P306 Serum tryptophan metabolites as a biomarker for disease severity in patients with IBD
Karakan, T.(1)*;Karatas, A.(2);Cindoruk, M.(2);Gulbahar, O.(3);
(1)Gazi University, Department of Gastroenterology, Ankara, Turkey;(2)Gazi University, Gastroenterology, Ankara, Turkey;(3)Gazi University, Biochemistry, Ankara, Turkey;
The levels of tryptophan (TRP) metabolites such as kynurenine (KYN), kynurenic acid (KYNA), quinaldic acid, 3-hydrocynynene, anthranilic acid, picolinic acid (PA) and xanthurenic were determined systematically in inflammatory bowel disease (IBD). Previous studies found a negative correlation with TRP levels and IBD disease activity. However, there is no data about serum levels of TRP metabolites and their correlation with severity of IBD. We aimed to determine the correlation between the levels of TRP, its metabolites and the clinical, laboratory, and endoscopic findings of the disease activation including fecal calprotectin.
A total of 115 patients, 77 (66.4%) with UC and 38 (33.6%) with CD, were included. Forty three % (n=49) of the patients were female. 57 % (n=66) were male. The mean age of females and males were 42.07±13.39 and 44.23± 10.04 years, respectively. Patients were categorized according to their disease activity: Sixty-five (57%) of the patients were in remission and 50 (43%) were active. The predictive value of the disease activity was evaluated by the levels of serum tryptophan, its metabolites and the fecal calprotectin levels.
At a cut-off value of ≤11328.41 ng/ml of tryptophan, the sensitivity to predict disease activation is 76.9% and the specificity is 71.7%. On the other hand, at a cut-off value of ≥89.60 µg/g of fecal calprotectin, the sensitivity of detecting disease activation was 88.1% and the specificity was 80.0%. Calprotectin, sedimentation, CRP, KYN/TRP values were found to be significantly higher in patients in the active period than in patients in remission (p<0.001, p<0.001, p<0.007 respectively). KYNA, TRP, and PA values were found to be statistically significantly lower in patients in the active phase compared to those in remission (p=0.01, p<0.001, p=0.022 respectively).
Serum TRP levels were lower in increased disease activity. Quinolinic acid levels did not differ between active patients and patients in remission. Quinolinic acid, which is the metabolite of TRP degradation, was increased with active disease. However, fecal calprotectin still had superior predictive value for IBD disease activity. Further studies are needed to assess the TRP pathway for the disease severity and disease course in IBD.