The etiology of interstitial cystitis (IC) is not yet fully clear, and the following hypotheses are proposed:
1. Vascular and Lymphatic Obstruction
It was proposed that bladder fibrosis may be caused by pelvic surgery or infection, leading to obstruction of lymphatic vessels in the bladder wall and causing thrombotic angiitis or persistent small artery spasm due to vasculitis, but there is insufficient evidence.
2. Infection
It was proposed that bacterial, viral, or fungal infection may be the cause of IC, but there have been no reports of detecting the above three pathogens in IC patients.
3. Neurohumoral Factors
Mast cells are increased in the bladder proper membrane and detrusor muscle of IC patients. Cold, neuropeptides, drugs, trauma, toxins, etc., can activate mast cells, release vasoactive substances to sensitize sensory neurons, which further activate mast cells by releasing neurotransmitters or neuropeptides; mast cells can also directly cause vasodilation or bladder mucosal damage, leading to inflammation.
4. Immune Factors
The disease responds well to corticosteroid therapy, and some patients may detect anti-bladder mucosal antibodies in the blood. Many scholars have also found that autoantibodies or immune complexes produced against vascular antigens can deposit in the vascular wall, activate the complement system, and participate in the pathogenesis of IC.
5. Mucosal Permeability
It is speculated that IC is caused by the dysfunction of the bladder epithelium, which increases its permeability and allows urine to leak into the bladder wall through the transitional epithelium, causing bladder inflammation. Some people have confirmed that IC patients have an increase in TH protein in the superficial epithelium of the bladder, indicating an increase in mucosal permeability.