Effect Of Intravesical Glycosaminoglycan Substitution Therapy On Bladder Pain Syndrome/Interstitial Cystitis

Main Category: Urology / Nephrology
Article Date: 17 Oct 2008 - 5:00 PDT

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UroToday.com - One theory of BPS is based on a disorder of the blood-urine barrier at the urothelial level. According to this theory, a functional disorder results in increased urothelial permeability for urinary compounds, especially potassium ions. These compounds induce typical BPS symptoms such as urge sensation and pain at inadequately small bladder-filling volumes, resulting in a clinical picture of frequent micturition. Instillation of a potassium solution into the bladder mimics this condition in BPS patients. Specificity and sensitivity of the potassium test is poor for BPS, and its use as a diagnostic test for the condition is highly questionable.

Lukas Daha and colleagues from Vienna and Baden, Austria undertook a study to fill the void of a lack of data on the influence of GAG substitution therapy on cystometric bladder capacity. They wanted to compare pre and post-treatment maximal bladder capacities with a saline and a 0.2M potassium chloride (KCl) solution after GAG substitution therapy. They looked at 100 BPS patients treated from 1999 through 2004 with intravesical GAG therapy, primarily hyaluronic acid. Twenty-seven patients volunteered for repeat comparative assessment of maximal bladder capacity with saline and KCl solutions. Of these, 13 had responded to GAG and 14 had not responded.

The investigators found that in responders, the average maximal bladder capacity increased by 17% with the saline solution and by 101.5% with the 0.2M KCl. In the 14 non-responders, post-therapeutic average maximal bladder capacity was decreased by 35% with the saline solution and remained unchanged with the potassium solution.

The authors concluded that in non-responders to GAG therapy, the blood-urine barrier disorder may not be a primary one that can be repaired at the urothelial level, but may instead be secondary to other disorders that lead to an increased potassium sensitivity and are resistant to intravesical therapies. Further investigation in this group is obviously needed.

Daha LK, Riedl CR, Lazar D, Simak R, Pfluger H
Scand J Urol Nephrol. 2008 Jan 8:1-4

Reported by UroToday.com Contributing Editor Philip M. Hanno, MD, MPH

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