Vol 117, No 2 (Supplement) 2012
Supplement abstract

Liver vitamin D receptor, CYP2R1 and CYP27A1 expression related to progression of metabolic and viral chronic liver damage

Published 2013-02-21

Keywords

  • Vitamin D receptor,
  • vitamin D 25-hydroxylases,
  • non-alcoholic steatohepatitis

How to Cite

Carotti, S., Barchetta, I., Vespasiani-Gentilucci, U., Onetti-Muda, A., Picardi, A., Cavallo, M., & Morini, S. (2013). Liver vitamin D receptor, CYP2R1 and CYP27A1 expression related to progression of metabolic and viral chronic liver damage. Italian Journal of Anatomy and Embryology, 117(2), 33. Retrieved from https://oajournals.fupress.net/index.php/ijae/article/view/4219

Abstract

Background and aim: Low serum 25(OH)vitamin D3 levels were associated with the presence and prognosis of liver diseases [1]. The biological effects of 1,25(OH)2 vitamin D3 are mediated by the vitamin D receptor (VDR) and VDR has been widely detected in liver, but its expression in the course of liver disease has never been investigated [2]. We aimed to evaluate the hepatic expression of VDR and vitamin D 25-hydroxylases in patients with chronic hepatitis C (CHC) or non-alcoholic steatohepatitis (NASH) and its relationship with liver histology and serum 25(OH) vitamin D3 levels. Methods: Patients affected by CHC or NASH who had undergone liver biopsy and subjects without liver disease were included. Expression of VDR, CYP2R1 and CYP27A1 was evaluated by immunohistochemistry. Results: In CHC subjects, fibrosis stage was associated with low hepatic CYP27A1 expression, whereas in patients with VDR-negative inflammatory cells and low VDR expression on hepatocytes, the portal inflammation was significantly higher (p<0.009 and p<0.03). In NASH patients, VDR expression on cholangiocytes was inversely correlated with steatosis severity (p<0.02), lobular inflammation (p<0.01) and NAS score (p<0.03). Conclusions: The liver of patients with viral and metabolic chronic liver disease expresses VDR in a manner inversely proportional to the severity of histological lesions and a role of the vitamin D/VDR system in the progression of chronic liver damage is suggested.