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)

A case of symptomatic hypobetalipoproteinemia (hypo-beta LP) with unusual distribution of apolipoprotein E (apo E) in a 68-year-old male patient with chronic heart failure and liver cirrhosis associated with low triiodothyronine (T3) syndrome is reported. There was nothing in the family history to suggest familial hypo-beta LP. In this case, levels of apo B and low-density lipoprotein were very low, and the fraction of beta lipoprotein on polyacrylamide-gel disc electrophoresis (PAGE) was only 7%. However, the triglyceride level was normal due to the presence of chylomicron, in spite of hypocholesterolemia and hypophospholipidemia. The mid-band lipoprotein on PAGE showed that Lp (a) lipoprotein concentration was normal (18.3 mg/dl). The activities of lecithin cholesterol acyltransferase, hepatic triglyceride lipase and lipoprotein lipase (LPL) were low. The concentrations of apo C-II, apo C-III and apo E were low, while those of apo A-I and apo A-II were normal. The author recently reported that the apo C of high-density lipoprotein (HDL-apo C) was detected in alpha lipoprotein, but that HDL-apo E was detected in the near alpha 2-globulin region behind alpha lipoprotein on agarose-gel immunofixation electrophoresis. The author therefore named it alpha 2-apo E, and later found that the fraction percentage of alpha 2-apo E depends on lipolysis and is inversely correlated to the concentration of apo B.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of symptomatic hypobetalipoproteinemia with unusual distribution of apolipoprotein E]. 179 46

Assessment of the relative transcription rates and mRNA steady-state levels for apolipoprotein genes E, A-I, and A-II has been performed in normal rat liver, during liver regeneration and following induction of cirrhosis, as well as in rats with inherited analbuminemia associated with hyperlipidemia. Apo E exhibits primarily transcriptional control with an additional component of posttranscriptional control, whereas Apo A-I is controlled primarily at the posttranscriptional level, thus indicating that these genes are regulated independently. The level of control for Apo A-II has not been determined, because of difficulty experienced in measuring the transcription rate of this gene. During liver regeneration, cirrhosis, and analbuminemia, there is a marked increase in the ratio of Apo A-I to Apo E mRNA, resulting from an increase in the Apo A-I mRNA steady-state level and a decrease in Apo E mRNA. These changes are similar in the three pathophysiologic states and seem to occur through a combination of transcriptional and posttranscriptional mechanisms.
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PMID:Transcriptional and posttranscriptional regulation of apolipoprotein E, A-I, and A-II gene expression in normal rat liver and during several pathophysiologic states. 212 16

Serum concentrations of lipids and apolipoprotein A-I, A-II and B were determined in patients with hepatic metastases of colorectal cancer, with primary liver cancer and with cirrhosis. In all three liver diseases, the HDL fraction and apolipoproteins A-I and A-II showed significantly low values, while apolipoprotein B was only increased in hepatic metastases. The decrease of apolipoprotein A-II levels was more prominent in cirrhosis, thereby enhancing the A-I/A-II ratio. This ratio is decreased in metastasis and normal in hepatomas. In patients with hepatic metastases a correlation was observed between alkaline phosphatase and apolipoprotein A-II (p less than 0.05), and between gamma-glutamyltransferase and the A-I/A-II ratio (p less than 0.05). The present work suggests that determination of apolipoproteins and lipids of the HDL fraction offers a new approach to the study of liver diseases.
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PMID:Serum apolipoproteins A-I, A-II and B in hepatic metastases. Comparison with other liver diseases: hepatomas and cirrhosis. 287 62

Serum apoprotein A-I and A-II levels were determined by electroimmunoassay in patients with liver diseases and cholestasis. Significant decreases in apoprotein A-I and A-II levels were observed in such patients. The decreases were especially pronounced in the early phase of acute hepatitis and cholestasis. The decreases in A-II levels were more prominent than the decreases in A-I in severe hepatic dysfunction or cholestasis. Accordingly, the A-I/A-II ratio showed no change in the convalescent phase of acute hepatitis or chronic hepatitis but increased significantly in the early phase of acute hepatitis, cirrhosis of the liver, hepatoma, and cholestasis. The results suggested the existence of a high density lipoprotein with an abnormal apoprotein composition or a more profound decrease of HDL3 than of HDL2 in severe hepatocellular dysfunction of cholestasis.
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PMID:Serum apoprotein A-I and A-II levels in liver diseases and cholestasis. 627 23

Apolipoproteins A-I, A-II and B were evaluated in 18 chronic active hepatitis and 27 liver cirrhotic patients. The latter were also divided into compensated and decompensated subgroups. Significantly low values of apolipoproteins A-II and B were seen in chronic active hepatitis and liver cirrhotic patients, while apolipoprotein A-I was decreased in liver cirrhotic patients only. Chronic active hepatitis had higher apolipoprotein values than liver cirrhosis and in the latter one decompensated subgroup showed lower apolipoprotein levels than the compensated one. Apolipoproteins A-I, A-II and B correlated also well with prothrombin activity (Normotest) in liver cirrhotic patients, especially the apolipoprotein A-II values. This study suggests that serum values of apolipoproteins are affected by the type of liver damage and that their decrease could be partly due to impaired liver synthesis.
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PMID:Apolipoproteins A-I, A-II and B in chronic active hepatitis and in liver cirrhotic patients. 642 13

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

The relationship between high-density lipoproteins (HDL) in plasma and hepatic structure and microsomal function has been investigated in 54 patients undergoing diagnostic liver biopsy. Plasma HDL cholesterol and major apoproteins were correlated with hepatic histology and microsomal enzyme activity assessed directly as liver cytochrome P-450 concentration and indirectly by plasma antipyrine clearance rate. HDL cholesterol, the concentrations of apoproteins A-I and A-II, the HDL cholesterol/total cholesterol ratio and cytochrome P-450 were low in subjects with moderate or severe hepatic fatty infiltration or cirrhosis when compared with the values for subjects with a normal live. HDL cholesterol and apoprotein A-I and the HDL cholesterol/total cholesterol ratio were directly proportional to the amount of non-fatty parenchyma in the livers. Subjects with a normal liver undergoing treatment with enzyme-inducing drugs, such as phenytoin, phenobarbital and primidone, had higher HDL cholesterol, apoproteins A-I and A-II, HDL cholesterol/total cholesterol ratio, cytochrome P-450 and antipyrine clearance rate than subjects not receiving such therapy. Treatment with inducers appeared to have compensated for the effect of liver disease in lowering plasma HLD. In the entire population, and also in subjects not taking inducing drugs, when considered separately, plasma HDL cholesterol, apoproteins A-I and A-II and the HDL cholesterol/total cholesterol ratio were significantly correlated with cytochrome P-450 concentration. In subjects on enzyme inducers, HDL cholesterol and apoprotein A-I levels and the HDL cholesterol/total cholesterol ratio were proportional to the magnitude of the induction. Serum triglycerides were inversely proportional to the measures of liver microsomal enzyme activity. The lipoprotein pattern, high HDL cholesterol and apoproteins A-I and A-II, and high HDL cholesterol/total cholesterol ratio that accompany microsomal induction are characterized by a reduced risk of atherosclerotic vascular disease and a prolonged expectation of life. The plasma changes presumably reflect the effect of enzyme inducers, such as phenytoin and phenobarbital on hepatic lipids and proteins.
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PMID:Plasma high-density lipoproteins and hepatic microsomal enzyme induction. Relation to histological changes in the liver. 717 98