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)

Lipoprotein particles were examined in plasma and ascitic fluid from nine patients (5 males and 4 females) with liver cirrhosis and in plasma from nine control subjects. LDL and HDL fractions were isolated by ultracentrifugation under rate flotation conditions in a zonal rotor. LDL size was analysed by non-denaturing polyacrylamide gradient gel electrophoresis. Plasma lipids in cirrhotic patients were markedly reduced compared to controls. Free cholesterol represented 45.3% of the total cholesterol in plasma and 70.4% of the total cholesterol in the ascitic fluid. The total cholesterol-triglyceride ratio was three times higher in the plasma than in the ascitic fluid of cirrhotic patients. The LDL particles had the same flotation properties in plasma from cirrhotic patients as in that from controls. In cirrhotic patients the IDL concentration was higher than that in controls. In ascitic fluid the LDL particles had a higher flotation rate than in the plasma. The LDL diameter as measured by gradient gel electrophoresis was similar in both plasma and ascitic fluid of the cirrhotic patients as well as in the plasma of controls. In plasma and ascitic fluid of cirrhotic patients only a single HDL subclass (HDL1) could be identified. HDL1 particles had a higher flotation rate than normal HDL particles. The plasma levels of all the apoproteins were reduced in cirrhotic subjects compared to controls, but to a variable degree; while apo CII level in cirrhosis represented only 9% of the control level, the apo E level represented 77% of the control level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The lipoprotein composition of plasma and ascitic fluid in liver cirrhosis. 778 59

The endotoxin inactivating action of plasma was evaluated in 62 patients with cirrhosis and 10 healthy subjects. Endotoxin from E. coli 0111:B4 was added to each plasma sample to a final concentration of 250 pg/ml and the percentage loss of endotoxin activity by incubation (37 degrees C for 1 h) was calculated as the endotoxin inactivating rate. The plasma endotoxin inactivating rate in cirrhotics was significantly greater than that in healthy subjects, although patients with Child C cirrhosis and marked hyperbilirubinemia had a significantly lower endotoxin inactivating rate than other cirrhotics. The plasma endotoxin inactivating rate was positively correlated to serum HDL-cholesterol levels. In patients with Child A and Child B cirrhosis, the endotoxin inactivating rate was positively correlated to the endotoxin binding capacity of plasma albumin. The present results support the assumption that the plasma of cirrhotics has a high endotoxin inactivating capacity. Its decrease may augment endotoxicity in patients with advanced liver cirrhosis.
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PMID:Endotoxin inactivating action of plasma in patients with liver cirrhosis. 779 38

An ultracentrifugal technique for separating and analyzing serum lipoproteins was evaluated in comparison with analyses by electrophoresis using agarose-gel and polyacrylamide-gel. In general, the percent of pre beta- and beta-lipoproteins in electrophoresis was estimated higher than the percent of VLDL and LDL in ultracentrifugal method, while the percentage of alpha-lipoprotein in the former was estimated lower than that of HDL in the latter. In cases with abnormal lipoproteinemias, various discrepancies arose between the methods. For examples, pre beta- and beta-lipoproteins were estimated too high by the analyses with electrophoresis. The cholesterol content in HDL decreases in hypertriglyceridemia accompanied by an increase in triglyceride content. Therefore, when HDL cholesterol is determined by a polyanion method to assess the net HDL concentration in such cases, it is estimated to be low. Such errors are not only found in the determination of HDL cholesterol, but also in apoproteins in liver cirrhosis, because the composition of HDL apoprotein is markedly altered. Since the heterogeneity of lipoproteins separated by ultracentrifugation is characteristic in hereditary disorders of lipoproteins such as LCAT deficiency, the centrifugal technique is essential for lipoprotein analysis in such disorders. The disadvantages in ultracentrifugation are cross-contaminations among fractions, and removals of lipids and apoproteins from lipoprotein particles. Apo A-I and E proteins, and phospholipids were removed from the particles more rapidly than other components. From the results of repeated ultracentrifugation of HDL, 3% of apo A-I was estimated to be lost from the HDL during the centrifuge procedure.
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PMID:[Evaluation and problems of ultracentrifugal technique for separation and analysis of serum lipoproteins: comparison with other analytical methods]. 836 Oct 44

We determine the concentration of proapolipoprotein (proapo) A-I and its ratio with total apolipoprotein (apo) A-I (proapo A-I/total apo A-I) in plasma of patients with liver disease; we used a noncompetitive sandwich method, an enzyme-linked immunosorbent assay. The mean (SD) proapo A-I concentrations in patients with decompensated or compensated liver cirrhosis were higher than in normal subjects: 88 (25), 105 (36), and 69 (25) mg/L, respectively. The mean (SD) ratio (expressed as %) for each of these types of liver cirrhosis was also higher than in normal subjects: 10.0 (3.5), 10.2 (3.9), and 4.6 (1.6), respectively. In the patients, the proapo A-I concentration was positively correlated with the concentration of high-density lipoprotein subtype 2 cholesterol (HDL2-C) (r = 0.736), and the proapo A-I/total apo A-I ratio was correlated inversely with the HDL3-C concentration (r = -0.609). The activity of proapo A-I converting enzyme in patients with liver cirrhosis (62 +/- 30 nmol/h per liter) was significantly (P < 0.01) lower than that in normal subjects (172 +/- 55 nmol/h per liter). The increases of the plasma proapo A-I concentration and ratio in patients with liver cirrhosis may be caused by a decreased production of the converting enzyme in the liver. The increase of plasma proapo A-I may thus also affect the circulating HDL subtypes.
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PMID:Increase of plasma proapolipoprotein A-I in patients with liver cirrhosis and its relationship to circulating high-density lipoproteins 2 and 3. 841 59

The association between chronic liver disease and plasmatic lipids and glucidic metabolism was studied. The liver was evaluated with biochemical variables, ultrasound and upper gastrointestinal endoscopy. 12 chronic liver diseases patients and 10 normal were studied. 83.3% of patients showed lipidic abnormalities, 66.6% on the cholesterol levels and 41.7%, reduced HDL. When patients received 100 gr of glucose the response was abnormal in 83.3%. These results were compared with other "liver function test". 75% had abnormal bilirubin, 58.3% abnormal albumin, prothrombin time 58.3%, aminotransferases 75%. Esophageal verices were found in 75% of cases and ultrasound abnormalities in 91.6% (27.3% cirrhosis, 54.4% diffuse abnormal patter and 18.2% splenomegaly). These findings show that lipidic and glucidic metabolism, and ultrasound, in chronic liver diseases are the more frequent abnormalities.
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PMID:[Metabolic markers of chronic liver disease]. 856 66

Historically, alcohol use by the diabetic patient has been controversial. Recent studies in the general population have shown an improvement in mortality with moderate alcohol intake (one to three drinks per day). This improved mortality is greatest in those individuals who have a higher risk of ischemic heart disease. The mechanisms of the beneficial effects of alcohol include positive effects on insulin resistance, HDL cholesterol, platelet aggregation, and fibrinolysis. Since the diabetic patient has an especially high risk of ischemic heart disease because of these factors, the use of a moderate amount of alcohol should not be discouraged. The short-term risks of heavy or continuous alcohol intake include hypoglycemia, glucose intolerance, and ketone and lactate accumulation. In the long term, heavy alcohol intake is associated with an increased prevalence of cancer, hypertension, cirrhosis of the liver, and symptomatic neuropathy. Moderate alcohol intake taken with a meal has been shown to have little or no effect on postprandial glycemic excursions.
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PMID:Alcohol and the NIDDM patient. 873 20

Liver disease is accompanied by major qualitative and quantitative disturbances in plasma lipoprotein metabolism, the extent and intensity of which depend on the degree of parenchymal damage, cholestasis, or both. The main objective of this study was to determine the cholesteryl ester transfer CETP activity and its association with the lipoprotein neutral lipid composition in patients with either liver cirrhosis or cholestasis, as compared to normal controls. Lipoproteins were isolated by ultracentrifugation, lipids and apolipoproteins were measured by conventional methods, and the fatty acid composition was established by gas chromatography; CETP activity in lipoprotein-deficient plasma was measured by determining the transfer of [3H]cholesteryl esters from HDL to VLDL. Lipoprotein lipase and hepatic lipase activities were measured in post-heparin plasma by radiochemical methods. In patients with liver cirrhosis, low levels of VLDL, HDL, apo B, and Lp(a) were observed, as well as a change in the composition of HDL particles, with increases in the relative proportion of triglyceride and free cholesterol. Respectively, the last two changes could be attributed in part to the low hepatic lipase activity observed in this study, and to the low lecithin:cholesterol acyltransferase activity previously observed by others. In patients with cholestasis, a moderate hyperlipidemia due to the elevation of LDL was found. In contrast, HDL and apo A-I levels were very low reflecting a low number of HDL particles, which also had altered compositions with increases in the triglyceride and free cholesterol contents relative to apo A-I and esterified cholesterol, respectively. As regards the fatty acid composition of lipoprotein lipids, the two groups of patients showed, in general, a lower proportion of linoleic acid and a compensating higher proportion of oleic acid as compared to the controls, changes that were observed in both cholesteryl esters and triglycerides. In contrast, the proportions of oleic and palmitoleic acids in phospholipids were increased, whereas that of stearic acid was decreased in patients as compared to controls. In patients with liver cirrhosis, as well as in controls, no changes were observed in the fatty acid compositions of cholesteryl ester, triglycerides, or phospholipids among the different lipoproteins, which probably reflects the equilibration reached by the action of CETP. In patients with cholestasis, no differences were observed in fatty acid composition among the lipoprotein phospholipids but, interestingly, cholesteryl esters from VLDL had a significantly lower linoleic acid content than those from HDL, whereas triglycerides from VLDL had significantly higher oleic acid and lower linoleic acid contents than those from HDL. This distinct fatty acid composition of the neutral lipids between lipoproteins was associated with a significant decrease (25%) in the cholesteryl ester transfer activity in patients with cholestasis. We suggest that fat malabsorption due to the biliary defect may induce a decrease in cholesteryl ester transfer protein synthesis or section, which in turn would slow the equilibration of the neutral lipids among plasma lipoproteins.
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PMID:Cholesteryl ester transfer activity in liver disease and cholestasis, and its relation with fatty acid composition of lipoprotein lipids. 874 May 80

Liver damage and alterations in the exocrine function of the gland lead to a profound alteration of the plasma lipoprotein profile. To determine whether hepatic disease results in changes in the lipoprotein fatty acid composition, i.e. to determine whether liver function influences the homeostasis of complex lipids in plasma, we studied the fatty acid profile of lipids from VLDL, LDL and HDL, as well as from total plasma, in thirty-one patients of both sexes with hepatobiliary pathology (compensated liver cirrhosis, uncompensated liver cirrhosis, primary biliary cirrhosis, other intrahepatic cholestasis, and acute viral hepatitis). We also studied a group of healthy adults as controls. We present the lipoprotein profile and the fatty acid composition (myristic C14, palmitic C16, palmitoleic C16: 1, stearic C18, oleic C18: 1, linoleic C18: 2, eicosatrienoic C20: 3 omega 6 and arachidonic C20: 4) of lipoprotein and total plasma triacylglycerols, cholesteryl esters and phospholipids. The main observation of this study is that, despite the profound changes in the lipoprotein profile and the lower abundance of polyunsaturated fatty acids in complex lipids, the composition of all triacylglycerols, cholesteryl esters and phospholipids is very similar for the corresponding lipoproteins of patients with hepatobiliary disease and of control subjects. This indicates that in the controls as in the studied patients, the exchange of lipids between plasmatic lipoproteins is very rapid and demonstrates the possible importance of the extrahepatic synthesis of cholesteryl ester transfer protein.
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PMID:Fatty acid composition of lipoprotein lipids in hepatobiliary diseases. 889 22

Over the last few years, lipoprotein(a) [Lp(a)] levels have been investigated because clinical studies have related it to increased cardiovascular and cerebrovascular risk. Although it is known that serum Lp(a) concentrations are controlled genetically, little is known about its metabolism. We studied changes in the lipid profile and Lp(a) values in 57 patients (34 males and 23 females) affected by cirrhosis of the liver subdivided into Child's classes in order to assess whether this lipoprotein is sensitive to reduced liver protein synthesis. The patients presented with low total cholesterol, normal HDL-cholesterol (HDL-c), LDL-cholesterol (LDL-c), triglycerides, apoprotein A1 (Apo-A1) and apoprotein B100 (Apo-B100) concentrations, while Lp(a) concentrations seemed elevated. Grouping the patients into Child's classes revealed that all the lipid parameters investigated reduced as the disease progressed. Lp(a) reduced significantly between Child's Classes I and II and seems to be correlated with the severity of cirrhosis and the clinical worsening of the patients' conditions. These findings suggest that Lp(a) is not only an index of atherosclerosis risk, but also plays a role in monitoring liver functions.
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PMID:Lipoprotein(a) in cirrhosis. A new index of liver functions? 901 Jun 14

Patients with homozygous beta-thalassemia show an abnormal lipoprotein profile. In asymptomatic heterozygotes the lipid pattern is less markedly affected but interestingly related to a diminished cardiovascular risk. The extent and significance of these findings are still a matter of debate and no data are available on lipoprotein(a) plasma levels. Seventy patients with homozygous beta-thalassemia (HT-P), 70 beta-thalassemia trait carriers (TT-C) and 70 sex and age-matched controls were investigated and their plasma lipoprotein profile and apo(a) phenotypes determined. In a subgroup of these same subjects (12 HT-P, 12 TT-C and 24 controls) and in 12 bone marrow-transplanted homozygous beta-thalassemic patients (BMT-P) plasma lipoprotein composition was assessed. HT-P disclosed significantly lower total-cholesterol, LDL-cholesterol, HDL-cholesterol, apo A-I, apo B plasma levels and higher triglyceride concentration than TT-C (-7, -11, -8, -8, -13 and +11%, respectively) or controls (-39, -50, -46, -32, -30 and + 35%, respectively). All lipoprotein subclasses were triglyceride-enriched, while LDLs were also protein-enriched and HDLs protein-depleted. TT-C disclosed a small but significant reduction in apo A-I and apo B plasma levels but only minor lipoprotein abnormalities with respect to the controls. BMT-P lipoprotein composition was intermediate between HT-P and normal subjects. Apo(a) plasma levels did not differ among the groups. A higher prevalence of 'small' apo(a) isoforms was present in HT-P. Within the same 'isoform group', apo(a) plasma levels were significantly lower in HT-P than in TT-C or controls. Since liver cirrhosis is almost always present in HT-P, it is conceivable that an altered hepatic apo(a) synthesis or catabolism due perhaps to diminished apolipoprotein glycation may be involved. In TT-C a partially improved cardiovascular risk profile was apparent (low hematocrit, low LDL-cholesterol and apo B), thus justifying the claim for a low prevalence of ischemic heart disease, but no Lp(a) plasma level modification could be detected.
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PMID:Plasma lipoprotein composition, apolipoprotein(a) concentration and isoforms in beta-thalassemia. 918 Feb 53


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