Vitamin D improves inflammatory bowel disease outcomes: basic science and clinical review

Krista M Reich, Richard N Fedorak, Karen Madsen, Karen I Kroeker, Krista M Reich, Richard N Fedorak, Karen Madsen, Karen I Kroeker

Abstract

Vitamin D deficiency is commonly diagnosed among patients with inflammatory bowel disease (IBD). Patients with IBD are at risk of low bone density and increased fractures due to low vitamin D levels, long standing disease, and frequent steroid exposures; as a result, it is well established that vitamin D supplementation in this population is important. There is increasing support for the role of vitamin D in strengthening the innate immune system by acting as an immunomodulator and reducing inflammation in experimental and human IBD. The active form of vitamin D, 1,25(OH)D3, acts on T cells to promote T helper (Th)2/regulatory T responses over Th1/Th17 responses; suppresses dendritic cell inflammatory activity; induces antibacterial activity; and regulates cytokine production in favor of an anti-inflammatory response. Murine and human IBD studies support a therapeutic role of vitamin D in IBD. Risk factors for vitamin D deficiency in this population include decreased sunlight exposure, disease duration, smoking, and genetics. Vitamin D normalization is associated with reduced risk of relapse, reduced risk of IBD-related surgeries, and improvement in quality of life. Vitamin D is an inexpensive supplement which has been shown to improve IBD outcomes. However, further research is required to determine optimal serum vitamin D levels which will achieve beneficial immune effects, and stronger evidence is needed to support the role of vitamin D in inducing disease response and remission, as well as maintaining this improvement in patients' disease states.

Keywords: Cytokines; Immune response; Inflammation; Inflammatory bowel disease; Supplementation; Vitamin D.

Figures

Figure 1
Figure 1
Vitamin D sources and metabolism[8]. Vitamin D can be obtained either from the diet or synthesized in the skin. Under solar ultraviolet (UVB) radiation, 7-dehydrocholesterol in the skin is converted into cholecalciferol (vitamin D3). Vitamin D from the diet enters chylomicrons, which transport it into circulation. Vitamin D is stored in adipose tissue, but when released into circulation, vitamin D binding proteins direct it to the liver where it is converted into its major circulating form, 25-hydroxyvitamin D3 [25(OH)D3] by 25-hydroxylase. In the kidneys, 25(OH)D3 is converted into 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3], the active form, by 1α-hydroxylase. It can now exert its biological effects including calcium absorption, resorption, and bone development. Parathyroid hormone released from the parathyroid glands upregulates hepatic conversion of 1,25(OH)2D3 by stimulating 1α-hydroxylase production; however, autoregulatory mechanisms suppress these actions through negative feedback loops. 1,25(OH)2D3 suppresses parathyroid hormone and 1α-hydroxylase production. Vitamin D is then catabolized by 24-hydroxylase and excreted as calcitroic acid. The recommended optimal range for vitamin D levels is 30-60 ng/mL (75-150 nmol/L). Copyright© 2007 Massachusetts Medical Society. All rights reserved; VDR: Vitamin D receptor; RXR: Retinoid X receptor.

Source: PubMed

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