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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There are many changes in the plasma, lipids, and lipoproteins in patients with liver disease. They have proved difficult to study but our understanding of these changes has increased greatly during recent years. In obstructive jaundice hyperlipidaemia is a fairly constant finding and this appears to be due to the regurgitation of phospholipid from the obstructed biliary tree. The plasma lipids tend to fall with parenchymal liver disease. The composition of the lipoproteins depends on the activity of the plasma enzyme lecithin: cholesterol acyl transferase. When LCAT activity is high the individual lipoprotein fractions are normal. When it is reduced all of the lipoprotein fractions are affected but the pattern found with obstruction is quite different from that found with parenchymal disease. The changes in plasma lipoproteins appear to be associated with change in the lipid composition of cellular membranes and this may have important functional implications.
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PMID:Plasma lipids and lipoproteins in liver disease. 35 66

Direct gas chromatographic method for quantitative determination of plasma neutral lipids was used for the study of cholesterol esterification in vitro. Fully automated computerized method permits the determination of lipid classes (free cholesterol, cholesteryl esters, and triglycerides), as well as their fractions according to the molecular weight, without previous derivatization. All components are determined from one analysis. The method is highly precise and accurate. The coefficient of variation for free and esterified cholesterol is 1.21 and 1.11% in the concentration range 30--430 and 75--545 mg/dl, respectively. The LCAT activity was determined as a decrease in the free cholesterol concentration after one hour's incubation; from the same analysis, the recovery control as an increase in the esterified cholesterol concentration was calculated. The mean difference was 1.06%, maximum difference did not exceed 4%. The LCAT activity in the reference group was 97.2 +/- 28.2 mumol/l/h and was significantly lower than that in hyperlipdemic one. Intravenous administration of heparin had an inhibition effect in subjects with hyperlipidemia of type IV, while only slight changes in the reference group and an increase in hyperlipidemia of type III were observed.
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PMID:Gas chromatographic study of cholesterol esterification during postheparin lipolysis in vitro in hypertriglyceridemia. 74 41

Vitamin E deficiency in two species of monkeys (capuchins and cynamolgus) reduced the in vitro cholesterol esterification by plasma lecithin-cholesterol acyltransferase. The reduction was greates in the most deficient species and in animals fed a diet rich in polyunsaturated fat (safflower oil) stripped of vitamin E. The best correlate of total esterification was the plasma concentration of free cholesterol which reflected the degree of hyperlipidemia, found to be greatest in capuchins fed coconut oil. A logical explanation for the decreased LCAT activity in vitamin E deficiency would be peroxidative damage of substrate (the PUFA of lecithin) or of sulfhydryl sited on lecithin-cholesterol acyltransferase itself. However, neither case was fully supported by the data suggesting that additional information concerning the nature of the reaction and the role of vitamin E is required.
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PMID:Depression of lecithin-cholesterol acyltransferase esterification in vitamin E-deficient monkeys. 80 56

The Spatholobus suberectus (SS) of hexue type, the Euonymus alatus (EA) of huoxue type and the Eupolyphaga sinensis (ES) of poxue type were selected and their influence on plasma lipid in the experimental hyperlipidemia quails was observed. The ES could raise plasma HDL-C/TC ratio and increase LCAT activity. The SS could raise plasma HDL2-C/HDL3-C ratio. The effect of EA on plasma HDL-C/TC, HDL2-C/HDL3-C and LCAT levels was between SS and ES. All the three huoxue huayu Chinese drugs could lower plasma HDL3-C level and slow down the progress of atherosclerosis to a certain degree. The above-mentioned results show that certain orders exist between the action range of huoxue huayu drugs and their effect on regulating plasma lipid.
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PMID:[Comparison of Spatholobus suberectus Dum, Euonymus alatus (Thunb.) Sieb. and Eupolyphaga sinensis Walker on regulation of plasma lipid]. 178

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

CAD results from atherosclerosis, a chronic disease process that has its origin in childhood. Children and adolescents can be at higher risk for CAD by virtue of being from families with premature CAD or familial dyslipoproteinemias. The plasma lipid and lipoprotein levels result from a number of complex metabolic processes that are under the control of genetic and environmental (e.g., diet) influences. The normal ranges of plasma lipids and lipoproteins in children are known, and children and adolescents with dyslipoproteinemia are ordinarily defined as those having levels of plasma total, LDL, or triglyceride above the 95th percentile or with a low HDL cholesterol below the 5th percentile. Children of a parent with documented dyslipoproteinemia or with family history of premature CAD may be screened in the fasting state any time after 2 years of age. Following the exclusion of secondary causes of dyslipoproteinemia, the diagnosis of primary dyslipoproteinemia can be made. Lipoprotein patterns are not diagnostic for a given genotype. Efforts to determine further the biochemical defects responsible for a given phenotype have led to the investigation of gene coding for the apolipoproteins, the key enzymes in the lipoproteins pathways (LPL, HDL, and LCAT) and the receptors that process lipoproteins, such as the LDL receptor and the chylomicron remnant receptor. From a practical standpoint, the diagnosis of the kind of dyslipoproteinemia in a child will depend upon the nature and severity of the dyslipoproteinemia, both in the child (or adolescent) and in parents and siblings. Marked increases in plasma total and LDL cholesterol in the child and in at least one of the parents often reflect the presence of familial hypercholesterolemia, an inherited dominant condition due to a defect in the LDL receptor gene. The triglyceride levels are often normal. If the child has a different dyslipoproteinemia pattern from siblings and parents, then the diagnosis of familial combined hyperlipidemia or hyperapobetalipoproteinemia should be considered. Most children with mild or borderline elevations in total and LDL cholesterol will have polygenic hypercholesterolemia. Triglyceride problems in children and adolescents are relatively uncommon, particularly the more severe hypertriglyceridemia such as that found in lipoprotein lipase and apoC-II deficiency, dysbetalipoproteinemia, and type V hyperlipoproteinemia. High levels of Lp(a) lipoprotein, in isolation or in combination with other dyslipoproteinemia, accelerate risk for CAD. Low levels of HDL cholesterol in the absence of other abnormalities suggest the diagnosis of hypoalphalipoproteinemia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diagnosis and management of familial dyslipoproteinemia in children and adolescents. 225 50

Hyperlipidemia is a common complication of PBC. Ten patients with serologically and histologically defined PBC were randomized to receive either oral cyclosporin A (CyA) or placebo for one year. Fasting blood samples were obtained from subjects at the beginning, and following one year of treatment, for plasma lipids, apolipoproteins AI (apo AI) and B (apo B), and lecithin-cholesterol acyltransferase (LCAT) activity. On entry to the study there were no significant differences between groups for serum concentrations of total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), free cholesterol (FC), total phospholipids (TPL), apo AI, apo B and LCAT activity. Compared to normal laboratory values, baseline TC was elevated in 5/10, LDL-C in 5/10, TPL in 6/10, while LCAT activity was decreased in 8/10 patients. The percent change after one year for CyA group vs the placebo group are as follows: total cholesterol, -22 vs -8%; LDL cholesterol -33 vs -25%; free cholesterol, -39 vs -14%; total phospholipids, -46 vs -23%; and LCAT activity, +/- 236 vs +/- 43%. The decrease in TC, LDL-C, FC, TPL with increase in LCAT activity suggests that CyA administration is associated with improvement in the lipid abnormalities of PBC.
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PMID:Effect of cyclosporin A on serum lipids in primary biliary cirrhosis patients. 261 91

The possible role of Mg in the pathogenesis of vascular disease has recently received increasing attention. Accumulating evidence indicates that Mg strongly influences vascular tone and responsiveness to pressor agents and that Mg deficiency may be associated with an increased risk of hypertension. Moreover, experimental Mg deficiency produces vascular lesions with calcifications while increasing the dietary intake of Mg has been shown to prevent atheroma and thrombotic complications. The modifications of lipid metabolism during experimental Mg deficiency have been recently characterized. Severe Mg deficiency in weanling rats produces a marked hypertriglyceridemia and a decrease in the percentage of cholesterol transported by high-density lipoprotein. The decreased clearance of circulating triglycerides appears to be the major mechanism contributing to hyperlipemia. The same animals were found to have a reduced insulin response after intravenous glucose challenge and a slight reduction in heparin release lipoprotein lipase. A marked reduction in plasma activity of LCAT and a significant decrease in esterified/total plasma cholesterol ratio have also been reported. Severe Mg deficiency in weanling rats produces marked changes in the fatty acid pattern of total plasma lipids, as shown by decreased levels of stearic acid, increased of oleic acid and linoleic acid, and decreased levels of arachidonic acid. Platelets from Mg-deficient rats become more sensitive to thrombin. Such an increased sensitivity of platelets may in turn play an important role in initiating the vascular lesion as well as in thrombotic complications. In view of these experimental data in animal models, more work seems necessary in man to assess the effect of Mg on lipid metabolism and vascular disease.
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PMID:Magnesium, lipids and vascular diseases. Experimental evidence in animal models. 352 56

The occurrence of hyperlipidemia and fat accumulation in certain tissues of premature newborn infants is known. Lecithin-cholesterol acyltransferase (LCAT) catalyzes esterification of free cholesterol and is important in the transport and disposal of lipids. Cord plasma LCAT activity of full-term newborn infants is nearly one-half of that present in the adult plasma. The present study also has found a significant positive correlation between cord plasma LCAT activity and gestational age of the newborn. The ratio of circulating cholesterol ester to free cholesterol was significantly lower only in newborn infants with gestational age less than 32 wk, in comparison to full-term newborn infants or adults. LCAT deficiency and decreased cholesterol ester formation may be responsible for the inadequate lipid clearance in premature newborn infants.
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PMID:Prematurity and lecithin-cholesterol acyltransferase deficiency in newborn infants. 396 14

In studies concerning risk factors for cardiovascular diseases, a number of reports have emphasized the influence of lipids, but the role of dietary minerals other than sodium has been less studied. However, epidemiological studies have suggested that dietary intake of magnesium and potassium may be involved in such pathogenesis. Studies of the influence of magnesium deficiency on arteriosclerosis include its effect on the initial lesion, altered metabolism of elastin, proliferation of collagen, calcification, lipid metabolism, platelet aggregation and hypertension. Magnesium and potassium metabolism are closely related and magnesium is required for maintaining the level of cellular potassium. As a consequence, magnesium and potassium deficiency frequently occur together and potassium deficiency may be an aggravating factor in pathogenesis. The development of the initial lesion in the arterial wall may be facilitated by loss of cellular magnesium and potassium. Experimental magnesium deficiency induces arterial damage, a loss of magnesium and potassium and an increase in the calcium and sodium content of the cell. Experimental models that have been used to produce cardiovascular lesions induce similar changes and losses of major intracellular cations may affect the main metabolic processes of the cell. This report summarizes the experimental evidence that magnesium deficiency may affect several different stages involved in arteriosclerosis and that potassium deficiency may exacerbate this. Magnesium deficiency results in vascular calcification. Experiments indicate that elastin is the site of the initial calcification and the metabolism of elastin is altered. This vascular lesion then brings about an increase in the collagen content of the wall. Low magnesium status could probably affect this process by slowing collagen resorption and lead to an irreversible accumulation of connective tissue. Results showing a different distribution of the various types of lipoprotein during experimental magnesium deficiency strongly suggest that lipid exchange between the vessel walls and blood can be modified. Severe magnesium deficiency in weanling rats produces a marked hypertriglyceridemia, a decrease in the percentage of cholesterol transported by HDL lipoprotein and a reduction in LCAT activity. The decreased clearance of circulatory triglycerides appears to be the major mechanism contributing to hyperlipemia. Magnesium deficiency could therefore contribute to accumulation of vascular lipid. Magnesium and potassium depletion have also been reported in diabetes and the vascular implications of this should be considered.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of magnesium and potassium in the pathogenesis of arteriosclerosis. 639 44


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