MP31-05 UROTHELIAL DYSFUNCTION AND CHRONIC INFLAMMATION IN PATIENTS WITH BLADDER OUTLET OBSTRUCTION AND DIFFERENT BLADDER DYSFUNCTION AND DIFFERENT BLADDER OUTLET OBSTRUCTION DEGREE

Abstract

You have accessJournal of UrologyBenign Prostatic Hyperplasia: Basic Research1 Apr 2015MP31-05 UROTHELIAL DYSFUNCTION AND CHRONIC INFLAMMATION IN PATIENTS WITH BLADDER OUTLET OBSTRUCTION AND DIFFERENT BLADDER DYSFUNCTION AND DIFFERENT BLADDER OUTLET OBSTRUCTION DEGREE Chung-Cheng Wang, Jia-Hui Chang, and Hann-Chorng Kuo Chung-Cheng WangChung-Cheng Wang More articles by this author , Jia-Hui ChangJia-Hui Chang More articles by this author , and Hann-Chorng KuoHann-Chorng Kuo More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2015.02.1360AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES The underlying mechanisms responsible for the bladder dysfunction in bladder outlet obstruction (BOO) remain poorly understood. The purpose of this study is to investigate the urothelial dysfunction and chronic inflammation in patients with BOO. METHODS In this prospective study, we enrolled those patients with LUTS. Based on their VUDS performances, it was categorized into 4 sub-groups: control, BOO with detrusor overactivity (DO), BOO with Detrusor underactivity (DU) and BOO with hypersenstivity bladder (HSB). Bladder tissues taken from these patients were analyzed. Immunofluorescence (IF) staining of junction protein E-cadherin, mast cell, TUNEL and zonula occludens 1(ZO-1) were performed. RESULTS A total of 44 men were enrolled in this study. There were 34 patients presented with BOO (DO: 12, DU: 11 and HSB: 11). The expression and cellular location of E-cadherin, mast cell, TUNEL and ZO-1 were illustrated in Fig. 1. The distribution of E-cadherin is significantly reduced in BOO with DU (8.37±9.50) (p<0.000), whereas exhibit highest number of TUNEL (3.60±3.43) (p<0.021). The tryptase signal in BOO with DO is significantly increased (19.05±6.14) (p<0.000)(Table 1). All these parameters do not show positive correlation with Abrams-Griffiths (AG) number. Increasing number of E-cadherin is associated with Pdet and Qmax. Tryptase/ mast cell is positively associated with FSF. CONCLUSIONS In this study, we have shown that LUTS secondary to BOO are associated with chronic urothelial inflammation and urothelial dysfunction. DU induced by BOO is associated with significant urothelial defection. This may imply that the loss of functional protein and urothelial cell apoptosis might contribute to the pathophysiology of bladder dysfunction in BOO. Table 1. The numbers of E-cadherin, tryptase, TUNEL and ZO-1 in different sub-groups Normal (N=10) BOO+DO (N=12) BOO+DU (N=11) BOO+HSB (N=11) P value E-cadherin 27.70±10.42 11.16±7.65 8.37±9.50 27.23±13.94 0.000 Tryptase (mast cell) 4.16±2.68 19.05±6.14 11.67±11.10 12.91±4.51 0.000 TUNEL 0.85±1.31 3.45±2.55 3.60±3.43 1.39±1.79 0.021 ZO-1 6.90±1.82 7.43±1.65 9.08±5.82 7.14±3.40 0.490 BOO: bladder outlet obstruction; DO: detrusor overactivity; DU: detrusor underactivity; HSB: hypersenstivity bladder; ZO-1: zonula occludens 1 © 2015 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 193Issue 4SApril 2015Page: e357 Advertisement Copyright & Permissions© 2015 by American Urological Association Education and Research, Inc.MetricsAuthor Information Chung-Cheng Wang More articles by this author Jia-Hui Chang More articles by this author Hann-Chorng Kuo More articles by this author Expand All Advertisement Advertisement PDF DownloadLoading ...