J. B. Anderson, FRCS, Research Fellow in Urology, Bristol Royal Infirmary
The Enigma of Interstitial Cystitis—an Autoimmune Disease?
Article first published online: 21 NOV 2008
British Journal of Urology
Volume 63, Issue 1, pages 58–63, January 1989
How to Cite
ANDERSON, J. B., PARIVAR, F., LEE, G., WALLINGTON, T. B., MacIVER, A. G., BRADBROOK, R. A. and GINGELL, J. C. (1989), The Enigma of Interstitial Cystitis—an Autoimmune Disease?. British Journal of Urology, 63: 58–63. doi: 10.1111/j.1464-410X.1989.tb05124.x
J. G. Gingell, FRCS, Consultant Urologist, Southmead Hospital
- Issue published online: 21 NOV 2008
- Article first published online: 21 NOV 2008
- Accepted for publication 4 April 1988
Summary— Interstitial cystitis (IC) is characterised by recurrent inflammation and destruction of bladder tissue without obvious cause. To determine whether this self-perpetuating disease is the result of an autoimmune disorder, we studied 26 patients with IC of mean duration 5 years and compared the results with those of a control group of similar age and sex with other urological complaints.
We performed a standard autoimmune profile and looked for specific antibodies to normal human bladder in the serum, using an indirect immunofluorescence technique. Deep bladder biopsies were examined by conventional histology and cryostat sections were studied with peroxidase-conjugated anti-human antibodies in a search for immunoglobulin deposition within the bladder.
Seventeen of 26 patients with IC (65%) and 5 of 14 controls (36%) demonstrated non-organ-specific antibodies; 40% of those with IC had anti-nuclear antibodies; 18 IC patients (75%) and 4 of 10 controls (40%) had anti-bladder antibodies present in the serum, but 5 healthy volunteers showed no such antibody activity. There was no statistically significant difference between the two groups for either type of antibody (Fisher's exact test). Only 5 of 17 patients with IC (29%) showed immunoglobulin deposition in the bladder epithelium, a similar proportion to controls (38%); 4 of these 5 had circulating anti-bladder antibodies present in the serum.
Although IC patients demonstrated a non-specific increase in antibody formation, this was not significantly different from a similar group of other urological patients. The lack of specificity makes this immunological response more likely to be a secondary phenomenon associated with inflammatory damage to the bladder rather than the primary cause of the disease.