Interstitial cystitis has an acute onset and progresses rapidly, but the disease usually remains stable without further exacerbation after the onset of typical symptoms. Even without treatment, more than half of patients will experience spontaneous remission, only to have another episode soon after. The symptoms can be divided into two symptom groups: bladder irritation and painful symptoms. The main symptoms are severe bladder irritation such as urinary frequency, urgency, painful urination and pain in the suprapubic area, but also urethral pain, perineal and vaginal pain, and painful intercourse in 60% of patients. The pain is very intense and is associated with bladder filling, and the symptoms may be relieved after urination. In some atypical patients, the symptoms may be manifested as lower abdominal cramping or pressure, and the symptoms are aggravated before menstruation or during ovulation. Physical examination is usually unremarkable. Some patients have pressure pain in the suprapubic area and tenderness in the bladder on vaginal palpation. Although interstitial cystitis (IC) has been known for a century, the etiology and pathogenesis of IC remain unclear. According to current research advances, there are several hypotheses in general: 1. Occult infection: Although no definite pathogens have been detected from patients, there is evidence that microorganisms (including bacteria, viruses, and fungi) in the urine of patients with IC are significantly higher than in normal controls. Most people now believe that infection may not be the primary cause of IC development, but it may act in conjunction with other pathogenic factors.
2, genetic factors: the incidence of IC in North Americans is significantly higher than in Japanese, the incidence in Jewish women is much higher than in other races, while blacks rarely suffer from IC, suggesting that IC may be related to race.
3, neurogenic inflammatory response: stress states such as cold, trauma, toxins, drugs, sympathetic excitation, release of vasoactive substances, causing local inflammation and nociceptive hypersensitivity; vasoactive substances can also further activate mast cells, causing vasodilation, bladder mucosal damage causing inflammatory response.
4, mast cell activation: the activation and aggregation of mast cells is the main pathophysiological changes of IC. Mast cells are mostly aggregated around the nerves. Under acute stress, mast cells are activated and degranulated, releasing a variety of vasoactive substances such as histamine, cytokines, prostaglandins, trypsin, etc., which can cause a severe inflammatory response. There is activation of mast cells in the bladder in 20% to 65% of patients.
5, autoimmune disease: IC is an autoimmune disease for the following reasons: (1) most often seen in women; (2) a high percentage of patients with other autoimmune diseases at the same time; (3) patients with drug allergies accounted for 26% to 70% of cases, and many patients can detect anti-nuclear antibodies; (4) histological examination with lesions of connective tissue; (5) the application of immunosuppressive therapy has some effect.
6, bladder mucosal barrier damage: the amino polysaccharide layer on the migrating epithelial cells has a protective layer that prevents urine and its harmful components from damaging the nerves and muscles under the mucosa. After bladder mucosal barrier damage epithelial cell dysfunction, permeability changes, as a result of which potentially toxic substances in urine enter bladder muscles, depolarizing sensory nerves and causing clinical symptoms such as urinary frequency, urinary urgency. This potentially toxic substance is mainly potassium ions, potassium ions do not damage or permeate the normal urinary epithelium, but have a toxic effect on the bladder muscle layer.
7, the toxic effects of urine: IC patients have specific toxic substances in urine to cause damage to the bladder, such as anti-proliferative factors.