Urethral function and failure: A review of current knowledge of urethral closure mechanisms, how they vary, and how they are affected by life events.

Urethral function and failure: A review of current knowledge of urethral closure mechanisms, how they vary, and how they are affected by life events.
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DOI:
10.1002/nau.24760
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发表时间:
2021-11
影响因子:
2
通讯作者:
DeLancey JOL
DeLancey JOL
中科院分区:
医学3区
文献类型:
--
作者:
Pipitone F;Sadeghi Z;DeLancey JOL

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最近的证据表明尿道在引起压力性和急迫性尿失禁中的作用,需要对关于女性尿道功能和功能障碍的文献进行严格的评价。使用从文献中选择的包含影响尿道功能和失败因素的机械数据的文章进行证据评估。压力性尿失禁(SUI)患者的最大尿道闭合压(MUCP)比正常对照组低40%。来自5名女性的证据显示横纹肌/平滑肌、血管丛、结缔组织对MUCP的贡献相对相等。MUCP在相似年龄的个体中变化2倍,即使在未经生育的妇女中,每十年也下降15%。年龄解释了MUCP中57%的方差。这与横纹肌/平滑肌损失和神经密度降低平行。人们对影响每分钟和每十年压力变化的因素知之甚少。尚未研究结缔组织变化。在产后持续9个月的新发SUI中,MUCP比年龄和产次匹配的对照组低25%。纵向研究未显示阴道分娩后尿道功能的显著变化,这表明出生后尿道支持的变化可能会暴露预先存在的括约肌无力并导致SUI。支持损伤、先前存在的尿道无力和神经病变之间的相互作用机制尚不清楚。尿道功能衰竭是SUI的主要原因,也是UUI的一个促成因素;这可能解释了为什么混合症状在流行病学研究中占主导地位。尿道闭合不良的突出特征是尿道相关的横纹肌缺失和相似年龄女性之间的差异。然而,结缔组织的变化,血管功能和复杂的相互作用的因素知之甚少。
A critical appraisal of the literature regarding female urethral function and dysfunction is needed in light of recent evidence showing the urethra’s role in causing stress and urge urinary incontinence. An evidence assessment was conducted using selected articles from the literature that contained mechanistic data on factors affecting urethral function and failure. Maximal urethral closure pressure (MUCP) is 40% lower in stress urinary incontinence (SUI) than normal controls. Evidence from 5 women shows relatively equal contributions to MUCP from striated/smooth muscle, vascular-plexus, connective tissue. MUCP varies 2-fold in individuals of similar age and declines 15% per decade even in nulliparous women. Age explains 57% of variance in MUCP. This parallels with striated/smooth muscle loss and reduced nerve density. Factors influencing pressure variation minute-to-minute and decade-to-decade are poorly understood. Connective tissue changes have not been investigated. MUCP in de novo SUI persisting 9-months postpartum is 25% less than in age and parity matched controls. Longitudinal studies do not show significant changes in urethral function after vaginal birth suggesting that changes in urethral support from birth may unmask pre-existing sphincter weakness and precipitate SUI. Mechanisms of interaction between support injury, pre-existing urethral weakness and neuropathy are unclear. Urethral failure is the predominant cause of SUI and a contributing factor for UUI; potentially explaining why mixed symptoms predominate in epidemiological studies. Age-related striated muscle loss and differences between women of similar age are prominent features of poor urethral closure. Yet, connective tissue changes, vasculature function and complex interactions among factors are poorly understood.
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