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)

The plasma lecithin: cholesterol acyltransferase was determined in patients with various liver diseases and the relationship between this enzyme activity and the other liver function tests were studied including long term observations. Lecithin: cholesterol acyltransferase activity in fulminant hepatitis and liver cirrhosis showed a significant decrease in comparison with normal volunteers. Although the enzyme activity of hepatoma showed significant decrease, they were ascribed to the influence of concomitant liver cirrhosis. The enzyme activity showed insignificant changes in the acute and chronic hepatitis and alcoholic liver disease. Lecithin: cholesterol acyltransferase activity was correlated with the concentration of cholesterolester rather than with the ratio of esters to cholesterol. In addition, it was well correlated with pseudocholine esterase and serum albumin. The lecithin: cholesterol acyltransferase activity in the cases during follow-up period varied in good parallel with cholesterol-esters concentration and pseudocholine esterase in the cases with acute hepatitis; with serum albumin in the cases with liver cirrhosis. Furthermore, it varied inversely with SGPT in the cases with acute hepatitis. In a case with hepatoma, lecithin: cholesterol acyltransferase activity decreased more sharply than the cholesterolesters concentration and serum albumin immediately before death.
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PMID:Plasma lecithin: cholesterol acyltransferase activity in liver disease. 23 Sep 93

For the evaluation of certain differences in the diminution of export proteins of the liver we examined some exactly defined groups of liver diseases with the aim of further differentiation of the pathogenetic mechanisms. We measured the activity of glutamate-oxalacetate transaminase, glutamate-pyruvate transaminase, glutamate dehydrogenase, lactate dehydrogenase, alkaline phosphatase, cholinesterase and lecithin-cholesterol acyltransferase, the Quick value, the coagulation factors I, II, V, VII, VIII, IX and X. Clotting factors were determined by a Schnitger-Gross Coagulometer. Prothrombin, antithrombin III, plasminogen, factor VIII associated antigen and activated factor XIII were measured by immunoelectrophoresis according to Laurell. Lipoprotein electrophoresis in agarose gel was performed to evaluate changes in lecithin-cholesterol acyltransferase activity. Except of the rising diminution of export proteins in the course of liver disease from acute hepatitis to cirrhosis we found also specific changes of the patterns of the plasma specific enzymes. These proteins were diminished dependent on their half life time and the inflammatory activity--measured as the height of the transaminases. Lecithin cholesterol acyltransferase and factor VIII did not participate in the general diminution of the most export proteins; some details were found to explain this differing behaviour. Results are critically discussed with regard to new aspects in the biochemistry of the damaged liver cell.
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PMID:[Correlations between the diminished secretion of export proteins from the liver and the plasmatic activity of liver cell enzymes (author's transl)]. 42 91

Most patients with stable cirrhosis of the alcoholic have "target" red cells; however, a minority have "spur" cells and severe hemolytic anemia. These two syndromes were studied in 27 patients with target cells and 17 patients with spur cells, all of whom had advanced cirrhosis. The cholesterol and phospholipid content of red cell membranes effectively distinguished target cells from spur cells. Target cells alone were rich in lecithin, and both the cholesterol/phospholipid and cholesterol/lecithin mole ratios were greater in spur cells. The cholesterol/phospholipid mole ratio of both types of red cells correlated closely with the free cholesterol saturation of serum lipoproteins, as defined by the amount of free cholesterol relative to phospholipid and protein in these lipoproteins. Lecithin: cholesterol acyltransferase (LCAT) activity was decreased in most patients with target cells and spur cells; however, the relationship between this activity and the lipid abnormalities observed was weak. Serum bile acid levels also correlated poorly with serum and cell lipids. However, in patients with target cells the amount of cholic and deoxycholic acids in serum was approximately equal to the amount of chenodeoxycholic acid, whereas in patients with spur cells chenodeoxycholic acid (the precursor of lithocholic acid) predominated.
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PMID:An analysis of lipoproteins, bile acids, and red cell membranes associated with target cells and spur cells in patients with liver disease. 464 Sep 53

Phosphatidylcholine (PC), especially dilinoleoyl-PC, has been reported to be effective in preventing hepatic fibrosis in chronically alcohol-fed baboons. Continuous hepatic inflammation predisposes the structure of the liver to fibrosis. Since n-3 polyunsaturated fatty acids (PUFA) have been shown to exhibit an anti-inflammatory effect, we tested the hypothesis that n-3 PUFA PC as a dietary supplement has a beneficial effect on chronic liver disease susceptible to fibrosis. Salmon roe phospholipids, 90% of which are PC, were extracted and encapsulated. Almost a third of the PC fatty acids were docosahexaenoic acid (22:6 n3) and 10% were eicosapentanoic acid (20:5 n3). About 1600 mg/day of the phospholipids was administered for six months to six chronic liver disease patients, four with hepatitis B infection (three with cirrhosis, one with chronic hepatitis), one with hepatitis C virus cirrhosis and one with alcoholic cirrhosis. There was no change in the results of blood chemistry studies related to liver function, except in globulin, which decreased from 3.80 g/dl to 3.67 g/dl (p < 0.05). Among the lipid parameters, HDL-cholesterol, apolipoprotein A-I and apolipoprotein E increased significantly. Although this was a small trial, n-3 PUFA PC may be beneficial in the treatment of chronic liver diseases.
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PMID:Beneficial effect of salmon roe phosphatidylcholine in chronic liver disease. 1062 24

Hepatitis E virus (HEV) infection in most individuals is known as a self-limiting, acute, icteric hepatitis, but evidence shows HEV is responsible for choric hepatitis and rapid progressed liver cirrhosis in immuno-compromised patients. We present the case of a patient whose diagnosis of acute graft failure was due to a HEV infection 7 years after his first liver transplantation because of Wilson's disease. The process showed severe jaundice with fatigue, poor appetite and continually rising serum aminopherase. The blood serum was found positive for the anti-HEV IgG antibody but negative for anti-HEV IgM or other infections. Cholangiole cholestasis was detected in graft biopsy. Triple hepato-protective drugs (Transmetil, Polyene Phosphatidylcholine, and Compound Ammonium Glycyrrhetate S) alongside five times Artificial Liver Support System (ALSS) did not improve the patient's condition, but the total bilirubin level rose to more than 900umol/L. So re-transplantation was performed. Blood testing shows normal liver enzymes and bilirubin with persisting anti-HEV IgG antibody positive at the 3-month follow-up.
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PMID:Hepatitis E virus infection results in acute graft failure after liver transplantation: a case report. 2451 38

Nonalcoholic fatty liver disease (NAFLD) is a term used to characterize a range of disease states that involve the accumulation of fat in the liver but are not associated with excessive alcohol consumption. NAFLD is a prevalent disease that can progress to organ damage like liver cirrhosis and hepatocellular carcinoma. Many animal models have demonstrated that one-carbon metabolism is strongly associated with NAFLD. Phosphatidylcholine is an important phospholipid that affects hepatic lipid homeostasis and de novo synthesis of this phospholipid is associated with NAFLD. However, one-carbon metabolism serves to support all cellular methylation reactions and catabolism of methionine, serine, glycine, choline, betaine, tryptophan, and histidine. Several different pathways within one-carbon metabolism that play important roles in regulating energy metabolism and immune function have received less attention in the study of fatty liver disease and fibrosis. This review examines what we have learned about hepatic lipid metabolism and liver damage from the study of one-carbon metabolism thus far and highlights unexplored opportunities for future research.
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PMID:One-Carbon Metabolism in Fatty Liver Disease and Fibrosis: One-Carbon to Rule Them All. 3211 38