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

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Summary

Introduction

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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