Objective: To determine the validity coefficient of the total prostate gland volume as an expression of the transition zone (TZ) volume. To test the hypothesis of hyperinsulinaemia as a causal factor for the development of benign prostatic hyperplasia (BPH).
Patients and methods: Three hundred and seven consecutive patients with lower urinary tract symptoms were studied. A subgroup of 114 patients were tested with regard to the validity coefficient between the total prostate gland volume and the TZ volume. In the total material of 307 men, a BPH risk factor analysis was performed in which groups of men with the following conditions were related to the annual BPH growth rate: men without or with metabolic disease; men with different components of the metabolic syndrome, and men with low or high fasting plasma insulin values. The prostate gland volume and the TZ volume were determined using ultrasound. The presence of non-insulin-dependent diabetes mellitus (NIDDM) and treated hypertension was obtained from the patients' medical records. Data on blood pressure, waist and hip measurement, body height and weight were collected and body mass index and waist/hip ratio were calculated. Blood samples were drawn from fasting patients to determine the insulin and HDL-cholesterol values.
Results: In the subgroup of men subjected to measurement of both the total prostate gland volume and the TZ volume, the correlation coefficient between total prostate gland volume and the TZ volume was r.s. = 0.97 (p < 0.0001) which, thus, constituted the validity coefficient. The median annual BPH growth rate in the total group was 1.03 ml/year. The median annual BPH growth rate was faster in men with metabolic disease (p < 0.0001), NIDDM (p < 0.0001), treated hypertension (p < 0.0001), obesity (p < 0.0001) and dyslipidaemia (p < 0.0001) than in men without metabolic disease. Moreover, the annual BPH growth rate correlated positively with the diastolic blood pressure (r.s. = 0.27; p < 0.001), the BMI (r.s. = 0.22; p < 0.001) and four other expressions of obesity, and negatively with the HDL-cholesterol level (r.s. = -0.15; p < 0.001). The median annual BPH growth rate was faster in men with a high than in men with a low fasting plasma insulin level (p = 0.019). When the patients were divided into quartiles, the median annual BPH growth rate increased statistically significantly with increasing fasting plasma insulin levels. The fasting plasma insulin values correlated with the annual BPH growth rates (p = 0.009). When performing a multivariate analysis using the total prostate gland volume as dependent variable, fasting plasma insulin (p = 0.001) and age (p < 0.001) became statistically significant.
Conclusion: The results of the present report suggest that the total prostate gland volume constitutes a valid expression of BPH. The findings support the hypothesis that hyperinsulinaemia is causally related to the development of BPH and generate the hypothesis of an increased sympathetic nerve activity in men with BPH.