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Interstitial cystitis: a neuroimmunoendocrine disorder

T C Theoharides1, X Pang, R Letourneau

  • 1Department of Pharmacology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA. ttheoharides@infonet.tufts.edu

Annals of the New York Academy of Sciences
|June 18, 1998
PubMed
Summary

Interstitial cystitis (IC) involves bladder pain and urinary urgency, potentially linked to immune and nerve responses. Activated mast cells and neurohormonal factors appear central to IC pathogenesis.

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Area of Science:

  • Urology
  • Immunology
  • Neuroscience

Background:

  • Interstitial cystitis (IC) is a chronic bladder condition primarily affecting women, causing pain and urinary frequency.
  • Symptoms worsen with ovulation and stress, suggesting neurohormonal involvement.
  • Key theories involve a compromised bladder lining and heightened mast cell activity.

Purpose of the Study:

  • To explore the complex pathophysiology of interstitial cystitis.
  • To investigate the role of mast cells, neurohormonal factors, and the bladder lining in IC.

Main Methods:

  • Review of existing theories on IC pathophysiology.
  • Analysis of the interaction between bladder mast cells, neurons, and hormones.
  • Consideration of animal models of stress and mast cell activation.

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Main Results:

  • A defective glycosaminoglycan (GAG) layer may permit irritant penetration, activating bladder mast cells.
  • Mast cell mediators can cause tissue damage and sensitize neurons.
  • Estradiol enhances mast cell activation via estrogen receptors, explaining ovulation-related symptom flares.
  • Stress-induced mast cell activation is linked to substance P and corticotropin-releasing hormone (CRH).

Conclusions:

  • Interstitial cystitis is likely a syndrome with integrated neural, immune, and endocrine components.
  • Activated mast cells play a pivotal role in the pathogenesis of IC.
  • Understanding these interactions may lead to novel therapeutic strategies for IC.