代谢综合征与良性前列腺增生症的相关性研究
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摘要
目的：
对老年病科良性前列腺增生症(benign prostatic hyperplasia,BPH)患者和BPH合并代谢综合征(metabolic syndrome, MS)的患者进行相关性研究,探讨代谢性指标如腰围(waist)、体重指数(body mass index, BMI)、血脂(lipids)、空腹血糖(free blood glucose, FBS)以及胰岛素抵抗(insuline resistance, IR)对BPH病程的影响,旨在揭示代谢综合征在良性前列腺增生症病程中的作用。
方法：
采用横断面研究方法,以2008年2月在湘雅二医院老年病科门诊和2009年3月在解放军163医院老年病科门诊就诊的≥60岁BPH患者为研究对象,对入选的101例BPH患者的代谢性指标包括：BMI、Waist、Lipids、FBS、空腹胰岛素(free-Insuline,FINS)与BPH评价指标包括：前列腺体积(prostate volume,PV)、血清前列腺特异性抗原(prostate specific antigen,PSA)、国际前列腺症状评分(international Prostate Symptom Score,IPSS)、BPH病程时间等进行统计,按照BPH和MS的诊断标准,将101例BPH患者分为单纯BPH组(45人)与合并MS的BPH组(56人),并根据患者的BMI、Waist、高密度脂蛋白胆固醇(high density lipoprotein cholesterol, HDL-C)、FBS、胰岛素抵抗指数(homeostasis model assessment of insuline resistance index,HOMA-IR)水平进行分组,分析各代谢性因素对BPH病程的影响。计量资料用均数±标准差(x±s)表示,组间均数比较采用独立样本的t检验,多组间均数比较采用单因素方差分析,两两比较采用LSD-t检验,计数资料采用百分比描述,两组构成比的比较用x2检验,相关性分析采用Pearson相关性分析和多元线性逐步回归分析。检验水准a=0.05(双侧)。
结果：
1.合并MS的BPH患者前列腺体积明显大于单纯BPH患者(51.19±25.64ml vs 38.34±13.67ml,P=0.003),BPH病程年数前者长于后者(14.46±6.32年vs 11.51±6.32年,P=0.046)。
2.超重与肥胖BPH患者前列腺体积(49.44±26.83ml,51.66±22.23ml)明显大于正常体重BPH患者(38.10±10.64 ml,P=0.021,P=0.043),血清PSA、BPH病程、IPSS两组比较均无显著性差异(P>0.05)。将BMI≥24kg/m2的BPH患者分为腹型肥胖组(腰围>90cm)与非腹型肥胖组(腰围≤90cm)比较,两组前列腺体积有显著性差异(50.26±26.51 ml vs 38.99±11.25ml,P=0.005),PSA、BPH病程、IPSS在两者之间均无显著性差异(P>0.05)。
3.低HDL-C水平(HDL-C≤1.04mmol/L)的BPH患者前列腺体积明显大于正常HDL-C水平的BPH患者(54.23±28.92 ml vs40.40±14.87ml,P=0.009),而PSA、IPSS、BPH病程等指标的两组间比较,未发现显著性差异。
4.FBS水平异常(FBS≥6.1mmol/L)的BPH患者前列腺体积(50.40±22.56 vs 41.16±20.80ml,P=0.035)、PSA水平(3.29±2.44 vs1.91±1.47ng/ml,P=0.013)超过正常FBS水平的BPH患者,而IPSS、BPH病程等指标在两组间比较,未发现显著性差异。
5.合并胰岛素抵抗(HOMA-IR>2.8)的BPH患者的前列腺体积明显大于胰岛素敏感的BPH患者(56.40±27.32 ml vs 39.41±15.67ml, P=0.001),BPH病程年数在胰岛素抵抗组明显高于胰岛素敏感的BPH患者组(16.61±7：73年vs 11.23±7.15年,P=0.001),PSA、IPSS在两组之间比较未发现显著性差异。
6.将所有BPH患者前列腺体积与Waist、BMI、FBS、餐后2小时血糖(2-hour postprandial blood glucose,2hPBG)、糖化血红蛋白、HDL-C、低密度脂蛋白胆固醇(low density lipoprotein cholesterol, LDL-C)、总胆固醇(totalcholesterol, TC)、甘油三酯(triglyceride, TG)、FINS、HOMA-IR进行相关性分析,显示前列腺体积与BMI(r=0.459, P=0.000)、FINS(r=0.421,P=0.001)、HOMA-IR(r=0.490, P=0.003)呈显著正相关；而与HDL-C(r=-0.378,P=0.000)呈显著负相关；与Waist、FBS、2hPBG、糖化血红蛋白、LDL-C、TC、TG无明显相关性。多元逐步回归分析显示前列腺体积与HOMA-IR关系最密切。
结论：
1.肥胖、腹型肥胖、高密度脂蛋白胆固醇降低、空腹血糖升高、具胰岛素抵抗的良性前列腺增生症患者前列腺体积增大程度更严重,空腹血糖升高者血清PSA更高,合并胰岛素抵抗的良性前列腺增生症患者病程更长。
2.体重指数、空腹胰岛素、胰岛素抵抗指数与前列腺体积呈正相关；高密度脂蛋白胆固醇与前列腺体积呈负相关,在众多的代谢性因素中,前列腺体积与胰岛素抵抗指数关系最密切
3.代谢综合征对良性前列腺增生症的发展具有明显的影响
Objectives
The purpose of this study was to evaluate the relationship between benign prostate hyperplasia(BPH) and metabolic syndrome(MS)in Geriatrics Department. To analyze the metabolic indexes including waist, body mass index(BMI), lipids, free blood glocuse(FBS), insuline resistance(IR) which affect BPH, so as to explore the effect of MS on the occurrence and development of BPH.
Methods
In the cross-sectional study,101 elderly BPH patients(aged≥60y) were recruited from Geriatrics Outpatients, Second XiangYa hospital in Feb,2008 and People's Liberation Army 163 hospital in March,2009. The metabolic indexes such as BMI, waist, lipids, FBS, free insuline(FINS)and BPH related datas containing prostate volume(PV), prostate specific antigen (PSA), international prostate symptom score(IPSS), course of BPH were collected and recorded, then were calculated statistically. All BPH patients were divided into two groups(the BPH with MS group and the BPH group) according whether they were diagnosed BPH and MS.The study was to compare the differences in indexes of prostatic hyperplasia in BPH with MS group and the BPH group.In addition, all patients were divided into differents groups according to level of BMI, waist, high density lipoprotein cholesterol (HDL-C),FBS,homeostasis model assessment of insuline resistance index (HOMA-IR) and assessed respectively the effect of these metabolic indexes on BPH. All descriptive data were reported as the mean±standard deviation(M±SD).The differences in the mean values between two groups were analyzed by Independent Samples T test, ANOVA, and LSD-test were used for multiple comparison. Enumeration data were reported as percentage, the analysis of correlation were used Pearson correlation and multiple liner regression.Significance was defined at the 5% level.
Results
1.The BPH with MS group showed significantly higher values of PV(51.19±25.64ml vs 38.34±13.67ml, P=0.003)and longer course of BPH(14.46±6.32y vs 11.51±6.32y, P=0.046) than in pure BPH group.
2.The overweight and the obese BPH patients had significantly higher levels of PV(49.44±26.83ml,51.66±22.23ml) (P=0.021, P=0.043) than BPH patients with normal weight (38.10±10.64ml), the differences in PSA, course of BPH, IPSS between two groups weren't statistically significant(P>0.05).Additionally, BPH patients with BMI≥24kg/m2 combined abdominal obesity group had significantly higher levels of PV(50.26±26.51ml vs 38.99±11.25ml, P=0.005)than BPH patients without abdominal obesity, the differences in PSA, history of BPH, IPSS between two groups weren't statistically significant(P>0.05).
3.BPH patients combined low levels of high density lipoprotein had significantly higher prostate volume than normal levels of high density lipoprotein BPH patients(54.23±28.92 vs 40.40±14.87ml, P=0.009), the differences in PSA, course of BPH, IPSS between two groups weren't statistically significant(P>0.05).
4.The values of PV(50.40±22.56 vs 41.16±20.80ml,P=0.035), PSA(3.29±2.44 vs 1.91±1.47ng/ml, P=0.013)in the BPH patients with elevated FBS were significantly higher than the BPH patients with normal value FBS.
5.BPH patients combined with IR (HOMA-IR>2.8) had higher values of PV than the insuline sensitive BPH patients(56.40±27.32 vs 39.41±15.67ml, P=0.001), the former group had longer courses of BPH than the latter group(16.61±7.73 vs 11.23±7.15y, P=0.001),the differences in PSA, IPSS weren't significant.
6.The values of PV of all patients were positively correlated with BMI(r=0.459, P=0.000), FINS(r=0.421, P=0.001), HOMA-IR(r=0.490, P=0.003)and negatively correlated with HDL-C(r=-0.378, P=0.000), and they had no significant correlation with waist, FBS,2-hour postprandial blood glucose(2hPBG), low density lipoprotein cholesterol(LDL-C),HbA1C,totalcholesterol(TC), triglyceride(TG). Multiple linear stepwise regression analysis showed that prostate volume was most closely correlated with HOMA-IR.
Conclusions
1.BPH patients combined with obesity, abdominal obesity, low levels of HDL-C, elevated FBS,IR had the larger values of prostate volume, BPH patients combined with IR had longer course of BPH.
2.Level of BMI, FINS,HOMA-IR were positively correlated with PV, and HDL-C was negatively correlated with PV.In numerous metabolic indexes, HOMA-IR was correlated with PV most closely.
3.MS had evident effect on the occurrence and development of BPH.
对老年病科良性前列腺增生症(benign prostatic hyperplasia,BPH)患者和BPH合并代谢综合征(metabolic syndrome, MS)的患者进行相关性研究,探讨代谢性指标如腰围(waist)、体重指数(body mass index, BMI)、血脂(lipids)、空腹血糖(free blood glucose, FBS)以及胰岛素抵抗(insuline resistance, IR)对BPH病程的影响,旨在揭示代谢综合征在良性前列腺增生症病程中的作用。
方法：
采用横断面研究方法,以2008年2月在湘雅二医院老年病科门诊和2009年3月在解放军163医院老年病科门诊就诊的≥60岁BPH患者为研究对象,对入选的101例BPH患者的代谢性指标包括：BMI、Waist、Lipids、FBS、空腹胰岛素(free-Insuline,FINS)与BPH评价指标包括：前列腺体积(prostate volume,PV)、血清前列腺特异性抗原(prostate specific antigen,PSA)、国际前列腺症状评分(international Prostate Symptom Score,IPSS)、BPH病程时间等进行统计,按照BPH和MS的诊断标准,将101例BPH患者分为单纯BPH组(45人)与合并MS的BPH组(56人),并根据患者的BMI、Waist、高密度脂蛋白胆固醇(high density lipoprotein cholesterol, HDL-C)、FBS、胰岛素抵抗指数(homeostasis model assessment of insuline resistance index,HOMA-IR)水平进行分组,分析各代谢性因素对BPH病程的影响。计量资料用均数±标准差(x±s)表示,组间均数比较采用独立样本的t检验,多组间均数比较采用单因素方差分析,两两比较采用LSD-t检验,计数资料采用百分比描述,两组构成比的比较用x2检验,相关性分析采用Pearson相关性分析和多元线性逐步回归分析。检验水准a=0.05(双侧)。
结果：
1.合并MS的BPH患者前列腺体积明显大于单纯BPH患者(51.19±25.64ml vs 38.34±13.67ml,P=0.003),BPH病程年数前者长于后者(14.46±6.32年vs 11.51±6.32年,P=0.046)。
2.超重与肥胖BPH患者前列腺体积(49.44±26.83ml,51.66±22.23ml)明显大于正常体重BPH患者(38.10±10.64 ml,P=0.021,P=0.043),血清PSA、BPH病程、IPSS两组比较均无显著性差异(P>0.05)。将BMI≥24kg/m2的BPH患者分为腹型肥胖组(腰围>90cm)与非腹型肥胖组(腰围≤90cm)比较,两组前列腺体积有显著性差异(50.26±26.51 ml vs 38.99±11.25ml,P=0.005),PSA、BPH病程、IPSS在两者之间均无显著性差异(P>0.05)。
3.低HDL-C水平(HDL-C≤1.04mmol/L)的BPH患者前列腺体积明显大于正常HDL-C水平的BPH患者(54.23±28.92 ml vs40.40±14.87ml,P=0.009),而PSA、IPSS、BPH病程等指标的两组间比较,未发现显著性差异。
4.FBS水平异常(FBS≥6.1mmol/L)的BPH患者前列腺体积(50.40±22.56 vs 41.16±20.80ml,P=0.035)、PSA水平(3.29±2.44 vs1.91±1.47ng/ml,P=0.013)超过正常FBS水平的BPH患者,而IPSS、BPH病程等指标在两组间比较,未发现显著性差异。
5.合并胰岛素抵抗(HOMA-IR>2.8)的BPH患者的前列腺体积明显大于胰岛素敏感的BPH患者(56.40±27.32 ml vs 39.41±15.67ml, P=0.001),BPH病程年数在胰岛素抵抗组明显高于胰岛素敏感的BPH患者组(16.61±7：73年vs 11.23±7.15年,P=0.001),PSA、IPSS在两组之间比较未发现显著性差异。
6.将所有BPH患者前列腺体积与Waist、BMI、FBS、餐后2小时血糖(2-hour postprandial blood glucose,2hPBG)、糖化血红蛋白、HDL-C、低密度脂蛋白胆固醇(low density lipoprotein cholesterol, LDL-C)、总胆固醇(totalcholesterol, TC)、甘油三酯(triglyceride, TG)、FINS、HOMA-IR进行相关性分析,显示前列腺体积与BMI(r=0.459, P=0.000)、FINS(r=0.421,P=0.001)、HOMA-IR(r=0.490, P=0.003)呈显著正相关；而与HDL-C(r=-0.378,P=0.000)呈显著负相关；与Waist、FBS、2hPBG、糖化血红蛋白、LDL-C、TC、TG无明显相关性。多元逐步回归分析显示前列腺体积与HOMA-IR关系最密切。
结论：
1.肥胖、腹型肥胖、高密度脂蛋白胆固醇降低、空腹血糖升高、具胰岛素抵抗的良性前列腺增生症患者前列腺体积增大程度更严重,空腹血糖升高者血清PSA更高,合并胰岛素抵抗的良性前列腺增生症患者病程更长。
2.体重指数、空腹胰岛素、胰岛素抵抗指数与前列腺体积呈正相关；高密度脂蛋白胆固醇与前列腺体积呈负相关,在众多的代谢性因素中,前列腺体积与胰岛素抵抗指数关系最密切
3.代谢综合征对良性前列腺增生症的发展具有明显的影响
Objectives
The purpose of this study was to evaluate the relationship between benign prostate hyperplasia(BPH) and metabolic syndrome(MS)in Geriatrics Department. To analyze the metabolic indexes including waist, body mass index(BMI), lipids, free blood glocuse(FBS), insuline resistance(IR) which affect BPH, so as to explore the effect of MS on the occurrence and development of BPH.
Methods
In the cross-sectional study,101 elderly BPH patients(aged≥60y) were recruited from Geriatrics Outpatients, Second XiangYa hospital in Feb,2008 and People's Liberation Army 163 hospital in March,2009. The metabolic indexes such as BMI, waist, lipids, FBS, free insuline(FINS)and BPH related datas containing prostate volume(PV), prostate specific antigen (PSA), international prostate symptom score(IPSS), course of BPH were collected and recorded, then were calculated statistically. All BPH patients were divided into two groups(the BPH with MS group and the BPH group) according whether they were diagnosed BPH and MS.The study was to compare the differences in indexes of prostatic hyperplasia in BPH with MS group and the BPH group.In addition, all patients were divided into differents groups according to level of BMI, waist, high density lipoprotein cholesterol (HDL-C),FBS,homeostasis model assessment of insuline resistance index (HOMA-IR) and assessed respectively the effect of these metabolic indexes on BPH. All descriptive data were reported as the mean±standard deviation(M±SD).The differences in the mean values between two groups were analyzed by Independent Samples T test, ANOVA, and LSD-test were used for multiple comparison. Enumeration data were reported as percentage, the analysis of correlation were used Pearson correlation and multiple liner regression.Significance was defined at the 5% level.
Results
1.The BPH with MS group showed significantly higher values of PV(51.19±25.64ml vs 38.34±13.67ml, P=0.003)and longer course of BPH(14.46±6.32y vs 11.51±6.32y, P=0.046) than in pure BPH group.
2.The overweight and the obese BPH patients had significantly higher levels of PV(49.44±26.83ml,51.66±22.23ml) (P=0.021, P=0.043) than BPH patients with normal weight (38.10±10.64ml), the differences in PSA, course of BPH, IPSS between two groups weren't statistically significant(P>0.05).Additionally, BPH patients with BMI≥24kg/m2 combined abdominal obesity group had significantly higher levels of PV(50.26±26.51ml vs 38.99±11.25ml, P=0.005)than BPH patients without abdominal obesity, the differences in PSA, history of BPH, IPSS between two groups weren't statistically significant(P>0.05).
3.BPH patients combined low levels of high density lipoprotein had significantly higher prostate volume than normal levels of high density lipoprotein BPH patients(54.23±28.92 vs 40.40±14.87ml, P=0.009), the differences in PSA, course of BPH, IPSS between two groups weren't statistically significant(P>0.05).
4.The values of PV(50.40±22.56 vs 41.16±20.80ml,P=0.035), PSA(3.29±2.44 vs 1.91±1.47ng/ml, P=0.013)in the BPH patients with elevated FBS were significantly higher than the BPH patients with normal value FBS.
5.BPH patients combined with IR (HOMA-IR>2.8) had higher values of PV than the insuline sensitive BPH patients(56.40±27.32 vs 39.41±15.67ml, P=0.001), the former group had longer courses of BPH than the latter group(16.61±7.73 vs 11.23±7.15y, P=0.001),the differences in PSA, IPSS weren't significant.
6.The values of PV of all patients were positively correlated with BMI(r=0.459, P=0.000), FINS(r=0.421, P=0.001), HOMA-IR(r=0.490, P=0.003)and negatively correlated with HDL-C(r=-0.378, P=0.000), and they had no significant correlation with waist, FBS,2-hour postprandial blood glucose(2hPBG), low density lipoprotein cholesterol(LDL-C),HbA1C,totalcholesterol(TC), triglyceride(TG). Multiple linear stepwise regression analysis showed that prostate volume was most closely correlated with HOMA-IR.
Conclusions
1.BPH patients combined with obesity, abdominal obesity, low levels of HDL-C, elevated FBS,IR had the larger values of prostate volume, BPH patients combined with IR had longer course of BPH.
2.Level of BMI, FINS,HOMA-IR were positively correlated with PV, and HDL-C was negatively correlated with PV.In numerous metabolic indexes, HOMA-IR was correlated with PV most closely.
3.MS had evident effect on the occurrence and development of BPH.
引文
[1].Wei Johnt,Calhown Elizabeth,Jacobsen StevevJ.Urologic disease in America project:Benign prostatic hyperplasia[J].J Urol,2005,173(4):1256-1261.
[2]于普林,郑宏,苏鸿学等.中国六城市老年人前列腺增生的患病率及相关因素[J].中华流行病学杂志,2000,21：276-278.
[3]National Health and Nutrition Examination Survey (NHANES):National center for Health Statistics.[accessed February 2007]. http://www.cdc.gov/nchs/nhanes.htm.
[4]Bjorn Hildrum, Arnstein Mykletun, Torstein Hole,etal. Age-specific prevalence of the metabolic syndrome defined by the International Diabetes Federation and the National Cholesterol Education Program the Norwegian HUNT 2 Study[J].BMC Public Health 2007,7:220-223.
[5]陈蕾,贾伟平,陆俊茜等.上海市成人代谢综合征流行调查[J].中华心血管杂志,2003,31：909-12.
[6]陆再英,钟南山.内科学[M].北京：人民卫生出版社,2008,第七版,813.
[7]贾伟平.中国人群有胰岛素抵抗的状况[J].国外医学.内分泌学分册,2002,22(4)：264-267.
[8]Lees,Min HG, Choi SH, etal.Central obesity as a risk factor for prostatic hyperplasia[J].Obesity,2006,14(1):172-9.
[9]J.Kellogg Parsons,H.Ballentine Cater, Alan W. Partin, etal.Metabolic Factors Associated with Benign Prostatic Hyperplasia[J].J Clin Endocrinol Metab,2006, 91(7):2562-2568.
[10]孙立军.前列腺体积与肥胖及血糖的相关性调查[J].中国误诊医学杂志,2007,7(27)：6704-6705.
[11]Weisman KM,Larijani GE,Goldstein MR.Relationship between Benign Prostatic Hyperplasia and history of Coronary artery disease in elderly men[J]. Pharamacotherapy,2000,20:383-386.
[12]梁飞宇,屈晓冰,赵晓昆.良性前列腺增生症和冠心病患者超敏C反应蛋白水平的检测[J].中国老年医学杂志,2007,1(27)：162-164.
[13]Jennifer L.St.Savver,Arunav Sarma,Debra J.Jacobson,etal.Associations between C-reactive protein and benign prostatic hyperplasia/lower urinary tract symptom outcomes in a population-based cohort[J].American Journal of epidemiology,2009,169(11):1281-90.
[14]Kozlowski R,Kershen RT,Siroky MB,etal. Chronic ischemia alters prostate structure and reactivity in rabbits[J].JUROL 2001,165(3):1019-1026.
[15]Hammarsten J,Hogstedt B.Hyperinsulinaemia as a risk factor for developing Benign Prostatic Hyperplasia[J].Eur Urol,2001,39(2):151-158.
[16]Hammarsten J,Hogstedt B,Holthuis N,etal.Components of the metabolic stndrome risk factors for the development of Benign Prostatic Hyperplasia[J].Prostate cancer Prostatic DIS,1998,1(3):157-162.
[17]李培军,张祥华,郭利君等.高脂血症与良性前列腺增生相关性的临床研究[J].中华外科杂志,2005,43(6)：387-389.
[18]沈文,李蓉,胡卫列.良性前列腺增生与动脉硬化症关系的初步探讨[J].医学临床研究,2007,24(4)：555-556.
[19]Padayatty SJ, Marcelli M, Shao TC, et al.Lavastatin-Induced Apoptosis in Prostate Stromal Cells[J].J Clin Endocrinol Metab.1997;82(5):1434-1439.
[20]Rees RW, Foxwell NA, Ralph DJ, et al. Y-27632, a Rhokinase inhibitor, inhibits proliferation and adrenergic contraction of prostatic smooth muscle cells[J].J Urol.2003;170:2517-22.
[21]Watts KL, Spiteri MA. Connective tissue growth factor expression and induction by transforming growth factor beta is abrogated by simvastatin via a Rho signaling mechanism[J].Am J Physiol Lung Cell Mol Physiol 2004;287:L1323-32.
[22]Escobart EL,Gomes-marcondes MC,Carvalho HF.Dietary fatty acid quality affects AR and PPARgamma levels and prostate growth[J].Prostate,2009,69(5):548-58.
[23]Hanefel DM,etal.Insuline secretion and insuline sensitivity patterns is different in isolated impaired glucose tolerance and impaired fasting glucose[J].Diabetes Care.2003,2:868-74.
[24]J.KelloggParsons,JaclynBergstrom,Elizabethconnor.Lipids,Lipoperteins,and risk of Benign prostatic hyperplasia in community dwelling men[J].BJU Int.2008,101(3):313-318.
[25]Wheatcroft, SB;Williams, IL; Shah, AM; Kearney, MT.Pathophysiological implications of insulin resistance on vascular endothelial function[J].Diabet Med. 2003;20:255-68.
[26]Berger AP,Bartsch QDeibl M. Atherosclerosis as a risk factor for Benign Prostatic Hyperplasia[J].BJU Int.2006,98:1038-1042.
[27]黄延焱,卢晓喆,俞茂华.老年代谢综合征患者血胰岛素样生长因子1与代谢综合征的关系[J].中华老年医学杂志,2006,25(7)：519-21.
[28]Steven E.Oliver,Barney Barrass,David J.Gunnell,etal.Serum insulin-like factors-II positively associated with serum prostate-specific antigen in middle-aged men without evidence of prostate cancer[J].Cancer Epidemiol.Biomarkers prev,2004,13:163.
[29]Mc Connell JD, Roehrborn CG,Bautista OM,etal.The long-term effect of doxazosin, finasteride,and combination therapy on the clinical progression of benign prostatic hyperplasia[J].N Engl J Med,2003,349(25):2387-2398.
[30]Wang W, Bergh A, Damber JE Chronic inflammation in BPH is associated with focal upregulation of cyclo-oxygenase-2, Bd-2 and cell proliferation in glandular epithelium[J].Prostate,2004,61:60-72
[31]Nandeesha H,Koher BC,Dorairajan LN,etal.Hyperinsulinemia and dyslipidemia in non-diabetic Benigne Prostata hyperplasie[J].Clin chim Acta,2006,370:89-93.
[32]Ozden C,Ozdal OL,Urqancioqiu Qetal.The correlation between metabolic synderom and prostatic growth in patients with Benigne Prostatahyperplasie[J].Eur Urol,2007,51:199-203.
[1].Michael k Brawer.Best of the 2009 AUA annuall meeting.Rev urol 2009;11(2):82-107.
[2].梁飞宇,屈晓冰,赵晓昆.炎症与良性前列腺增生症[J].国外医学.老年医学分册,2005,26(5)：193-196.
[3].陆再英,钟南山.内科学[M].北京：人民卫生出版社,2008,第七版.831.
[4].National Health and Nutrition Examination Survey (NHANES):National center for Health Statistics.[accessed February 2007]. http://www.cdc.gov/nchs/nhanes.htm
[5].Bjorn Hildrum, Arnstein Mykletun, Torstein Hole,etal. Age-specific prevalence of the metabolic syndrome defined by the International Diabetes Federation and the National Cholesterol Education Program the Norwegian HUNT 2 Study. BMC Public Health 2007,7:220-223.
[6].屈晓冰,谢景超,赵晓昆.良性前列腺增生症和冠心病的关系研究现状[J].中华老年医学杂志,2004,23(1)：46-47。
[7].Nandeesha H,Koher BC,Dorairajan LN,etal.Hyperinsulinemia and dyslipidemia in non-diabetic Benigne Prostata hyperplasie[J].Clin chim Acta,2006,370:89-93.
[8].Ozden C,Ozdal OL,Urqancioqiu Qetal.The correlation between metabolic synderom and prostatic growth in patients with Benigne Prostatahyperplasie[J].Eur Urol,2007,51:199-203.
[9].]Michel MC,HeemannU, SchumacherH,etal.Association of hypertension with symptoms of benign prostatichyperplasia[J].Jurol,2004,172:1390-3.
[10]Kevi NT,Mcvary,Alfred rademaker,etal.Autonomic nervous system overtactivity in men with lower urinary tract symptoms secondary to benign prostatic hyperplasia[J].The Journal of urology,2005,174:1327-1333.
[11]郭利君,张祥华,李培军等.高血压对良性前列腺增生组织中血管新生影响的研究[J].中华医学杂志,2005,9：606-609.
[12]Gunther Wennemuth, Gerhard Aumuller.Angiotensin Ⅱ-mediated Calcium signals and mitogenesis in human prostate stromal cell line hpcps[J].Br J pharmacol,2005144(1):3-10.
[13]Weisman KM,Larijani GE,Goldstein MR.Relationship between Benign Prostatic Hyperplasia and history of Coronary artery disease in elderly men[J]. Pharamacotherapy,2000,20:383-386.
[14].梁飞宇,屈晓冰,赵晓昆.良性前列腺增生症和冠心病患者超敏C反应蛋白水平的检测[J].中国老年医学杂志,2007,1(27)：162-164.
[15].Jennifer L.St.Savver,Arunav Sarma,Debra J.Jacobson,etal.Associations between C-reactive protein and benign prostatic hyperplasia/lower urinary tract symptom outcomes in a population-based cohort[J].American Journal of epidemiology, 2009,169(11):1281-90.
[16]Kozlowski R,Kershen RT,Siroky MB,etal.Chronic ischemia alters prostate structure and reactivity in rabbits[J].JUROL 2001,165(3):1019-1026.
[17].Hammarsten J,Hogstedt B.Hyperinsulinaemia as a risk factor for developing Benign Prostatic Hyperplasia[J].Eur Urol,2001,39(2):151-158.
[18]Hammarsten J,Hogstedt B,Holthuis N,etal.Components of the metabolic stndrome risk factors for the development of Benign Prostatic
Hyperplasia[J].Prostate cancer Prostatic DIS,1998,1(3):157-162.
[19].李培军,张祥华,郭利君等.高脂血症与良性前列腺增生相关性的临床研究[J].中华外科杂志,2005,43(6)：387-389.
[20]沈文,李蓉,胡卫列.良性前列腺增生与动脉硬化症关系的初步探讨[J].医学临床研究,2007,24(4)：555-556.
[21]Padayatty SJ, Marcelli M, Shao TC, et al Lavastatin-Induced Apoptosis in Prostate Stromal Cells[J].J Clin Endocrinol Metab.1997;82(5):1434-1439.
[22]Rees RW, Foxwell NA, Ralph DJ, et al.Y-27632, a Rhokinase inhibitor, inhibits proliferation and adrenergic contraction of prostatic smooth muscle cells[J].J Urol.2003;170:2517-22.
[23]Watts KL, Spiteri MA. Connective tissue growth factor expression and induction by transforming growth factor beta is abrogated by simvastatin via a Rho signaling mechanism[J]. Am J Physiol Lung Cell Mol Physiol 2004;287:L1323-32.
[24]Escobart EL,Gomes-marcondes MC,Carvalho HF.Dietary fatty acid quality affects AR and PPARgamma levels and prostate growth[J].Prostate, 2009,69(5):548-58.
[25].Cohen PGBenign prostatic hyperplasia:the hypogondal-obesity-prostate connection[J].Med hypotheses,2009,73(2):142-3.
[26]J.Kellogg Parsons,H.Ballentine Cater,Alan W.Partin,etal.Metabolic Factors Associated with Benign Prostatic Hyperplasia[J].J Clin Endocrinol Metab, 2006,91(7):2562-2568.
[27]Lees,Min HG, Choi SH,etal.Central obesity as a risk factor for prostatic hyperplasia[J].Obesity,2006,14(l):172-9.
[28]孙立军.前列腺体积与肥胖及血糖的相关性调查[J].中国误诊医学杂志,2007,7(27)：6704-6705.
[29].Gupta A,GUPTAS,Pavuk M,etal.Anthoropometric and Metabolic factors and risk of Benign Prostat hyperplasie:a prospective cohort study of Air Force Veterans[J].Ur logy,2006,68:1198-205.
[30].Wheatcroft, SB;Williams, IL; Shah, AM; Kearney, MT. Pathophysiological implications of insulin resistance on vascular endothelial function[J].Diabet Med. 2003;20:255-68.
[31]Berger AP,Bartsch G,Deibl M. Atherosclerosis as a risk factor for Benign Prostatic Hyperplasia. BJU Int.2006,98:1038-1042.
[32]黄延焱,卢晓喆,俞茂华.老年代谢综合征患者血胰岛素样生长因子-1与代谢综合征的关系.中华老年医学杂志,2006,25(7)：519-21.
[33].Steven E.Oliver,Bamey Barrass,David J.Gunnell,etal.Serum insulin-like factors-II positively associated with serum prostate-specific antigen in middle-aged men without evidence of prostate cancer.Cancer Epidemiol.Biomarkers prev,2004,13:163.
[34]Demirtunc Refik, Duman, Dursun,etal. Effects of Doxazosin and Amlodipine on Mean platelet volume and serum serotonin level in patients with Metabolic Syndrome:A Randomised controlled study. Clinical Drug Investigation.2007,27(6):435-441.
[35]马妮娜,沈璐华.氯沙坦对高血糖合并高血压患者胰岛素敏感性的影响.中国全科医学,2008,11：2019-2020.
[2]于普林,郑宏,苏鸿学等.中国六城市老年人前列腺增生的患病率及相关因素[J].中华流行病学杂志,2000,21：276-278.
[3]National Health and Nutrition Examination Survey (NHANES):National center for Health Statistics.[accessed February 2007]. http://www.cdc.gov/nchs/nhanes.htm.
[4]Bjorn Hildrum, Arnstein Mykletun, Torstein Hole,etal. Age-specific prevalence of the metabolic syndrome defined by the International Diabetes Federation and the National Cholesterol Education Program the Norwegian HUNT 2 Study[J].BMC Public Health 2007,7:220-223.
[5]陈蕾,贾伟平,陆俊茜等.上海市成人代谢综合征流行调查[J].中华心血管杂志,2003,31：909-12.
[6]陆再英,钟南山.内科学[M].北京：人民卫生出版社,2008,第七版,813.
[7]贾伟平.中国人群有胰岛素抵抗的状况[J].国外医学.内分泌学分册,2002,22(4)：264-267.
[8]Lees,Min HG, Choi SH, etal.Central obesity as a risk factor for prostatic hyperplasia[J].Obesity,2006,14(1):172-9.
[9]J.Kellogg Parsons,H.Ballentine Cater, Alan W. Partin, etal.Metabolic Factors Associated with Benign Prostatic Hyperplasia[J].J Clin Endocrinol Metab,2006, 91(7):2562-2568.
[10]孙立军.前列腺体积与肥胖及血糖的相关性调查[J].中国误诊医学杂志,2007,7(27)：6704-6705.
[11]Weisman KM,Larijani GE,Goldstein MR.Relationship between Benign Prostatic Hyperplasia and history of Coronary artery disease in elderly men[J]. Pharamacotherapy,2000,20:383-386.
[12]梁飞宇,屈晓冰,赵晓昆.良性前列腺增生症和冠心病患者超敏C反应蛋白水平的检测[J].中国老年医学杂志,2007,1(27)：162-164.
[13]Jennifer L.St.Savver,Arunav Sarma,Debra J.Jacobson,etal.Associations between C-reactive protein and benign prostatic hyperplasia/lower urinary tract symptom outcomes in a population-based cohort[J].American Journal of epidemiology,2009,169(11):1281-90.
[14]Kozlowski R,Kershen RT,Siroky MB,etal. Chronic ischemia alters prostate structure and reactivity in rabbits[J].JUROL 2001,165(3):1019-1026.
[15]Hammarsten J,Hogstedt B.Hyperinsulinaemia as a risk factor for developing Benign Prostatic Hyperplasia[J].Eur Urol,2001,39(2):151-158.
[16]Hammarsten J,Hogstedt B,Holthuis N,etal.Components of the metabolic stndrome risk factors for the development of Benign Prostatic Hyperplasia[J].Prostate cancer Prostatic DIS,1998,1(3):157-162.
[17]李培军,张祥华,郭利君等.高脂血症与良性前列腺增生相关性的临床研究[J].中华外科杂志,2005,43(6)：387-389.
[18]沈文,李蓉,胡卫列.良性前列腺增生与动脉硬化症关系的初步探讨[J].医学临床研究,2007,24(4)：555-556.
[19]Padayatty SJ, Marcelli M, Shao TC, et al.Lavastatin-Induced Apoptosis in Prostate Stromal Cells[J].J Clin Endocrinol Metab.1997;82(5):1434-1439.
[20]Rees RW, Foxwell NA, Ralph DJ, et al. Y-27632, a Rhokinase inhibitor, inhibits proliferation and adrenergic contraction of prostatic smooth muscle cells[J].J Urol.2003;170:2517-22.
[21]Watts KL, Spiteri MA. Connective tissue growth factor expression and induction by transforming growth factor beta is abrogated by simvastatin via a Rho signaling mechanism[J].Am J Physiol Lung Cell Mol Physiol 2004;287:L1323-32.
[22]Escobart EL,Gomes-marcondes MC,Carvalho HF.Dietary fatty acid quality affects AR and PPARgamma levels and prostate growth[J].Prostate,2009,69(5):548-58.
[23]Hanefel DM,etal.Insuline secretion and insuline sensitivity patterns is different in isolated impaired glucose tolerance and impaired fasting glucose[J].Diabetes Care.2003,2:868-74.
[24]J.KelloggParsons,JaclynBergstrom,Elizabethconnor.Lipids,Lipoperteins,and risk of Benign prostatic hyperplasia in community dwelling men[J].BJU Int.2008,101(3):313-318.
[25]Wheatcroft, SB;Williams, IL; Shah, AM; Kearney, MT.Pathophysiological implications of insulin resistance on vascular endothelial function[J].Diabet Med. 2003;20:255-68.
[26]Berger AP,Bartsch QDeibl M. Atherosclerosis as a risk factor for Benign Prostatic Hyperplasia[J].BJU Int.2006,98:1038-1042.
[27]黄延焱,卢晓喆,俞茂华.老年代谢综合征患者血胰岛素样生长因子1与代谢综合征的关系[J].中华老年医学杂志,2006,25(7)：519-21.
[28]Steven E.Oliver,Barney Barrass,David J.Gunnell,etal.Serum insulin-like factors-II positively associated with serum prostate-specific antigen in middle-aged men without evidence of prostate cancer[J].Cancer Epidemiol.Biomarkers prev,2004,13:163.
[29]Mc Connell JD, Roehrborn CG,Bautista OM,etal.The long-term effect of doxazosin, finasteride,and combination therapy on the clinical progression of benign prostatic hyperplasia[J].N Engl J Med,2003,349(25):2387-2398.
[30]Wang W, Bergh A, Damber JE Chronic inflammation in BPH is associated with focal upregulation of cyclo-oxygenase-2, Bd-2 and cell proliferation in glandular epithelium[J].Prostate,2004,61:60-72
[31]Nandeesha H,Koher BC,Dorairajan LN,etal.Hyperinsulinemia and dyslipidemia in non-diabetic Benigne Prostata hyperplasie[J].Clin chim Acta,2006,370:89-93.
[32]Ozden C,Ozdal OL,Urqancioqiu Qetal.The correlation between metabolic synderom and prostatic growth in patients with Benigne Prostatahyperplasie[J].Eur Urol,2007,51:199-203.
[1].Michael k Brawer.Best of the 2009 AUA annuall meeting.Rev urol 2009;11(2):82-107.
[2].梁飞宇,屈晓冰,赵晓昆.炎症与良性前列腺增生症[J].国外医学.老年医学分册,2005,26(5)：193-196.
[3].陆再英,钟南山.内科学[M].北京：人民卫生出版社,2008,第七版.831.
[4].National Health and Nutrition Examination Survey (NHANES):National center for Health Statistics.[accessed February 2007]. http://www.cdc.gov/nchs/nhanes.htm
[5].Bjorn Hildrum, Arnstein Mykletun, Torstein Hole,etal. Age-specific prevalence of the metabolic syndrome defined by the International Diabetes Federation and the National Cholesterol Education Program the Norwegian HUNT 2 Study. BMC Public Health 2007,7:220-223.
[6].屈晓冰,谢景超,赵晓昆.良性前列腺增生症和冠心病的关系研究现状[J].中华老年医学杂志,2004,23(1)：46-47。
[7].Nandeesha H,Koher BC,Dorairajan LN,etal.Hyperinsulinemia and dyslipidemia in non-diabetic Benigne Prostata hyperplasie[J].Clin chim Acta,2006,370:89-93.
[8].Ozden C,Ozdal OL,Urqancioqiu Qetal.The correlation between metabolic synderom and prostatic growth in patients with Benigne Prostatahyperplasie[J].Eur Urol,2007,51:199-203.
[9].]Michel MC,HeemannU, SchumacherH,etal.Association of hypertension with symptoms of benign prostatichyperplasia[J].Jurol,2004,172:1390-3.
[10]Kevi NT,Mcvary,Alfred rademaker,etal.Autonomic nervous system overtactivity in men with lower urinary tract symptoms secondary to benign prostatic hyperplasia[J].The Journal of urology,2005,174:1327-1333.
[11]郭利君,张祥华,李培军等.高血压对良性前列腺增生组织中血管新生影响的研究[J].中华医学杂志,2005,9：606-609.
[12]Gunther Wennemuth, Gerhard Aumuller.Angiotensin Ⅱ-mediated Calcium signals and mitogenesis in human prostate stromal cell line hpcps[J].Br J pharmacol,2005144(1):3-10.
[13]Weisman KM,Larijani GE,Goldstein MR.Relationship between Benign Prostatic Hyperplasia and history of Coronary artery disease in elderly men[J]. Pharamacotherapy,2000,20:383-386.
[14].梁飞宇,屈晓冰,赵晓昆.良性前列腺增生症和冠心病患者超敏C反应蛋白水平的检测[J].中国老年医学杂志,2007,1(27)：162-164.
[15].Jennifer L.St.Savver,Arunav Sarma,Debra J.Jacobson,etal.Associations between C-reactive protein and benign prostatic hyperplasia/lower urinary tract symptom outcomes in a population-based cohort[J].American Journal of epidemiology, 2009,169(11):1281-90.
[16]Kozlowski R,Kershen RT,Siroky MB,etal.Chronic ischemia alters prostate structure and reactivity in rabbits[J].JUROL 2001,165(3):1019-1026.
[17].Hammarsten J,Hogstedt B.Hyperinsulinaemia as a risk factor for developing Benign Prostatic Hyperplasia[J].Eur Urol,2001,39(2):151-158.
[18]Hammarsten J,Hogstedt B,Holthuis N,etal.Components of the metabolic stndrome risk factors for the development of Benign Prostatic
Hyperplasia[J].Prostate cancer Prostatic DIS,1998,1(3):157-162.
[19].李培军,张祥华,郭利君等.高脂血症与良性前列腺增生相关性的临床研究[J].中华外科杂志,2005,43(6)：387-389.
[20]沈文,李蓉,胡卫列.良性前列腺增生与动脉硬化症关系的初步探讨[J].医学临床研究,2007,24(4)：555-556.
[21]Padayatty SJ, Marcelli M, Shao TC, et al Lavastatin-Induced Apoptosis in Prostate Stromal Cells[J].J Clin Endocrinol Metab.1997;82(5):1434-1439.
[22]Rees RW, Foxwell NA, Ralph DJ, et al.Y-27632, a Rhokinase inhibitor, inhibits proliferation and adrenergic contraction of prostatic smooth muscle cells[J].J Urol.2003;170:2517-22.
[23]Watts KL, Spiteri MA. Connective tissue growth factor expression and induction by transforming growth factor beta is abrogated by simvastatin via a Rho signaling mechanism[J]. Am J Physiol Lung Cell Mol Physiol 2004;287:L1323-32.
[24]Escobart EL,Gomes-marcondes MC,Carvalho HF.Dietary fatty acid quality affects AR and PPARgamma levels and prostate growth[J].Prostate, 2009,69(5):548-58.
[25].Cohen PGBenign prostatic hyperplasia:the hypogondal-obesity-prostate connection[J].Med hypotheses,2009,73(2):142-3.
[26]J.Kellogg Parsons,H.Ballentine Cater,Alan W.Partin,etal.Metabolic Factors Associated with Benign Prostatic Hyperplasia[J].J Clin Endocrinol Metab, 2006,91(7):2562-2568.
[27]Lees,Min HG, Choi SH,etal.Central obesity as a risk factor for prostatic hyperplasia[J].Obesity,2006,14(l):172-9.
[28]孙立军.前列腺体积与肥胖及血糖的相关性调查[J].中国误诊医学杂志,2007,7(27)：6704-6705.
[29].Gupta A,GUPTAS,Pavuk M,etal.Anthoropometric and Metabolic factors and risk of Benign Prostat hyperplasie:a prospective cohort study of Air Force Veterans[J].Ur logy,2006,68:1198-205.
[30].Wheatcroft, SB;Williams, IL; Shah, AM; Kearney, MT. Pathophysiological implications of insulin resistance on vascular endothelial function[J].Diabet Med. 2003;20:255-68.
[31]Berger AP,Bartsch G,Deibl M. Atherosclerosis as a risk factor for Benign Prostatic Hyperplasia. BJU Int.2006,98:1038-1042.
[32]黄延焱,卢晓喆,俞茂华.老年代谢综合征患者血胰岛素样生长因子-1与代谢综合征的关系.中华老年医学杂志,2006,25(7)：519-21.
[33].Steven E.Oliver,Bamey Barrass,David J.Gunnell,etal.Serum insulin-like factors-II positively associated with serum prostate-specific antigen in middle-aged men without evidence of prostate cancer.Cancer Epidemiol.Biomarkers prev,2004,13:163.
[34]Demirtunc Refik, Duman, Dursun,etal. Effects of Doxazosin and Amlodipine on Mean platelet volume and serum serotonin level in patients with Metabolic Syndrome:A Randomised controlled study. Clinical Drug Investigation.2007,27(6):435-441.
[35]马妮娜,沈璐华.氯沙坦对高血糖合并高血压患者胰岛素敏感性的影响.中国全科医学,2008,11：2019-2020.