Botulinum Toxin A and Lower Urinary Tract Dysfunction: Pathophysiology and Mechanisms of Action
Botulinum Toxin A and Lower Urinary Tract Dysfunction: Pathophysiology and Mechanisms of Action
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The use of onabotulinumtoxinA (BoNT-A) for the treatment of lower urinary tract diseases (LUTD) has increased markedly in recent years.The indications for BoNT-A treatment of LUTD now include neurogenic or idiopathic detrusor overactivity, interstitial cystitis/bladder pain AEG IDK84451IB - 83cm Induction Hob with Integrated Hood - Black - 942 150 636 syndrome and voiding dysfunction.The mechanisms of BoNT-A action on LUTDs affect many different aspects.Traditionally, the effects of BoNT-A were believed to be attributable to inhibition of acetylcholine release from the presynaptic efferent nerves at the neuromuscular junctions in the detrusor or urethral sphincter.BoNT-A injection in the bladder also regulated sensory nerve function by blocking neurotransmitter release and reducing receptor expression in the urothelium.
In addition, recent studies revealed an anti-inflammatory effect for BoNT-A.Substance P and nerve growth factor in the urine and bladder tissue decreased after BoNT-A injection.Mast cell activation in the bladder also decreased.BoNT-A-induced improvement of urothelium function plays an important mitigating role in bladder dysfunction.Vascular endothelial growth factor expression in urothelium decreased after BoNT-A injection, as did apoptosis.
Studies also revealed increased apoptosis in the prostate after BoNT-A injection.Although BoNT-A injection has been widely used to treat different LUTDs refractory to conventional treatment, currently, onabotulinumtoxinA has been proven effective only Figure Skating - Skates - Womens on urinary incontinence due to IDO and NDO in several large-scale clinical trials.The effects of onabotulinumtoxinA on other LUTDs such as interstitial cystitis, benign prostatic hyperplasia, dysfunctional voiding or detrusor sphincter dyssynergia have not been well demonstrated.