Urinary Uronate and Sulfated Glycosaminoglycan Levels: Markers for Interstitial Cystitis Severity

Abstract

The majority of urinary GAGs likely exist as small oligosaccharides. Urinary uronate and sulfated GAG levels are increased in patients with IC who have severe disease. They may become useful markers for monitoring IC.

The significance of potassium chloride sensitivity test and urinary uronic acid level in the diagnosis of chronic pelvic pain syndrome

“…Therefore, increased uronic acid in the urine might serve as an indirect laboratory indicator of IC [9][10][11][12]. However, Hurst reported lower values for macromolecular GAGs in IC [13], whereas Lokeshwar reported higher values [10].…”

Evaluation of the metabolism of glycosaminoglycans in patients with interstitial cystis

“…Urinary GAG content in PBS/IC patients has been shown to be decreased (25,26), similar (27,28) and increased (4,13,18). Our results showed a significant decrease in urinary excretion of sulfated GAG of patients with PBS/IC compared to the controls.…”

“…Urine and tissue levels of GAG have been studied in PBS/IC and in animal models but their results are not uniform (2,(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18). Such variation suggests that there is no complete understanding of how and why GAG is produced and degraded in PBS/IC, if GAG expression is the cause or the reaction for PBS/IC.…”

Urinary Glycosaminoglycan Levels as a Marker of Renal Amyloidosis in Patients with Familial Mediterranean Fever

“…[14] As such, Lokeshwar et al have reported that GAG levels (protective for bladder's urothelium) increase in severe interstitial cystitis, and that this modality can be used both in the diagnosis and screening of the patients. [7] There are studies in the available medical literature that used parameters other than urinary GAG excretion for the same purpose. Duzova et al have studied the role of SAA in the screening of colchicine dose and subclinical inflammation and reported that SAA is the most useful marker in the determination of subclinical inflammation, that its levels decrease immediately should there be an increase in the dose of colchicines, and that this parameter can be used to screen the dose of the medication.…”

“…[4][5][6] Family history is commonly positive. [7,8] The FMF gene has been localized to the short arm of chromosome 16 and is know as the MEFV gene. The pyrine dysfunction due to mutation in MEFV gene is suggested as the most important factor in the pathogenesis of the disease.…”