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Abstract

Interstitial cystitis (IC) is a disease of mystery. This disease causes increased bladder sensitivity, decreased bladder capacity, and a painful bladder, whether empty or full. Recently, most physicians have concluded that IC is an inflammatory disease that can progress if not treated. However, the effects of treatment aiming at protection of the urothelium have usually been limited. 1 Nickel J.C. Barkin J. Forrest J. et al. Randomized, double-blind, dose-ranging study of pentosan polysulfate sodium for interstitial cystitis. Urology. 2005; 65: 654-658 Abstract Full Text Full Text PDF PubMed Scopus (141) Google Scholar Botulinum toxin type A (BTX-A) injection provides a novel treatment of IC, decreasing bladder sensitivity by reducing the sensory receptors, such as P2X3 and transient receptor potential vanilloid 1, 2 Apostolidis A. Papat R. Yiangou Y. et al. Decreased sensory receptors P2X3 and TRPV1 in suburothelial nerve fibers following intradetrusor injection of botulinum A toxin for human detrusor overactivity. J Urol. 2005; 173: 977-983 Abstract Full Text Full Text PDF Scopus (359) Google Scholar increasing bladder capacity by paralyzing the detrusor, 3 Kuo H.C. Urodynamic evidence of effectiveness of botulinum A toxin injection in treatment of detrusor overactivity refractory to anticholinergic agents. Urology. 2004; 63: 868-872 Abstract Full Text Full Text PDF PubMed Scopus (173) Google Scholar and decreasing bladder pain by suppressing the release of calcitonin gene-related peptide and other neuropeptides. 4 Rapp D.E. Turk K.W. Bales G.T. et al. Botulinum toxin type A inhibits calcitonin gene-related peptide release from isolated rat bladder. J Urol. 2006; 175: 1138-1142 Abstract Full Text Full Text PDF PubMed Scopus (143) Google Scholar The actual mechanism of effective BTX-A treatment has not been elucidated. It is possibly through inhibition of the inflammatory process. This letter-to-editor points out the underlying molecular mechanism of BTX-A affects on the proinflammatory pathway, which further modulates the secretion of nerve growth factor from the bladder wall. By inhibiting the inflammatory process in the suburothelium or urothelium, BTX-A not only might decrease the apoptosis of urothelial cells, but also could reestablish the integrity of the injured urothelium. However, because the inflammatory process in IC might involve the corresponding spinal cords, 5 Cui M. Aoki K.R. Botulinum toxin type A (BTX-A) reduces inflammatory pain in the rat formalin model. Cephalalgia. 2000; 20: 414-418 Crossref Google Scholar the therapeutic result of BTX-A on IC through detrusor injection cannot last for long. Repeated BTX-A injections might provide long-term desensitization to the inflammation of the central nervous system in IC and a better treatment outcome. Intravesical Botulinum Toxin A Injections Plus Hydrodistension Can Reduce Nerve Growth Factor Production and Control Bladder Pain in Interstitial Cystitis: A Molecular MechanismUrologyVol. 72Issue 2PreviewI read with great interest the article by Liu and colleagues.1 This work shows that botulinum toxin markedly reduces nerve growth factor (NGF) compared with a placebo. I would like to complete the discussion of Liu and coworkers1 by suggesting a major route through which botulinum toxin could reduce NGF. Full-Text PDF