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Vitamin D Supplement improve SVR in Chronic Hepatitis C (Genotype 1) Naïve Patients treated with Peg Interferon and Ribavirin
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Reported by Jules Levin
European Association for the Study of the Liver (EASL)
Vienna, Austria
April 16, 2010
S. Abu Mouch1,2,3, Z. Fireman3,4, J. Jarchovsky2,4, N. Assy3,5
1Hepatology Unit, 2Internal Medicine B, Hillel Yaffe Medical Center, Hadera, 3Faculty of Medicine, Technion, Haifa, 4Gastroenterology, Hillel Yaffe Medical Center, Hadera, 5Liver Unit, Ziv Medical Center, Safed, Israel. *saif@hy.health.gov.il
1. Andrew et al. N Engl. J Med 2004;350:2265-71.
2. Hugo et al. Hepatology 2007;46:350-358.
Rodriguez-Torre et al. N Engl J Med 2009;360:257-67
Rodriguez-Torre et al. N Engl. J Med 2009;360:257-67.
Am J Clin. Nutr. 2008;88(suppl.):558S- 64S
Am J Clin Nutr 2008;88(suppl):558S- 64S
Holick M. N Engl J Med 2007;357:266-281
Figure 2. Metabolism of 25-Hydroxyvitamin D to 1,25-Dihydroxyvitamin D for Nonskeletal Functions. When a macrophage or monocyte is stimulated through its toll-like receptor 2/1 (TLR2/1) by an infectious agent such as Mycobacterium tuberculosis or its lipopolysaccharide, the signal up-regulates the expression of vitamin D receptor (VDR) and 25-hydroxyvitamin D-1{alpha}-hydroxylase (1-OHase). A 25-hydroxyvitamin D [25(OH)D] level of 30 ng per milliliter (75 nmol per liter) or higher provides adequate substrate for 1-OHase to convert 25(OH)D to its active form, 1,25 dihydroxyvitamin D [1,25(OH)2D]. 1,25(OH)2D travels to the nucleus, where it increases the expression of cathelicidin, a peptide capable of promoting innate immunity and inducing the destruction of infectious agents such as M. tuberculosis. It is also likely that the 1,25(OH)2D produced in monocytes or macrophages is released to act locally on activated T lymphocytes, which regulate cytokine synthesis, and activated B lymphocytes, which regulate immunoglobulin synthesis. When the 25(OH)D level is approximately 30 ng per milliliter, the risk of many common cancers is reduced. It is believed that the local production of 1,25(OH)2D in the breast, colon, prostate, and other tissues regulates a variety of genes that control proliferation, including p21 and p27, as well as genes that inhibit angiogenesis and induce differentiation and apoptosis. Once 1,25(OH)2D completes the task of maintaining normal cellular proliferation and differentiation, it induces expression of the enzyme 25-hydroxyvitamin D-24-hydroxylase (24-OHase), which enhances the catabolism of 1,25(OH)2D to the biologically inert calcitroic acid. Thus, locally produced 1,25(OH)2D does not enter the circulation and has no influence on calcium metabolism. The parathyroid glands have 1-OHase activity, and the local production of 1,25(OH)2D inhibits the expression and synthesis of parathyroid hormone. The 1,25(OH)2D produced in the kidney enters the circulation and can down-regulate renin production in the kidney and stimulate insulin secretion in the beta islet cells of the pancreas.
Mol Aspects Med. 2008 December ; 29(6): 369-375. doi:10.1016/j.mam.2008.04.004
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