ESPU Congress 2018 - Abstract Book

11 11–14 APRIL, 2018, HELSINKI, FINLAND CONCLUSIONS Our findings provide evidence of a broad range of histologic alterations of the exstrophic bladder. Persistent and partly progressing structural, inflammatory and proliferative changes are present in a substantial proportion of patients despite succesful repair in early infancy. Importantly, intestinal metaplasia, a potentially premalignant change, was not observed in any biopsy taken at primary bladder closure, but only years thereafter during subsequent procedures. Since the natural history of this lesion in the exstrophic bladder is unknown, these patients require lifelong surveillance. 13:33–13:36 S1-2 (PP) PERSISTENT UROTHELIAL DIFFERENTIATION CHANGES IN THE RECONSTRUCTED EXSTROPHIC BLADDER: A PRIMARY STRUCTURAL DEFICIT? Peter RUBENWOLF  1 , Fabian EDER  2 , Stefanie GOETZ  3 , Martin PROMM  4 and Wolfgang H. ROESCH  4 1) University Hospital Frankfurt, Urology, Frankfurt, GERMANY - 2) University Hospital Regensburg, Pathology, Regensburg, GERMANY - 3) University Hospital Regensburg, Urology, Regensburg, GERMANY - 4) University Hospital Regensburg, Pediatric Urology, Regenburg, GERMANY PURPOSE To investigate whether the urothelial differentiation changes observed in the unclosed bladder template persist after succesful delayed bladder closure in early infancy. MATERIAL AND METHODS Bladder biopsies from 34 children obtained during secondary reconstructive procedures were examined by immunohistochemistry for expression cytokeratin 20, cytokeratin 13, claudin 4 and uroplakin IIIa, all well characterised markers associated with the terminally differentiated urothelial phenotype (group 1). Findings were compared with both bladder tissues harvested at the time of primary delayed repair (group 2) and appropriate (non-exstrophy) controls (group 3). RESULTS 32 % of bladder specimen from children having previously undergone succesful primary bladder closure displayed a regular urothelial morphology including umbrella cells and a fully differentiated urothelial phenotype with regular expression of all 4 markers, as opposed to 4 % of bladders at the time of primary reconstruction. Detailed results are presented in Table 1. Group/Marker (regular expression, %) Cytokeratin 13 Cytokeratin 20 Claudin 4 Uroplakin IIIa Regular expression of all 4 markers Group 1: reconstructed bladder (n=34) 47 35 71 35 32 Group 2: unclosed bladder (n=32) 34 4 48 4 4 Group 3: controls (no exstrophy; n=16) 93 97 89 95 89 CONCLUSIONS Our finding provide prima facie evidence of persisting structural and phenotypic changes in two- thirds of exstrophic bladders despite early bladder closure. In accordance with current genetic findings, we hypothesize a primary genetically-determined structural and functional urothelial deficit alongside a maturational delay and acquired secondary changes due to inflammatory and me- chanical irritation of the unclosed urothelium. The translational value of our findings as regards the developemental potential of the bladder needs to be established in future studies.