Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum lipids, apoprotein and lecithin-cholesterol acyltransferase activities were studied in 27 renal transplant recipients with stable and normal renal function (serum creatinine 0.16 mM/l or less) sustained for more than 1 year following grafting. Hypertriglyceridemia, which was characteristic of hyperlipidemia in 18 hemodialyzed patients with chronic renal failure, was no longer manifest in transplant recipients. On the other hand, de novo hypercholesterolemia was observed posttransplant with mean serum levels of 5.82 +/- 1.34 versus 5.01 +/- 0.88 mM/l in 575 normal controls. As to the high-density lipoprotein metabolism, the cholesterol content (1.72 +/- 0.56 mM/l) was significantly higher in transplant patients than in hemodialyzed patients (0.82 +/- 0.31 mM/l). In contrast, no variation in apoprotein A-I levels was found between both groups of patients, which produced an elevated high-density lipoprotein cholesterol:apoprotein A-I ratio. Thus, derangement in the serum lipid profile, although qualitatively different, continued to be present following transplantation, and its relevance to the cardiovascular morbidity in these patients remains to be evaluated.
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PMID:De novo development of hypercholesterolemia and elevated high-density lipoprotein cholesterol: apoprotein A-I ratio in patients with chronic renal failure following kidney transplantation. 641 53

Bilateral corneal opacities are the first clinical sign of a familial lecithin-cholesterol acyltransferase (LCAT) deficiency and can be found in early childhood. Familial LCAT deficiency includes the following typical clinical findings: corneal opacification, proteinuria, anemia, turbid or milky plasma, very low plasma HDL, very low plasma cholesterol esters and lysolecithin, hyperlipidemia, and very low or absent LCAT enzymatic activity. Several patients have had fundus findings including angioid streaks and papilledema. This disease is autosomal recessive and has been reported in a total of 19 patients previously. Progression of the disease has resulted in premature atherosclerosis, renal failure and transplantation, decreasing visual acuity and corneal transplantation.
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PMID:Corneal opacification and lecithin-cholesterol acyltransferase (LCAT) deficiency: a case report. 647 90

An esterifying activity of blood plasma (lecithin-cholesterol-acyl transferase, LCAT) was decreased in men with ischemic heart disease (IHD) and coronary atherosclerosis as compared with patients without any symptoms of IHD; the decrease of the activity was most distinct in patients with low level of cholesterol in high density lipoproteins (HDL) and with hyperlipidemia. In these patients phospholipid composition of HDL subfractions was altered: a decrease in the lecithin ratio, increase in the content of sphingomyelin and corresponding decrease in the ratio lecithin/sphingomyelin. Decrease in content of HDL cholesterol and in concentration of apo A-I in blood, plasma, alterations in phospholipid composition of HDL subfractions and in the rate of fatty acids unsaturation of HDL phospholipids in the patients with IHD were considered as factors responsible for the decrease of LCAT activity, which may aggravate the atherosclerotic impairment of arteries.
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PMID:[Esterifying activity of the plasma in patients with ischemic heart disease]. 652 15

Lipids of HDL (high density lipoproteins) and their subfractions (HDL2 and HDL3), and LCAT activity (lecithin: cholesterol acyltransferase) were determined in hepatobiliary diseases without severe hyperbilirubinemia (less than 10 mg/dl). The decrease in major lipid constituents (cholesterol and phospholipids) of HDL was mainly attributable to the decrease in those of HDL3, except in some liver diseases of acute or severe stage (acute hepatitis in an acute stage and hepatoma) which were accompanied with a simultaneous moderate decrease in those of HDL2 and in fatty liver which showed a preferential decrease in those of HDL2. The LCAT activity also decreased in several diseases. Some of the hepatobiliary diseases, on the contrary, showed an increase in HDL-triglycerides (mostly in HDL3 and in some diseases also in HDL2) which might participate to some extent in secondary hyperlipidemia in the liver parenchymal diseases, although they were the minor lipid constituents of HDL. From results that HDL3- but not HDL2-cholesterol levels significantly correlated with serum total protein, albumin and choline esterase, it was suggested that the decrease in large constituents of HDL, particularly of HDL3, is caused by hepatocellular dysfunction which causes inhibition of protein and lipid syntheses in the liver in most of the hepatobiliary diseases except for fatty liver which has a preferential decrease in HDL2 lipids.
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PMID:Changes in high density lipoproteins in patients with hepatobiliary diseases. Levels and lipid composition of HDL2 and HDL3 and LCAT reaction. 685 43

In this review we have endeavored to emphasize the central role of the liver in normal lipoprotein metabolism and to demonstrate how derangements in these metabolic processes can lead to abnormalities characteristic of liver disease. Since changes in the concentration and composition of plasma lipids and lipoproteins occur frequently in liver disease, these findings may be useful in following the clinical course of patients with liver disease of various causes. It should be emphasized that elevated plasma triglycerides and cholesterol are due to underlying defects in lipoprotein metabolism and should not be confused with primary hyperlipidemia. Impaired cholesterol esterification, abnormal lipoprotein electrophoretic patterns and lipoprotein compositional changes, all reflect abnormalities of lipoprotein metabolism that are secondary to hepatocellular injury or cholestasis. These abnormalities are very sensitive indicators of fundamental metabolic defects that are related in part to LCAT and apoprotein activator deficiencies, impaired H-TGL and LPL activity and, perhaps, defective remnant lipoprotein clearance by the liver. Since these abnormalities tend to improve with clinical recovery they have proved to be reliable and sensitive indicators of hepatic function and thus, are useful in the assessment of liver disease.
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PMID:Lipoprotein metabolism in liver disease. 698 38

Effects of 5-methyl-7-diethylamino-s-triazolo-1, 5-a) pyrimidine (trapidil, Rocornal), a therapeutic agent for ischemic heart disease, on various types of experimental hyperlipemias were studied. With administration of trapidil, elevation of serum high density lipoprotein cholesterol (HDL-C) levels and reduction in serum total cholesterol (TC), low density lipoprotein and very low density lipoprotein cholesterol (LDL-C) and the ratio of HDL-C to LDL-C (LDL-C/HDL-c) were observed in most disease models. Changes in HDL-C levels and LDL-C/HDL-C in the hyperlipemia induced by lipid-enriched diet in mice and in the hyperlipemia induced by high cholesterol diet in Japanese quails were of statistical significance. Also, amelioration of reduction in HDL-C induced by high fat emulsion plus 6-n-propyl-2-thiouracil in rats was observed to be significant. Moreover, trapidil significantly reduced TC, LDL-C levels and LDL-C/HDL-C in the hyperlipemia in hamsters. To investigate possible mechanisms of therapeutic effects of trapidil, blood enzyme activities in Japanese quails with hyperlipemia were assayed. Trapidil showed increases in plasma lipoprotein lipase and serum lecithin-cholesterol acyltransferase activities. These results suggest that trapidil may be an effective chemotherapeutic agent for treating ischemic heart disease.
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PMID:[Effects of 5-methyl-7-diethylamino-s-triazolo-(1, 5-a) pyrimidine (trapidil) on various experimental hyperlipemias (author's transl)]. 720 81

Diminished autologous LCAT activity was found in patients with proteinuria. This was due to substrate limitation and albumin appeared the most likely limiting factors. It is suggested that low albumin can contribute to the hyperlipidaemia of nephrotic syndrome through its role on the LCAT reaction. Evidence of the ability of triglyceride to enhance homologous LCAT activity was also noted.
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PMID:The mechanism of hyperlipidaemia in nephrotic syndrome--role of low albumin and the LCAT reaction. 738 46

Arterial hypertension is a dominant pathogenetic factor for glomerulosclerosis. Nevertheless metabolic factors such as hyper- or dyslipoproteinemia may significantly modify and accelerate the process of glomerular scarring. Hyperlipidemia and lipoprotein abnormalities are often encountered in patients with nephrotic syndrome and chronic renal disease. Although the significance of lipid deposition in renal tissue and the role of lipoproteins in the pathogenesis of renal disease in man has not yet been clearly defined, experimental and clinical data indicate a damaging effect of disturbed lipid metabolism on the kidney. In humans glomerular lipid deposition is observed in several genetic diseases, including lecithin-cholesterol acyltransferase activity deficiency. Studies on animals with reduced renal mass, diabetes mellitus or arterial hypertension have shown that hypercholesterolemia increases the incidence of glomerulosclerosis. Especially the interaction of arterial hypertension and dyslipoproteinemia leads to a rapid and pronounced development of glomerulosclerosis. As most of these studies have been performed in the rat, which has a different lipoprotein profile than man, these results should be carefully interpreted with regard to their relevance for humans. In vitro cell culture studies on human glomerular cells have provided insight into the possible cellular mechanisms of lipid-induced glomerular damage. Apoprotein E containing lipoproteins that are pathologically elevated in many renal diseases are avidly taken up by human glomerular cells. Mesangial cells seem to play a central role in the initiation of glomerulosclerosis by proliferation and production of excess extracellular matrix. Lipoproteins are able to stimulate DNA synthesis in these cells and increase the synthesis of mitogens and matrix proteins. The pathogenetic role of modified, oxidized lipoproteins has not yet been elucidated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Arterial hypertension and hyperlipidemia as determinants of glomerulosclerosis. 830 44

Hyperlipidemias are grouped according to their lipid levels in hypercholesterolemia, hypertriglyceridemias, and mixed hyperlipidemias. Among these, hypercholesterolemia has the strongest correlation to the risk for coronary heart disease. Based on the results from epidemiologic studies and intervention trials several expert panels have defined cholesterol values with low and high cardiovascular risk and cholesterol target levels for treatment. In the presence of hyperlipidemia additional parameters like LDL cholesterol, HDL cholesterol, and Lp(a) may be determined depending on the individual patient's risk profile. For classification of familial lipid disorders, analysis of relatives and the determination of special parameters may be necessary. These include apolipoproteins (concentration, isoforms, mutants), enzyme activities (lipases, LCAT), LDL receptor activity, oratypical lipoproteins.
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PMID:[Classification of hyperlipoproteinemias and interpretation of laboratory parameters]. 865 Sep 32

To study the pathophysiology of hyperlipidemia in nephrotic syndrome, we compared lipid metabolism in the nephrotic stage (stage 1) and in stage 2, when albuminuria had subsided, in 11 patients with minimal-change disease treated with corticosteroid. High-density lipoprotein (HDL) levels were decreased and HDL contained more cholesterol and triglyceride per unit of protein in stage 1 in the patients than in age-matched healthy controls. The urinary protein level was positively correlated only with low-density lipoprotein (LDL) levels, suggesting that the increased albumin clearance stimulated LDL production. Serum cholesterol levels were positively correlated with apolipoprotein E levels and were negatively correlated with lecithin-cholesterol acyltransferase activity in the nephrotic stage; the opposite correlations were seen in controls. Although triglycerides in HDL had normalized at stage 2, triglycerides in LDL and very-low-density lipoprotein did not return toward normal until stage 3, when serum cholesterol levels were normalized.
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PMID:Lipoprotein derangement during steroid treatment in minimal-change nephrotic syndrome. 885 59


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