Related Experiment Videos
Autorosette inhibition factor: a positive acute phase reactant in interstitial cystitis
B Frandsen1, G Lose, M Holm-Bentzen
1Department of Clinical Chemistry, Kolding Hospital, Denmark.
European Urology
|January 1, 1988
Summary
Interstitial cystitis (IC) patients show elevated urinary eosinophil cationic protein (ECP) and complement C3d. A positive correlation between autorosette inhibition factor (AIF) and C3d suggests AIF
Area of Science:
- Urology
- Immunology
- Pathophysiology
Background:
- Painful bladder disease, including interstitial cystitis (IC), presents complex diagnostic challenges.
- Biomarkers in urine, such as autorosette inhibition factor (AIF), complement C3d, and eosinophil cationic protein (ECP), are being investigated for their role in IC.
Purpose of the Study:
- To investigate the concentrations of urinary AIF, C3d, and ECP in patients with painful bladder disease.
- To explore potential correlations between these biomarkers and the diagnosis of interstitial cystitis (IC).
Main Methods:
- Urine samples were collected from 28 patients diagnosed with painful bladder disease.
- Levels of AIF, C3d, and ECP were measured in all urine samples.
- Statistical analysis was performed to identify correlations and significant differences between patient groups, particularly those with confirmed IC (detrusor mastocytosis).
Main Results:
- A significant positive correlation (r = 0.73, p < 0.01) was observed between urinary AIF and C3d in patients with IC.
- Urinary ECP median concentration was significantly elevated in IC patients.
- Urinary C3d median concentration was significantly elevated in both IC patients and other painful bladder disease patients.
- AIF demonstrated characteristics of a positive acute phase reactant in IC.
Conclusions:
- Urinary AIF, C3d, and ECP are elevated in patients with interstitial cystitis.
- The positive correlation between AIF and C3d in IC suggests a potential role in the inflammatory process.
- AIF may influence bladder epithelial barrier function, contributing to IC pathogenesis.