The aim of this study was to use a systematic schedule, including urodynamics, to describe the rate of coexisting overactive bladder (OB) in patients with bladder outlet obstruction (BOO) caused by benign prostatic hyperplasia (BPH). We also identified differences between the patients with pure BOO compared with those with BOO combined with OB (BOO + OB). One hundred and sixty-two men referred to our clinic due to LUTS were included. Patients with a history that might affect their bladder function were excluded. After cystometry and pressure-flow studies, the patients were divided into pure BOO and BOO + OB. Of the 162 men, 55% had pure BOO. BOO + OB was found in 45%. Age, s-PSA, voided volume, and obstruction grade differed significantly between the groups. The patients with BOO + OB were older, had a higher s-PSA, voided smaller volumes, and were more obstructed. We found no differences in TRUS-volume, Q-max, IPS score, or PVR. There was a strong association between OB and BOO, the percentage of OB increasing with increased obstruction. TRUS-volume, Q-max, IPS score, and PVR did not predict whether the patients had a combined BOO + OB or not. These findings indicate that BOO is a progressive disease, which in time causes pronounced obstruction and perhaps in itself contributes to the development of OB.
These data confirm that prostate volume and serum PSA concentration are significantly correlated and increase with advanced age. The correlations between uroflowmetry (Qmax) and age, prostate volume, serum PSA and IPSS were also significant. However, there was no relationship between symptoms and objective measures of BPE. The increase in different parameters of the severity of benign prostatic hyperplasia with advanced age is not continuous. The prostate volume alone is not useful in the estimation of disease severity.
The aetiology of benign prostatic hyperplasia (BPH) remains unclear. The objective of the present study was to test the insulin, oestradiol and metabolic syndrome hypotheses as promoters of BPH. The design was a risk factor analysis of BPH in which the total prostate gland volume was related to endocrine and anthropometric factors. The participants studied were 184 representative men, aged 72-76 years, residing in Gö teborg, Sweden. Using a multivariate analysis, BPH as measured by the total prostate gland volume correlated statistically significantly with fasting serum insulin (b ¼ 0.200, P ¼ 0.028), free oestradiol (b ¼ 0.233, P ¼ 0.008) and lean body mass (b ¼ 0.257, P ¼ 0.034). Insulin and free oestradiol appear to be independent risk factors for BPH, confirming both the insulin and the oestradiol hypotheses. Our findings also seem to confirm the metabolic syndrome hypothesis. The metabolic syndrome and its major endocrine aberration, hyperinsulinaemia, are possible primary events in BPH.
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