Journal
WORLD JOURNAL OF GASTROENTEROLOGY
Volume 20, Issue 17, Pages 4934-4947Publisher
BAISHIDENG PUBLISHING GROUP INC
DOI: 10.3748/wjg.v20.i17.4934
Keywords
Vitamin D; Inflammatory bowel disease; Immune response; Inflammation; Cytokines; Supplementation
Categories
Funding
- Center of Excellence for Gastrointestinal and Immunity Research (CEGIIR)
- Alberta Innovates-Health Solutions Inflammatory Bowel Disease Consortium
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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. (C) 2014 Baishideng Publishing Group Co., Limited. All rights reserved.
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