Despite all of the accolades that vitamin D has received, the fact that low vitamin D is associated with worse outcomes, in a number of disease states, does not prove causality. A recent article indicates that vitamin D is likely more of a marker of disease activity than a mediator of disease activity in inflammatory bowel disease (IBD), and specifically Crohn’s disease (CD) (Inflamm Bowel Dis 2014; 20: 856-60).
Background: Binding sites for the vitamin D receptor (VDR) have been “identified in genes associated with CD, and vitamin D has been shown to enhance the production of interleukin-10 (IL-10) and induction of regulatory T-cells.”
Design:The authors prospectively collected samples of 37 CD patients; the mean age in those with active disease (n=20) was 34 years and it was 30 years in those with inactive disease. In 8 patients with active disease, vitamin D levels were measured at the time of active inflammation (day 0) and at 14 days after receiving infliximab (day 14).
- Key finding in these 8 patients: Vitamin D (25-OH) was 23 ng/mL on day 0 and 40 ng/mL 2 weeks later. Only 1 of these 8 patients was taking a vitamin D supplement.
- Key finding in the entire cohort: in the active disease group mean vitamin D level was 27 ng/mL compared with 38 ng/mL in those in remission (P=0.02).
Take-home point: There is an inverse relationship between vitamin D levels and disease activity. However, the early increases in vitamin D levels with clinical response to anti-TNF therapy suggests that a major mechanism of vitamin D deficiency is related to the burden of systemic inflammation. Hence, repeat testing when patients are in remission may obviate the need for vitamin D supplementation in many patients.
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