C反应蛋白、尿微量白蛋白、载脂蛋白与老年糖尿病并脑梗死的相关性
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摘要
目的：
分析老年糖尿病并脑梗死患者C反应蛋白、尿微量白蛋白与载脂蛋白的水平变化,探讨其与老年糖尿病患者发生脑梗死之间的关系。
方法：
1、研究对象：
研究人群来自2009年11月～2010年4月在齐鲁医院老年科的住院患者共90例,分为老年糖尿病并发急性脑梗死组(Ⅰ组)30例、老年非糖尿病性急性脑梗死组(Ⅱ组)30例、老年糖尿病无脑梗死组(Ⅲ组)30例。另选择同期在本院查体的健康人群25例作为对照组(Ⅳ组)。其中所有脑梗死患者均符合1995年第4届全国脑血管病学术会议修订的脑血管病诊断标准；所有糖尿病患者均符合WH01999年制定的糖尿病诊断标准。所有研究对象均无急慢性感染、肝功能异常、肾功能衰竭、恶性肿瘤、自身免疫性疾病、慢性心功能衰竭、急性冠脉事件及既往心肌梗死病史。
2、研究方法：
所有受检对象均测量身高、体质量、腰围、臀围,计算体质量指数(BMI)=体质量(kg)/身高2(m2)、腰臀比(WHR)=腰围/臀围。询问病程,了解有无吸烟史,测血压。空腹采集肘静脉血测定空腹血糖(FBG),糖化血红蛋白(HbA1C),血清总胆固醇(TC)、甘油三酯(TG),高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白A-I(ApoA-I)、载脂蛋白B(ApoB),高敏C反应蛋白(hs-CRP)。同日留取中段晨尿,取2ml检测尿微量白蛋白(MAU)。
3、统计学处理：
使用SPSS10.0软件包进行数据处理。正态分布的计量资料用X±s表示；正态分布两组间均数的比较采用t检验,显著性检验采用双侧检验,P<0.05为差异有统计学意义。两变量相关分析运用非参数Spearman等级相关检验。并对以上指标进行logistic回归分析。
结果：
1.一般资料比较：各组年龄、性别比、吸烟、BMI等因素经统计学检验,两两之间无明显差异(P>0.05),具有可比性。
2. hs-CRP值在年龄、男性比、吸烟、BMI等因素差异上均无统计学意义,具有可比性。Ⅰ、Ⅱ、Ⅲ组hs-CRP水平均高于Ⅳ组(P<0.01,P<0.05),且Ⅰ组hs-CRP水平高于Ⅱ、Ⅲ组(P<0.05)。多元线性回归分析表明,hs-CRP浓度与TC、LDL-C、ApoB均无相关性,但与TG、MAU呈正相关(P<0.05),与HDL-C、ApoA-I呈显著负相关(P<0.01)。
3.Ⅰ、Ⅱ、Ⅲ组MAU水平均明显高于Ⅳ组(P<0.01),且Ⅰ组MAU水平高于Ⅱ、Ⅲ组(P<0.01),Ⅱ组MAU水平低于Ⅲ组(P<0.01)。相关分析提示,MAU水平和FBG、HbAIC呈正相关(P<0.05),与血脂(TC、TG、HDL-C、LDL-C)均无相关性。
4.Ⅰ、Ⅱ、Ⅲ组TC、TG、LDL-C、ApoB水平均高于Ⅳ组(P<0.01), HDL-C、ApoA-I水平均低于Ⅳ组(P<0.01),且Ⅰ组TC、TG、LDL-C、ApoB水平高于Ⅱ、Ⅲ组(P<0.01,P<0.05), HDL-C、ApoA-I水平低于Ⅱ、Ⅲ组(P<0.01,P<0.05)。Ⅱ组TG、LDL-C水平低于Ⅲ组(P<0.05)。
结论：
1.hs-CRP的浓度变化与糖尿病发生脑梗死的危险性密切相关。
2.MAU水平与糖尿病并发脑血管事件密切相关。
3.TC、TG、LDL-C、ApoB水平升高与HDL-C、ApoA-I水平降低是糖尿病合并脑血管病变的危险因素。
意义：
本课题进一步阐明C反应蛋白、尿微量白蛋白、载脂蛋白与老年糖尿病患者发生脑梗死之间的关系,对有效预防老年糖尿病患者脑梗死的发生、减少脑血管终点事件有重要的临床意义和应用价值。
Objective:
To investigate the changes of C-Reactive Protein、Microalbuminuria and Apolipoprotein in elderly diabetic patients complicated with cerebral infarction.
Methods:
1.Objects of study:
From November 2009 to April 2010 in Geriatrics of Qilu Hospital,Ninty cases were Collected.All the patients were in-patients and were divided into three groups:30 cases of old DM group with acute cerebral infarction(I group),30 cases of Non-DM elderly acute cerebral infarction(II group),30 cases of old DM group without cerebral infarction(III group).25 normal persons served as healthy controls.All the cerebral infarction patients were consistent with cerebrovascular disease diagnostic criteria;All the DM patients were consistent with diabetes mellitus diagnostic criteria.All of the subjects had no acute or chronic infection,liver dysfunction, kidney failure, cancer,autoimmune disease,chronic heart failure,acute coronary events and history of previous myocardial infarction.
2. Methods of study:
The levels of height、body weight、waistline、hipline be measured,body mass index、waist-to-hip ratio be calculated.Ask the course and find out the smoking history,test blood pressure.Fasting elbow venous blood were collected to measure fasting blood glouse(FBG),glycated hemoglobin(HbA1C),total cholesterol(TC),triglycerides(TG),high density lipoprotein cholesterol(HDL-C),low density lipoprotein cholesterol(LDL-C), apolipoprotein A-I (ApoA-I),apolipoprotein B (ApoB) and high-sensitivity C-reactive protein. Morning urine specimens was leaved to detect Microalbuminuria (MAU).
3. Statistical analysis:
All data were statistically dealled by SPSS 10.0 package.Measurement data of normal distribution was showed by x±s;the mean of normal distribution between the two groups was compared using the t test number,test of significance using two-sided test,P<0.05 was considered as statistically significant.Correlation analysis of two variables using non-parametric Spearman rank correlation test. And the above-mentioned indicators were analyzed by logistic regression analysis.
Results:
1.Comparison of general information:age, sex, smoking, BMI and other factors of each group was tested by statistical test, there was no significant difference between any two (P> 0.O5) and be comparable.
2.hs-CRP values in age,gender ratio,smoking,BMI and other factors were no statistically significant difference.The level of hs-CRP in I II III groups was higher than that of IV group(P<0.01,.P<0.05),near regression analysis indicated that hs-CRP was no correlation with TC、LDL-C and ApoB,but was positive correlation with TG、MAU(P<0.05),and was significantly negative correlation with HDL-C、ApoA-I(P<0.01).
3.The level of MAU in I II III groups was much higher than that of IV group(P<0.01),the level of MAU in I groups was higher than that ofⅡⅢgroup(P<0.01),and the level of MAU inⅡgroups was lower than that of III group(P<0.01).Simple correlation analysis indicated that MAU was positive correlation with FBG and HbA1C,but was no correlation with TC、TG、HDL-C andLDL-C.
4.The levels of TC、TG、LDL-C、ApoB were higher than that of IV group(P<0.01), the levels of HDL-C、ApoA-I were lower than that of IV group(P<0.01),and the level of TC、TG、LDL-C and ApoB in I groups were higher than that ofⅡⅢgroup(P<0.01,P<0.05), the level of HDL-C、ApoA-I in I groups were lower than that ofⅡⅢgroup(P<0.01,P<0.05), the level of TG、LDL-C in II groups were lower than that of III group(P<0.05).
Conclusions:
1.The concentrations of hs-CRP is closely related to the risk of diabetes cerebral infarction.
2. The levels of MAU is closely related to the occurred of cerebral vascular events in diabetes.
3.The increased levels of TC,TG,LDL-C,ApoB and the reduced levels of HDL-C,ApoA-I are the risk factors to diabetes mellitus with cerebral vascular disease.
Significance:
This issue further clarifies the relationship between C-reactive protein, Microalbuminuria,Apolipoprotein and cerebral infarction in elderly diabetic patients, that has important clinical significance and applications Value to the effective prevention of cerebral infarction and deseasing cerebral vascular end point in patients with diabetes.
分析老年糖尿病并脑梗死患者C反应蛋白、尿微量白蛋白与载脂蛋白的水平变化,探讨其与老年糖尿病患者发生脑梗死之间的关系。
方法：
1、研究对象：
研究人群来自2009年11月～2010年4月在齐鲁医院老年科的住院患者共90例,分为老年糖尿病并发急性脑梗死组(Ⅰ组)30例、老年非糖尿病性急性脑梗死组(Ⅱ组)30例、老年糖尿病无脑梗死组(Ⅲ组)30例。另选择同期在本院查体的健康人群25例作为对照组(Ⅳ组)。其中所有脑梗死患者均符合1995年第4届全国脑血管病学术会议修订的脑血管病诊断标准；所有糖尿病患者均符合WH01999年制定的糖尿病诊断标准。所有研究对象均无急慢性感染、肝功能异常、肾功能衰竭、恶性肿瘤、自身免疫性疾病、慢性心功能衰竭、急性冠脉事件及既往心肌梗死病史。
2、研究方法：
所有受检对象均测量身高、体质量、腰围、臀围,计算体质量指数(BMI)=体质量(kg)/身高2(m2)、腰臀比(WHR)=腰围/臀围。询问病程,了解有无吸烟史,测血压。空腹采集肘静脉血测定空腹血糖(FBG),糖化血红蛋白(HbA1C),血清总胆固醇(TC)、甘油三酯(TG),高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白A-I(ApoA-I)、载脂蛋白B(ApoB),高敏C反应蛋白(hs-CRP)。同日留取中段晨尿,取2ml检测尿微量白蛋白(MAU)。
3、统计学处理：
使用SPSS10.0软件包进行数据处理。正态分布的计量资料用X±s表示；正态分布两组间均数的比较采用t检验,显著性检验采用双侧检验,P<0.05为差异有统计学意义。两变量相关分析运用非参数Spearman等级相关检验。并对以上指标进行logistic回归分析。
结果：
1.一般资料比较：各组年龄、性别比、吸烟、BMI等因素经统计学检验,两两之间无明显差异(P>0.05),具有可比性。
2. hs-CRP值在年龄、男性比、吸烟、BMI等因素差异上均无统计学意义,具有可比性。Ⅰ、Ⅱ、Ⅲ组hs-CRP水平均高于Ⅳ组(P<0.01,P<0.05),且Ⅰ组hs-CRP水平高于Ⅱ、Ⅲ组(P<0.05)。多元线性回归分析表明,hs-CRP浓度与TC、LDL-C、ApoB均无相关性,但与TG、MAU呈正相关(P<0.05),与HDL-C、ApoA-I呈显著负相关(P<0.01)。
3.Ⅰ、Ⅱ、Ⅲ组MAU水平均明显高于Ⅳ组(P<0.01),且Ⅰ组MAU水平高于Ⅱ、Ⅲ组(P<0.01),Ⅱ组MAU水平低于Ⅲ组(P<0.01)。相关分析提示,MAU水平和FBG、HbAIC呈正相关(P<0.05),与血脂(TC、TG、HDL-C、LDL-C)均无相关性。
4.Ⅰ、Ⅱ、Ⅲ组TC、TG、LDL-C、ApoB水平均高于Ⅳ组(P<0.01), HDL-C、ApoA-I水平均低于Ⅳ组(P<0.01),且Ⅰ组TC、TG、LDL-C、ApoB水平高于Ⅱ、Ⅲ组(P<0.01,P<0.05), HDL-C、ApoA-I水平低于Ⅱ、Ⅲ组(P<0.01,P<0.05)。Ⅱ组TG、LDL-C水平低于Ⅲ组(P<0.05)。
结论：
1.hs-CRP的浓度变化与糖尿病发生脑梗死的危险性密切相关。
2.MAU水平与糖尿病并发脑血管事件密切相关。
3.TC、TG、LDL-C、ApoB水平升高与HDL-C、ApoA-I水平降低是糖尿病合并脑血管病变的危险因素。
意义：
本课题进一步阐明C反应蛋白、尿微量白蛋白、载脂蛋白与老年糖尿病患者发生脑梗死之间的关系,对有效预防老年糖尿病患者脑梗死的发生、减少脑血管终点事件有重要的临床意义和应用价值。
Objective:
To investigate the changes of C-Reactive Protein、Microalbuminuria and Apolipoprotein in elderly diabetic patients complicated with cerebral infarction.
Methods:
1.Objects of study:
From November 2009 to April 2010 in Geriatrics of Qilu Hospital,Ninty cases were Collected.All the patients were in-patients and were divided into three groups:30 cases of old DM group with acute cerebral infarction(I group),30 cases of Non-DM elderly acute cerebral infarction(II group),30 cases of old DM group without cerebral infarction(III group).25 normal persons served as healthy controls.All the cerebral infarction patients were consistent with cerebrovascular disease diagnostic criteria;All the DM patients were consistent with diabetes mellitus diagnostic criteria.All of the subjects had no acute or chronic infection,liver dysfunction, kidney failure, cancer,autoimmune disease,chronic heart failure,acute coronary events and history of previous myocardial infarction.
2. Methods of study:
The levels of height、body weight、waistline、hipline be measured,body mass index、waist-to-hip ratio be calculated.Ask the course and find out the smoking history,test blood pressure.Fasting elbow venous blood were collected to measure fasting blood glouse(FBG),glycated hemoglobin(HbA1C),total cholesterol(TC),triglycerides(TG),high density lipoprotein cholesterol(HDL-C),low density lipoprotein cholesterol(LDL-C), apolipoprotein A-I (ApoA-I),apolipoprotein B (ApoB) and high-sensitivity C-reactive protein. Morning urine specimens was leaved to detect Microalbuminuria (MAU).
3. Statistical analysis:
All data were statistically dealled by SPSS 10.0 package.Measurement data of normal distribution was showed by x±s;the mean of normal distribution between the two groups was compared using the t test number,test of significance using two-sided test,P<0.05 was considered as statistically significant.Correlation analysis of two variables using non-parametric Spearman rank correlation test. And the above-mentioned indicators were analyzed by logistic regression analysis.
Results:
1.Comparison of general information:age, sex, smoking, BMI and other factors of each group was tested by statistical test, there was no significant difference between any two (P> 0.O5) and be comparable.
2.hs-CRP values in age,gender ratio,smoking,BMI and other factors were no statistically significant difference.The level of hs-CRP in I II III groups was higher than that of IV group(P<0.01,.P<0.05),near regression analysis indicated that hs-CRP was no correlation with TC、LDL-C and ApoB,but was positive correlation with TG、MAU(P<0.05),and was significantly negative correlation with HDL-C、ApoA-I(P<0.01).
3.The level of MAU in I II III groups was much higher than that of IV group(P<0.01),the level of MAU in I groups was higher than that ofⅡⅢgroup(P<0.01),and the level of MAU inⅡgroups was lower than that of III group(P<0.01).Simple correlation analysis indicated that MAU was positive correlation with FBG and HbA1C,but was no correlation with TC、TG、HDL-C andLDL-C.
4.The levels of TC、TG、LDL-C、ApoB were higher than that of IV group(P<0.01), the levels of HDL-C、ApoA-I were lower than that of IV group(P<0.01),and the level of TC、TG、LDL-C and ApoB in I groups were higher than that ofⅡⅢgroup(P<0.01,P<0.05), the level of HDL-C、ApoA-I in I groups were lower than that ofⅡⅢgroup(P<0.01,P<0.05), the level of TG、LDL-C in II groups were lower than that of III group(P<0.05).
Conclusions:
1.The concentrations of hs-CRP is closely related to the risk of diabetes cerebral infarction.
2. The levels of MAU is closely related to the occurred of cerebral vascular events in diabetes.
3.The increased levels of TC,TG,LDL-C,ApoB and the reduced levels of HDL-C,ApoA-I are the risk factors to diabetes mellitus with cerebral vascular disease.
Significance:
This issue further clarifies the relationship between C-reactive protein, Microalbuminuria,Apolipoprotein and cerebral infarction in elderly diabetic patients, that has important clinical significance and applications Value to the effective prevention of cerebral infarction and deseasing cerebral vascular end point in patients with diabetes.
引文
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36. Pasceri V, Chang J, Willerson JT, et al. Modulation of C-reactive protein mediate monocyte chemo attractant protein induction in human endothelial cells by anti-atherosclerosis drugs[J]. Circulation,2001,103:531-534.
37. Nederkoom PJ, Gram Y, Hunink MG. Duplex ultrasound and magnetic resonance angiography compared with digital subtraction angiography in carotid artery stenos is:A systematic review[J]. Stroke,2003,34:1324-1334.
38. Dziedzic T, Gryz EA, Turai W, et al. Serum interleukin-6 soluble receptor in relation to interleukin-6 in stroke patients[J]. J Mol Neu. rosci,2004,24(2):293-298.
39. Kawanami D, Maemura K, Takeda N. C-reactive protein induces VCAM-1 gene expression through NF-kappa B activation in vascular endothelial cells[J]. Atherosclerosis,2006,185(1):39-46.
40. Kim CS, Park HS, Kawada T. Circulating levels of MCP-1and IL-8 are elevated in human obese subjects and associated with obesity-related parameters[J]. Int J Obes(Lond),2006: 1-5.
41. Boulman N, kvy Y, Leiba R, et al. Increased C-reactive protein levels in the polycystic ovary syndrome:a marker of cardiovascular disease[J]. J Clin Endocrinol Metab,2004, 89:2160-2165.
42. Pence S, Yilmaz G, Yilmaz N, et al. Determination of plasma fibronectin and seium C-reactive protein in patients with cerebrovascular events[J]. Int J Clin Pract,2003, 57(2):91-95.
43.张萍.血清超敏C反应蛋白检测在脑血管疾病中的应用[J].中国血液流变学杂志,2004,14：254-255.
44. Short RA, Johnson RJ, Tuttle KR, et al. Uric acid microalbuminria and cardiovascular events in high risk patients[J]. Am J Nephro 1,2005,25:36-44.
45.索丽霞,余叶蓉,喻红玲.2型糖尿病患者胰岛素抵抗、血管内皮细胞功能与微量白蛋白尿.中华内分泌杂志,2004,20：26-29.
46.许曼音.糖尿病学[J]上海：上海科学技术出版社.2003：180-187.
47. Murtaugh MA, Jacobs DR Correlates of urinary albumin execration in young adult blacks and whites:The coronary artery risk development in young adults study [J]. Am J Epidemiol,2003,158:676-686.
48. Araki S, Haneda M, Koya D. Reduction in microalbuminuria as an integrated indicator for renal and cardiovascular risk reduction in patients with type 2 diabetes. Diabetes, 2007,56(6):1727-1730.
49.李博一,文磊,宋一惠,等.2型糖尿病慢性血管病变与尿MA的关系.实用糖尿病杂志,2007,3(2)：11-12.
50. Cosson E, Pham I, Valensi P, et al. Impaired coronary endothelium dependent vasodilatation is associated with microalbuminuria in patients with type 2 diabetes and angiographic ally normal coronary arteries[J]. Diabetes Care,2006,29:107-112.
51. Erbagci AB, Tarakcioglu M, Coskun Y, et al. Mediators of in flammationin children with type 1 diabetes mellitus:cytokines in type 1 diabetic children [J]. Clin Biochem,2001, 34:645-650.
52. Schalkwijk CG, Stehouwer CD. Vascular complications in diabetes mellitus:the role of endothelial dysfunction. Clin Sci (Lond),2005,109(2):143-159.
1 Gaede P, Vedel P, Larsen N, et al. Multifactorial intervention and cardiovascular disease in patients with type 2 diabetes. N Engl J Med,2003; 348:383-393.
2 Pradhan AD, Manson J E, Rifai N, et al.C-reactive protein interleukin-6, and risk of developing type 2 diabetes melitus. JAMA,2001; 286(3):327-334.
3李国娟,文芳.2型糖尿病患者超敏CRP水平与IMT关系初探[J].实用糖尿病杂志,2006；2(Ⅰ)：892-894.
4陈文力,严研,王巧云.冠心病患者血清C-反应蛋白水平及其与牙周病的关系[J].中国全科医学,2004；7(3)：168-169.
5 Harry Yu, Nader Rifai. High-sensitivity C-reactive protein and atherosclerosis:from theory to the reply [J]. Clinical Bio chemistry,2000; 33 (8):601-601.
6 Pepys MB. C-reactive protein fifty years on [J]. Lancet,1981; 1:653-657.
7 Devaraj S, Singh U, Jialal I, et al. The evolving role of C-reactive protein in stherothrombosis [J]. Clin Chem.2009; 55(2):229-238.
8 Bang R, MarnellL, Mold C, et al. Analysis of binding sites in human C-reactive Protein for Fcgamma R I, Fcgamma by site-directed mutagenesis [J]. J B iol Chem.2005; 280(26):25095-25102.
9王凯,王涛,金凤.颈动脉狭窄与细胞因子和基因表达[J].内蒙古医学院学报,2006；28(6)：596-599.
10 Bickel C, Ruppreeh H J B lank enb erg S, et al. Relation of markers of inflammation (C reactive protein, fibrinogen, von Will brand factor, and leukocyte count) and stat in therapy to long-term mortality in patients with anginographically proven coronary artery disease[J]. Am JC ardio,2002; 89(8):901-908.
11 Blake GJ, Ridker PM. Novel clinical markers of vascular wall inflammation[J]. Circ Res,2001,89(9):763-771.
12 Torzewski J, Torzewski M, Bowyer DE, et al. C reactive protein frequently co localizes with the terminal complement complex in the intimae of early atherosclerotic lesion of human coronary artery[J]. Arteroscler Thumb Vase Biol,1998,18:1386.
13 Boulman N, kvy Y, Leiba R, et al. Increased C-reactive protein levels in the polycystic ovary syndrome:a marker of cardiovascular disease[J]. J Clin Endocrinal Metal,2004, 89:2160-2165.
14 Tamam Y, Iltumur K, Apak I. Assessment of acute phase proteins in acute ischemic stroke[J]. Tohoku J Exp Med,2005,206(2):91-98.
15张国瑾,赵增荣.国外脑血管病研究进展[M].北京：中国医药科技出版社,2000.116-124.
16 Hashimoto H, Kitagawa K, Hoecake H, et al. Relationship between C-reactive protein and progression of early carotid atherosclerosis in hypertensive subjects[J]. Stroke, 2004,35:1625-1630.
17 Highlander P, Shaw G P. Current pharmacotherapeutic concepts for the treatment of cardiovascular disease in Diabetics [J]. Ther Adv Cardiovasc Dis,2010; 4(1):43-54.
18 Wild S, Roglic G, Green A, et al. Global prevalence of diabetes:estimates for the year 2000 and projections for 2030[J]. Diabetes Care,2004; 27(5):1047-1053.
19 BRUNO G, FORNENGOP, NOVELLI G, et al. C-reactive protein and 5-year survival in type 2 diabetes:the castle monferrato study [J]. Diabetes,2009; 58(4):926-933.
20 Visser M, Bouter LM, Mcquillan GM, et al. Elevated C-reactive protein levels in overweight and obe8e adults. JAMA,1999; 282:2131-2135.
21 Krakofl J, Funahashi T, Stehouwer CD, et al. Inflammatory markers, adiponectin, and risk of type 2 diabetes in the Pima Indian. Diabetes Care,2003; 26:1745-1751.
22 Hu D Y, Pan C Y. Cross-sectional study on the prevalence of abnormal glucose metabolism in patients with coronary artery disease in China-China heart survey [J]. Chin J Endocrinal Metab,2006; 22(1):7-10.
23 Celermajer D S. Endothelial dysfunction:does it matter? Is it reversible? J Am Coil Cardiol,1997; 30:325-333.
24 Kintscher U, Wakino S, Kim S, et al. Angiotensin II induces migration and Pyk2/ paxillin phosphorylation of human mooneyes. Hypertension,2001; 37:587-593.
25 Williams B. Angiotensin II and the path physiology of cardiovascular remodeling. Am J Cardiol,2001; 87:10C-17C.
26 Reddy KG,Nair RN, Sheehan HM, et al. Evidence that selective endothelial dysfunction may occur in the absence of angiographer ultrasound atherosclerosis in patients with risk factors for atherosclerosis. J Am Coil Cardiol.1994; 23:833-843.
27 Yasojima K, Schwab C, MeGeer EG, et al. Generation of C-reactive protein and complement components in atherosclerotic plaques. Am J Path.2001; 158:1039-1051.
28 Venugopal SK, Devaraj S, Yuharma I, et al. Demonstration that C-reactive protein decreases eons expression and bioactivity in human aortic endothelial cells. Circulation.2002; 106:1439-1441.
29 Kawanami D, Maemura K, Takeda N. C-reactive protein induces VCAM-1 gene expression through NF-kappa B activation in vascular endothelial cells[J]. Atherosclerosis,2006,185(1):39-46.
30 Kim CS, Park HS, Kawada T. Circulating levels of MCP-land IL-8 are elevated in human obese subjects and associated with obesity related parameters[J]. Int J Obes(Lond),2006:1-5.
31 Guldiken S, Demir M, Arikan E. The levels of circulating markers of atherosclerosis and inflammation in subjects with different degrees of body mass index; Soluble CD40 legend and high-sensitivity C-reactive protein[J]. Thromb Res,2006,1-5.
32杨胜利,何秉贤.C-反应蛋白与冠心病.中华心血管病杂志,2001.29：187-188.
33 Patrick L, Uzick M. Cardiovascular disease:C-reactive protein and the inflammatory disease paradigm:HMG-CoA reductase inhibitors, alphatocopherol, red yeast rice, and olive oil polyphenols. A review of the literature [J]. Altem Med Rev,2001,6(3): 248-271.
34 Wilson AM, Swan JD, Din H, et al. Widespread vascular production of C-reactive protein and a relationship between serum CRP, plaque CRP and intimal hypertrophy [J]. Atherosclerosis.2007,191(1):175-181.
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27. Pradhan AD, Manson J E, Rifai N, et al. C-reactive protein interleukin-6, and risk of developing type 2 diabetes melitus. JAMA,2001,286(3):327-334.
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33. Hashimoto H, Kitagawa K, Hoecake H, et al. Relationship between Creactive protein and progression of early carotid atherosclerosis in hypertensive subjects[J]. Stroke,2004, 35(7):1625-1630.
34. Patrick L, Uzick M. Cardiovascular disease:C reactive protein and the inflammatory disease paradigm:HMG-CoA reductase inhibitors, alphatocopherol, red yeast rice, and olive oil polyphenols. A review of the literature [J]. Altem Med Rev,2001,6(3):248-271.
35. Napoli M, papa F, Bocola V, et al. C-reactive protein in ischemic stroke, an independent prognostic fator[J]. Stroke,2001,32:917-924.
36. Pasceri V, Chang J, Willerson JT, et al. Modulation of C-reactive protein mediate monocyte chemo attractant protein induction in human endothelial cells by anti-atherosclerosis drugs[J]. Circulation,2001,103:531-534.
37. Nederkoom PJ, Gram Y, Hunink MG. Duplex ultrasound and magnetic resonance angiography compared with digital subtraction angiography in carotid artery stenos is:A systematic review[J]. Stroke,2003,34:1324-1334.
38. Dziedzic T, Gryz EA, Turai W, et al. Serum interleukin-6 soluble receptor in relation to interleukin-6 in stroke patients[J]. J Mol Neu. rosci,2004,24(2):293-298.
39. Kawanami D, Maemura K, Takeda N. C-reactive protein induces VCAM-1 gene expression through NF-kappa B activation in vascular endothelial cells[J]. Atherosclerosis,2006,185(1):39-46.
40. Kim CS, Park HS, Kawada T. Circulating levels of MCP-1and IL-8 are elevated in human obese subjects and associated with obesity-related parameters[J]. Int J Obes(Lond),2006: 1-5.
41. Boulman N, kvy Y, Leiba R, et al. Increased C-reactive protein levels in the polycystic ovary syndrome:a marker of cardiovascular disease[J]. J Clin Endocrinol Metab,2004, 89:2160-2165.
42. Pence S, Yilmaz G, Yilmaz N, et al. Determination of plasma fibronectin and seium C-reactive protein in patients with cerebrovascular events[J]. Int J Clin Pract,2003, 57(2):91-95.
43.张萍.血清超敏C反应蛋白检测在脑血管疾病中的应用[J].中国血液流变学杂志,2004,14：254-255.
44. Short RA, Johnson RJ, Tuttle KR, et al. Uric acid microalbuminria and cardiovascular events in high risk patients[J]. Am J Nephro 1,2005,25:36-44.
45.索丽霞,余叶蓉,喻红玲.2型糖尿病患者胰岛素抵抗、血管内皮细胞功能与微量白蛋白尿.中华内分泌杂志,2004,20：26-29.
46.许曼音.糖尿病学[J]上海：上海科学技术出版社.2003：180-187.
47. Murtaugh MA, Jacobs DR Correlates of urinary albumin execration in young adult blacks and whites:The coronary artery risk development in young adults study [J]. Am J Epidemiol,2003,158:676-686.
48. Araki S, Haneda M, Koya D. Reduction in microalbuminuria as an integrated indicator for renal and cardiovascular risk reduction in patients with type 2 diabetes. Diabetes, 2007,56(6):1727-1730.
49.李博一,文磊,宋一惠,等.2型糖尿病慢性血管病变与尿MA的关系.实用糖尿病杂志,2007,3(2)：11-12.
50. Cosson E, Pham I, Valensi P, et al. Impaired coronary endothelium dependent vasodilatation is associated with microalbuminuria in patients with type 2 diabetes and angiographic ally normal coronary arteries[J]. Diabetes Care,2006,29:107-112.
51. Erbagci AB, Tarakcioglu M, Coskun Y, et al. Mediators of in flammationin children with type 1 diabetes mellitus:cytokines in type 1 diabetic children [J]. Clin Biochem,2001, 34:645-650.
52. Schalkwijk CG, Stehouwer CD. Vascular complications in diabetes mellitus:the role of endothelial dysfunction. Clin Sci (Lond),2005,109(2):143-159.
1 Gaede P, Vedel P, Larsen N, et al. Multifactorial intervention and cardiovascular disease in patients with type 2 diabetes. N Engl J Med,2003; 348:383-393.
2 Pradhan AD, Manson J E, Rifai N, et al.C-reactive protein interleukin-6, and risk of developing type 2 diabetes melitus. JAMA,2001; 286(3):327-334.
3李国娟,文芳.2型糖尿病患者超敏CRP水平与IMT关系初探[J].实用糖尿病杂志,2006；2(Ⅰ)：892-894.
4陈文力,严研,王巧云.冠心病患者血清C-反应蛋白水平及其与牙周病的关系[J].中国全科医学,2004；7(3)：168-169.
5 Harry Yu, Nader Rifai. High-sensitivity C-reactive protein and atherosclerosis:from theory to the reply [J]. Clinical Bio chemistry,2000; 33 (8):601-601.
6 Pepys MB. C-reactive protein fifty years on [J]. Lancet,1981; 1:653-657.
7 Devaraj S, Singh U, Jialal I, et al. The evolving role of C-reactive protein in stherothrombosis [J]. Clin Chem.2009; 55(2):229-238.
8 Bang R, MarnellL, Mold C, et al. Analysis of binding sites in human C-reactive Protein for Fcgamma R I, Fcgamma by site-directed mutagenesis [J]. J B iol Chem.2005; 280(26):25095-25102.
9王凯,王涛,金凤.颈动脉狭窄与细胞因子和基因表达[J].内蒙古医学院学报,2006；28(6)：596-599.
10 Bickel C, Ruppreeh H J B lank enb erg S, et al. Relation of markers of inflammation (C reactive protein, fibrinogen, von Will brand factor, and leukocyte count) and stat in therapy to long-term mortality in patients with anginographically proven coronary artery disease[J]. Am JC ardio,2002; 89(8):901-908.
11 Blake GJ, Ridker PM. Novel clinical markers of vascular wall inflammation[J]. Circ Res,2001,89(9):763-771.
12 Torzewski J, Torzewski M, Bowyer DE, et al. C reactive protein frequently co localizes with the terminal complement complex in the intimae of early atherosclerotic lesion of human coronary artery[J]. Arteroscler Thumb Vase Biol,1998,18:1386.
13 Boulman N, kvy Y, Leiba R, et al. Increased C-reactive protein levels in the polycystic ovary syndrome:a marker of cardiovascular disease[J]. J Clin Endocrinal Metal,2004, 89:2160-2165.
14 Tamam Y, Iltumur K, Apak I. Assessment of acute phase proteins in acute ischemic stroke[J]. Tohoku J Exp Med,2005,206(2):91-98.
15张国瑾,赵增荣.国外脑血管病研究进展[M].北京：中国医药科技出版社,2000.116-124.
16 Hashimoto H, Kitagawa K, Hoecake H, et al. Relationship between C-reactive protein and progression of early carotid atherosclerosis in hypertensive subjects[J]. Stroke, 2004,35:1625-1630.
17 Highlander P, Shaw G P. Current pharmacotherapeutic concepts for the treatment of cardiovascular disease in Diabetics [J]. Ther Adv Cardiovasc Dis,2010; 4(1):43-54.
18 Wild S, Roglic G, Green A, et al. Global prevalence of diabetes:estimates for the year 2000 and projections for 2030[J]. Diabetes Care,2004; 27(5):1047-1053.
19 BRUNO G, FORNENGOP, NOVELLI G, et al. C-reactive protein and 5-year survival in type 2 diabetes:the castle monferrato study [J]. Diabetes,2009; 58(4):926-933.
20 Visser M, Bouter LM, Mcquillan GM, et al. Elevated C-reactive protein levels in overweight and obe8e adults. JAMA,1999; 282:2131-2135.
21 Krakofl J, Funahashi T, Stehouwer CD, et al. Inflammatory markers, adiponectin, and risk of type 2 diabetes in the Pima Indian. Diabetes Care,2003; 26:1745-1751.
22 Hu D Y, Pan C Y. Cross-sectional study on the prevalence of abnormal glucose metabolism in patients with coronary artery disease in China-China heart survey [J]. Chin J Endocrinal Metab,2006; 22(1):7-10.
23 Celermajer D S. Endothelial dysfunction:does it matter? Is it reversible? J Am Coil Cardiol,1997; 30:325-333.
24 Kintscher U, Wakino S, Kim S, et al. Angiotensin II induces migration and Pyk2/ paxillin phosphorylation of human mooneyes. Hypertension,2001; 37:587-593.
25 Williams B. Angiotensin II and the path physiology of cardiovascular remodeling. Am J Cardiol,2001; 87:10C-17C.
26 Reddy KG,Nair RN, Sheehan HM, et al. Evidence that selective endothelial dysfunction may occur in the absence of angiographer ultrasound atherosclerosis in patients with risk factors for atherosclerosis. J Am Coil Cardiol.1994; 23:833-843.
27 Yasojima K, Schwab C, MeGeer EG, et al. Generation of C-reactive protein and complement components in atherosclerotic plaques. Am J Path.2001; 158:1039-1051.
28 Venugopal SK, Devaraj S, Yuharma I, et al. Demonstration that C-reactive protein decreases eons expression and bioactivity in human aortic endothelial cells. Circulation.2002; 106:1439-1441.
29 Kawanami D, Maemura K, Takeda N. C-reactive protein induces VCAM-1 gene expression through NF-kappa B activation in vascular endothelial cells[J]. Atherosclerosis,2006,185(1):39-46.
30 Kim CS, Park HS, Kawada T. Circulating levels of MCP-land IL-8 are elevated in human obese subjects and associated with obesity related parameters[J]. Int J Obes(Lond),2006:1-5.
31 Guldiken S, Demir M, Arikan E. The levels of circulating markers of atherosclerosis and inflammation in subjects with different degrees of body mass index; Soluble CD40 legend and high-sensitivity C-reactive protein[J]. Thromb Res,2006,1-5.
32杨胜利,何秉贤.C-反应蛋白与冠心病.中华心血管病杂志,2001.29：187-188.
33 Patrick L, Uzick M. Cardiovascular disease:C-reactive protein and the inflammatory disease paradigm:HMG-CoA reductase inhibitors, alphatocopherol, red yeast rice, and olive oil polyphenols. A review of the literature [J]. Altem Med Rev,2001,6(3): 248-271.
34 Wilson AM, Swan JD, Din H, et al. Widespread vascular production of C-reactive protein and a relationship between serum CRP, plaque CRP and intimal hypertrophy [J]. Atherosclerosis.2007,191(1):175-181.