Abstract

You have accessJournal of UrologyBladder and Urethra: Anatomy, Physiology and Pharmacology II1 Apr 2015MP21-14 UROTHELIAL DYSFUNCTION IN DIABETIC PATIENTS WITH OVERACTIVE BLADDER Chung-Cheng Wang, Jing-Hui Lin, and Hann-Chorng Kuo Chung-Cheng WangChung-Cheng Wang More articles by this author , Jing-Hui LinJing-Hui Lin 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.2015.02.966AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Diabetes mellitus (DM) and overactive bladder (OAB) are common health problems that markedly increase the incidence and prevalence with advancing age. Epidemiological study has showed that DM is an independent factor for OAB. The pathophysiology of diabetic bladder dysfunction is complex and multifactorial diseases. Recent studies have focused mainly on detrusor, smooth muscle, bladder vasculature and innervation, whereas the effect of DM on the urothelium is rarely known. This study explored the urothelial dysfunction and suburothelial inflammation in DM patients with OAB compared with OAB non-diabetic patients and controls based on the immunohistochemistry study. METHODS Junction protein E-cadherin, tryptase (to assess mast cell activation) and TUNEL (to assess urothelial apoptosis) were performed in bladder tissues from 19 OAB diabetic patients, 14 OAB non-diabetic patients and 10 controls. The fluorescence intensity of E-cadherin was measured using the ImageJ method. The percentage of apoptotic cells, proliferated cells and activated mast cells were measured and quantified as positive cells per area unit (4 µm2). RESULTS Immunofluorescence showed a significantly lower distribution of E-cadherin in OAB bladder tissue compared with that of control patients (Table 1). However, E-cadherin in OAB diabetic patients and OAB non-diabetic patients were similar (22.2±15.1 and 24.9±17.1, p=0.72). The tryptase signal was significantly stronger and TUNEL staining revealed a significantly higher number of apoptotic cells in the OAB bladder tissues than those of control patients. But, the differences of tryptase signal (23.3±7.6 and 19.6±5.0, p=0.16) and TUNEL staining (5.2±5.6 and 5.6±4.7, p=0.60) were not significant between OAB diabetic patients and OAB non-diabetic patients. Clinical parameters including Hba1c, DM duration, DM treatment and serum creatinine did not correlate with E-cadherin, tryptase signal or TUNEL staining. CONCLUSIONS Our result suggests that OAB patients have increased cell apoptosis, increased mast cell activity and impaired bladder barrier function. However, Diabetes itself doesnot increase the severity of cell apoptosis and bladder inflammation. Table 1. Immunofluorescence data of controls, OAB patients with and without DM Control (N=10) OAB without DM (N=14) OAB with DM (N=19) P-value P* value P** value E-cadherin 42.7±20.3 24.9±17.1 22.2±15.1 0.04 0.01 0.72 Tryptase 3.99±3.38 19.6±5.04 23.3±7.58 <0.001 <0.001 0.16 TUNEL 0.73±0.97 5.62±4.71 5.21±5.63 0.008 0.09 0.6 ZO-1 21.5±6.4 6.69±5.02 11.2±7.25 0.02 0.65 0.05 DM: Diabetes mellitus; OAB: overactive bladder; ZO-1: zonulaoccludents 1 © 2015 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 193Issue 4SApril 2015Page: e238 Advertisement Copyright & Permissions© 2015 by American Urological Association Education and Research, Inc.MetricsAuthor Information Chung-Cheng Wang More articles by this author Jing-Hui Lin More articles by this author Hann-Chorng Kuo More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

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