A Comprehensive Review of Overactive Bladder Pathophysiology: On the Way to Tailored Treatment.
Gonadal Steroid Hormones
/ deficiency
Humans
Metabolic Syndrome
/ metabolism
Microbiota
Mood Disorders
/ psychology
Muscle, Smooth
/ innervation
Urethra
/ physiopathology
Urinary Bladder
/ physiopathology
Urinary Bladder, Neurogenic
/ physiopathology
Urinary Bladder, Overactive
/ metabolism
Urodynamics
Urothelium
/ physiopathology
Detrusor overactivity
Overactive bladder
Urinary incontinence
Urodynamics
Journal
European urology
ISSN: 1873-7560
Titre abrégé: Eur Urol
Pays: Switzerland
ID NLM: 7512719
Informations de publication
Date de publication:
06 2019
06 2019
Historique:
received:
06
10
2018
accepted:
28
02
2019
pubmed:
30
3
2019
medline:
6
10
2020
entrez:
30
3
2019
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 30922690
pii: S0302-2838(19)30186-1
doi: 10.1016/j.eururo.2019.02.038
pii:
doi:
Substances chimiques
Gonadal Steroid Hormones
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
988-1000Commentaires et corrections
Type : CommentIn
Type : CommentIn
Type : CommentIn
Type : CommentIn
Informations de copyright
Copyright © 2019 European Association of Urology. Published by Elsevier B.V. All rights reserved.