Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increasing prevalence of nonalcoholic fatty liver disease (NAFLD) in parallel with the obesity epidemic has been a major public health concern. NAFLD is the most common chronic liver disease in the United States, ranging from fatty liver to steatohepatitis, fibrosis and cirrhosis in the liver. In response to chronic liver injury, fibrogenesis in the liver occurs as a protective response; however, prolonged and dysregulated fibrogenesis can lead to liver fibrosis, which can further progress to cirrhosis and eventually hepatocellular carcinoma. Interplay of hepatocytes, macrophages and hepatic stellate cells (HSCs) in the hepatic inflammatory and oxidative milieu is critical for the development of NAFLD. In particular, HSCs play a major role in the production of extracellular matrix proteins. Studies have demonstrated that bioactive food components and natural products, including astaxanthin, curcumin, blueberry, silymarin, coffee, vitamin C, vitamin E, vitamin D, resveratrol, quercetin and epigallocatechin-3-gallate, have antifibrotic effects in the liver. This review summarizes current knowledge of the mechanistic insight into the antifibrotic actions of the aforementioned bioactive food components.
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PMID:Food components with antifibrotic activity and implications in prevention of liver disease. 2926 6

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.
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PMID:[MALABSORPTION FAT-SOLUBLE VITAMINS AND PROSPECTS OF THEIR USE IN LIVER DISEASES]. 3028 30

Nonalcoholic steatohepatitis (NASH) is a frequent liver disease that can progress to cirrhosis and for which effective therapy is still lacking. Despitean important role of oxidative stress in the pathogenesis of NASH, antioxidant approaches have not been investigatedsufficiently. The aim of the study was to compare the efficacy of ursodeoxycholic acid (UDCA) versus vitamin E plus vitamin C in non-diabetic patients with nonalcoholic steatohepatitis. Patients with elevated aminotransferase levels and drinking, less than 40 g alcohol/week with NASH diagnose were randomly assigned to receive either UDCA 15 mg/per kg/day (group A) or vitamin E 800mg/day plus vitamin C 500 mg/day (group B) for 12 months and control group,which did not receive any medical treatment. Lifestyle modification was advised to all groups. The primary study endpoint was improvement in alanine transaminase (ALT) levels, secondary endpoints were improvement in steatosis score and improvement in fibrosis score. Baseline characteristics were not significantly different between groups. After 12 months treatment with vitamin E plus C, as compared with UDCA, was associated with a significant reduction ofmean alanineaminotransferase (ALT) levels. Similarly, there was significant reduction of both mean steatosis score and fibrosis score. Vitamin E plus C combination is aneffective, safe and inexpensive treatmentoption in patients with NASHand may be useful to reduce damage from oxidative stress and slow the process leading to cirrhosis.
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PMID:COMPARATIVE ANALYSIS OF EFFICIENCY OF URSODEOXYCHOLIC ACID AND COMBINATION OF VITAMIN E AND VITAMIN C IN TREATMENT OF NON-DIABETIC NONALCOHOLIC STEATOHEPATITIS. 3110 82


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