Reich Krista M, Fedorak Richard N, Madsen Karen, Kroeker Karen I
Krista M Reich, Richard N Fedorak, Karen Madsen, Karen I Kroeker, Division of Gastroenterology, University of Alberta, Edmonton, Alberta T6G 2X8, Canada.
World J Gastroenterol. 2014 May 7;20(17):4934-47. doi: 10.3748/wjg.v20.i17.4934.
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.
维生素D缺乏在炎症性肠病(IBD)患者中很常见。由于维生素D水平低、病程长以及频繁使用类固醇,IBD患者存在骨密度低和骨折风险增加的情况;因此,在这一人群中补充维生素D很重要,这一点已得到充分证实。越来越多的证据支持维生素D在通过作为免疫调节剂增强先天免疫系统和减轻实验性及人类IBD炎症方面的作用。维生素D的活性形式1,25(OH)D3作用于T细胞,促进T辅助(Th)2/调节性T反应超过Th1/Th17反应;抑制树突状细胞的炎症活性;诱导抗菌活性;并调节细胞因子产生以利于抗炎反应。小鼠和人类IBD研究支持维生素D在IBD中的治疗作用。该人群维生素D缺乏的风险因素包括阳光照射减少、病程、吸烟和遗传因素。维生素D水平正常化与复发风险降低、IBD相关手术风险降低以及生活质量改善相关。维生素D是一种价格低廉的补充剂,已被证明可改善IBD的治疗效果。然而,需要进一步研究以确定能产生有益免疫效果的最佳血清维生素D水平,并且需要更有力的证据来支持维生素D在诱导疾病反应和缓解以及维持患者病情改善方面的作用。