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Intravesical Therapy and Its Evolution Over Three Decades, A European View

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Bladder Pain Syndrome – An Evolution
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Abstract

The finding of an effective and specific therapy for IC/BPS remains a challenge because of the lack of a consensus regarding the causes and the inherent difficulties in the diagnosis. One of the last recent hypothesis is that IC/BPS could be pathophysiologically related to a disruption of the bladder mucosa surface layer with consequent loss of glycosaminoglycans (GAGs). This class of mucopolysaccharides has hydrorepellent properties and their alteration expose the urothelium to many urinary toxic agents (GAGs). The urothelium consist of three layers of cells [1–3] (basal, intermediate and apical or umbrella cells) This outer layer comprises the main impermeable and protective barrier against urine. The barrier function is comprised also of other defensive mechanism such as: tight junctions, uroplakin and a dense layer of glycosaminoglycan (GAG) on the apical surface. The removal of GAG layer causes loss of the apical cells within 24 h and leads to enhanced permeability. When these substances penetrate the bladder wall a chain is triggered in the submucosa. Here nerve terminals produce inflammatory mediators causing mast cell degranulation and histamine secretion with consequent vasodilatation and inflammatory exudate. The consequence of this inflammatory response is the stimulation of C fibers with mast cell activation and histamine release. This produce consequent bladder pain and release of neuropetides with a consequent damage to the mucosa and fibrosis of the submucosa [4–6].

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Correspondence to Mauro Cervigni .

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Cervigni, M. (2018). Intravesical Therapy and Its Evolution Over Three Decades, A European View. In: Hanno, P., Nordling, J., Staskin, D., Wein, A., Wyndaele, J. (eds) Bladder Pain Syndrome – An Evolution. Springer, Cham. https://doi.org/10.1007/978-3-319-61449-6_22

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  • DOI: https://doi.org/10.1007/978-3-319-61449-6_22

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