| Abstract: | In a review article considers issues of efficiency and tactics of the purpose of fat-soluble vitamins, as in cholestatic and noncholestatic liver disease, as well as water-soluble vitamins, particularly vitamin C cholelithiasis. Oxidative stress due to chronic inflammation is one of the major conversion mechanisms of liver fibrosis in cirrhosis. The imbalance between production of reactive oxygen species and antioxidant defense causes a number of pathophysiological changes in the liver, including activation of hepatic stellate cells. The carriers of the I148M PNPLA3 mutation was not observed concentration reduction in liver vitamin A with increasing severity of the disease, but the observed decrease in the level of circulating retinyl palmitate and retinol-binding protein. To the appointment of vitamin A in liver disease should be approached with caution. Hypervitaminosis A leads to accelerated liver fibrosis and stimulates carcinogenesis. Currently actively studied the possibility of using vitamin E as an antioxidant, in patients with non-alcoholic fatty liver disease. His presence in the membranes phospholipid bilayer allows cells to prevent non-enzymatic oxidation of cell components by free radicals. Vitamin E can suppress the profibrotic processes. In patients with chronic cholestatic liver disease is common, vitamin K deficiency, even when administered, and is associated with the degree of cholestasis and severity of disease. The vitamin D deficiency, liver disease is also associated with the severity of disease correlated with the severity of liver failure and infectious complications. Vitamin D is an independent prognostic parameter for mortality risk in patients with liver cirrhosis. |
