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)

In 101 alcoholic patients, plasma apolipoproteins A-I, A-II and B, and lipids were studied in relation to liver function tests, albumin and bilirubin. As compared with controls, the entire population revealed a slight increase in triglycerides, transaminases and bilirubin, and a marked increase in gamma glutamyl transferase. The population was divided into 3 groups according to histological liver microscopy: no lesion, steatosis and cirrhosis. In group 1, apo A-I, A-II and HDL-C were significantly increased. In steatosis, apo A-I, apo A-II and HDL-C had almost normal levels. In cirrhosis, the 3 parameters were significantly decreased, but the apo A-I/apo A-II ratio was increased in relation to the predominant decrease in apo A-II. Liver enzymes were not discriminative, not even gamma GT, which was increased in all 3 groups. Apolipoprotein B, total cholesterol and LDL-cholesterol were insensitive to the degree of hepatic involvement, but a low apo A-I/B ratio might be indicative of a cardiovascular risk. It is suggested that apoproteins and their ratios be used as new markers for the degree of alcoholic intoxication and the risk of cardiovascular complications.
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PMID:Plasma levels of apolipoproteins A-I, A-II and B in alcoholism. Relation to the degree of histological liver damage, and to liver function tests. 642 88

Considering liver cirrhosis a limit model, and therefore a condition suitable for the analysis of changes of lipid metabolism in liver disorders generally, the authors examined the L-CAT pattern, total and free cholesterol, HDL-cholesterol and APO-A in sixty-five subjects; fifty-three were suffering from liver cirrhosis, and were subdivided into those who were diabetic in addition, and those who were not, as well as according to the severity and duration of the liver disease; the remaining twelve were healthy controls. Analysis of the findings showed L-CAT to diminish significantly as the metabolic changes due to liver injury worsen. Contrary to the other parameters studied, L-CAT was the only one for which significant changes were found on analysis of variance comparing non-diabetic cirrhotics of varying severity. Further comparison suggested the idea that the reduction of L-CAT activity was correlated to the rate of progression of the disease rather than to the temporary condition of compensation or decompensation, so much so as to suggest itself as a valid parameter for the prognosis of liver cirrhosis.
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PMID:Pattern of lecithin-cholesterol-acyl-transferase (L-CAT) activity in the course of liver cirrhosis. 661 81

To elucidate the role of the liver in the metabolism of HDL subfractions, the levels of HDL2 and HDL3 were determined in the sera obtained from patients with liver disease. The determinations were carried out either by zonal ultracentrifugation or by gradient gel electrophoresis combined with HDL cholesterol measurement. Mean HDL3 cholesterol level in patients with liver cirrhosis was about one third of the normal controls whereas no significant changes were observed in HDL2 cholesterol concentration. HDL3 cholesterol levels in patients with chronic hepatitis were about a half of the controls. The levels of HDL3 cholesterol correlated significantly to the levels of serum albumin and to choline esterase activities. The results suggest either that HDL3 is synthesized in the liver or that there is a metabolic defect in the conversion of HDL2 to HDL3 in liver disease.
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PMID:Quantitative determinations of HDL2 and HDL3 in patients with liver disease. 683 48

In order to further investigate plasma lipoproteins abnormalities secondary to serious liver damage, we studied plasma lipids and lipoproteins, and in particular HDL subfractions (HDL2, HDL3), in 12 patients with cirrhosis of the liver and in 12 sex, age and weight matched healthy volunteers. Enzymatic methods were used to determine total cholesterol and triglycerides, while the extractive method of Abell et al. was used for the determination of HDL-cholesterol levels after LDL and VLDL precipitation with polyanions (MnCl2 and Na-heparin) and of HDL3-cholesterol values after HDL2 precipitation with dextran-sulphate 15,000 m.w. Total cholesterol and HDL-cholesterol levels were significantly lower in cirrhotic patients compared to normal subjects. We must emphasize that only HDL3-cholesterol was decreased in cirrhotics, whereas HDL2-cholesterol values were normal or high. We suggest that a diminished activity of hepatic triglyceride lipase might account for the decrease in HDL3-cholesterol in liver cirrhosis.
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PMID:[HDL2 and HDL3 cholesterol in hepatic cirrhosis]. 686 Apr 95

The plasma lipid and apoprotein concentrations were monitored in a group of 12 patients with chronic alcohol abuse entering an abstinence program for 3 weeks. 6 of them had a normal liver function as expressed by the levels of liver enzymes gamma GT, GOT, GPT, while 6 had elevated plasma liver enzyme concentrations. None had evidence of either cirrhosis or alcohol hepatitis. Patients with abnormal liver enzymes had elevated HDL-cholesterol, apo AI and apo AII concentrations in plasma, with normal total cholesterol and apo 8 concentrations. In the group of patients with normal liver enzyme concentrations, the apoproteins and lipids did not significantly differ from the control group. In the course of the abstinence treatment a parallel decrease of apoproteins, HDL-cholesterol and liver enzyme concentrations was observed. The values normalized after 10-15 days. These data indicate that the effect of alcohol on the plasma apoprotein and lipids occurs mostly in the HDL fraction, that it correlates with the state of hepatic function and that it can be reversed by an abstinence treatment.
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PMID:Plasma apoproteins levels in chronic alcohol abuse. 710 48

Changes in lipoprotein fractions HDL and LDL-VLDL were investigated in 84 chronic alcoholic patients and attempts were made to correlate these changes with the severity of liver damage. In 40 patients with undetectable hepatic lesions the lipoprotein fractions were not reduced but a rapidly reversible increase in HDL was noted in 15%. The 14 patients with steatosis and alcoholic hepatitis showed a fall in HDL, often associated with an increase in plasma triglycerides; these changes regressed during weaning. The 30 patients with cirrhosis of the liver had irreversibly low HDL and LDL levels.
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PMID:[Serum lipoproteins in chronic alcoholics. Changes in HDL, VLDL and LDL as a function of the degree of hepatic involvement]. 717 34

Total serum cholesterol (C) and triglyceride (TG) levels, C and TG-VLDL, C-LDL and C-HDL, total apoprotein B (apo B) and albumin (alb.) have been studied in three groups of patients with liver cirrhosis (CE), persistent hepatitis (EPS) and alcoholic chronic liver disease (EA) divided in two sub-groups of 4 EPS and 4 CE, and have been compared with controls values. In all cases the diagnosis was made on liver biopsy C, C-LDL and C-HDL levels were significantly lower in EPS, C and C-LDL in EA and CE; comparing the three groups each other, the only statistically significant difference was found for C-HDL values, more elevated in the 4 cases of EPS with alcoholism than in CE and EPS without alcoholism.
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PMID:[Serum lipoprotein fractions in chronic liver diseases with and without alcoholism]. 730 12

In 214 patients with different chronic liver diseases and in 31 controls the plasma lipids (total and esterified cholesterol, HDL cholesterol, triglycerides) and lipoproteins have been evaluated. The liver patients were classified not only according to traditional diagnostic criteria, but also using a functional classification based on the evaluation of biosynthetic alteration and cholestatic damage, separately assessed in all patients. Parenchimal liver diseases and cholestatic diseases show different and specific plasma lipids and lipoprotein abnormalities. In parenchimal diseases (notably cirrhosis) a reduction of the plasmatic level of total, esterified and HDL cholesterol, without significant changes of triglycerides and lipoproteins was observed. As documented by functional classification, the reduction of total and esterified cholesterol correlates significantly with the degree of biosynthetic alteration. This finding may be related to the reduced hepatic cholesterol synthesis, probably associated with a decreased serum activity of the lecithin cholesterol acyl transferase (LCAT), due to impaired hepatic enzyme synthesis.
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PMID:[Changes in plasma lipids and lipoproteins in chronic liver diseases]. 734 33

In a group of 80 patients (50 male and 30 female) aged between 44 and 65, affected by alcoholic liver disease (46 with steatosis and 34 with liver cirrhosis) the Authors examined the relationship between the plasma lipid, in particular of Lp(a), and the incidence of vascular atherosclerotic plaques. The results were compared with those found in the controls (50 subjects of similar age, social and working status to that of the above patients but nondrinkers without liver or other metabolic disease). In the patients with steatosis we found a moderate increase in plasma lipid fractions including total, HDL and LDL cholesterol, but low levels of Lp(a), with an incidence of arterial plaques of 10.86%. In those with liver cirrhosis the findings were characterized by low levels of lipids and in particular of Lp(a), with an incidence of arterial plaques of 8.82%, decidedly less marked than in the controls (16%). In both cases the low incidence of vascular involvement appears to be in some way linked with low levels of Lp(a) and the severity of liver disease and not with the behaviour of HDL cholesterol.
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PMID:Lp(a) levels and reduced risk of vascular atheromatosis in patients with alcoholic liver disease. 748 Sep 70

Out of 665 patients after liver biopsy performed during 14 years of the work of the Clinic, 35 cases of patients with non-alcoholic liver steatosis and hyperlipoproteinaemia were selected and analysed retrospectively. The cases of patients with the presence of HBV or HCV infection markers were excluded. The histological material was divided according to the intensity of steatosis expressed as the per cent of hepatocytes with the features of fatty degeneration and also according to the following classification: I--steatosis, II--steatosis with hepatitis, III--steatosis with portal fibrosis, IV--steatotic cirrhosis. In the patients in whom the per cent of hepatocytes with fatty degeneration in biopsy examination exceeded 60%, the mean serum triglyceride concentration was 5.53 mmol/l and was over twice higher than that in the group with steatosis not exceeding 30% of hepatocytes. Similarly, in the patients with steatosis and accompanying hepatitis (steatohepatitis), the mean triglyceride concentration was 5.28 mmol/l and was over twice higher than that in the patients with steatosis with accompanying portal fibrosis. The patients with steatohepatitis had significantly lower HDL concentrations than those with the remaining types of histological changes.
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PMID:[Fatty liver assessed by histologic examination in patients with hyperlipoproteinemia]. 748 18


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