Hammarsten Jan, Högstedt Benkt
Department of Urology, Halland, Varberg Hospital, Varberg, Sweden.
Scand J Urol Nephrol. 2002;36(5):330-8. doi: 10.1080/003655902320783827.
Whether there is an association between the development of benign prostatic hyperplasia (BPH) and clinical prostate cancer is controversial. The present report tests the hypothesis of an association between BPH growth and the development of clinical prostate cancer by examining stage, grade and PSA-level in men with recently discovered clinical prostate cancer with slow or fast-growing BPH. If the hypothesis is true, men with fast-growing BPH would have a more advanced clinical prostate cancer.
Two hundred and twenty patients in whom a clinical prostate cancer was diagnosed were consecutively included. The prevalence of atherosclerotic disease, non-insulin-dependent diabetes mellitus (NIDDM) or treated hypertension was provided by the respective patient's medical history. Tallness, body weight, waist measurement, hip measurement and blood pressure were determined. The body mass index (BMI) and waist/hip ratio (WHR) were calculated. Blood samples were drawn to determine triglycerides, total cholesterol, HDL-cholesterol, LDL-cholesterol, uric acid, ALAT and the fasting plasma insulin level. The prostate gland volume was measured using transrectal ultrasound. The annual BPH growth rate was calculated, assuming that the total prostate gland volume was 20 mL at the patient age of forty. The prostate cancer diagnosis was established using the technique of transrectal ultrasound-guided automatic needle biopsy of the prostate.
Men with clinical prostate cancer, PSA <50 ng/mL, and with fast-growing BPH had a higher systolic (p = 0.009) and diastolic (p = 0.020) blood pressure, were taller (p < 0.001) and more obese, as determined by body weight (p < 0.001), BMI (p = 0.005), waist measurement (p < 0.001) and hip measurement (p = 0.003). They also had a higher fasting plasma insulin level (p = 0.014) and a lower HDL-cholesterol level (p = 0.067) than men with slow-growing BPH. Moreover, men with clinical prostate cancer, PSA <50 ng/mL, and fast-growing BPH had more pronounced clinical prostate cancer, as measured by grade (p = 0.029) and PSA-level (p = 0.016), than men with slow-growing BPH. In the total material, including men with clinical prostate cancer, PSA >/=50 ng/mL, men with fast-growing BPH also had a higher prevalence of NIDDM (p = 0.039) and a borderline statistical significance for higher stage (p = 0.09) than men with slow-growing BPH. The BPH growth rate was significantly associated with the clinical prostate cancer grade (p = 0.018) and PSA-level (p = 0.002) but not with the clinical cancer stage in a multivariate statistical analysis.
This report confirms findings in previous studies that fast-growing BPH is a risk factor for NIDDM, hypertension, tallness, obesity, dyslipidaemia and hyperinsulinaemia. The present report extends this list of risk factors to include atherosclerotic disease manifestations, hyperuricaemia and higher ALAT levels. The study suggests that fast-growing BPH is a risk factor for developing clinical prostate cancer and, thus, supports the hypothesis of an association between the development of BPH and clinical prostate cancer. The study generates the hypothesis that clinical prostate cancer is a component of the metabolic syndrome and that insulin is a promoter of clinical prostate cancer.
良性前列腺增生(BPH)的发展与临床前列腺癌之间是否存在关联存在争议。本报告通过检查近期发现临床前列腺癌且伴有缓慢或快速生长的BPH的男性患者的分期、分级和前列腺特异性抗原(PSA)水平,来检验BPH生长与临床前列腺癌发展之间存在关联的假设。如果该假设成立,那么快速生长的BPH男性患者的临床前列腺癌病情会更严重。
连续纳入220例被诊断为临床前列腺癌的患者。根据各自患者的病史提供动脉粥样硬化疾病、非胰岛素依赖型糖尿病(NIDDM)或经治疗的高血压的患病率。测量身高、体重、腰围、臀围和血压。计算体重指数(BMI)和腰臀比(WHR)。采集血样以测定甘油三酯、总胆固醇、高密度脂蛋白胆固醇(HDL-胆固醇)、低密度脂蛋白胆固醇(LDL-胆固醇)、尿酸、丙氨酸转氨酶(ALAT)和空腹血浆胰岛素水平。使用经直肠超声测量前列腺体积。假设患者40岁时前列腺总体积为20 mL,计算BPH的年生长率。采用经直肠超声引导下前列腺自动穿刺活检技术进行前列腺癌诊断。
临床前列腺癌、PSA<50 ng/mL且伴有快速生长的BPH的男性患者,收缩压(p = 0.009)和舒张压(p = 0.020)更高,身高更高(p < 0.001),且更肥胖,这由体重(p < 0.001)、BMI(p = 0.005)、腰围(p < 0.001)和臀围(p = 0.003)确定。与伴有缓慢生长的BPH的男性患者相比,他们的空腹血浆胰岛素水平更高(p = 0.014),HDL-胆固醇水平更低(p = 0.067)。此外,临床前列腺癌、PSA<50 ng/mL且伴有快速生长的BPH的男性患者,根据分级(p = 0.029)和PSA水平(p = 0.016),其临床前列腺癌比伴有缓慢生长的BPH的男性患者更严重。在包括临床前列腺癌、PSA≥50 ng/mL的男性患者的整个样本中,伴有快速生长的BPH的男性患者NIDDM的患病率也更高(p = 0.039),且与伴有缓慢生长的BPH的男性患者相比,在分期更高方面有边缘统计学意义(p = 0.09)。在多变量统计分析中,BPH生长率与临床前列腺癌分级(p = 0.018)和PSA水平(p = 0.002)显著相关,但与临床癌症分期无关。
本报告证实了先前研究中的发现,即快速生长的BPH是NIDDM、高血压、身高较高、肥胖、血脂异常和高胰岛素血症的危险因素。本报告将该危险因素列表扩展至包括动脉粥样硬化疾病表现、高尿酸血症和更高的ALAT水平。该研究表明,快速生长的BPH是发生临床前列腺癌的危险因素,因此支持了BPH发展与临床前列腺癌之间存在关联的假设。该研究提出了一个假设,即临床前列腺癌是代谢综合征的一个组成部分,且胰岛素是临床前列腺癌的一个促进因素。