良性前列腺增生与肥胖相关性研究
량성전렬선증생여비반상관성연구
Study on the association between benign prostatic hyperplasia and obesity
  • 万方数据
    中华老年医学杂志 중화노년의학잡지
    Chinese Journal of Geriatrics
    2011年 3期 211-215 ,共5页

    毕夫景%林青%赵咏桔

    필부경%림청%조영길

    前列腺增生%肥胖症 前列腺增生%肥胖癥
    전렬선증생%비반증
    Prostatic hyperplasia%Obesity
    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.
    목적 탐토량성전렬선증생(BPH)여비반혹중심성비반적관계.방법 선택노년남성환자109례,분위BPH조(59례)화비BPH조(50례),검측혈청전렬선특이성항원(PSA)급성격소、혈지등상관생화지표;측량신고、체질량、요위등물리지표;경복초성측량전렬선체적,병수방지소3차.결과 비반조BPH환병솔(73.33%)급초체질량조BPH환병솔(64.28%)균교정상조(26.67%)증고(x2분별위13.991,6.836,균P＜0.002),중심성비반조BPH환병솔(71.19%)교비중심성비반조(36.00%)명현증고(x2=12.156,P＜0.001);BPH조요위신고지수、요위、체질량、체질지수、둔위[0.56±0.05、(93.6±8.8)cm、(72.6±9.7)kg、(25.7±3.4)kg/m2화(100.2±6.6)cm]명현고우비전렬선증생조[0.52±0.06、(87.0±10.1)cm、(64.5±9.3)kg、(23.1±2.9)kg/m2화(95.6±8.1)cm](t분별=-3.30,-3.65,-4.38,-4.17,-3.18,균P＜0.01);비반조전렬선총체적고우정상조[(40.8±23.5)ml여(20.1±6.1)ml,t=-2.82,P＜0.01),중심성비반조명현고우비중심성비반조[(42.8±25.6)ml여(26.9±11.2)ml],(t=-3.93,P＜0.001);중심성비반조자이순/총고동(E2/TT)비치、이도소저항지수(HOMA-IR)(9.06±4.36、2.81±2.80)고우비중심성비반조(7.38±3.11、1.55±0.76)(t분별=-2.02,-4.24,균P＜0.05),혈청TT、성격소결합단백(SHBG)칙저우비중심성비반조[(4.54±1.54)nmol/L대(5.20±1.54)nmol/L,(45.8±17.24)nmol/L대(59.6±26.09)nmol/L,균t분별=2.16,2.79,P＜0.05];Logistic축보회귀분석표명,요위시영향전렬선체적적주요인소(x2=19.52,P=0.000);전렬선총체적적년증장솔재비반조동양고우정상조[(7.14±8.09)ml여(1.49±5.14)ml,t=-2.19,P＜0.05],재중심성비반조명현고우비중심성비반조[(7.96±13.81)ml여(1.35±5.36)m1,t=-3.28,P＜0.01];중심성비반조적전렬선특이성항원밀도(PSAD)저우비중심성비반조(0.048±0.036대0.090±0.093,t=2.02,P＜0.05);비반조적PSAD저우정상조(0.052±0.039여0.091±0.080,t=3.13,P＜0.01).결론 BPH적발생여비반,우기시중심성비반밀절상관,기궤제가능여비반환자체내성격소실형、생장격소-이도소양생장인자축적문란유관.
    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.
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