Abstract

The standard treatment for overactive bladder starts with patient education and behavior therapies, followed by antimuscarinic agents. For patients with urgency urinary incontinence refractory to antimuscarinic therapy, currently both American Urological Association (AUA) and European Association of Urology (EAU) guidelines suggested that intravesical injection of botulinum toxin A should be offered. The mechanism of botulinum toxin A includes inhibition of vesicular release of neurotransmitters and the axonal expression of capsaicin and purinergic receptors in the suburothelium, as well as attenuation of central sensitization. Multiple randomized, placebo-controlled trials demonstrated that botulinum toxin A to be an effective treatment for patients with refractory idiopathic or neurogenic detrusor overactivity. The urinary incontinence episodes, maximum cystometric capacity, and maximum detrusor pressure were improved greater by botulinum toxin A compared to placebo. The adverse effects of botulinum toxin A, such as urinary retention and urinary tract infection, were primarily localized to the lower urinary tract. Therefore, botulinum toxin A offers an effective treatment option for patients with refractory overactive bladder.

Highlights

  • IntroductionOveractive bladder (OAB) is a clinical diagnosis defined by the International Continence

  • Overactive bladder (OAB) is a clinical diagnosis defined by the International ContinenceSociety as “urgency, with or without urge incontinence, usually with frequency and nocturia” [1].The overall prevalence of OAB was 12%–17% in the general population and it poses a great impact on daily activities and quality of life (QOL) [2,3,4,5]

  • Both American Urological Association (AUA) and European Association of Urology (EAU) guidelines suggested that intravesical injection of botulinum toxin A (BoNT/A) should be offered to patients with urgency urinary incontinence (UUI) refractory to antimuscarinic and beta3-adrenoceptor agonist therapy, and the FDA approved dose was 100 U of BoNT/A for idiopathic detrusor overactivity (IDO) and 200 U for neurogenic detrusor overactivity (NDO) [7,14]

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Summary

Introduction

Overactive bladder (OAB) is a clinical diagnosis defined by the International Continence. Antimuscarinic agents are widely used but associated with adverse effects such as dry mouth, constipation, and blurred vision [7,8]. Both AUA and EAU guidelines suggested that intravesical injection of BoNT/A should be offered to patients with urgency urinary incontinence (UUI) refractory to antimuscarinic and beta3-adrenoceptor agonist therapy, and the FDA approved dose was 100 U of BoNT/A for idiopathic detrusor overactivity (IDO) and 200 U for neurogenic detrusor overactivity (NDO) [7,14]. In this article we will review the mechanism of BoNT/A in the treatment of OAB and evaluate randomized, placebo-controlled trials for the applicability of BoNT/A in IDO and NDO

Mechanism of Action
Idiopathic Detruosr Overacitity
Injection Method
Neurogenic Detruosr Overacitity
Adverse Events
Findings
Conclusions
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