O144: Vitamin D deficiency and hepatitis C

Abstract

Patients with chronic hepatitis C are at high risk of severe vitamin D insufficiency and deficiency, defined as 25-hydroxyvitamin D [25(OH)D3] serum levels <20 ng/mL and <10 ng/mL, respectively. Though advanced liver fibrosis and cirrhosis are determinants of hepatitis C virus (HCV)- related vitamin D deficiency, even patients without liver fibrosis have a significantly higher prevalence of vitamin D deficiency than uninfected individuals. Increasing evidence indicates that vitamin D deficiency in the general population not only negatively affects bone health, but also promotes metabolic disorders like the metabolic syndrome or steatosis and inflammatory diseases like type I diabetes. Importantly, a recent large prospective study in the general population has revealed an association between intact vitamin D metabolism and overall survival. Interestingly, we have shown recently in a large study that an impaired vitamin D metabolism may also promote the risk of hepatocellular carcinoma development related to HCV infection. Furthermore, clinical and in vitro studies suggest a functional role of vitamin D signaling in the response to interferon-alfa-based therapies of chronic hepatitis C. In this regard, it appears important to point out that serum concentration of 25(OH)D3, the precursor of the bioactive vitamin D metabolite calcitriol, is not a reliable predictor of treatment outcome, though some studies have suggested an association between 25(OH)D3 serum levels and treatment outcome. Collectively, vitamin D supplementation appears highly relevant in many patients with chronic hepatitis C as it may prevent significant adverse clinical endpoints. Furthermore, it appears likely that vitamin D metabolism plays a role in the outcome of antiviral therapy of chronic hepatitis C, but it currently remains unclear whether administration of vitamin D metabolites could be useful in improving treatment outcome.