S. Keay et al., CONCENTRATIONS OF SPECIFIC EPITHELIAL GROWTH-FACTORS IN THE URINE OF INTERSTITIAL CYSTITIS PATIENTS AND CONTROLS, The Journal of urology, 158(5), 1997, pp. 1983-1988
Purpose: Interstitial cystitis (IC) is a chronic bladder disease for w
hich the etiology is unknown. Because the bladder epithelium is often
abnormal in IC, we determined whether the levels of specific urine gro
wth factors postulated to be important for bladder epithelial prolifer
ation are altered in IC. Materials and Methods: ELISAs were used to de
termine levels of epidermal growth factor (EGF), insulin-like growth f
actor 1 (IGF1), insulin-like growth factor binding protein 3 (IGFBP3),
and heparin binding epidermal growth factor-like growth factor (HB-EG
F) in urine specimens from women with IC, asymptomatic women without b
ladder disease, and women with bacterial cystitis. Results: Urine HB-E
GF levels were specifically and significantly decreased in IC patients
as compared to asymptomatic controls or patients with bacterial cysti
tis, whether expressed as concentration (amount per volume of urine) o
r the amount relative to urine creatinine in each specimen. In contras
t, urine EGF, IGF1, and IGFBP3 levels were all significantly elevated
in IC patients compared to asymptomatic controls. Further, the amounts
of urine EGF and IGF1 were also elevated in IC patients as compared t
o patients with bacterial cystitis, and urine IGFBP3 levels were signi
ficantly elevated when expressed per milligram of urine creatinine. Co
nclusions: These findings indicate that complex changes in the levels
of urine epithelial cell growth factors (EGF, IGF1, and HB-EGF) and a
growth factor binding protein (IGFBP3) are associated with IC. While E
GF, IGF1, and IGFBP3 levels are either the same or increased in the ur
ine of IC patients as compared to patients with bacterial cystitis or
asymptomatic controls, HB-EGF levels are significantly decreased in th
e urine of IC patients. Understanding the reasons for these changes ma
y lead to understanding the pathogenesis of this disorder.