Background: A previous study revealed elevated serum Immunoglobulin E (IgE) in ketamine related cystitis (KC) patients. IgE might participate the pathogenesis of different types of bladder pain syndromes, including KC and interstitial cystitis (IC).
Objectives: To investigate the IgE expression in KC and IC bladder tissue.
Study design: Prospective evaluation.
Setting: The study was conducted in a tertiary teaching hospital, Hualien Tzu Chi Hospital.
Methods: We investigated the bladder IgE with immunofluorescence staining and quanti?cation. The active mast cells were measuring using tryptase. The symptoms and urodynamic study results were recorded. Double immunofluorescence staining of tryptase and IgE was also performed. Sixteen KC patients, 10 ulcerative IC patients, and 20 non-ulcerative IC patients participated. The history and urodynamic parameters were investigated in these patients. The bladder mucosa was biopsied during cystoscopic hydrodistention. Bladder biopsies were also taken from 22 patients with bacterial cystitis and 12 healthy controls.
Results: Bladder IgE was positive in 15 (93.8%) KC patients, 9 (90%) ulcerative IC patients, one (5%) non-ulcer IC patient, 8 (36.4%) bacterial cystitis patients, and 2 (16.7%) controls (P < .001). The bladder IgE was greater in the patients with KC than in the others (P < .001). After excluding KC patients, bladder IgE was significantly higher in the patients with ulcerative IC than the others (P < .001). The bladder IgE was significantly correlated with pain on a visual analogue scale (r2 = 0.156, P = .017) and maximum bladder capacity (r2 = 0.423, P < .001). Tryptase expression did not show a significant difference between KC, ulcer IC, and non-ulcer IC (P = 0.222). Double immunofluorescence staining showed co-expression of tryptase and IgE.
Conclusions: IgE-mediated inflammation played a significant role in the pathogenesis of KC and ulcerative IC.
Key words: Immunoglobulin E, ketamine cystitis, interstitial cystitis.