Interstitial cystitis (IC) is a chronic inflammatory disease of the bladder characterized by clinical symptoms of urinary frequency, dysuria and bladder pain. Interstitial cystitis was proposed as early as 1887, but the disease was not recognized by most physicians for nearly 100 years. Many physicians do not even believe that the disease exists, and even if they agree that it may exist, it is difficult to diagnose; even if it can be diagnosed, it is difficult to confirm with conclusive evidence and no specific effective treatment is available. The complexity of interstitial cystitis is demonstrated not only by the variety of clinical symptoms, but also by the lack of a definitive etiology, the poorly understood pathophysiologic manifestations, and the absence of a single effective treatment; research data on interstitial cystitis often leave scholars with a sense of frustration as conflicting findings continue to emerge, simply adding to the complexity of understanding interstitial cystitis. Because of the complexity of the diagnosis of interstitial cystitis, the NIDDK first developed diagnostic criteria regarding interstitial cystitis in the United States in 1987 (see table for details). As this diagnostic criteria was originally introduced with the aim of rigorously diagnosing interstitial cystitis in order to conduct relevant clinical studies. A growing number of scholars now believe that the diagnostic criteria are too strict and may result in 60% of patients with associated symptoms and pathophysiologic changes not being diagnosed accordingly.
From current studies, the symptoms of interstitial cystitis are associated with the urologic, gynecologic, gastrointestinal, and pelvic floor, so that pain can occur from the bladder, urethra, prostate, vagina, and pelvic floor. The pathogenesis of interstitial cystitis is not yet clear, although there are various theories including autoimmunity, the main pathophysiological feature is the disruption of the blood-urinary barrier of the bladder and the leakage of various harmful substances such as potassium ions in the urine into the submucosa causing a series of symptoms. The pathogenesis of interstitial bladder, characterized by Hunner’s ulcer, especially pathology showing significant mast cell infiltration, may be related to allergy or autoimmunity, and the effectiveness of antihistamines in treating interstitial cystitis with mast cell infiltration supports this possibility. In recent years, it has been found that urinary anti-value-added factor (APF) is significantly elevated and HB-EGF is significantly reduced in patients with interstitial cystitis, suggesting that some mechanism may be present in the urine that inhibits the growth of the bladder mucosa and that the blood-urinary barrier is thus disrupted.
The diagnostic criteria of the Institute of Diabetes, Digestive and Kidney Diseases study on interstitial cystitis meet both of the following criteria: 1. Painful or urgent bladder 2. Typical Hunner’s ulcer, or erythroderma Either of the following can be excluded 1. Bladder volume >350 ml in the awake state 2. Bladder volume up to 150 ml without intense urgency 3. Urodynamics showing non-random bladder contractions 4. Duration of symptoms