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)

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

The behaviour of LCAT was examined in acute viral hepatitis and post-hepatic cirrhosis. In the former case, the enzyme was also investigated during remissions. The influence of cholestasis on LCAT activity was evaluated. Depression was noted in cirrhosis and the acute stage of hepatitis, whereas enhanced values were observed during remissions. Depression of the enzyme by cholestasis is explained in a variety of ways.
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PMID:[The behavior of lecithin cholesterol acyltransferase (LCAT) in acute viral hepatitis and post-hepatitis cirrhosis]. 44 Jun 18

C4b-binding protein (C4bp), a glycoprotein involved in regulating the classical pathway of the complement system, binds the activated form of C4b and accelerates the decay rate of the C4b, C2a complex. Recently, sequence analysis of the cDNA for proline-rich protein (PRP) demonstrated that PRP is identical with C4bp. We measured the concentration of C4bp in serum by single radial immunodiffusion in patients with various liver diseases. Concentration of C4bp was significantly lower in hepatic cirrhosis (P = 0.001) and higher in fatty liver (P = 0.0002) than the control values, after adjusting for age, sex, and concentration of total cholesterol, triglyceride, and C-reactive protein. Significant positive correlations were observed between the concentration of C4bp in serum and total protein, albumin, cholinesterase level, and lecithin-cholesterol acyltransferase activity. Immunohistochemical analysis of human liver with specific antiserum to human C4bp demonstrated reaction endproducts in the hepatocytes around the central veins. These observations provide evidence that C4bp is synthesized by hepatocytes.
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PMID:Evidence that C4b-binding protein (proline-rich protein) is synthesized by hepatocytes. 204 87

Hepatic diseases differ from most other causes of secondary dyslipidaemia in that the circulating lipoproteins are not only present in abnormal amounts but they frequently also have abnormal composition, electrophoretic mobility and appearance. Pre-beta and alpha bands can be absent on electrophoresis in all types of liver disease although material in the VLDL and HDL ranges can be isolated in the ultracentrifuge. Cholestatic liver disease has been the most extensively studied and the hyperlipidaemia can be extreme with marked elevations of free cholesterol and phospholipids. This results largely from the presence of LP-X, an abnormal LDL, with a vesicular structure that appears in rouleaux formation under the electron microscope. It is virtually specific for cholestasis and familial LCAT deficiency. The LDL, however, is heterogeneous and may also contain a large triglyceride-rich particle (LP-Y) as well as more normal-looking particles, which are none the less depleted in cholesteryl esters and rich in triglycerides. Indeed, when patients with cholestasis are hypertriglyceridaemic the excess triglyceride is to be found predominantly in these two LDL fractions rather than in VLDL. HDL in cholestasis may contain disc-like particles, similar to those newly secreted by the liver and intestine, as well as more normal-looking spherical particles. In extrahepatic obstruction concentrations of HDL and its major apolipoproteins, apoAI and apoAII, are frequently reduced, although a subfraction rich in apoE is often found. In all but the latest stages of chronic intrahepatic cholestasis due to primary biliary cirrhosis, however, HDL, especially HDL2, concentrations are increased, probably due to the presence of a circulating inhibitor of HL. Many of these lipoprotein changes found in cholestasis resemble those of familial LCAT deficiency, although the hyperlipidaemia is not usually so severe in the latter condition. Indeed, in patients with cholestasis but well-preserved LCAT activity many of the characteristic lipoprotein changes, such as LP-X, LP-Y and discoidal HDL, may not be seen. In acute hepatocellular disease, such as alcoholic or viral hepatitis, it is not unusual for the patient to go through a cholestatic phase and many of the same lipoprotein changes may be seen. In cirrhosis without cholestasis the patients are not usually significantly hyperlipidaemic and in advanced cases cholesterol and apoB levels may be reduced. Although LCAT activity and the proportion of plasma cholesterol esterified may also be markedly reduced, LP-X is not usually seen, possibly because the flux of free cholesterol and phospholipid (lecithin), the LCAT substrates, is relatively low. Discoidal HDLs are often present.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Dyslipoproteinaemia of liver disease. 208 7

The disappearance rate of indocyanine green (K.ICG) and the maximum removal rate (Rmax) usually correlate with each other. However, in some cases it was shown there was a dissociation between them. We investigated the relationship between the two rates in 146 subjects. K.ICG and Rmax correlated strongly with a correlation coefficient of 0.749 (p less than 0.001). Sixty-six cases were included in the limits of 95% confidence, and the other 80 cases outside the limits were defined as dissociated cases. Among them a lower Rmax rate as compared to the K.ICG rate was found in many cases of obstructive jaundice. Particularly a lower K.ICG rate compared to the Rmax rate was found in many cases of liver cirrhosis accompanied by esophageal varices and idiopathic portal hypertension. On the other hands, we performed multiple regression analysis on 12 other liver function tests. K.ICG was strongly related to platelet count, circulatory blood volume, and albumin, all factors relating to portal hypertension. Rmax largely depended on LCAT, A/G ratio, and cholinesterase, which are Therefore, the dissociation between K.ICG and Rmax was caused by differences in the characteristic of each disease.
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PMID:[Evaluation of correlation between the disappearance rate of indocyanine green and the maximum removal rate]. 223 72

The activity of LCAT (the controlling enzyme for cholesterol esterification in plasma) is known to be reduced in alcoholic cirrhosis, while little is known about early stage (liver steatosis) alcoholics. In this study, LCAT activity was assayed by Stokke and Norum's method, before and after a 15-day sobriety period, in liver steatosis and in cirrhosis alcoholics. Before alcohol withdrawal, LCAT activity was depressed in both groups. After the sobriety period, LCAT activity was significantly raised in liver steatosis patients, but was still lower than in controls; in cirrhosis patients, it was increased, but not significantly. According to our results, LCAT activity impairment in alcoholic liver disease is sustained by both the hypothesized mechanisms, alcohol-related metabolic disorders and lowered LCAT-enzyme production, but to different degrees, depending on the stage of the disease. In liver steatosis, metabolic disorders play a major role, as a liver-impairment-induced decrease in LCAT production seems rather unlikely, and increased LCAT activity is more likely to be sustained by metabolic normalisation than by any recovery of the damaged liver. However, the lack of improvement in about 20% of patients, and the fairly wide scattering of individual data, suggest a minor LCAT production impairment in liver steatosis too. In cirrhosis, the major role seems to be played by a permanent decrease in LCAT production, as no significant rise in LCAT activity was observed after alcohol withdrawal. However the restored LCAT activity observed in some patients could be related to improvement in the metabolic disorder, thus confirming the effectiveness of this mechnism in cirrhosis too.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lecithin: cholesterol-acyltransferase (LCAT) activity in alcoholic liver disease. 272 87

Serum apoproteins A and B and LCAT activities were estimated in 80 patients, 46 with posthepatic cirrhosis and 34 with alcoholic cirrhosis. The cirrhosis patients were also divided into compensated, decompensated, and hepatic coma subgroups. Apo-A and LCAT activities were significantly decreased in both cirrhotic groups without any significant difference between posthepatitic and alcoholic cirrhotic groups, while Apo-B was decreased in hepatic coma patients only. The decompensated cirrhosis patients showed lower Apo-A levels than the compensated cirrhosis patients and hepatic coma patients showed still lower levels compared to decompensated subgroup, while no significant decrease was observed in LCAT activities between compensated and decompensated cirrhosis patients. Apo-A level was correlated more significantly with serum albumin level than the LCAT activity. The study confirms that Apo-A level is highly related to the degree of liver injury and also suggests that this decrease may be mainly due to impaired liver synthesis and that the serum levels of Apo-A and Apo-B can be utilized in the differential diagnosis of chronic liver diseases.
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PMID:Serum apoproteins A and B and the lecithin: cholesterol acyl transferase activities in liver cirrhosis and hepatic coma patients. 323 86

A ninth Japanese patient afflicted with lecithin-cholesterol acyltransferase (LCAT) deficiency is described with emphasis on renal pathology. The most striking feature is massive deposition of lipid material in the glomeruli, particularly in the glomerular basement membrane (GBM) and in the mesangial region. The glomerular changes appear to be similar to that seen in some cases with cirrhosis of the liver. Lipid material contains a large amount of apolipoprotein-B detected by immunohistology. In two renal biopsies, taken three years apart, renal pathology is essentially the same and glomerular pathology is most characteristic. It is suggested that lipid deposition in glomeruli in this patient is rather slow. Family study of the present case reveals consanguinous marriages in the previous two generations suggesting the exaggerated gene expression of LCAT deficiency in this family.
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PMID:Nephropathy of familial lecithin-cholesterol acyltransferase deficiency: report of a case. 351 May 35

12 patients with unequivocal post-alcoholic end-stage liver cirrhosis were compared with 12 healthy controls with regard to the plasma concentrations of lipids, lipoproteins (by rate zonal ultra-centrifugation) and apolipoproteins of high-density-lipoproteins (HDL) (by disc electrophoresis), as well as to the activities of lecithin-cholesterol acyltransferase (LCAT) in plasma and of hepatic lipase (HL) in post-heparin plasma. The cirrhotic group showed the following differences (all significant at the p less than 0.01 level) from the control group: Total cholesterol, HDL-cholesterol, very-low-density-lipoproteins (VLDL), HDL, and HL were decreased. Intermediate-density-lipoproteins (IDL) were not detectable in the cirrhotic group. Low-density-lipoproteins (LDL) did not differ significantly from controls. However, LDL from cirrhotic patients contained more triglycerides but less esterified and free cholesterol (all p less than 0.01). The percentage apolipoprotein composition of HDL did not differ significantly between controls and cirrhotics. Surprisingly, LCAT activity in plasma as well as the ratios between esterified and free cholesterol in plasma, LDL, and HDL were nearly identical in both groups. It seems likely that LCAT activity decreases only in the states of acute or subacute liver injury or of biliary obstruction. Severe chronic liver injury or of biliary obstruction. Severe chronic liver damage as in our cases of end-stage liver cirrhosis without any signs of acute liver injury exhibits apparently no defect in cholesterol esterification.
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PMID:Lipoproteins, HDL-apolipoproteins, activities of hepatic lipase and lecithin-cholesterol acyltransferase in the plasma of patients with post-alcoholic end-stage liver cirrhosis. 663 32

Serum lipids and lipoproteins were analyzed after an overnight fast, and following a fatty meal in 10 patients with cirrhosis, 5 with fatty liver, and 5 normal subjects. Cirrhotic patients were divided into two groups of five on the basis of serum lecithin-cholesterol acyltransferase activity. Fasting triglyceride levels were similar in all four groups. In all but cirrhotic patients with low lecithin-cholesterol acyltransferase activity, most fasting triglyceride was found in very low density lipoproteins; in the latter group, most of it was found in low density lipoproteins. We confirmed that patients with fatty liver have a higher serum triglyceride response to fat feeding than normal subjects, but we did not find higher levels in cirrhotic patients. Cirrhotic patients with "normal" lecithin-cholesterol acyltransferase activity had a normal triglyceride response to dietary fat. In patients with cirrhosis and low lecithin-cholesterol acyltransferase activity, the increase in triglyceride was less than in normal subjects. In this group, most of the extra triglyceride was carried in low density lipoprotein, and not in chylomicrons and very low density lipoprotein, as in the other groups.
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PMID:Plasma lipid and lipoprotein response to fat feeding in alcoholic liver disease. 684 Jun 80


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