Department of Urology, University Hospital of Rennes, Rennes, France.
Department of Urology, Sheffield Teaching Hospitals, Sheffield, UK.
Eur Urol. 2019 Jun;75(6):988-1000. doi: 10.1016/j.eururo.2019.02.038. Epub 2019 Mar 26.
Current literature suggests that several pathophysiological factors and mechanisms might be responsible for the nonspecific symptom complex of overactive bladder (OAB).
To provide a comprehensive analysis of the potential pathophysiology underlying detrusor overactivity (DO) and OAB.
A PubMed-based literature search was conducted in April 2018, to identify randomised controlled trials, prospective and retrospective series, animal model studies, and reviews.
OAB is a nonspecific storage symptom complex with poorly defined pathophysiology. OAB was historically thought to be caused by DO, which was either "myogenic" (urgency initiated from autonomous contraction of the detrusor muscle) or "neurogenic" (urgency signalled from the central nervous system, which initiates a detrusor contraction). Patients with OAB are often found to not have objective evidence of DO on urodynamic studies; therefore, alternative mechanisms for the development of OAB have been postulated. Increasing evidence on the role of urothelium/suburothelium and bladder afferent signalling arose in the early 2000s, emphasising an afferent "urotheliogenic" hypothesis, namely, that urgency is initiated from the urothelium/suburothelium. The urethra has also recently been regarded as a possible afferent origin of OAB-the "urethrogenic" hypothesis. Several other pathophysiological factors have been implicated, including metabolic syndrome, affective disorders, sex hormone deficiency, urinary microbiota, gastrointestinal functional disorders, and subclinical autonomic nervous system dysfunctions. These various possible mechanisms should be considered as contributing to diagnostic and treatment algorithms.
There is a temptation to label OAB as "idiopathic" without obvious causation, given the poorly understood nature of its pathophysiology. OAB should be seen as a complex, multifactorial symptom syndrome, resulting from multiple potential pathophysiological mechanisms. Identification of the underlying causes on an individual basis may lead to the definition of OAB phenotypes, paving the way for personalised medical care.
Overactive bladder (OAB) is a storage symptom syndrome with multiple possible causes. Identification of the mechanisms causing a patient to experience OAB symptoms may help tailor treatment to individual patients and improve outcomes.
目前的文献表明,多种病理生理因素和机制可能与膀胱过度活动症(OAB)的非特异性症状有关。
全面分析逼尿肌过度活动(DO)和 OAB 的潜在病理生理学。
2018 年 4 月,基于 PubMed 的文献检索,以确定随机对照试验、前瞻性和回顾性系列、动物模型研究和综述。
OAB 是一种具有定义不明确病理生理学的非特异性储尿症状综合征。OAB 历史上被认为是由 DO 引起的,DO 要么是“肌源性”(逼尿肌的自主收缩引起的紧迫性),要么是“神经源性”(中枢神经系统发出信号引起逼尿肌收缩)。在尿动力学研究中,许多 OAB 患者并未发现客观的 DO 证据;因此,已经提出了 OAB 发展的替代机制。在 21 世纪初,越来越多的证据表明尿路上皮/下皮和膀胱传入信号的作用,强调了传入的“尿路上皮源性”假说,即紧迫性是由尿路上皮/下皮发起的。最近,尿道也被认为是 OAB 的可能传入起源——“尿道源假说”。其他几个病理生理因素也被牵涉其中,包括代谢综合征、情感障碍、性激素缺乏、尿微生物群、胃肠道功能障碍和亚临床自主神经系统功能障碍。这些不同的可能机制应被视为有助于诊断和治疗算法。
鉴于其病理生理学性质尚不清楚,将 OAB 标记为“特发性”而无明显病因,这很诱人。OAB 应被视为一种复杂的、多因素的症状综合征,由多种潜在的病理生理机制引起。在个体基础上确定潜在病因可能会导致 OAB 表型的定义,为个性化医疗铺平道路。
膀胱过度活动症(OAB)是一种具有多种潜在原因的储尿症状综合征。确定导致患者出现 OAB 症状的机制可能有助于针对个体患者量身定制治疗方法并改善治疗效果。