Abstract
BackgroundVitamin D is required to maintain the integrity of the intestinal barrier and inhibits inflammatory signaling pathways.ObjectiveVitamin D deficiency might be involved in cirrhosis-associated systemic inflammation and risk of hepatic decompensation in patients with liver cirrhosis.MethodsOutpatients of the Hepatology Unit of the University Hospital Frankfurt with advanced liver fibrosis and cirrhosis were prospectively enrolled. 25-hydroxyvitamin D (25(OH)D3) serum concentrations were quantified and associated with markers of systemic inflammation / intestinal bacterial translocation and hepatic decompensation.ResultsA total of 338 patients with advanced liver fibrosis or cirrhosis were included. Of those, 51 patients (15%) were hospitalized due to hepatic decompensation during follow-up. Overall, 72 patients (21%) had severe vitamin D deficiency. However, patients receiving vitamin D supplements had significantly higher 25(OH)D3 serum levels compared to patients without supplements (37 ng/mL vs. 16 ng/ml, P<0.0001). Uni- and multivariate analyses revealed an independent association of severe vitamin D deficiency with the risk of hepatic decompensation during follow-up (multivariate P = 0.012; OR = 3.25, 95% CI = 1.30–8.2), together with MELD score, low hemoglobin concentration, low coffee consumption, and presence of diabetes. Of note, serum levels of C-reactive protein, IL-6 and soluble CD14 were significantly higher in patients with versus without severe vitamin D deficiency, and serum levels of soluble CD14 levels declined in patients with de novo supplementation of vitamin D (median 2.15 vs. 1.87 ng/mL, P = 0.002).ConclusionsIn this prospective cohort study, baseline vitamin D levels were inversely associated with liver-cirrhosis related systemic inflammation and the risk of hepatic decompensation.
Highlights
Vitamin D is a key hormone in the regulation of bone metabolism [1]
Uni- and multivariate analyses revealed an independent association of severe vitamin D deficiency with the risk of hepatic decompensation during follow-up, together with MELD score, low hemoglobin concentration, low coffee consumption, and presence of diabetes
Serum levels of C-reactive protein, IL-6 and soluble CD14 were significantly higher in patients with versus without severe vitamin D deficiency, and serum levels
Summary
Vitamin D receptor (VDR) signaling has been shown to impact on the expression of more than 9000 genes, and accumulating evidence suggests that these genomic effects of calcitriol, the bioactive form of vitamin D, execute important non-classical (in contrast to bone metabolism) functions of vitamin D such as regulation of immune responses or cell proliferation [2]. A large prospective study has shown that baseline vitamin D deficiency is associated with an increased risk of inflammatory bowel disease during follow-up [6]. This might be explained by direct effects of VDR signaling on tight junctions and integrity of intestinal epithelial cells [7,8]. Vitamin D is required to maintain the integrity of the intestinal barrier and inhibits inflammatory signaling pathways
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