ABSTRACT
Our aim was to study the association between menstrual cycle characteristics, the use of female hormones and urinary incontinence (UI) in an age-stratified random population sample of 2158 premenopausal women who answered a questionnaire on urinary incontinence. Episodes of UI during 1997 were reported by 18.3% and one or more episodes of UI the preceding year by 3.9%. Based on multiple logistic regression, self-reported UI the day before answering the questionnaire was found to be associated with current hormone use for menstrual disorders (OR 2.7, 95% CI 1.2-6.6), a recent decrease in bleeding duration (OR 2.2, 95% CI 1.3-3.7), being on days 11-15 before the expected end of the menstrual cycle the preceding day (OR 2.6, 95% CI 1.3-5.0), and with general UI risk factors, i.e. vaginal childbirth, childhood enuresis, BMI >/=530 and exposure to abdominal and/or gynecologic surgery. The findings are in accordance with a hypothesis of hormonal variation being a risk indicator of UI in premenopausal women.
Subject(s)
Contraceptives, Oral, Hormonal , Menstrual Cycle , Premenopause , Urinary Incontinence/physiopathology , Adult , Female , Humans , Logistic Models , Risk Factors , Urinary Incontinence/epidemiology , Urinary Incontinence/etiologyABSTRACT
In a population sample, the period prevalence of urinary incontinence (UI) during pregnancy was found to be 19.9% and 24.1% among 352 nulliparous and 290 primiparous women, respectively. The first UI episode ever was experienced by 16.7% and 7.0% during the two last trimesters of the first and second pregnancies, respectively. None of the pregnancy-specific risk factors, such as emesis and birthweight, was significantly associated with UI during pregnancy. Previous UI was a significant risk factor for period prevalent UI during pregnancy, explaining 34% and 83% of pregnancy UI for the nulliparous and the primiparous, respectively. The present data suggest pregnancy UI not to be provoked by the mere onset of pregnancy, but by increasing hormonal concentrations or local tissue changes caused by hormones, whereas there was no support for a theory based on increasing pressure on the bladder caused by the weight of the fetus.
