Interstitial Cystitis/Painful Bladder Syndrome

Alis Kolter Panzera, MSN, CRNP

Disclosures

Urol Nurs. 2007;27(1):13-19. 

In This Article

Pathology

Although the exact cause of PBS/IC is still unknown, several theories exist. No single theory has been proven to be the cause in all cases; however, many consider PBS/IC to be multifactorial in nature. One popular hypothesis is that the bladder lining (epithelium) is deficient and therefore permeable to urinary irritants (Parsons, 1996a). This theory has been expanded to state that the bladder epithelial glycocalyx is deficient. In a normal bladder, large, negatively charged molecules called glycoproteins and glycosaminoglycans (GAG) line the epithelium and provide an impermeable barrier. A defect in the GAG layer allows leakage and absorption of urinary solutes to occur; the major solute being potassium. Ongoing exposure of the bladder wall to potassium causes inflammation, tissue irritation and injury, mast cell degranulation, and sensory nerve depolarization (see Figure 1). This process results in symptoms associated with PBS/IC including urinary frequency, urgency, and pain (Parsons, 2003). Recent studies suggest that mast cells, containing histamine-rich granules, are involved in a variety of neuroinflammatory diseases (Theoharides & Cochrane, 2004) Mast cell activation and the subsequent histamine release can be stimulated by acetylcholine, stress, and hormonal fluctuations which may, in turn, play a role in the flares and seasonal symptoms that often occur with PBS/IC (Stanford, 2001).

Figure 1.

Role of GAG Layer in IC: Defective Urothelial Barrier.

An alternate hypothesis is that an initial insult to the bladder occurs (for example, a urinary tract infection), which excites sensory nerves located in the bladder wall. This excitation triggers an inflammatory response, or neurogenic inflammation. This in turn releases the neuropeptide substance P, causing the release of mast-cell mediators, histamines, leukotrienes (resulting in local inflammation), cell and tissue damage, and fibrosis (Elbadawi, 1997). Ultimately, there is a wind-up of the nervous system with neuroplasticity (c-fibers) and visceral allodynia, and pain beyond the bladder occurs (Butrick, 2003).

PBS/IC has also been theorized to be an autoimmune condition because some clinical features resemble a dysregulation of the immune system. Examples include the chronicity, the exacerbations and remissions, and response to immunosuppressants seen in PBS/IC (Sant, 2002). It also appears that PBS/IC may have a yet unexplained association with autoimmune diseases and pain syndromes such as vulvar vestibulitis, fibromyalgia, Hashimoto's thyroiditis, and irritable bowel syndrome (Myers & Arya, 2000; Ochs & Tan, 1997).

Although numerous underlying causes have been proposed and investigated, none fully explain all the manifestations of this disorder. Most experts agree that PBS/IC is a heterogeneous clinical syndrome that may be the consequence of several different pathophysiologic processes (Bradley & Singh, 2000). A multifactorial etiology may also explain the difficulty in objectively defining, diagnosing, and treating PBS/IC.

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