P431 Vitamin D binding protein in the limelight: IBD-related inflammation and circulating levels of vitamin D binding protein, total, free and bioavailable 25-hydroxyvitamin D
A. Aksan1,2,3, K. Böttger2,4, N. Hein4, Y. Caicedo-Zea5, I. Diehl6, C. Schumann5, F.P. Armbruster7, J.M. Stein1,2,4
1J. W Goethe University, Institute of Pharmaceutical Chemistry, Frankfurt am Main, Germany, 2Interdisciplinary Crohn-Colitis Centre Rhein-Main, Clinical and Scientific Research, Frankfurt am Main, Germany, 3Justus-Liebig-Universität, Institute of Nutritional Science, Giessen, Germany, 4DGD Clinics Frankfurt-Sachsenhausen, Gastroenterology and Clinical Nutrition, Frankfurt/Main, Germany, 5Immundiagnostik AG, Vitamin D Research, Bensheim, Germany, 6Immundiagnostik AG, Immunoassays, Bensheim, Germany, 7Immundiagnostik AG, Managing Director, Bensheim, Germany
Background
Vitamin D deficiency occurs frequently in patients with Crohn’s disease (CD) and ulcerative colitis (UC). While recent cohort studies support an association of vitamin D with important clinical parameters and outcomes in IBD, the complex interplay of inflammation with vitamin D metabolism in IBD poses a viscious circle. We sought to further illucidate the relation between inflammation and different vitamin D parameters. To the best our knowledge, this was the first study to focus on the relationship between vitamin D binding protein (VDBP), circulating total, free, and bioavailable 25-hydroxyvitamin D (25(OH)D), and inflammation, in adult IBD patients.
Methods
This was a comparative, single-centred, cross-sectional study in patients with IBD aged 18–65 years. Full blood count, transferrin, albumin and hsCRP were determined by standard methods. The presence/absence of inflammation was assessed based on serum hsCRP levels (cutoff <5mg/l). VDBP levels were determined by ELISA, and 25(OH)D by LCMS. Free and bioavailable vitamin D levels were calculated using the validated formula. IBM SPSS version 25.0 was used for statistical analysis.
Results
In total, 129 subjects with IBD (70 male/59 female; 82 CD/47 UC; mean age 41.7 ± 12.6 years) were enrolled. Of these, 38/129 had inflammation (19 m/19 f; 26 CD/12 UC; 39.6 ± 12.9 years) while 91/129 had no inflammation (40 m/51 f; 56 CD/35 UC; 42.5 ± 12.5 years). Subjects with disease activity had significantly higher leukocyte, erythrocyte sedimentation rate (ESR) and hsCRP, but lower transferrin, transferrin saturation (TSAT) and albumin levels than those without inflammation (
Conclusion
High levels of circulating VDBP were associated with inflammatory activity. Moreover, free/total 25(OH)D ratio was inversely associated with inflammation. Other vitamin D parameters including total, free and bioavailable 25(OH)D showed no association with inflammation. These findings suggest that VDBP may play a bigger role than thought as a modulator of vitamin D and inflammation, and that simultaneous detection and investigation of plasma VDBP may provide additional insights into this complex interaction.