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)

Using with the newly modified perchloric acid pretreatment method and endotoxin specific assay (Endospecy), the plasma endotoxin in the patients with liver cirrhosis was investigated. The mean value of plasma endotoxin in control (n = 20) was below 9.8 pg/ml. The plasma endotoxin level in liver cirrhosis was 5.7 +/- 5.3 pg/ml (n = 70, mean +/- SD), and 20% of the patients (15 cases) showed above 9.8 pg/ml. Endotoxin level significantly correlated with the severity of liver function based on the Child-Turcotte classification (p less than 0.01). Plasma endotoxin positively correlated with total bilirubin (r = 0.417) and ICG clearance test (r = 0.298) and negatively correlated with prothrombin time (%) (r = 0.497) and HDL-cholesterol (r = 0.578) in the patients with liver cirrhosis. There was no correlation between esophageal varices and plasma endotoxin level. Plasma endotoxin was slightly detected in the patients with decompensated cirrhosis, and these data suggest that plasma endotoxin level in cirrhosis is not so elevated.
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PMID:[Plasma endotoxin measured by the combination of new perchloric acid pretreatment method and endotoxin specific assay in liver cirrhosis]. 132 Jan 42

Plasma lipid and lipoprotein profile was determined in 12 cirrhotics, 15 patients with cirrhosis and hepatocellular carcinoma (HCC) and 20 healthy volunteers. When compared with controls plasma total cholesterol (TC), high density lipoprotein cholesterol (HDLC), high density lipoprotein phospholipids (HDLPL), HDLPL/PL levels were low, phospholipid (PL) was normal and HDLC/TC and PL/TC were high in cirrhosis. In cirrhotics with HCC, TC, PL, PL/TC levels were elevated while HDLC, HDPL, HDLC/TC and HDLPL/PL were normal. A comparison within the patient groups showed that in cirrhosis alone, the levels of TC, HDLC, PL, HDLPL and HDLPL/PL were lower and PL/TC level was higher than in cirrhotics with HCC. Plasma albumin levels showed a negative correlation with PL/TC and a positive correlation with HDL-cholesterol in cirrhosis. In cirrhosis with HCC plasma, phospholipid levels showed a significant negative correlation with total bilirubin and alanine aminotransferase. The variations in the level of plasma lipids and lipoproteins may assist in describing the nature of these two forms of liver disease.
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PMID:Abnormal lipid and lipoprotein patterns in liver cirrhosis with and without hepatocellular carcinoma. 133 73

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

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 effects of propranolol on liver functions of healthy rats were studied administering daily doses of 1 mg/kg. Beta receptor blockade has been investigated in carbontetrachloride induced liver cirrhosis. Normal liver functions were unchanged with the exception of an increase in Glucos-6-Phosphatase. The severe cirrhotic injuries were counteracted or moderated when propranolol administration started the same day as CCl4 injection. The amount and function of mixed-function-monooxygenases were normalised. Carbohydrate and protein metabolism impairments were moderated. Serum triglyceride and HDL-cholesterin levels were however uninfluenced. The metabolic properties of propranolol seem to be advantageous in chronic liver impairments.
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PMID:[Beta receptor blockade and liver function]. 254 Jun 15

It is known that chronic alcoholics and type II diabetics show hyperlipidemia, characterized by hypertriglyceridemia and in a minor degree by hypercholesterolemia. The mechanisms underlying the effect of ethanol and carbohydrates on plasma lipids seem to be different; therefore in diabetic subjects chronic alcohol consumption could produce a more severe hyperlipidemia and so accelerate atherosclerotic events. In order to verify it we have measured plasma cholesterol, HDL-cholesterol, and triglycerides and investigated the presence of micro- and macroangiopathy in two groups of non-insulin-dependent diabetics, differing each other for daily alcohol intake (18 chronic male alcoholics and 30 male subjects consuming respectively more than 150 g and less than 50 g of alcohol daily). In alcoholics, no clinical features, laboratory and echographic findings of cirrhosis and pancreatic disease were present. In order to avoid a possible interference of other factors on the metabolism of plasma lipids, in our study patients were selected with the following criteria: 1) only male subjects; 2) age 40-60 years; 3) nonsmokers; 4) moderate coffee drinkers; 5) average physical activity; 6) with BMI less than 28; 7) in good diabetic control (HbA1c less than 6%, n.v. 4.4%-5.6%); 8) normal kidney function (plasma creatinine less than 1.3 mg%) and 24 hr proteinuria absent;) 9) in treatment with diet alone or diet plus low doses of sulphonylureas or biguanides. The data were analyzed by Student's "t" and chi-squared tests. No significant differences could be detected (alcoholics/occasional drinkers, means +/- 1 SD) either in the plasma levels of cholesterol (181.7 +2- 39.3/198.2 +/- 32.5), HDL-cholesterol (43.4 +/- 12.7/38.5 +/- 11.9), and triglycerides (105.5 +/- 56.4/159.7 +/- 114.8) and in the frequency of micro (22.2%/16.6%) and macroangiopathy (16.6%/26.6%) between the two studied groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of chronic alcohol consumption on blood lipid levels and angiopathy in diabetics]. 274 71

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

The molecular nature of serum (from normal subjects and from patients affected by various hepatobiliary diseases) gamma-glutamyltranspeptidase (GGT) isoenzymes has been studied by selective lipoprotein precipitation. Some fractions co-precipitate with LDL + VLDL (pre-beta-, beta-, beta/gamma-, gamma-, and dep-GGT fractions) or with HDL (partial precipitation of alpha 1-GGT in cirrhosis). Alpha 1-GGT + alpha 2-GGT in normal subjects, and Alb-GGT did not precipitate with either of the precipitation treatments. Total GGT and its isoenzymes were stable at 4 degrees C and at -20 degrees C for at least 20 days, with the exception of Alb-GGT which at -20 degrees C decreased by 20%. The percentage of GGT associated with LDL + VLDL appeared to be a possible marker to discriminate liver tumors from cirrhosis. A cut-off value of 20 U/L of this marker yielded a diagnostic sensitivity of 87% and a diagnostic specificity of 85%.
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PMID:Gamma-glutamyltranspeptidase isoenzyme forms and lipoproteins in normal and pathological sera. 290 Feb 24

APO A-1 and B HDL cholesterol in 15 cases of acute hepatitis and 13 cases of hepatic cirrhosis were comparatively studied with different biochemical parameters. The decrease in APO A-1 and HDL revealed an alteration of the hepatic function. When the APO A-1 and HDL returned to normal a recovery of the hepatic function was observed.
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PMID:[Importance of apolipoproteins A-1 and B in acute viral hepatitis and hepatic cirrhosis]. 357 19

It is now possible to pinpoint the biochemical processes responsible for liver damage in alcoholics and to monitor detoxication from a biological point of view. Cirrhosis of the liver is a direct consequence of chronic alcoholism in 60-80 % of cases, and most alcoholics, after several years of drinking, cannot escape the ravages of alcohol, although it is not yet known why a small proportion are not affected biochemically. Psychological deterioration can be explained biochemically, due to the neurotoxic effects of acetaldehyde, formed by alcohol but 20-30 times more toxic, which acts on catecholamines and serotonin with, inter alia, depressant, habit-forming, hallucinogenic and convulsive properties. Hepatic symptoms depend on the stage the alcholic has reached - acute, subacute or the chronic and final stage of cirrhosis of the liver, and include disturbances of transaminases, gamma-GT, serum proteins, immunoglobulins, specific proteins, lipids (including very interestingly an increase in cholesterol-HDL which needs to be investigated further) and hematic changes with FDP and thrombocytes affected, and often anaemia.
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PMID:[Biological profile of liver damage in alcoholics (author's transl)]. 611 Mar 11


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