A hypothesis for the etiology of interstitial cystitis.

Abstract

Interstitial cystitis (IC) is a chronic inflammatory disease of the bladder wall. The etiology is obscure.18,19,35,44,47,56 Several theories for the etiology of IC have been proposed over the years, including infection,6,56 immunological etiology,1 leaky urothelium resulting from a deficiency of its surface coat of glycosaminoglycans,41,42 activated mast cells,6,49 and neurogenic etiology.6,17 However, none of these theories have been proven beyond doubt.6 The rapid onset of IC, its appearance in mid-life, and the absence of strong family association have suggested to us8–11 and many others6 that IC could be an acquired disease, possibly caused by injury. Recurrent exposure to bacterial infection, which is common in the bladder, has been proposed as a putative mechanism of injury.47,56 Earlier studies were based on the assumption that the sole avenue for the interaction of noxious agents with the bladder is exposure of terminally differentiated “umbrella” cells to agents in the lumen. However, mere exposure of the superficial layer to injury, such as bacterial infection, may not result in chronic changes in the urothelium. These terminally differentiated cells are often shed in response to infectious agents,2,38 and unexposed progenitors of urothelial cells located in the basal layer (stem cells) divide and re-epithelize the injured area.