Vitamin D (25(OH)D) deficiency occurs in active Crohn's disease (CD) and may be secondary to reduced sunlight exposure and oral intake. Vitamin D–binding protein (VDBP) levels, however, fluctuate less with season and sunlight. The aim, therefore, was to examine patients with CD in remission and determine any associations between VDBP, serum 25(OH)D, and the calculated free 25(OH)D concentrations with the risk of disease flare.
Subjects were identified from prospectively maintained inflammatory bowel disease databases at 3 teaching hospitals in Australia. Patients were in steroid-free clinical remission at the time of blood draw and were followed for at least 12 months. Total and epimer-25(OH)D3, VDBP concentrations, and genotypes were determined.
A total of 309 patients with CD (46% men) met the inclusion criteria. A disease flare occurred in 100 (32.4%). Serum 25(OH)D3 was deficient (<50 nmol/L) in 36 (12%) and insufficient (50–75 nmol/L) in 107 (35%) patients. Total, free, and epimer-25(OH)D3 serum levels did not predict disease flare. Higher VDBP concentrations, however, significantly correlated with increased risk of disease flare (hazard ratio 1.2, 95% CI, 1.0–1.5). On multivariate analysis, VDBP concentration, low albumin, and medication-induced remission were significantly more associated with disease flare. VDBP genotypes were significantly associated with 25(OH)D and VDBP concentrations but not disease flare.
Vitamin D deficiency was uncommon in our patients with CD in remission, and serum 25(OH)D3 did not predict disease flare, whereas higher VDBP concentrations were significantly associated with disease flare. Further investigations to explore the possible mechanisms for this association are warranted.
Article first published online 22 August 2016.
*Harry Perkins Institute of Medical Research, School of Medicine and Pharmacology, University of Western Australia, Murdoch, Western Australia, Australia;
†Telethon Kids Institute, University of Western Australia, Subiaco, Western Australia, Australia;
‡UWA Centre for Applied Statistics, University of Western Australia, Western Australia, Crawley, Australia;
§Department of Gastroenterology and Hepatology, Flinders Medical Centre, South Australia, Adelaide, Australia;
‖Department of Gastroenterology and Hepatology, Royal Brisbane and Women's Hospital, Queensland, Brisbane, Australia; and
¶Centre for Inflammatory Bowel Diseases, Saint John of God Hospital, Subiaco, Western Australia, Australia.
Address correspondence to: Simon Ghaly, FRACP, Harry Perkins Institute of Medical Research, School of Medicine and Pharmacology, University of Western Australia, 102-118 Murdoch Drive, Murdoch WA 6150, Australia (e-mail: email@example.com).
The study was funded by the GESA-Ferring IBD Clinician Establishment Award 2015.
The authors have no conflict of interest to disclose.
Received June 01, 2016
Accepted June 2, 2016