| Interstital Cystitis | |
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Introduction >> |
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Symptoms >> |
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Etiology >> |
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Diagnosis >> |
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Epidemiology >> |
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General Management >> |
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Treatment >> |
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Medications >> |
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Direct Bladder Therapy >> |
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Surgical Treatments >> |
ETIOLOGY
The cause of IC still remains unclear and over the years many various theories such as infections, toxic and autoimmune etiologies were that were entertained were not substantiated. Presently the predominant theory speculates that a defect within the internal lining of the bladder is causing the IC symptoms. This theory, championed by Dr. Lowell Parson from San Diego, describes a possible abnormality or deficiency within the glycosaminoglycans (GAG) layer of the wall of the bladder. The abnormality within the GAG layer underneath the transitional epithelium (inner most layer of the bladder) may lead to local inflammation and exposure of the terminal nerve endings at the bladder wall to the acid urine and it was therefore termed the “urinary leakage” theory. Other authors hypothesized the possibility that IC is caused by a general “pelvic floor disorder” with aberrant firing of electro-neurological stimuli where the bladder is only one of the affected organs. This theory provides an explanation for the extra-vesical (not bladder) symptoms such as the bloated lower abdomen, pelvic pain and even and the irritable bowel syndrome (IBS) that have been reported by many IC patients.
Approximately 5 – 10% of IC patients are also found to have autoimmune conditions such as Systemic Lupus Erythematosus (SLE), Sjögren’s Syndrome, Fibromyalgia and Chronic Fatigue Syndrome (CFS) as well as IBS. This association raised the question of autoimmune etiology for IC, yet so far it remains just a theory.
Updated June 23rd, 2007