Update on the Pathophysiology of Interstitial Cystitis /Bladder Pain Syndrome

Purpose of Review Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic, potentially debilitating condition characterized by lower urinary tract symptoms and pain perceived to be related to the bladder. The etiology of IC/BPS has been rigorously studied for more than a century, but remains unknown. IC/BPS comprises a wide variety of clinical phenotypes with different potential etiologies. Recently, the importance of IC/BPS subtyping has become recognized. In this review, we revisit current hypotheses on IC/BPS pathophysiology and discuss the most likely causes of IC/BPS according to current research. Recent Findings Recent histological and genomic analyses revealed that IC/BPS with Hunner lesions is a distinct inflammatory disorder characterized by epithelial denudation and frequent clonal expansion of infiltrating B cells, in association with biological processes involved in immune responses and infectious disease. Meanwhile, IC/BPS without Hunner lesions is an unrelated, non-inflammatory disorder with few histological changes, and which is potentially associated with systemic neurophysiological/endocrine abnormalities. Recent evidence has also cast doubt on the importance of features that have been conventionally considered significant in IC/BPS pathophysiology, such as mast cell infiltration or glomerulation. IC/BPS with Hunner lesions should be considered IC, and IC/BPS without Hunner lesions should be considered BPS. Clear and proper phenotyping of IC/BPS is necessary for the successful diagnosis and treatment of IC/BPS and to facilitate future research on IC/BPS pathophysiology.