Vitamin D in chronic liver disease
Liver International Dec 2012
Caroline S. Stokes 1, Dietrich A. Volmer 2, Frank Grünhage 1, Frank Lammert 1,*
1 Department of Medicine II, Saarland University Medical Center, Homburg, Germany
2 Institute of Bioanalytical Chemistry, University of Saarland, Saarbrücken, Germany
* Corresponding author: Prof. Dr. med. Frank Lammert, Department of Medicine II
Saarland University Medical Center, Kirrberger Str. 100, 66421 Homburg, Germany
Phone: +49-6841-16-23201; Fax: +49-6841-16-23267; Email: firstname.lastname@example.org
© 2012 John Wiley & Sons A/S
Chronic liver disease (CLD) and several related extrahepatic manifestations such as hepatic osteodystrophy are associated with deficiency of vitamin D, which has therefore been suggested as therapeutic target. Vitamin D undergoes hepatic 25-hydroxylation, rendering the liver critical to the metabolic activation of this vitamin. Vitamin D deficiency is highly prevalent in CLD patients, and vitamin D levels are inversely related to the severity of CLD. Declining levels of carrier proteins such as albumin and vitamin D binding protein might also be critical in CLD. Intervention studies report improvements of CLD following supplementation, and benefits to health outcomes in particular with respect to hepatitis C virus infection have recently been documented.
We discuss vitamin D sources, functions and metabolism with a focus on the inherent complications of analytical measurements, such as the interference of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D C-3 epimers. Global discrepancies in the definition of optimal serum 25-hydroxyvitamin D levels are covered, and the prevalence of vitamin D deficiency in CLD is reviewed. We also address the functional mechanism underlying this deficiency, and refer to associations between genetic variation in vitamin D metabolism and CLD. Lastly, we focus on health implications of a vitamin D deficiency in CLD and consider therapeutic options.
Herein, we focus on the epidemiological and functional relationships between vitamin D deficiency and CLD, followed by a discussion of the potential implications for therapeutic interventions in clinical practice.
Provisional PDF is attached at the bottom of this page