Vitamin D deficiency has been proved to be associated with many chronic liver diseases. We read with great interest the recent article by Petta et al.1 in which they reported that low vitamin D serum level is related to severe fibrosis and low response to antiviral therapy in patients with genotype 1 (G1) chronic hepatitis C (CHC). The authors also provided important information that low serum vitamin D levels may possibly result from the reduced cytochrome P27A1 expression in patients with G1 CHC.1 However, further investigations are needed to understand the causal association between vitamin D deficiency and fibrosis in patients with CHC.
According to the recent significant finding that vitamin D is crucial to activating the immune defenses,2 I would like to propose that low serum vitamin D level may favor progression of fibrosis in patients with CHC. It was found that the killer cells of the immune system—human T cells—depend on vitamin D in order to be activated. Under the condition of vitamin D deficiency, T cells will not be able to react to and kill foreign pathogens in the body.2 Thus, it is conceivable that a low vitamin D serum level will make T cells remain inactive to hepatitis C virus and aggravate the fibrosis in patients with CHC.1 Moreover, in view of the prevalence of vitamin D deficiency in many chronic liver diseases,3, 4 the finding that vitamin D controls activation of human T cells has important implications for future studies concerning the potential role of vitamin D in the treatment of chronic liver diseases.