Abstract

Abstract Background A consistent finding in inflammatory bowel disease (IBD) is an altered composition of fecal bile acids, with an increase in primary bile acids and a decrease in secondary bile acids. It is less clear, whether fecal bile acids could prove to be biomarkers for IBD diagnosis and disease activity. The study aimed to determine correlations between eighteen fecal bile acid species and IBD entity as well as disease severity. Methods Eighteen fecal bile acid species were quantified from stool samples of 62 IBD patients and 17 controls using LC-MS/MS and stable isotope dilution. Bile acid levels were normalized to the dry weight of the fecal homogenates. For calculations, normalized bile acid concentrations and ratios of individual bile acid species to total bile acid levels were used. The p-values were corrected for multiple comparisons. Results In accordance with previous data, we showed that patients with IBD had more primary and less secondary bile acids in their stool compared to healthy controls, with greater differences when comparing healthy controls with ulcerative colitis (UC) than with Crohn´s disease (CD). In CD patients’ fecal calprotectin showed no correlations with any of the bile acids. In UC negative correlations between fecal calprotectin levels and two secondary bile acids, glycine conjugated lithocholic acid (GLCA) and hyodeoxycholic acid (HDCA), and thus total levels of secondary bile acids, existed. Comparing patients with low calprotectin levels (<50 µg/g) and patients with high calprotectin levels (>500 µg/g) in UC revealed that the latter group had lower GLCA and HDCA. Fecal bile acid levels of CD patients did not change with higher calprotectin. Moreover, serum C-reactive protein negatively correlated with the secondary bile acids HDCA, ursodeoxycholic acid, lithocholic acid, taurine conjugated lithocholic acid, deoxycholic acid and its taurine conjugated form in UC but not CD patients. Conclusion To distinguish between IBD subtypes, it may be helpful to note that impaired fecal bile acid homeostasis is specific to patients with active UC.

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