Diagnosis
- Primarily a diagnosis of exclusion
- Symptoms of unremitting frequency, sensory urgency, and/or pelvic pain associated with the bladder in the absence of other causes suggest IC.
- Bladder biopsy is necessary only if needed to rule out other etiologies of the patient's symptoms.
- Bladder distention to 80cm water pressure under anesthesia can be helpful in confirming the diagnosis
- Glomerulations, while not specific for IC, are suggestive of diagnosis
- Provides short-term symptom relief in one-third of patients
- May effect treatment algorithm if Hunner's ulcer is identified upon distention (approximately 10% of cases), or bladder capacity under anesthesia is less than 200mL.
- Need for cystoscopy in the absence of microhematuria is controversial.
- Urodynamics can differentiate sensory from motor urgency.
Etiology
- May be multifactorial, and a syndrome or symptom complex rather than specific disease
- Infection
- Not considered a likely etiologic factor
- No evidence of bacterial, viral, or fungal infection
- Abnormality in bladder lining
- Possible deficiency or abnormality of glycosaminoglycan layer allowing molecular leaks of urinary constituents into the bladder wall
- Intravesical potassium instillation causes significantly more pain in the following conditions compared to controls: IC, urinary infection, radiation cystitis, and in 25% of patients with detrusor instability
- Possible deficiency or abnormality of glycosaminoglycan layer allowing molecular leaks of urinary constituents into the bladder wall
- A toxic component in the urine may be responsible
- Pain in augmented bladders and neobladders as well as pouches can develop years after diversion for IC
- An antiprolilferative factor in the urine of IC patients has been identified that appears to be made or activated in the distal ureter or urinary bladder. Such a factor, that inhibits normal bladder epithelial regeneration, could be causally related to IC and may prove to be a reliable marker for the disorder in the near future.
- Mast cell release of vasoactive and nociceptive substances with secondary sentization of sensory neurons -- may be a primary or secondary etiologic agent
- Autoimmunity
- Suggested by relationship of systemic problems including Sjogrens syndrome, inflammatory bowel disease, systemic lupus in a minority of patients