Androgens and bladder outlet obstruction: a correlation with pressure-flow variables in a preliminary study

OBJECTIVES To determine the relationship between androgens, lower urinary tract symptoms (LUTS) and urodynamic variables of bladder outlet obstruction (BOO) in patients with LUTS/benign prostatic hyperplasia (BPH), as androgens are important in the pathogenesis of LUTS. PATIENTS AND METHODS Twenty-five men with symptomatic BPH were enrolled in the study and had a complete urodynamic investigation, establishing BOO. Age, prostate-specific antigen level, prostate volume and postvoid residual volume were recorded and the International Prostate Symptom Score (IPSS) was estimated. Detrusor pressure at maximum flow (P(det)Q(max)), at urethral closure (PdetCl, the pressure at the end of urinary flow) and maximum detrusor pressure (P-detmax) was recorded, while detrusor overactivity (DO) was noted when present. Blood samples were collected to measure total testosterone (T), and free T (FT) was calculated. Patients were grouped according to FT levels as low (< 72 pg/mL) and normal (FT >= 72 pg/mL). RESULTS Ten patients had a low FT level, with a mean (SD) of 54.3 (16.5) pg/mL, and 15 a normal level of FT, of 90.5 (11) pg/mL. FT was negatively correlated with PdetCl, and P(det)Q(max); the mean PdetCl and P(det)Q(max) differed significantly between patients with low and normal FT levels. Fourteen patients had DO and they had significantly lower levels of FT than those with no DO. All patients with a FT level of < 60 pg/mL had DO, and the presence of instability differed significantly from the rest of the group. CONCLUSIONS Low T levels in clinical BOO correlated negatively with PdetCl and P(det)Q(max), while promoting DO. Androgen seems to have an ameliorating role in lower urinary tract function

The effect of alpha-blocker treatment on bladder hypoxia inducible factor-1 alpha regulation during lower urinary tract obstruction

AIMS: To determine whether α1-blocker treatment, in chronic bladder outlet obstruction (BOO), influences bladder tissue ischemia. MATERIALS AND METHODS: This prospective study included 60 patients with BOO, of which 40 were under α1-blocker medication and 20 without treatment. Patients underwent transurethral resection of the prostate (TURP) or suprapubic prostatectomy (SPP). Ten patients with non-muscle invasive bladder cancer underwent transurethral resection of the bladder tumor and served as the control group. Tissue specimens were immunohistochemically stained for hypoxia inducible factor-1α (HIF-1α). RESULTS: Bladder tissue from obstructed subjects showed high immunoreactivity to HIF-1α. The specimens from the control group, showed no or weak, mainly cytoplasmic immunoreactivity to HIF-1α. Patients under α -blocker treatment did not differ in the number of HIF-1α positive cells compared to subjects with no treatment (median number 86.8 [20-150] and 88.6 [0-175], respectively) (p > 0.05). The lowest bladder pressure at which HIF-1α was up regulated, was detected at detrusor pressure Qmax (PdetQmax) = 60 cm H2O. CONCLUSIONS: Treatment with α-blockers in obstructed patients considered as non-responders, does not result in HIF-1α down regulation, thus bladder continues to be under chronic stress

The Effect of Alpha-Blocker Treatment on Bladder Hypoxia Inducible Factor-1 Alpha Regulation during Lower Urinary Tract Obstruction

Aims: To determine whether alpha 1-blocker treatment, in chronic bladder outlet obstruction (BOO), influences bladder tissue ischemia. Materials and Methods: This prospective study included 60 patients with BOO, of which 40 were under alpha 1-blocker medication and 20 without treatment. Patients underwent transurethral resection of the prostate (TURF) or suprapubic prostatectomy (SPP). Ten patients with non-muscle invasive bladder cancer underwent transurethral resection of the bladder tumor and served as the control group. Tissue specimens were immunohistochemically stained for hypoxia inducible factor-1 alpha (HIF-1 alpha). Results: Bladder tissue from obstructed subjects showed high immunoreactivity to HIF-1 alpha. The specimens from the control group, showed no or weak, mainly cytoplasmic immunoreactivity to HIF-1 alpha. Patients under alpha -blocker treatment did not differ in the number of HIF-1 alpha positive cells compared to subjects with no treatment (median number 86.8 [20-150] and 88.6 [0-175], respectively) (p > 0.05). The lowest bladder pressure at which H1F-1 alpha was up regulated, was detected at detnisor pressure Qmax (PdetQmax) = 60 cm H2O. Conclusions: Treatment with alpha-blockers in obstructed patients considered as non-responders, does not result in HIF-1 alpha down regulation, thus bladder continues to be under chronic stress