),与T2DM组差异无统计学意义(P>0.05);T2DM+COPD组高于COPD组(P<0.05);T2DM+AECOPD组高于AECOPD组(P<0.05)。结论:患者瘦素与IL-6含量可作为T2DM合并COPD患者的临床治疗及检测的指标。

Objective: To investigate the change level of leptin in patients with COPD with T2DM and its clinical significance. Methods: Collected the information of 110 patients. Serum LP and IL-6 concentrations were examined in healthy control group (10 cases), AECOPD group (20 cases), COPD group (20 cases), T2DM (20 cases) group, COPD with T2DM group (20 cases), AECOPD with T2DM group (20 cases) by ELISA. Results: the level of leptin in serum of patients with:COPD group was lower than the other groups (P<0.05); AECOPD is lower than T2DM+AECOPD group (P<0.05), higher than that of the control group (P<0.05), in comparison with T2DM group no statistical significance (P>0.05); T2DM+COPD group higher than control group, the difference was not statistically significant (P>0.05), higher than COPD group (P<0.05); T2DM+AECOPD higher than control group (P<0.01), COPD group (P<0.05) and T2DM group (P<0.05); T2DM group is higher than that of the control group (P<0.05). Serum level of IL-6 in the control group was lower than that of the other groups (P<0.05); COPD group and T2DM were no statistical significance (P>0.05), COPD group was lower than the other groups (P<0.05); AECOPD group was lower than that of T2DM+AECOPD group (P<0.05), in comparison with T2DM group no statistical significance (P>0.05); T2DM+COPD group higher than COPD group (P<0.05); T2DM+AECOPD group was higher than AECOPD group (P<0.05). Conclusion: LP and IL-6 contents can be used as the index of clinical treatment and detection of patients with T2DM and COPD.

参考文献:

[1] 文世林.糖尿病流行的全球趋势和国内现状[J].河南诊断与治疗杂志,2002,1(16):14-17.
[2] 代庆红,王忠东.中国糖尿病的现状调查[J].中国医药指南,2011,9(13):206-208.
[3] ANTONELLⅡNCALZ R,FUSO L,PITOCCO D,et al.Decline of neuroadrenergic bronchial innervation and respiratory function in type I diabetes mellitus:a longitudinal study[J].Diabetes Metab Resv,2007,23(4):311-316.
[4] ZHONG N,WANG C,YAO W,et al.Prevalence of chronic obstructive pulmonary disease in china:a large population-based survey[J].Am J Respir Crit Care Med,2007,176(8):753-760.
[5] JONES S A.Directing transition from innate to acquired immunity:defining a role for IL-6[J].J Immunol,2005,175(6):3463-3468.
[6] 赵雪峰,王红阳,杨万杰.COPD患者血细胞因子水平与肺功能的相关性分析[J].安徽医学,2010,31(6):559-562.
[7] WEDZICHA J A,SEEMUNGAL T A,MACCALLUM P K,et al.Acute exacerbations of chronic obstructive pulmonary disease are accompanied by elevations of plasma fibrinogen and serum IL-6 levels[J].Thromb Haemost,2000,84(2):210-215.
[8] GAN W Q,MAN S F P,SENTHILSELVAN A,et al.Association between chronic obstructive pulmonary disease and systemic inflammation:a systematic review and a meta-analysis[J].Thorax,2004,59(7):574-580.
[9] 杨立勇.低度慢性炎症与2型糖尿病[J].中华糖尿病杂志,2013,5(9):527-530.
[10] PRADHAN A D,MANSON J A E,RIFAI N,et al.C-reactive protein,interleukin 6,and risk of developing type 2 diahetes mellitus[J].JAMA,2001,286(3):327-334.
[11] SPRANGER J,KROKE A,MOHLIG M,et al.Inflammatory cytokines and the risk to develop type 2 diabetes results of the prospective population-based European Prospective Investigation into Cancer and Nutrition(EPIC) -Potsdam Study[J].Diabetes,2003,52(3):812-817.
[12] BOLTON C E,EVANS M,IONESCU A A,et al.Insulin resistance and inflammation:a further systemic complication of COPD[J].COPD,2007,4(2):121-126.
[13] SINDEN N J,STOCKLEY R A.Systemic inflammation and comorbidity in COPD:a result of ‘overspill’ of inflammatory mediatorn from the lungs? review of the evidence[J].Thorax,2010,65(10):930-936.
[14] BERK E S,KOVERA A J,BOOZER C N,et al.Adiponectin levels during low-and high-fat eucaloric diets in lean and obese women[J].Obes Res,2005,13(9):1566-1571.
[15] UERMAN J P,WISSE B E,THALER J P,et al.Leptin deficiency causes insulin resistanceinduced by uncontrolled diabetes[J].Diabetes,2010,59(7):1626.
[16] NISHIO K,SAKURAI M,KUSUYAMA T,et al.A randomized comparison of pioglitazone to inhibit restenosis after coronary stenting in patients with type 2 diabetes[J].Diabetes Care,2006,29(1):101.
[17] MALMSTROM R,TASKINEN M R,KARONEN S L,et al.Insulin increases plasma leptin concentrations in normal subjects and patients with NIDDM[J].Diabetologia,1996,39(8):993-996.
[18] KARAKAS S,KARADAG F,KARUL A B,et al.Circulating leptin and body composition in chronic obstructive pulmonary disease[J].Int J Clin Pract,2005,59(10):1167-1170.
[19] MARTIN-ROMERO C,SANTOS-ALVAREZ J,GOBERNA R,et al.Human leptin enhances activation and proliferation of human circulating T lymphocytes[J].Cell Immunol,2000,199(1):15-24.
[20] ANNA C G,FREDDY G E,WAGNER R M,et al.Exogenous leptin restores in vitro T cell proliferation and cytokine synthesis in patients with common variable immunodeficiency syndrome[J].Clin Immunol,2005,114(2):147-153.
[21] SANTOS-ALVAREZ J,GOBERNA R,SANCHEZ-MARGALET V.Human leptin stimulates proliferation and activation of human circulating monocytes[J].Cell Immunol,1999,194(1):6-11.
[22] SWEENEY G.Leptin signaling[J].Cell Signaling,2002,14(8):655-663.
[23] SHIRSHEV S V,ORLOVA E G.Molecular mechanisms of regulation of functional activity of mononuclear phagocytes by leptin[J].Biochemistry(Moscow),2005,70(8):841-847.
[24] 孔令霞.COPD合并2型糖尿病患者血清IL-10、IL-18表达水平的研究[D].长春:吉林大学,2013.

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