trial impact
Click here to Register

Diagnosis of Interstitial Cystitis : Ahead of its Time! :


Interstitial cystitis (IC) has continued to be an unresolved problem in clinical urology despite intense investigation over the past 16 or more years. The diagnosis of IC/PBS is based upon the presence of characteristic symptoms, provided that no symptoms or signs of other conditions are present.

The physical examination is important in making a diagnosis. On observation, many patients will be tearful and appear fatigued and/or depressed. Variable tenderness of the abdominal wall, hip girdle, soft tissues of the buttocks, pelvic floor, bladder base and urethra is almost universally present, probably due to sensitization of afferent nerve fibers in the dermatomyotomes (thoracolumbar and sacral) to which the bladder refers. In males, scrotal and penile tenderness can be present.

Pelvic ultrasound can be helpful for assessing the pelvic organs in these patients. It is important to remember that allodynia (perception of non-noxious stimuli, such as light touch, as being noxious or painful) can be present in any patient who has been in chronic pain, and that adequate pelvic examination may be possible in the patient.

Recent development suggests that pathogenesis can be helpful in diagnosis of IC. As known for years, the etiology and pathogenesis of IC are still undetermined, and its pathologic diagnosis is essentially one of exclusion, with no specific or clear criteria. In this review, current concepts of the etiology/pathogenesis and pathology are critically analyzed, new pathologic observations summarized, and a proposal of neurogenic inflammation as the primary pathogenetic factor is presented in the context of all currently available information.

No specific or diagnostic light microscopic pathologic features are provided by either routine histopathology or immunohistochemistry. Increasingly, it has been recognized that detrusor mast cell count has little or no diagnostic value. On the other hand, electron microscopy has provided important new observations:

  • Presence of mast cells, activated by piecemeal degranulation, in close proximity to intrinsic nerves—particularly in suburothelium.
  • Distinctive pathologic changes in urothelium, suburothelium, and muscularis in biopsy samples obtained after diagnostic bladder hydrodistension.
  • Constant associated changes in venules, capillaries, and neural elements in the same biopsy samples.
  • Diffuse involvement of bladder wall, with the most evident and profound pathologic changes in posthydrodistension biopsy samples obtained from cystoscopically obvious lesions (glomerulations).

These features are sufficiently distinctive to allow definitive pathologic diagnosis of IC, and provide a firm basis for primary involvement of neurogenic inflammation in its pathogenesis. A proposal is presented regarding the mechanisms invoked by neurogenic inflammation. This proposal revolves around sensory nerve excitation, the release of neuropeptides, and activated differential secretion of potent mast cell mediators. This proposal can account for the heterogeneity and variability of observed pathologic features, and upholds the tacit acceptance of IC as a disease of pluricausal etiology and multifactorial pathogenesis.

The approaches to the diagnosis of interstitial cystitis (IC) are evolving as a result of recent advances in the knowledge of the disease. With increasing awareness of IC prevalence and presentation, clinicians are identifying cases of IC earlier in the disease process. A diagnosis of IC can now be established without applying each step of the traditional diagnostic paradigm, which was designed to identify “classic” cases of IC.


  1. Panzera AK. Interstitial cystitis/Painful bladder syndrome. Urol Nurs. 2007;27(1):13-19.
  2. Carr LK, Corocs J, Njckel C, Teichman J. Diagnosis of Intersitial cystitis June 2007. Can Urol Assoc J. 2009;3(1):81-86.
  3. Van de Merve JP, Nordling J, Bouchelouche P, et al. Diagnostic criteria, classification, and nomenclaturefor painful bladder syndrome/interstitial cystitis: An ESSIC proposal. European Urology. 2008;53(1):60-67.
  4. Hanno PM. Interstitial cystitis - Epidemiology, Diagnostic criteria, Clinical Markers. Rev Urol. 2002;4(1):S3-S8.
  5. Heck BN. Interstitial cystitis:Enhancing early identification in primary care settings. JNP. 2007;3(8):509-519.
  6. Mattox TF. Interstitial cystitis in adolscents and children:a review. J Pediatr Adolesc Gynecol. 2004;17:7-11.
  7. Teichman JMH, Parsons CL. Contemporary clincal presentation of interstitial cystitis. Urology. 2007;69(4A):41-47.
  8. Association of Reproductive Health Professionals. Screening, treatment, and management of IC/PBS. www arhp org. Accessed March 9, 2009.
  9. Evans RJ. Pathophysiology and clinical presentation of interstitial cystitis. Avd Stud Pharm. 2005;8-14.
  10. National Kidney and Urologic diseases Information Clearinghouse(NKUDIC). Interstitial cystitis/ painful bladder syndrome. www kidney niddk nih gov. Accessed March 9, 2009.