Abstract
Background and objectivesThe hydroxylation to 25-hydroxy vitamin D (25(OH)D) occurs in the liver and the impact of liver disease on vitamin D is unclear. This study evaluated the relationship between vitamin D concentrations and hepatic histopathology, seasonality and patient characteristics in well-characterized patients having undergone a liver biopsy.Method25(OH)D was measured post-hoc in pre-treatment serum from 331 North European patients with chronic HCV genotype 2 or 3 infection (NORDynamIC study). Liver biopsies were scored for fibrosis and inflammation according to the Ishak protocol, and graded for steatosis. Non-invasive markers of hepatic fibrosis as well as baseline viral and host characteristics, including genetic polymorphisms rs2228570, rs7975232, and rs10877012 were also evaluated.ResultsMean 25(OH)D concentration was 59 ±23 nmol/L, with 41% having values <50 nmol/L and 6% were <30 nmol/L. 25(OH)D correlated with fibrosis (r = -0.10, p ≤0.05) in univariate but not in multivariate analyses. No association was observed between 25(OH)D and hepatic inflammation, but with steatosis in HCV genotype 2 infected patients. None of the genetic polymorphisms impacted on 25(OH)D levels or fibrosis. 25(OH)D levels were significantly inversely correlated to BMI (r = -0.19, p = 0.001), and was also associated with season and non-Caucasian ethnicity.ConclusionFibrosis was not independently associated with 25(OH)D concentration and no association was seen with hepatic inflammation, but HCV genotype 2 infected patients with moderate-to-severe steatosis had lower 25(OH)D levels compared to those without steatosis. A high percentage had potential risk of 25(OH)D deficiency, and BMI, seasonality and ethnicity were independently associated with 25(OH)D as previously reported.
Highlights
Vitamin D is essential for bone mineralization by regulating calcium and phosphate levels in blood, and deficiency can lead to rickets and osteomalacia [1]
None of the genetic polymorphisms impacted on 25(OH)D levels or fibrosis. 25(OH)D levels were significantly
Fibrosis was not independently associated with 25(OH)D concentration and no association was seen with hepatic inflammation, but hepatitis C virus (HCV) genotype 2 infected patients with moderateto-severe steatosis had lower 25(OH)D levels compared to those without steatosis
Summary
Vitamin D is essential for bone mineralization by regulating calcium and phosphate levels in blood, and deficiency can lead to rickets and osteomalacia [1]. As UV radiation in the northern latitudes is insufficient for production during winter, stored vitamin D, sufficient dietary intake, and/or supplementation are needed for maintenance of adequate levels during this season [5]. Calcitriol signals through the vitamin D receptor (VDR), influences the expression of a multitude of genes, and is expressed in most human cell types indicating a broader effect than regulation of bone mineralization [6]. This study evaluated the relationship between vitamin D concentrations and hepatic histopathology, seasonality and patient characteristics in wellcharacterized patients having undergone a liver biopsy
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