良性前列腺增生与肥胖相关性研究

目的 探讨良性前列腺增生(BPH)与肥胖或中心性肥胖的关系.方法 选择老年男性患者109例,分为BPH组(59例)和非BPH组(50例),检测血清前列腺特异性抗原(PSA)及性激素、血脂等相关生化指标;测量身高、体质量、腰围等物理指标;经腹超声测量前列腺体积,并随访至少3次.结果 肥胖组BPH患病率(73.33%)及超体质量组BPH患病率(64.28%)均较正常组(26.67%)增高(x2分别为13.991,6.836,均P＜0.002),中心性肥胖组BPH患病率(71.19%)较非中心性肥胖组(36.00%)明显增高(x2=12.156,P＜0.001);BPH组腰围身高指数、腰围、体质量、体质指数、臀围0.56±0.05、(93.6±8.8)cm、(72.6±9.7)kg、(25.7±3.4)kg/m2和(100.2±6.6)cm]明显高于非前列腺增生组0.52±0.06、(87.0±10.1)cm、(64.5±9.3)kg、(23.1±2.9)kg/m2和(95.6±8.1)cm](t分别=-3.30,-3.65,-4.38,-4.17,-3.18,均P＜0.01);肥胖组前列腺总体积高于正常组(40.8±23.5)ml与(20.1±6.1)ml,t=-2.82,P＜0.01),中心性肥胖组明显高于非中心性肥胖组(42.8±25.6)ml与(26.9±11.2)ml],(t=-3.93,P＜0.001);中心性肥胖组雌二醇/总睾酮(E2/TT)比值、胰岛素抵抗指数(HOMA-IR)(9.06±4.36、2.81±2.80)高于非中心性肥胖组(7.38±3.11、1.55±0.76)(t分别=-2.02,-4.24,均P＜0.05),血清TT、性激素结合蛋白(SHBG)则低于非中心性肥胖组(4.54±1.54)nmol/L对(5.20±1.54)nmol/L,(45.8±17.24)nmol/L对(59.6±26.09)nmol/L,均t分别=2.16,2.79,P＜0.05];Logistic逐步回归分析表明,腰围是影响前列腺体积的主要因素(x2=19.52,P=0.000);前列腺总体积的年增长率在肥胖组同样高于正常组(7.14±8.09)ml与(1.49±5.14)ml,t=-2.19,P＜0.05],在中心性肥胖组明显高于非中心性肥胖组(7.96±13.81)ml与(1.35±5.36)m1,t=-3.28,P＜0.01];中心性肥胖组的前列腺特异性抗原密度(PSAD)低于非中心性肥胖组(0.048±0.036对0.090±0.093,t=2.02,P＜0.05);肥胖组的PSAD低于正常组(0.052±0.039与0.091±0.080,t=3.13,P＜0.01).结论 BPH的发生与肥胖,尤其是中心性肥胖密切相关,其机制可能与肥胖患者体内性激素失衡、生长激素-胰岛素样生长因子轴的紊乱有关.

Abstract：

Objective To explore the relationship between benign prostatic hyperplasia (BPH)and obesity. Methods The 109 elder men were divided into two groups: BPH group (n=59) and non-BPH group (n= 50). The blood samples were collected for the detections of prostate specific antigen (PSA), triglyceride (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), fasting blood glucose (FBG), insulin,androgen, estrogen, sex hormone binding globulin (SHBG) and dehydroepiandrosterone(DHEA).The anthropometric indexes including height, body weigh, waist circumference (WC), hip circumference (HC), systolic blood pressure (SBP), diastolic blood pressure (DBP), body mass index (BMI), waist-to-height ratio (WHtR) and waist-to-hip ratio (WHR) were measured and calculated. The total prostate volume (TPV) were measured by transabdominal ultrasonography three times at least. Results The morbidity rate of BPH was significantly higher in obesity group and over weight group than in health control group (73.33% and 64.28% vs. 26. 67%, x2 = 13. 991 and 6. 836, both P＜0. 002). So was in central obesity group versus in health control group (71.19% vs.36.00%, x2 =12. 156, P＜0. 001). The waist-height index, waist circumference, body weight, BMI and hip circumference were significantly higher in BPH group than in non-BPH group (0. 56±0. 05)vs. (0.52±0.06), (93. 6±8.8) cm vs. (87.0± 10. 1) cm; (72.6±9.7) kg vs. (64.5±9.3) kg;(25.7±3.4) kg/m2 vs. (23.1±2.9) kg/m2; (100.2±6.6) cm vs. (95.6±8. 1) cm; t=-3.3, -3. 65, -4.38, -4. 17 and -3.18, respectively, all P＜0.01]. The TPV was higher in obesity groupthan in normal group (40.8± 23.5 ) ml vs. (20. 1 ± 6.1 ) ml, t = - 2.82, P＜ 0. 002] and obviously higher in central obesity group than in non-central obesity group (42.8±25.6)ml vs. (26. 9±11.2)ml, t= -3. 93, P＜0. 001]. The ratio of E2/TT and HOMA-IR were higher in central obesity group (9. 06±4.36) and (2.81 ±2. 80)] than in non-central obesity group (7. 38±3. 11) and (1. 55±0.76), t= -2.02 and -4.24, both P＜0. 05]. Inversely, the TT and SHBG were lower in central obesity group than in non-central obesity group (4.54 ± 1.54) nmol/L vs. (5.20 ± 1.54) nmol/L,(45.8± 17.24) nmol/L vs. (59.6 ± 26.09) nmol/L, t = 2.16 and 2.79, both P＜ 0. 05]. Logistic regression analysis showed that waist circumference was a major factor affecting TPV (x2= 19.52, P=0. 000). The annual growth rate of TPV was significantly higher in obesity group and central obesity group than in health control group (7. 14±8. 09)ml vs. (1. 49±5.14)ml, (7. 96±13.81)mlvs. (1. 35±5.36)ml, t=-2.19 and -3.28, both P＜0. 05]; The PSAD was significantly lower in central obesity group than in health control group (0. 048±0. 036) vs. (0. 090±0. 093), t=2.02, P＜0. 05], and lower in obesity group than in health control group (0. 052 ±0. 039) vs. (0. 091 ±0. 080), t= 3. 13, P＜0. 01]. Conclusions The occurrence of BPH is closely related to obesity,especially central obesity. Its mechanism may be related to sex hormone imbalance and the GH/IGF-1 axis disorders in obese patients.

Study on the association between benign prostatic hyperplasia and obesity

Objective To explore the relationship between benign prostatic hyperplasia (BPH)and obesity. Methods The 109 elder men were divided into two groups: BPH group (n=59) and non-BPH group (n= 50). The blood samples were collected for the detections of prostate specific antigen (PSA), triglyceride (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), fasting blood glucose (FBG), insulin,androgen, estrogen, sex hormone binding globulin (SHBG) and dehydroepiandrosterone(DHEA).The anthropometric indexes including height, body weigh, waist circumference (WC), hip circumference (HC), systolic blood pressure (SBP), diastolic blood pressure (DBP), body mass index (BMI), waist-to-height ratio (WHtR) and waist-to-hip ratio (WHR) were measured and calculated. The total prostate volume (TPV) were measured by transabdominal ultrasonography three times at least. Results The morbidity rate of BPH was significantly higher in obesity group and over weight group than in health control group (73.33% and 64.28% vs. 26. 67%, x2 = 13. 991 and 6. 836, both P＜0. 002). So was in central obesity group versus in health control group (71.19% vs.36.00%, x2 =12. 156, P＜0. 001). The waist-height index, waist circumference, body weight, BMI and hip circumference were significantly higher in BPH group than in non-BPH group (0. 56±0. 05)vs. (0.52±0.06), (93. 6±8.8) cm vs. (87.0± 10. 1) cm; (72.6±9.7) kg vs. (64.5±9.3) kg;(25.7±3.4) kg/m2 vs. (23.1±2.9) kg/m2; (100.2±6.6) cm vs. (95.6±8. 1) cm; t=-3.3, -3. 65, -4.38, -4. 17 and -3.18, respectively, all P＜0.01]. The TPV was higher in obesity groupthan in normal group (40.8± 23.5 ) ml vs. (20. 1 ± 6.1 ) ml, t = - 2.82, P＜ 0. 002] and obviously higher in central obesity group than in non-central obesity group (42.8±25.6)ml vs. (26. 9±11.2)ml, t= -3. 93, P＜0. 001]. The ratio of E2/TT and HOMA-IR were higher in central obesity group (9. 06±4.36) and (2.81 ±2. 80)] than in non-central obesity group (7. 38±3. 11) and (1. 55±0.76), t= -2.02 and -4.24, both P＜0. 05]. Inversely, the TT and SHBG were lower in central obesity group than in non-central obesity group (4.54 ± 1.54) nmol/L vs. (5.20 ± 1.54) nmol/L,(45.8± 17.24) nmol/L vs. (59.6 ± 26.09) nmol/L, t = 2.16 and 2.79, both P＜ 0. 05]. Logistic regression analysis showed that waist circumference was a major factor affecting TPV (x2= 19.52, P=0. 000). The annual growth rate of TPV was significantly higher in obesity group and central obesity group than in health control group (7. 14±8. 09)ml vs. (1. 49±5.14)ml, (7. 96±13.81)mlvs. (1. 35±5.36)ml, t=-2.19 and -3.28, both P＜0. 05]; The PSAD was significantly lower in central obesity group than in health control group (0. 048±0. 036) vs. (0. 090±0. 093), t=2.02, P＜0. 05], and lower in obesity group than in health control group (0. 052 ±0. 039) vs. (0. 091 ±0. 080), t= 3. 13, P＜0. 01]. Conclusions The occurrence of BPH is closely related to obesity,especially central obesity. Its mechanism may be related to sex hormone imbalance and the GH/IGF-1 axis disorders in obese patients.