Aims: The aims of this study were to investigate whether endogenous steroid hormones are (1) related to pathogenesis of stress urinary incontinence after menopause, (2) are related to severity of stress urinary incontinence, and (3) are related to prognostic parameters of stress urinary incontinence.
Methods: Twenty post-partum women with clinically diagnosed stress urinary incontinence and 20 age-matched postmenopausal women without stress urinary incontinence (control group) were evaluated. We compared urinary profile of the endogenous steroid hormones patients with stress urinary incontinence and controls, and between grade I and grade II of stress urinary incontinence. We also investigated the relationship between urinary profile of the endogenous steroid hormones and prognostic parameters of stress urinary incontinence (maximal urethral closure pressure, functional urethral length, Valsalva leak point pressure, cough leak point pressure, posterior urethrovesical angle, bladder neck descent, and stress urethral axis). The ages of the patients and those in the control group were 64.3 +/- 5.6 and 57.5 +/- 3.8 years old and the body mass indexes were 24.96 +/- 3.14 and 22.11 +/- 2.73 kg/m2 in patients and in normal subjects, respectively. Nine patients were grade I and 11 were grade II. Estrone and 17beta-estradiol only were detected in all subjects, regardless of control or patient group. It is noteworthy that there were no significant differences (P > 0.05) in the levels of estrone and 17beta-estradiol in the urine of postmenopausal normal subjects compared with in the urine of postmenopausal patients with urinary incontinence. E2/E1 ratio was not different between the two groups (P > 0.05). Among the objective steroids, DHEA, Delta4-dione, Delta5-diol, Te, DHT, 16alpha-DHT, 11-keto An, THDOC, and THB were not detected either in the urine of normal subjects and nor in the urine of the patients. After comparing androgen levels between normal subjects and patients, no significant differences (P>0.05) were detected, except for 5alpha-THB and 5alpha-THF. Neither 5alpha-THB or 5alpha-THF were detected in the patients' urine. Et/An (11beta-OH Et/11beta-OH An) concentration ratios were not significantly different between the two groups, either (P > 0.05). There were not significant differences of concentrations (micromol/g creatinine) of urinary steroids between grade I and grade II of stress urinary incontinence. Pregnanediol was significantly related to bladder neck descent in supine and sitting positions (R = 0.79, P = 0.01, and R = 0.73, P = 0.03, respectively), and pregnanetriol was significantly related to maximal urethral closure pressure and functional urethral length (R = 0.68, P = 0.04, and R = -0.79, P = 0.01, respectively). Androsterone was significantly related to bladder neck descent in supine and sitting positions (R = 0.68, P = 0.04, and R = 0.78, P = 0.01, respectively). 5-AT was significantly related to bladder neck descent in sitting position and stress urethral axis (R = 0.72, P = 0.03, and R = -0.71, P = 0.03). 11-keto Et was significantly related to bladder neck descent in supine and sitting positions and related to stress urethral axis (R = 0.82, P = 0.01, and R = 0.81, P = 0.01, R = -0.67, P = 0.04, respectively). THS was significantly related to bladder neck descent in supine and sitting positions and related to stress urethral axis (R = 0.76, P = 0.02, and R = 0.74, P = 0.02, R = -0.68, P = 0.04, respectively). THE was significantly related to bladder neck descent in sitting position (R = 0.67, P = 0.04).beta-Tetrahydrocortisol/alpha-tetrahydrocortisol (beta-THF/alpha-THF) and alpha-cortol were significantly related to maximal urethral closure pressure and functional urethral length (R = 0.74, P = 0.02, and R = -0.92, P = 0.01; R = 0.71, P = 0.36, and R = -0.87, P = 0.000, respectively). 17beta-estradiol (E2) was significantly related to bladder neck descent in supine position (R = -0.62, P = 0.04) and 17beta-estradiol/estrone (E2/E1) was significantly related to cough leak point pressure (R = 0.79, P = 0.01). In conclusion, the urinary concentrations of endogenous steroid metabolites in postmenopausal patients with stress urinary incontinence were not significantly different from normal patients and were not significantly different between grade I and grade II patients with stress urinary incontinence. Some endogenous steroid metabolites were positively or negatively significantly related to prognostic parameters of stress urinary incontinence.