Pd25-12 Two Bladder-Centric Phenotypic Subgroups Within Interstitial Cystitis/Bladder Pain Syndrome Patients With Low Bladder Capacity

You have accessJournal of UrologyInfections/Inflammation/Cystic Disease of the Genitourinary Tract: Interstitial Cystitis (PD25)1 May 2024PD25-12 TWO BLADDER-CENTRIC PHENOTYPIC SUBGROUPS WITHIN INTERSTITIAL CYSTITIS/BLADDER PAIN SYNDROME PATIENTS WITH LOW BLADDER CAPACITY Raymond Xu, Dylan Wolff, Trang Simon, Sarah Wachtman, Robert Evans, Gopal Badlani, and Stephen Walker Raymond XuRaymond Xu , Dylan WolffDylan Wolff , Trang SimonTrang Simon , Sarah WachtmanSarah Wachtman , Robert EvansRobert Evans , Gopal BadlaniGopal Badlani , and Stephen WalkerStephen Walker View All Author Informationhttps://doi.org/10.1097/01.JU.0001008584.88541.ff.12AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: The underlying pathophysiology behind a bladder-centric phenotype in interstitial cystitis/bladder pain syndrome (IC/BPS) is poorly understood. Given that Hunner lesions (HL) are a predominant feature of the bladder-centric phenotype, as is a low anesthetic bladder capacity (BC), the objective of this study was to determine the contribution of HL to gene expression differences in bladder mucosa from low BC patients. METHODS: Gene expression profiles were measured in mucosal bladder biopsies from women with IC/BPS (N=22) and a low anesthetic BC (≤ 400cc); biopsy samples from non-IC/BPS patients (N=16) served as controls. Low BC IC/BPS samples were further stratified into HL positive (HL+; N=8) and HL negative (HL-; N=14). Total RNA was extracted from all biopsy tissues and gene expression profiles were generated using the Nanostring nCounter Fibrosis Panel, comprised of 770 genes related to inflammation and fibrosis. Differentially expressed genes (DEG) were identified between each of the two IC/BPS subgroups, compared to controls. Comparison of these two DEG lists was used to identify differential gene expression common to all low BC patients, as well as genes uniquely associated with either the HL+ or HL- phenotype. RESULTS: There was significant overlap (86 genes) between DEGs in HL+ and HL- groups. The HL+ subgroup had 186 unique DEGs associated with active inflammation and fibrotic pathways including TGF-β signaling. In contrast, the HL- group had 28 unique DEG's which were associated primarily with fibrotic pathways including WNT/β-catenin signaling. These data are summarized in Table 1. CONCLUSIONS: Regardless of Hunner lesion status, IC/BPS patients with a low BC bladder-centric phenotype exhibit significant differential gene expression in pathways involved in fibrosis. HL+ patients exhibit a gene expression profile that is suggestive of a significantly active inflammatory state. These results suggest that distinct pathophysiologic mechanisms may underlie these two similar, but distinct, bladder-centric IC/BPS subgroups. Source of Funding: NIDDK 1R01DK124599-01 © 2024 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 211Issue 5SMay 2024Page: e541 Advertisement Copyright & Permissions© 2024 by American Urological Association Education and Research, Inc.Metrics Author Information Raymond Xu More articles by this author Dylan Wolff More articles by this author Trang Simon More articles by this author Sarah Wachtman More articles by this author Robert Evans More articles by this author Gopal Badlani More articles by this author Stephen Walker More articles by this author Expand All Advertisement PDF downloadLoading ...