Vitamin D and Inflammatory Bowel Disease

Abstract EN

Vitamin D deficiency has been recognized as an environmental risk factor for Crohn’s disease since the early 80s.

Initially, this finding was correlated with metabolic bone disease.

Low serum 25-hydroxyvitamin D levels have been repeatedly reported in inflammatory bowel diseases together with a relationship between vitamin D status and disease activity.

Subsequently, low serum vitamin D levels have been reported in various immune-related diseases pointing to an immunoregulatory role.

Indeed, vitamin D and its receptor (VDR) are known to interact with different players of the immune homeostasis by controlling cell proliferation, antigen receptor signalling, and intestinal barrier function.

Moreover, 1,25-dihydroxyvitamin D is implicated in NOD2-mediated expression of defensin-β2, the latter known to play a crucial role in the pathogenesis of Crohn’s disease (IBD1 gene), and several genetic variants of the vitamin D receptor have been identified as Crohn’s disease candidate susceptibility genes.

From animal models we have learned that deletion of the VDR gene was associated with a more severe disease.

There is a growing body of evidence concerning the therapeutic role of vitamin D/synthetic vitamin D receptor agonists in clinical and experimental models of inflammatory bowel disease far beyond the role of calcium homeostasis and bone metabolism.