Newswise — As the definition of Interstitial cystitis (IC) has become wider and wider, reflected in dramatically increasing prevalence figures, it has become more rather than less difficult to grasp this symptom complex - from an etiologic/pathogenetic as well as therapeutic point of view. No doubt are we dealing with a heterogeneous and poorly defined spectrum of disorders, and trial and error remains the leading treatment principle. Few methods reach a high degree of recommendation.

What can be learned from the present situation? This survey seems to support various hypothesis of pathogentic mechanisms like epithelial dysfunction, supported by good evidence for oral and intravesical pentosan polysulfate sodium treatment; neural dysfunction, supported by results of amitriptyline and hydroxyzine treatment; and immunologic abnormalities, supported by good responses to cyclosporine A and again support for hydroxyzine. It has to be assumed that methods as different as those are not useful in all patients, but rather in more or less specific situations. By very carefully identifying characteristics of patients responding to various principles, observations can be made giving clues to distinctive biological marks that may help when trying to design rational treatment for various categories.

Already at this stage, as emphasized before, the classic form of IC (with Hunner lesions) stands out as a well defined disease that deserves special attention, but there are certainly other distinctive categories to be identified and described. When we have learned better why and what we are doing, an improved situation as to evidence will follow.

Written byMagnus Fall, MD, PhD, as part of Beyond the Abstract on UroToday.com.

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CITATIONS

Eur Urol. 2008 Jul;54(1):65-78 (Jul-2008)