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Gastroenterology Research and Practice
Volume 2013 (2013), Article ID 602321, 12 pages
Review Article

The Role of Vitamin D in Primary Biliary Cirrhosis: Possible Genetic and Cell Signaling Mechanisms

Vietnamese American Medical Research Foundation, 14971 Brookhurst Street, Westminster, CA 92683, USA

Received 26 June 2012; Revised 8 November 2012; Accepted 12 November 2012

Academic Editor: P. Malfertheiner

Copyright © 2013 Khanh vinh quốc Lương and Lan Thi Hoàng Nguyễn. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Primary biliary cirrhosis (PBC) is an immune-mediated chronic inflammatory disease of the liver of unknown etiology. Vitamin D deficiency is highly prevalent in patients with PBC, and many studies have demonstrated the significant effect of calcitriol on liver cell physiology. Vitamin D has antiproliferative and antifibrotic effects on liver fibrosis. Genetic studies have provided an opportunity to determine which proteins link vitamin D to PBC pathology (e.g., the major histocompatibility complex class II molecules, the vitamin D receptor, toll-like receptors, apolipoprotein E, Nramp1, and cytotoxic T lymphocyte antigen-4). Vitamin D also exerts its effect on PBC through cell signaling mechanisms, that is, matrix metalloproteinases, prostaglandins, reactive oxygen species, and the transforming growth factor betas. In conclusion, vitamin D may have a beneficial role in the treatment of PBC. The best form of vitamin D for use in the PBC is calcitriol because it is the active form of vitamin metabolite, and its receptors are present in the sinusoidal endothelial cells, Kupffer cells, and stellate cells of normal livers, as well as in the biliary cell line.