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The Enigma of Interstitial Cystitis—an Autoimmune Disease?
Author(s) -
ANDERSON J. B.,
PARIVAR F.,
LEE G.,
WALLINGTON T. B.,
MacIVER A. G.,
BRADBROOK R. A.,
GINGELL J. C.
Publication year - 1989
Publication title -
british journal of urology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.773
H-Index - 148
eISSN - 1464-410X
pISSN - 0007-1331
DOI - 10.1111/j.1464-410x.1989.tb05124.x
Subject(s) - antibody , interstitial cystitis , medicine , autoimmune disease , pathology , immunology , inflammation , immunofluorescence , gastroenterology , urinary system
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.