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Can Botulinum Toxin A Still Have a Role in Treatment of Lower Urinary Tract Symptoms/Benign Prostatic Hyperplasia Through Inhibition of Chronic Prostatic Inflammation?
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Promise and the Pharmacological Mechanism of Botulinum Toxin A in Chronic Prostatitis Syndrome

Department of Urology 1, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung 83301, Taiwan
Department of Urology, University of Pittsburgh School of Medicine2, Pittsburgh, PA 15213, USA
Author to whom correspondence should be addressed.
Toxins 2019, 11(10), 586;
Received: 14 August 2019 / Revised: 4 October 2019 / Accepted: 9 October 2019 / Published: 11 October 2019
Chronic prostatitis/chronic pelvic pain syndrome (CP/ CPPS) has a negative impact on the quality of life, and its etiology still remains unknown. Although many treatment protocols have been evaluated in CP/CPPS, the outcomes have usually been disappointing. Botulinum neurotoxin A (BoNT-A), produced from Clostridium botulinum, has been widely used to lower urinary tract dysfunctions such as detrusor sphincter dyssynergia, refractory overactive bladder, interstitial cystitis/bladder pain syndromes, benign prostatic hyperplasia, and CP/ CPPS in urology. Here, we review the published evidence from animal models to clinical studies for inferring the mechanism of action underlying the therapeutic efficacy of BoNT in CP/CPPS. Animal studies demonstrated that BoNT-A, a potent inhibitor of neuroexocytosis, impacts the release of sensory neurotransmitters and inflammatory mediators. This pharmacological action of BoNT-A showed promise of relieving the pain of CP/CPPS in placebo-controlled and open-label BoNT-A and has the potential to serve as an adjunct treatment for achieving better treatment outcomes in CP/CPPS patients. View Full-Text
Keywords: Botulinum toxin; chronic prostatitis Botulinum toxin; chronic prostatitis
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Chen, C.-H.; Tyagi, P.; Chuang, Y.-C. Promise and the Pharmacological Mechanism of Botulinum Toxin A in Chronic Prostatitis Syndrome. Toxins 2019, 11, 586.

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