Urinary incontinence in women

Norton, Peggy; Brubaker, Linda

doi:10.1016/s0140-6736(06)67925-7

Cited by 419 publications

(334 citation statements)

References 125 publications

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“…[19][20][21][22] Obesity, particularly in the abdominal area, may cause incontinence through increased intra-abdominal pressure. 23,24 Given rising childhood and adolescent obesity, 25 and as high body mass index (BMI) is likely to persist over the life course, important questions remain regarding the influence of weight trajectories, in terms of the duration or timing of overweight/obese status, on urinary incontinence.…”

Section: Introductionmentioning

confidence: 99%

Body weight through adult life and risk of urinary incontinence in middle-aged women: results from a British prospective cohort

et al. 2008

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Objectives: To determine whether the onset and duration of being overweight or obese are associated with symptoms of urinary incontinence. Design: Nationally representative cohort study. Subjects: A total of 1201 women followed-up since their birth in 1946 and annually from 48 to 54 years. Measurements: The body mass index (BMI) at the age of 20, 26, 36 and 43, and symptoms of stress, urge and severe incontinence at seven consecutive years from age 48 to 54. Results: In each year from age 48 to 54, almost half (46-49%) reported symptoms of stress incontinence, urge incontinence rose from 22 to 25% and severe incontinence from 8 to 11%. At the age of 20, 26, 36 and 43, BMI was positively associated with stress symptoms and severe incontinence in midlife. BMI transition was found to have accumulation effects on symptoms of severe incontinence; women who were overweight/obese since age 20 years were more likely to report severe incontinence than women whose BMI remained below 25 kg/m 2 (odds ratio (95% confidence interval): 2.30 (1.36-3.93)) or who became overweight or obese at 43 years (1.85 (0.97-3.51)). These relationships existed beyond the effects of aging, childhood enuresis, kidney infection, childbirth characteristics, menopause, educational attainment, general practitioner consultations and smoking status. BMI was not associated with symptoms of urge incontinence. Conclusions: Across adult life, higher BMI for women was linked with subsequent symptoms of stress and severe incontinence in midlife; those who were overweight or obese since early in adult life more than doubled their risk of severe incontinence. Women, and especially young women, should be encouraged to keep their weight in a normal range throughout adult life.

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Section: Introductionmentioning

confidence: 99%

Body weight through adult life and risk of urinary incontinence in middle-aged women: results from a British prospective cohort

et al. 2008

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“…UP TO 50% OF WOMEN ARE REPORTED to suffer from urinary incontinence or overactive bladder (22). Lower urinary tract function is intimately interrelated to physiological estradiol (E 2 ) variations, as illustrated by the transitory increase in urethral pressure at the peak of E 2 secretion at midcycle (32), its gradual increase during pregnancy (15), and the prevalence of urinary bothers after menopause (6).…”

mentioning

confidence: 99%

Estradiol increases urethral tone through the local inhibition of neuronal nitric oxide synthase expression

Gamé¹,

Allard²,

Escourrou³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Gamé X, Allard J, Escourrou G, Gourdy P, Tack I, Rischmann P, Arnal J-F, Malavaud B. Estradiol increases urethral tone through the local inhibition of neuronal nitric oxide synthase expression. Am J Physiol Regul Integr Comp Physiol 294: R851-R857, 2008. First published January 9, 2008 doi:10.1152/ajpregu.00467.2007.-Estrogens are known to modulate lower urinary tract (LUT) trophicity and neuronal nitric oxide synthase (nNOS) expression in several organs. The aim of this study was to explore the effects of endogenous and supraestrus levels of 17␤-estradiol (E2) on LUT and urethral nNOS expression and function. LUT function and histology and urethral nNOS expression were studied in adult female mice subjected either to sham surgery, surgical castration, or castration plus chronic E2 supplementation (80 g ⅐ kg Ϫ1 ⅐ day Ϫ1 , i.e., pregnancy level). The micturition pattern was profoundly altered by long-term supraestrus levels of E2 with decreased frequency paralleled by increased residual volumes higher than those of ovariectomized mice. Urethral resistance was increased twofold in E2-treated mice, with no structural changes in urethra, supporting a pure tonic mechanism. Acute nNOS inhibition by 7-nitroindazole decreased frequency and increased residual volumes in ovariectomized mice but had no additive effect on the micturition pattern of long-term supraestrus mice, showing that longterm supraestrus E2 levels and acute inhibition of nNOS activity had similar functional effects. Finally, E2 decreased urethral nNOS expression in ovariectomized mice. Long-term supraestrus levels of E2 increased urethral tone through inhibition of nNOS expression, whereas physiological levels of E2 had no effect. estrogen; neurourology; urethra UP TO 50% OF WOMEN ARE REPORTED to suffer from urinary incontinence or overactive bladder (22). Lower urinary tract function is intimately interrelated to physiological estradiol (E 2 ) variations, as illustrated by the transitory increase in urethral pressure at the peak of E 2 secretion at midcycle (32), its gradual increase during pregnancy (15), and the prevalence of urinary bothers after menopause (6).In woman, estrogen therapy has been shown to prevent postmenopausal cystitis (8) and urinary atrophy and overactive bladder (6). Moreover, clinical data suggest that estrogens partly improve lower urinary tract functioning by improving local trophicity (13). However, regarding urinary incontinence, estrogens either failed to show any effect on stress urinary incontinence (24) or actually increased (in a large multicentric study) the incidence and severity of all types of urinary incontinence (12).The intricate relationship between urine storage and micturition involves a reciprocal balance in the muscle tone of bladder and urethra, which are under spinal and supraspinal controls. Autonomic regulation of the lower urinary tract physiology is driven by all three components of the autonomic nervous system. Nitric oxide (NO), the key neurotransmitter of the nonadrenergic, noncholinergic nerves ...

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“…23 However, what we know about UI are conclusions obtained from studies and observations on late stage of the condition. 24 ICS has set a crucial distinction on the UI condition, symptoms, signs and urodynamic diagnosis which are shown in Table 1. 24 Table 1: Terminology for urinary incontinence.…”

Section: Prevalence and Classificationmentioning

confidence: 99%