UMLS:C0020473 - FACTA Search

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

These are the preliminary data of an open multicenter trial of antihypertensive treatment with isradipine as monotherapy (dose, 4.55 +/- 0.56 mg twice daily; n = 11) or isradipine (7.5 +/- 0.63 mg twice daily) in combination with bopindolol (1.16 +/- 0.12 mg once daily; n = 30) administered for 3 years to patients with essential hypertension (WHO classification I or II). Blood pressure was significantly decreased in both treatment groups and there was no indication of resistance to therapy. Plasma levels of total cholesterol and triglycerides were decreased by the end of the second year of treatment, and there was a tendency toward increase in plasma levels of high-density lipoprotein cholesterol (HDL2 or HDL3). The atherogenic index (ratio between total cholesterol and HDL2 plus HDL3) was also decreased. Blood glucose levels remained unchanged in both normoglycemic patients and those with non-insulin-dependent diabetes mellitus (NIDDM) during 3 years of therapy. It is concluded that isradipine is safe and effective when administered long-term in the treatment of hypertensive patients with either hyperlipidemia or NIDDM.
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PMID:Hungarian Isradipine Study (HIS): long-term (3-year) effects on blood pressure and plasma lipids. 794 81

Plasma triglycerides are increased in the majority of patients with advanced renal failure but cholesterol is not. HDL cholesterol is reduced while LDL IDL and VLDL cholesterol is increased. Lecithin:cholesterol acyltransferase (LCAT), an enzyme necessary for HDL maturation, is reduced in chronic renal failure (CRF). As a consequence, while all subtypes of HDL are reduced, the small HDL3 subtype is relatively enriched at the expense of the larger, more functional HDL2 subtype. Triglycerides are increased in all lipoprotein fractions. HDL-associated apolipoproteins, apo A-I and A-II are decreased, while apo B is increased. Lipoprotein catabolic rate is reduced, but the cause of hyperlipidemia is multifactorial; reduced lipoprotein lipase (LPL) activity, increased concentration of apo C-III (a specific inhibitor of LPL) in plasma, secondary hyperparathyroidism, insulin resistance. Hyperlipidemia is not corrected by dialysis. Lipid levels are somewhat higher in CAPD patients, possibly as a consequence of increased glucose absorption or as a consequence of transperitoneal HDL losses. Triglycerides decrease and cholesterol increases following transplantation. Oxidized lipids are increased in plasma of patients with CRF. Plasma polyunsaturated fatty acids are decreased and saturated fatty acids increased. The same changes occur in the lipid bilayers composing leukocytes and red blood cell membranes. These changes result in altered membrane fluidity, and are corrected by dialysis. While atherosclerotic disease is a leading cause of death in dialysis patients, it is not certain that the specific lipid disorders of CRF are responsible for this morbidity, nor is it recommended at this time that qualitative abnormalities be treated pharmacologically in the absence of increased lipid levels.
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PMID:Hyperlipidemia of chronic renal failure. 798 78

The purpose of this study was to examine the effect of one bout of low-intensity exercise on the lipemic response to a high-fat meal. Twelve (six women, six men) normolipidemic adults aged 25.8 +/- 1.2 years (mean +/- SEM) took part in two trials. In the exercise trial, subjects walked for 2 hours on a treadmill at 30.9% +/- 1.6% of maximal oxygen uptake (VO2 max) 15 hours before ingestion of the test meal. In the control trial, subjects rested the day before the test meal. After a 12-hour fast, blood samples were obtained by venous cannulation before ingestion and hourly after ingestion for 6 hours. Serum was analyzed for triacylglycerol (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and HDL2-C, apolipoproteins (apos) A-I and B, free fatty acids (FFA), free glycerol, glucose, and insulin. TG values were corrected for free glycerol. Fasting serum TG and peak TG concentrations were lower (Wilcoxon, P < .05) for the exercise trial than for the control trial (0.74 +/- 0.03 v 0.92 +/- 0.08 and 1.98 +/- 0.18 v 2.59 +/- 0.32 mmol.L-1, respectively). The total lipemic response (area under the TG/time curve, normalized to the 0-hour level) was 31% +/- 7% lower in the exercise trial (4.28 +/- 0.66 v 6.46 +/- 1.08 mmol.L-1.h, P < .01). No differences were found between trials in the other parameters. These results show that a single bout of low-intensity exercise reduces the extent of postprandial lipemia in normolipidemic young adults. One possible mechanism is enhanced lipoprotein lipase (LPL) activity in the exercised skeletal muscle.
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PMID:The effect of a single bout of brisk walking on postprandial lipemia in normolipidemic young adults. 802 6

Hyperlipidemia so commonly complicates heavy proteinuria that it has come to be regarded as an integral feature of the nephrotic syndrome (NS). Characteristically, total plasma cholesterol and triglyceride levels are elevated, as are very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) cholesterol. Although high-density lipoprotein (HDL) concentrations may be normal, HDL subtypes are abnormally distributed, with a reduction of HDL2 and an increase in HDL3. In addition, lipoprotein (a) [Lp (a)] levels may be elevated. The mechanisms underlying these abnormalities are multifactorial, involving both increased rates of lipoprotein synthesis and defective clearance and catabolism of circulating particles. Although recent dietary and therapeutic studies have demonstrated that nephrotic hyperlipidemia can be effectively treated, the need for such intervention has not been clearly established. This pattern of lipoprotein abnormality is associated with an increased risk of cardiovascular disease in the general population, and several studies have suggested that nephrotic individuals are more likely to develop atherosclerosis. However, no prospective trials have evaluated the relationship between deranged lipid metabolism and coronary or cerebral artery disease in patients with NS. In addition, although recent experimental studies suggest that lipid abnormalities may accelerate renal injury and that lipid-lowering agents may protect renal function, there is little current evidence to suggest that such intervention is of value in preserving residual renal function in humans. Further studies are clearly required to assess the potential long-term benefits of lipid-lowering intervention in individuals with NS. In the meantime, based on data generated from other population groups, a rational approach to the clinical management of hyperlipidemia in these patients is presented.
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PMID:Lipid abnormalities in the nephrotic syndrome: causes, consequences, and treatment. 812 33

To gain insight into metabolic determinants of high density lipoproteins (HDL) containing apolipoproteins A-I and A-II (LpA-I/A-II) and those containing A-I, but devoid of A-II (LpA-I), the plasma concentration of LpA-I and LpA-I/A-II within the HDL2 and HDL3 density spectrum was measured in 14 normolipidemic male subjects on a standardized diet. Apolipoprotein plasma concentrations of HDL subspecies were compared with the magnitude of postprandial lipemia, activities of lipoprotein lipase and hepatic lipase in postheparin plasma, plasma lecithin:cholesterol acyltransferase (LCAT) activity, and cholesteryl ester transfer protein (CETP) mass. Plasma levels of LpA-I/A-II were 2.5 times higher than levels of LpA-I (123 +/- 20 vs. 48.3 +/- 22.1 mg protein/dl) and the partition of LpA-I and LpA-I/A-II between HDL2 and HDL3 differed in that the proportion of LpA-I associated with HDL2 was greater than that of LpA-I/A-II (23 +/- 19 vs. 6 +/- 6%, P < 0.002). With increasing levels of HDL2, the proportion of LpA-I in HDL2 increased (P < 0.002). Furthermore, levels of LpA-I and LpA-I/A-II were strongly correlated within the HDL2 but not within the HDL3 density region. Plasma levels of LpA-I, but not LpA-I/A-II, were inversely correlated with the magnitude of postprandial lipemia. However, activities of lipoprotein lipase and hepatic lipase tended to show stronger associations with the partition of LpA-I/A-II between HDL2 and HDL3 than with that of LpA-I. Within the HDL3, but not the HDL2 density spectrum, LpA-I/A-II exhibited a positive association with plasma LCAT activity, while LpA-I displayed an inverse association with plasma CETP mass. These results are consistent with differences in substrate properties of LpA-I and LpA-I/A-II for lipoprotein modifying enzymes and imply different, but overlapping metabolic pathways of LpA-I and LpA-I/A-II.
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PMID:High density lipoproteins with differing apolipoproteins: relationships to postprandial lipemia, cholesteryl ester transfer protein, and activities of lipoprotein lipase, hepatic lipase, and lecithin: cholesterol acyltransferase. 816 33

The effect of different fat loads on postprandial lipemia and hemostatic activity was examined in 10 middle-aged men using 3 different meals. One meal was rich in saturated fatty acids (cream), the other rich in n-6 polyunsaturated fatty acids (sunflower oil) and the third was fat-free containing only carbohydrates. Lipoprotein lipids and hemostatic parameters were measured during fasting and 2, 4, 6 and 8 h after the test meal. In fasting samples, several hemostatic parameters were significantly associated with lipoprotein lipids. Most notable were the strong associations of fibrinolysis parameters tissue plasminogen activator antigen and plasminogen activator inhibitor activity (PAI-1) with total and very low density lipoprotein (VLDL) triglycerides. During lipemia, the associations were approximately similar or slightly weaker than in the fasting state. Both fat loads resulted in similar postprandial lipid responses: VLDL and high density lipoprotein (HDL) triglycerides reached maximum at 4 h after the meal. VLDL cholesterol also increased 4 and 6 h after the fat loads. HDL3 cholesterol declined after the fatty meals but no change was observed in the HDL2 fraction. The fat-free meal gave no significant lipid changes during the time course studied. Factor VII activity (F VII:C) increased 6 and 8 h after the fatty meals, whereas a decrease was observed after the fat-free meal. The changes (+/- S.D.) at 8 h after cream, sunflower oil and fat-free meal were 5.2 +/- 3.3, 3.3 +/- 4.2 and -5.8 +/- 7.9 percentage points, respectively, and the effect of the meal on the changes was statistically significant (F (8,99) = 2.99, P = 0.0048). F VII antigen (F VII:Ag) tended to decline during the day but there was no difference between the meals. Factor VIII activity (F VIII:C) was highest after the polyunsaturated fat meal and lowest after the fat-free meal. PAI-1 declined during the day and the decline tended to be steepest after the fat-free morning meal. The effect of the meal on the changes in lipoprotein lipids and hemostatic factors varied significantly between individuals. In conclusion, postprandial lipemia after a single fatty meal was associated with procoagulatory change in F VII:C but there was no difference between saturated fat and n-6 polyunsaturated fat.
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PMID:The effects of saturated fat and n-6 polyunsaturated fat on postprandial lipemia and hemostatic activity. 828 Jan 80

In 16 members of two Austrian families affected by a missense mutation at codon 188 of the lipoprotein lipase (LPL) gene (8 heterozygous and 8 normal subjects), carrier status for the mutation as determined by DNA analysis was related to LPL activity in postheparin plasma, to the magnitude of postprandial lipemia, and to concentration, composition, and size of the major lipoprotein classes of postabsorptive plasma. Carriers exhibited clearly reduced LPL activity, normal fasting triglycerides, but pronounced postprandial lipemia. The carriers' impaired triglyceride tolerance, as evident in the postprandial state of challenge only, was associated with a fasting lipoprotein constellation characterized by (a) enrichment of HDL2 with triglycerides, (b) reduced HDL2-cholesterol, (c) enrichment of VLDL and intermediate density lipoprotein (IDL) with cholesteryl esters, (d) elevated IDL levels, and (e) small-sized LDL. Within any given individual, the degrees of expression of these characteristics were quantitatively and continuously related with each other as well as with the magnitude of lipemia and with LPL activity.
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PMID:Heterozygous lipoprotein lipase deficiency due to a missense mutation as the cause of impaired triglyceride tolerance with multiple lipoprotein abnormalities. 843 54

Plasma lipid/lipoprotein changes were monitored after a fat load (65 g fat per square meter body surface area) in six carriers of the apolipoprotein A-IMilano (A-IM) variant and six age- and sex-matched control subjects. The magnitude of postprandial lipemia, calculated as the area under the curve (AUC) described by plasma triglyceride (TG) level versus time, was threefold higher in the A-IM carriers; however, after correction for the different baseline TG levels, it was similar to control subjects. Moreover, the magnitude of postprandial lipemia was positively correlated with baseline TG in both A-IM carriers (r = 0.77) and control subjects (r = 0.80), indicating that fasting TGs are a major determinant of postprandial response in all subjects. Postprandial lipemia was also inversely correlated with high density lipoprotein (HDL) and HDL2 cholesterol in both groups (A-IM, r = -0.81 and -0.79; control subjects, r = -0.87 and -0.94). Different from those in control subjects, the plasma apo A-I levels in the A-IM carriers decreased progressively while apo B increased up to 4 hours but decreased thereafter. Postprandial rises of low density lipoprotein TG but not of HDL-TG AUC were significantly higher in the A-IM carriers, even after normalization for the different fasting concentrations. These data show that the low plasma HDL levels of A-IM carriers, which are secondary to a primary structural alteration of the major HDL apolipoprotein, are associated with elevated fasting and postprandial TG levels and an anomalous postprandial redistribution of TG among lipoprotein classes.
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PMID:Increased postprandial lipemia in Apo A-IMilano carriers. 846 88

Hyperlipidemia associated with non-insulin-dependent diabetes mellitus (NIDDM) and insulin resistance is characterized by high triglyceride levels; raised levels of total low-density lipoprotein (LDL), which is made up of small, dense, cholesterol-rich particles; low levels of high-density lipoprotein (HDL); and glycosylation of apolipoproteins. Optimal drug therapy for this lipid profile is controversial. To test whether a fibrinic acid derivative (gemfibrozil) or a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor (lovastatin) would produce better results in these patients, a crossover study was performed. Gemfibrozil 600 mg twice daily and, after a washout period, lovastatin 20 to 40 mg twice daily were administered to nine patients with NIDDM. Gemfibrozil significantly decreased triglyceride, very-low-density lipoprotein (VLDL), and intermediate-density lipoprotein (IDL) levels, the total cholesterol:HDL ratio, and the IDL plus VLDL;HDL ratio, and significantly increased levels of HDL, HDL2, and HDL3. Lovastatin significantly decreased levels of total cholesterol, calculated LDL, directly measured LDL, IDL, total triglycerides, VLDL, and the ratios of LDL:HDL, total cholesterol:HDL, and directly measured LDL:HDL and significantly increased total HDL and HDL3 levels. Gemfibrozil was significantly more effective than lovastatin in raising total HDL and HDL3 levels and in lowering the IDL plus VLDL:HDL ratio. Lovastatin was significantly more effective than gemfibrozil in lowering total cholesterol, LDL, directly measured LDL, and the LDL:HDL and directly measured LDL:HDL ratios. In the absence of malignant hypertriglyceridemia, an HMG-CoA reductase inhibitor, rather than a fibrinic acid derivative, is indicated for the treatment of patients with dyslipidemia associated with NIDDM and insulin resistance.
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PMID:A comparison of lovastatin, an HMG-CoA reductase inhibitor, with gemfibrozil, a fibrinic acid derivative, in the treatment of patients with diabetic dyslipidemia. 859 42

The relative content of various fatty acids in serum lipoproteins was determined in patients with type IIa (38), IIb (49) and IV (77) of hyperlipoproteinemia and compared with 52 controls. Significant changes were found in hyperlipoproteinemia associated with hypertriglyceridemia (type IV) but not in "pure" hypercholesterolemia (type IIa). In all lipoprotein fractions (VLDL, LDL, HDL) in type IV of hyperlipoproteinemia the increased oleic and linolenic acid proportions were found, while proportions of linoleic, arachidonic and docosahexaenoic acids were decreased. The saturated fatty acids (myristic, palmitic and stearic) were found increased in LDL. Linear regression analysis has shown positive correlation between the content of arachidonic and docosahexaenoic acids in HDL and LDL and the serum levels of total HDL-cholesterol, HDL2-cholesterol, HDL3-cholesterol and ApoA1, while a negative correlation between these fatty acids and serum triglycerides level appeared. These findings can be explained partly by increased content of triglycerides and free fatty acids in lipoproteins. Possible differences concerning mechanisms of accelaration of atherogenesis in various types of hyperlipidemia are discussed.
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PMID:Serum lipoprotein fatty acid patterns in various types of familiar combined hyperlipidemia. 868 53

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