Interstitial Cystitis (cont.)
Melissa Conrad Stöppler, MD
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
In this Article
- Interstitial cystitis facts
- Overview of urinary function
- What is interstitial cystitis (IC)?
- What is the cause of interstitial cystitis?
- What are the signs and symptoms of interstitial cystitis?
- How is interstitial cystitis diagnosed?
- What is the treatment of interstitial cystitis?
- Are lifestyle modifications of value in managing interstitial cystitis?
- Are there any special concerns about interstitial cystitis?
- What is the prognosis (outcome) of interstitial cystitis?
- Find a local Urologist in your town
What is the cause of interstitial cystitis?
No one knows what causes PBS/IC, but doctors believe that it is a real physical problem and not a result, symptom, or sign of an emotional problem. Because the symptoms of PBS/IC are varied, most researchers believe that it represents a spectrum of disorders rather than one single disease.
One area of research on the cause of PBS/IC has focused on the layer that coats the lining of the bladder called the glycocalyx, made up primarily of substances called mucins and glycosaminoglycans (GAGs). This layer normally protects the bladder wall from toxic effects of urine and its contents. Researchers have found that this protective layer of the bladder is "leaky" in about 70% of PBS/IC patients and have hypothesized that this may allow substances in urine to pass into the bladder wall where they might trigger PBS/IC, making these patients susceptible to chemicals in the urine, including those from foods or beverages.
Along with altered permeability of the bladder wall, researchers are also examining the possibility that PBS/IC results from decreased levels of protective substances in the bladder wall. Reduced levels of GAGs (discussed previously) or other protective proteins might also be responsible for the damage to the bladder wall seen in PBS/IC.
No matter what the mechanism for disruption of the bladder lining, potassium is one substance that may be involved in damage to the bladder wall. Potassium is present in high concentrations in urine and is normally not toxic to the bladder lining. However, if the tissues lining the inside of the bladder (urothelium) are disrupted or are abnormally leaky, potassium could then penetrate the lining tissues and enter the muscle layers of the bladder where it can cause damage and promote inflammation.
Researchers have isolated a substance known as antiproliferative factor (APF) that appears to block the normal growth of cells that make up the lining of the bladder. APF has been identified almost exclusively in the urine of people suffering with PBS/IC. Research is under way to clarify the potential role of APF in the development of PBS/IC.
Increased activation of sensory nerves (neurologic hypersensitivity) in the bladder wall is also thought to contribute to the symptoms of PBS/IC. Cells known as mast cells, which play a role in the body's inflammatory response to injury, release chemicals that are believed to be capable of contributing to the symptoms of PBS/IC.
Other theories about the cause of PBS/IC are that it is a form of autoimmune disorder or that infection with an unidentified organism may be producing the damage to the bladder and the accompanying symptoms.
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