Increased pentosidine, an advanced glycation end-product, in urine and tissue reflects disease activity in inflammatory bowel diseases.

Background:  Under inflammatory conditions with strong oxidative stresses, advanced glycation end-products (AGE), carbonyl compounds, are produced. The concentration of pentosidine, an AGE, reportedly correlates with complications of diabetes mellitus and worsening of rheumatoid arthritis, but its role in the pathogenesis of inflammatory bowel diseases (IBD) is unclear. Methods:  Immunohistochemistry was performed with antibodies against pentosidine, and 8-OH-2-deoxyguanosine. The urinary concentration of pentosidine was also quantified by enzyme-linked immunosorbent assay method. Results:  Pentosidine expression was up-regulated in the inflamed tissue of IBD. The expression of both pentosidine and 8-OH-2-deoxyguanosine was similar and increased in the inflamed epithelium and infiltrating cells (neutrophils and lymphocytes). The urinary concentration of pentosidine in active ulcerative colitis was significantly greater than that in inactive ulcerative colitis (0.12 ± 0.15 vs 0.021 ± 0.011 µg/mg of Cr, P < 0.05), and was greater in active Crohn's disease than in inactive Crohn's disease (0.071 ± 0.086 vs 0.039 ± 0.023 µg/mg of Cr). Conclusions:  The urinary pentosidine level correlated with the activity of ulcerative colitis and may be a marker for disease activity in ulcerative colitis.