P668 Does biotin deficiency play a role in the pathogenesis of Inflammatory Bowel Disease? Preliminary results of a cross-sectional study

Erbach, J.(1);Arnold, A.(2);Bonn, F.(2);Stein, J.M.(1,3,4);Schröder, O.(1,3);Aksan, A.(1,5);

(1)Interdisciplinary Crohn Colitis Centre Rhein-Main, Clinical Research, Frankfurt am Main, Germany;(2)Immundiagnostik AG, LC/MS Department, Bensheim, Germany;(3)DGD Clinics Frankfurt-Sachsenhausen, Gastroenterology and Clinical Nutrition, Frankfurt am Main, Germany;(4)Goethe University Frankfurt, Institute of Pharmaceutical Chemistry, Frankfurt am Main, Germany;(5)Justus-Liebig University Giessen, Institute of Nutritional Science, Giessen, Germany


Biotin, a water-soluble B-vitamin, has been shown to have anti-inflammatory properties. A biotin-deficient diet was recently shown to induce a colitis-like phenotype in mice, alleviated by biotin substitution. Mice with DSS colitis showed biotin deficiency and significantly reduced levels of SDMT, a protein involved in biotin absorption. Oral biotin substitution reversed DSS colitis and induced remission by inhibiting NF-κB, a transcription factor that hinders inflammatory cytokine expression and plays a role in intestinal barrier integrity and IBD. We investigated for the first time a possible clinical role of biotin status in IBD.


In a comparative, cross-sectional study, serum samples of IBD patients were compared with samples of 80 healthy blood donors (40f;18-65y). CBC, albumin and hsCRP were determined by standard tests and samples assessed for presence/absence of inflammation (serum hsCRP, cutoff <5mg/L). Since its known that serum biotin levels does not accurately reflect biotin status, serum 3-hydroxyisovaleryl carnitine (3HIAc) levels were determined by LC-MS/MS.


138 IBD patients (67f;72 CD/66 UC;42.5±14.3y) were enrolled. Of these, 83/138 had inflammation (39f;43CD/40UC;42.5±14.6y) and 55/138 no inflammation (28f;29CD/26UC;42.5±13.9y). In IBD patients, mean serum 3HIAc levels were significantly higher vs. controls but similar with vs. without inflammation (Table 1). The reference serum 3HIAc level was calculated as 11.0-27.3 nmol/L from controls; biotin deficiency was defined as >27.3 nmol/L 3HIAc (90thPC), since no validated cut-off exists. Biotin deficiency in IBD patients was significantly greater than in controls (Table 1).


High serum 3HIAc levels were associated with IBD. In line with preclinical studies, biotin deficiency was more pronounced in IBD patients than controls. No relation was found with inflammatory activity or disease type. Our findings suggest that biotin may have a bigger role than thought in IBD; whether as a cause or effect in IBD pathogenesis warrants investigation. Routine assessment and correction of biotin status may ameliorate IBD and help maintain intestinal integrity.

Table 1: 3-hydroxyisovaleryl carnitine levels and biotin deficiency