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题名糖皮质激素治疗前后AECOPD患者血清IL-13、TNF-a、血浆vWF含量表达及临床意义
其他题名Changes of IL-13、TNF-a and vWF before and after treatment with systemic Glucocorticoids in Patients with AECOPD
作者
学位类型硕士
导师陈少贤 ; 陈彦凡 ; 叶进燕
答辩日期2010-06-06
学位授予单位温州医科大学
学位专业内科学
关键词慢性阻塞性肺疾病,糖皮质激素, IL-13,TNF-a,vWF
摘要目的:通过检测AECOPD(慢性阻塞性肺疾病急性加重)患者全身糖皮质激素治疗前后血清TNF-、IL-13、血浆vWF水平变化,探讨糖皮质激素在AECOPD治疗中作用及对各类细胞因子影响,为临床治疗提供实验依据。方法:选择2007年11月至2008年4月收住我院呼吸内科的慢性阻塞性肺疾病急性加重期(AECOPD)患者30例,均符合AECOPD诊断标准,男20例,女10例,年龄54~83(60.33±7.12)岁,其中伴II型呼吸衰竭患者8例。门诊健康体检者30例,男15例,女15例,年龄57~76岁(56.67±6.11)岁,用ELISA法检测治疗组(静脉注射糖皮质激素治疗前、后)及对照组血清IL-13、TNF-及血浆vWF含量。用spss软件分析。结果:1、血清IL-13的测定结果:AECOPD组糖皮质激素治疗前血清IL-13浓度(44.96±5.91 pg/mL)、治疗后血清IL-13浓度(30.62±4.81 pg/mL)显著高于对照组(25.83±3.91 pg/mL)(p<0.01),治疗后血清IL-13浓度(30.62±4.81 pg/mL)较治疗前(44.96±5.91 pg/mL)明显降低(p<0.01)2、血清TNF-的测定结果:AECOPD组糖皮质激素治疗前血清TNF-浓度(38.85±7.01 pg/mL)、治疗后血清TNF-浓度(29.86±5.20 pg/mL)显著高于对照组(9.14±1.60 pg/mL)(p<0.01),治疗后血清TNF-浓度(29.86±5.20 pg/mL)较治疗前(38.85±7.01 pg/mL)明显降低(p<0.01)3、血浆vWF的测定结果:AECOPD组糖皮质激素治疗前血浆vWF浓度(275.93±20.91%)、治疗后血浆vWF浓度(256.25±30.52)显著 高于对照组(171.94±33.94%)(p<0.01),治疗后血浆vWF浓度(256.25±30.52%)较治疗前(275.93±20.91%)明显降低(p<0.01)结论:COPD急性加重期血清IL-13、TNF-及血浆vWF明显升高,全身糖皮质激素治疗后明显下降,提示多种炎症因子参与急性炎症反应,AECOPD患者内皮细胞损伤加重,存在不同程度的凝血和纤溶系统的激活。糖皮质激素对控制病情进展有一定作用,联合抗炎、抗凝治疗对AECOPD患者预后有指导意义。
其他摘要Objective: To observe the levels of serum Interleukin-13 (IL-13), Tumor Necrosis Factor-a (TNF-a) and plasma Von Willbrand factor (vWF) in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) before and after treatment with systemic Glucocorticoids. Assess the efficacy of glucocorticoids with AECOPD and its influence on cytokines, provide experimental basis for clinical treatment.Methods: Thirty AECOPD hospitalizations were recruited into the study during 2007 November to 2008 April. All were according to the diagnostic standards with the AECOPD,male 20, female 10, age 54 years old ~83 years old,average(60.33±7.12)years old,8 with respiratory failure type II. 30 health people from clinic healthy examination , male 15, female 15, age 57 years old ~76 years old,average(56.67±6.11)years old, IL-13、TNF-a in serum and vWF in plasma were measured by ELISA. The data were analysised among AECOPD group (before and after treatment with systemic glucocorticoids ) and control group. The data were analysised by SPSS softwareResults:1.The concentrations of IL-13 in serum: The level of IL-13 in AECOPD group before treatment(44.96±5.91 pg/mL)and after treatment(30.62±4.81 pg/mL) were significantly higher than these of control group(25.83±3.91 pg/mL)(p<0.01).The level of IL-13 in AECOPD group after systemic Glucocorticoids((30.62±4.81 pg/mL)was significantly lower than that group before systemic Glucocorticoids(44.96±5.91 pg/mL)(p<0.01).2. The concentrations of TNF-a in serum: The level of TNF-a in AECOPD group before treatment(38.85±7.01 pg/mL)and after treatment(29.86±5.20 pg/mL) were significantly higher than these of control group(9.14±1.60 pg/mL)(p<0.01).The level of TNF-a in AECOPD group after systemic Glucocorticoids(29.86±5.20 pg/mL)was significantly lower than that group before systemic Glucocorticoids(38.85±7.01 pg/mL)(p<0.01).3. The concentrations of vWF in plasma: The level of vWF in AECOPD group before treatment(275.93±20.91%)and after treatment(256.25±30.52 %) were significantly higher than these of control group(171.94±33.94%)(p<0.01).The level of vWF in AECOPD group after systemic Glucocorticoids(256.25±30.52 %)was significantly lower than that group before systemic Glucocorticoids(275.93±20.91%)(p<0.01).Conclusions: IL-13、TNF-a in serum and vWF in plasma express highly in acute exacerbation of chronic obstructive pulmonary disease, and decrease significantly after treatment with systemic Glucocorticoids. It showed various inflammation factors participate and interact together ,vascular endothelial cell injury and activation of coagulation and fibrinolysis existed in AECOPD. Systemic Glucocorticoids has good efficacy on patients. If coagulation and inflammation are treated simultaneously,it can provide a good prognosis for the therapy of AECOPD.
语种中文
学号20061094
发布年限2010-05-27
毕业论文分类号0R05
原始专题第一临床学院
学位论文研究方向呼吸系统疾病
参考文献参考文献 [1]. 中华医学会呼吸病学分会慢性阻塞性肺疾病学组.COPD诊治指南(2007年修订版).继续医学教育 2007, 21(2):31-42. [2]. Peter J. BARNES, D.S. CHRONIC OBSTRUCTIVE PULMONARY DISEASE. The New England Journal of Medicine,2000 343(4): 269 - 80. [3]. James C. Hogg, M.D., Fanny Chu, et al. The Nature of Small-Airway Obstruction in Chronic Obstructive Pulmonary Disease. 2004 Jun 24; 350 (26): 2645 - 53. [4].Garrod R, Marshall J, Barley E, et al. The relationship between inflammatory makers and disability in chronic obstructive pulmonary disease (COPD).primary Care Respiratory Journal (2007); 16(4): 236 - 240. [5].Joppa P, Petrasova D, Stancak B, et al. Systemic Inflammation in Patients With COPD and Pulmonary Hypertension. Chest 2006; 130; 326 - 333. [6].Sevenoaks MJ and Stockley RA, Chronic Obstructive Pulmonary Disease, inflammation and co-morbidity – a common inflammatory phenotype ? Respir Res. 2006; May 2; 7:70. [7]. Lee JS, Rosengart MR, Kondragunta V, et al. Inverse association of plasma IL-13 and inflammatory chemokines with lung function impairment in stable COPD: a cross-sectional cohort study. Respiratory Research 2007, 8: 64. [8].Palatli M, Cakir A, Cildag O, et al. Microalbuminuria, von Willebrand factor and fibrinogen levels as markers of the severity in COPD exacerbation. Thromb Thrombolysis 2007 Jul 10. [9]. Belvisi M. G. and Bottomley K. M. The role of matrix metalloproteinases (MMPs) in the pathophysiology of chronic obstructive pulmonary disease (COPD): a therapeutic role for inhibitors of MMPs? Inflamm res. 52 (2003) 95–100. [10].Corbel M, Belleguic M, Boichot E, et al. Involvement of gelatinases (MMP-2 and MMP-9) in the development of airway inflammation and pulmonary fibrosis. Cell Biology and Toxicology 2002, 18: 51 - 61. 11.黎东明,陈琼,何惠娟,等 慢性阻塞性肺疾病发病中的中性粒细胞凋亡作用研究,中国基层医药, 2005, 12 (5) : 517 – 5191 12. DaviesL,Angus RM, Calverley PM. Oral corticosteroids in patients admitted to hospitalwith exacerbationsof chronic obstructive pulmonary disease: a prospective randomised controlled trial [J ].Lancet, 1999,354 (9177 ):456-460. 13. NiewoehnerDE, ErblandML, Deupree RH, et al. Effect of systemic glucocorticoids on exacerbations of chronic obstructive pulmonary disease, Department of Veterans Affairs Cooperative study group [J] 1999:340 (25 ):1941-1947. 14. Carswell EA, Old LJ, Kassel RL, et al. An endotoxin-induced serum factor that causes necrosis of tumors. Proc Natl Acad Sci U S A ,1975,72 (9):3666-70 15. Shalaby M R, Pennica D, Palladino M A. An overview of thehistory and biological properties of tumor necrosis factor. Springe Semin Immun, 1986,9(1):33-37 16. Seiichiro S ,Koichiro T ,Hideto S ,et al.Association of tumor necrosis factor-α gene promoter Polymorphism with lowAttenuatio areas on highresolution CT in patients with COPD.[J] .Chest ,2002 ,122(2):416-420. 17. Sakao S ,Tatumi K,Igari H , et al . Association of tumor necrosis factor-α gene pro-moter polymorphism with the presence of COPD [J].Am J Respir Crit Care Med, 2001,163(2):420-422. 18. Eid AA ,Ionescu AA ,Nixon LS. Inflammatory response and body composition in chronic obstructive pulmonary disease[J ] . AmJ Respir Crit Care Med Vol ,2004 ,164 (8 Pt 1) :1414-1418. 19. Andrew C, Jin D. Hsin T tumor necrosis factor is central to acute cigarette smoke- Induced inflammation and connective tissue breakdown. J.AM J Respir Crit Care Med Vol, 2002, 166(6) :849-854. 20. Bochaer BS , Klunk DA , Sterbinsky SA , et al. Interleukin-13 selectively induces vascular adhesion molecule-1(VCAM-1) expression in human endothelial cells. J .J Immunol , 2000, 164:799-803. 21. Zhen g T , Zhou Zhu ,Zhongde Wang et al. Inducible targeting of IL-13 to the adult lung causes matrix metal oproteinase - and cathepsin – dependent emphysema. J Clin Invest, 2001 ,106:1081-1093. 22. Van der Pouw Kraan TC , van Veen A, Boeije LC, et al. An IL-13 promoter polymorphism associated with increased risk of allergic asthma. Genes Immun ,1999, 1: 61-65. 23. Peinado VI , Barbera JA , Ramirez J , et al . Endot helial dysfunction in pulmonary arteries of patient s wit h mild COPD. Am J Physiol (Lung Cell Mol Physiol) ,1998 ,274 :9082913. 24. Voelkel NF , Cool CD. Pulmonary vascular involvement in chronic obstructive pulmonary disease. Eur Respir J , 2003 , 22 (Suppl 46) :28s232s. 25. Santos S, Peinado VI, Ramirez J, et al. Characterization of pulmonary vascular remodelling in smokers and patients with mild COPD. Eur Respir J ,2002 ,19 :632-638. 26. Ogawa S ,Sheeniwas R,Brett T, et al. The effect of hypoxia on capillary endothelial cell function: modulation of barrier and coagulant function. Br T Haematol, 1990, 75:517. 27. Song L, Dong X, Zhou Y. Changes of vWF in vascular endothelial cells with acute hypoxia. Zhonghua Xue Ye Xue Za Zhi,2000,21:4752477. 28. 汪建新,王辰,庞宝森,等.高浓度二氧化碳致大鼠肺脏和右心室损伤的病理组织学观察. 中华结核和呼吸杂志,2001,7:410-413 29. Cella G,Bellotto F,Tona F,et al.Plasma markers of endothelial dysfunction in pulmonary hypertension.Chest ,2001,120:1226-1230. 30. Isermann B, Hendrickson SB,Zogg M,et al.Endothelium specific loss of Murine thrombomodulin disrupts the protein C anticoagulant pathway and causes juvenile onset thrombosis. Clin Invest,2001,108:537-546
全文文件名20061094李恒妍2009内科学.pdf|20061094李恒妍2009内科学.pdf
文献类型学位论文
条目标识符https://kms.wmu.edu.cn/handle/3ETUA0LF/119870
专题温州医科大学
作者单位
溫州医科大学第一临床学院
推荐引用方式
GB/T 7714
李恒妍. 糖皮质激素治疗前后AECOPD患者血清IL-13、TNF-a、血浆vWF含量表达及临床意义&#61537;[D]. 温州医科大学,2010.

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