Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Significant risk factors for premature coronary heart disease include: (1) family history, (2) elevated low density lipoprotein (LDL) cholesterol level > or = 160 mg/dl, l, (3) decreased high density lipoprotein (HDL) cholesterol level < 35 mg/dl, l, (4) cigarette smoking, (5) high blood pressure and (6) diabetes mellitus. All of these risk factors are common in patients with premature heart disease. Common familial lipid disorders associated with premature heart disease include familial lipoprotein(a) excess, familial dyslipidemia (elevated triglycerides and decreased HDL cholesterol), familial combined hyperlipidemia (elevations of LDL cholesterol and triglycerides, and often decreased HDL cholesterol), familial hypoapobetalipoproteinemia (elevated apolipoprotein B levels), familial hypoalphalipoproteinemia (low HDL cholesterol levels), and familial hypercholesterolemia (elevated LDL cholesterol levels). All these disorders have been characterized using age and gender specific 90th and 10th percentile values from the normal population. The diagnosis and potential management of these disorders is reviewed.
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PMID:Familial lipoprotein disorders and premature coronary artery disease. 780 28

Dyslipidemia is one of the first metabolic dysfunction observed among patients with end stage renal disease. It can also induce acceleration of renal tissue damage. Kidney transplantation may cause recovery of some dysfunction in lipid metabolism while influencing deterioration of others. The aim of this study was to monitor dynamics of basic lipid parameters in the first year after kidney transplantation. The sample included 25 patients (9W, 16M), aged 18-59, avg. 36. We have measured concentration of the following parameters in blood serum: triglycerides (TG), total cholesterol (CH-C) and apolipoprotein B (Apo B). Simultaneously, functions of transplanted kidney were tested with use of routine methods. The immunosuppressive treatment of patients followed the scheme: cyclosporine + prednisolone + azathioprine. The treatment influence on lipid disorders was measured by relevant correlation coefficients. The obtained results point to the observation that in the first year after kidney transplantation the TG concentration gradually decreases, with simultaneous continuous increase of CH-C concentration, mainly due to LDL concentration increase. No influence of immunosuppressive treatment on lipid parameters was observed. However, lipid dysfunction, especially TG, correlated with kidney function.
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PMID:[Dynamics of changes in lipid metabolism during the first year after kidney transplantation]. 780 32

Using a stable isotope method, we measured the hepatic secretion rate of very-low-density lipoprotein apolipoprotein B-100 (VLDL apoB) in a 26-year-old women who had dyslipidemia due to cholesteryl ester storage disease (CESD) and in five normolipidemic subjects. [1-13C]Leucine was administered by a primed constant intravenous infusion and the enrichment of VLDL apoB was determined by gas chromatography-mass spectrometry. The absolute secretion rate (ASR) of VLDL apoB in the patient was more than twice the mean ASR of the normolipidemic group (17.1 vs 8.0 +/- 0.8 mg/kg body wt. per day). The plasma mevalonic acid concentration, a measure of intrahepatic cholesterol synthesis, was also greater in the patient than in the normolipidemic subjects (8.3 vs 4.4 +/- 1.8 micrograms/L). The findings are consistent with the hypothesis that in CESD increased intrahepatic synthesis of cholesterol stimulates hepatic secretion of VLDL apoB and this may partly account for the dyslipidemia.
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PMID:Increased hepatic secretion of very-low-density lipoprotein apolipoprotein B-100 in cholesteryl ester storage disease. 781 57

Coronary artery disease (CAD) patients (n = 235), comprising minimal (CAD-, n = 124) and severe (CAD+, n = 111) CAD, were recruited on the basis of their angiographic scores. Male control subjects (n = 123) were selected randomly from the Caerphilly Heart Study cohort. Subjects were genotyped for the Ser447-Ter mutation and HindIII/Pvu II restriction fragment length polymorphisms of the lipoprotein lipase gene and investigated for associations with severity and development of CAD and lipid and lipoprotein levels. The Ser447-Ter mutation showed no significant associations with CAD or dyslipidemia but was related to favorable lipid and lipoprotein profiles. The H2H2 genotype (P < .05) and H2 allele (P = .05) were significantly more frequent in CAD+ versus CAD- and control subjects versus CAD-. H2H2 subjects, among the entire male cohort, had significantly higher levels of apolipoprotein B (P = .0002), total cholesterol (P < .004), and triglycerides (P < .04) than alternative genotypes. P2P2 associated with significantly lower high-density lipoprotein cholesterol levels (P < .01). The H2 allele had most significant associations with raised apolipoprotein B levels compared with other biochemical parameters. Our data suggest that the H2 allele may be a linkage marker for an etiologic mutation for dyslipidemia and the severity and development of atherosclerosis; this is not the Ser447-Ter mutation.
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PMID:DNA variants at the LPL gene locus associate with angiographically defined severity of atherosclerosis and serum lipoprotein levels in a Welsh population. 791 49

The lipid and lipoprotein profiles including apolipoprotein A1 and B100 are measured in 50 idiopathic nephrotic patients (males 26, females 24) with mean age of 32 + 13.6 yrs, serum creatinine 1.32 +/- 0.43 mg/dl compared with 50 age matched normal controls. The renal histology consist of IgM nephropathy 70 per cent, membranous 12 per cent, and IgA 2 per cent. The serum cholesterol, triglycerides, LDL- cholesterol, VLDL-cholesterol, apolipoprotein B (521.6 +/- 201.6, 291.4 +/- 156.2, 438.8 +/- 207.4, 58.3 +/- 31.2, 265.1 +/- 119.8) are statistically significantly higher than controls (p < 0.001). The HDL-cholesterol (30.2 +/- 16.1) is also significantly lower than controls (p < 0.001) but apolipoprotein A is not different from normal subjects. The most common hyperlipoprotein type is type IIb (66%), less common are type IIa (22%), IV (6%) and III (4%) respectively. There is no correlation between serum lipids, lipoproteins and urinary protein, serum albumin, and histological diagnosis. The ratio of cholesterol: HDL, LDL: HDL and Apo A1: B are all significantly higher than normal control (p < 0.001) and correlate with urinary protein levels. This study shows that the nephrotic patients who have persistent heavy proteinuria have dyslipidemia which is highly atherogenic and probably increases the incidence of coronary heart disease.
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PMID:Lipoprotein abnormalities in adult nephrotic syndrome. 796 58

Plasma lipoprotein levels and carotid-femoral pulse wave velocity, used as a marker of aortic rigidity, were evaluated in 53 young subjects with borderline hypertension by comparison with normotensive controls of the same age and body surface area. Subjects with body weight excess, exaggerated alcohol intake, and/or tobacco consumption were excluded from the study. Borderline hypertensive patients were characterized by significantly higher values of pulse wave velocity and plasma levels of glucose, total cholesterol, high density lipoprotein subfraction HDL3, apolipoprotein B, and lipoprotein (a). There were no group/sex interactions. A significant dyslipidemia was observed in 13 males of the 53 borderline hypertensive subjects. Only in this subgroup did subjects exhibit a strong positive relationship between pulse wave velocity and either plasma total cholesterol or apolipoprotein B. The correlation was observed even after adjustment for blood pressure. The study provides evidence that, in young males with borderline hypertension, some abnormalities of plasma lipoproteins requiring treatment may be present and are associated with an increased stiffness of the arterial wall.
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PMID:Abnormalities of lipid metabolism and arterial rigidity in young subjects with borderline hypertension. 817 14

Hyperlipidemia is common in renal allograft recipients. To elucidate the role of cyclosporine in posttransplant hyperlipidemia, we measured lipids, lipoprotein lipids, and apolipoproteins of thirty-five renal allograft recipients and evaluated their relation to trough cyclosporine blood levels. All patients were on a triple immunosuppressive regimen with equal doses of prednisone and azathioprine, and had stable graft function. Cyclosporine blood levels were significantly correlated to total plasma cholesterol (P = 0.028), low-density lipoprotein cholesterol (P = 0.022), apolipoprotein B (P = 0.017), and the cholesterol/high-density lipoprotein cholesterol ratio (P < 0.002), but not to plasma triglycerides. Significant inverse correlations were found between cyclosporine blood levels and high-density lipoprotein cholesterol (P = 0.034), high-density lipoprotein3 cholesterol (P = 0.025), and apolipoprotein A-1 (P = 0.047), but not high-density lipoprotein2 cholesterol. The independent relation of cyclosporine blood levels to each of the measured lipid parameters was investigated by a stepwise regression model including age, body mass index, interval from transplantation, diabetes mellitus, plasma creatinine, and intake of diuretics and beta-blockers. After correction for these 7 variables, cyclosporine blood levels remained significantly associated with high-density lipoprotein cholesterol, high-density lipoprotein3 cholesterol, apolipoprotein A-1, apolipoprotein B, low-density lipoprotein cholesterol, and the cholesterol/high-density lipoprotein cholesterol ratio. These data suggest that cyclosporine causes atherogenic dyslipidemia.
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PMID:Relation of cyclosporine blood levels to adverse effects on lipoproteins. 819 11

Four-year-old schoolchildren with a positive family history for atherogenic dyslipidemia and/or clinical atheroma before 55 years of age were screened for hypercholesterolemia. Investigations included determination of serum levels of total cholesterol, triglycerides, HDL cholesterol, apolipoprotein A1, apolipoprotein B, and Lp(a); an agarose lipidogram; acrylamide gradient electrophoresis; and determination of LDL composition by ultracentrifugation. Normal values were defined as values under the 90th centile, i.e., 1.97 g/l for total cholesterol, 0.89 g/l for triglycerides, 1.36 g/l for LDL-cholesterol, and 1.26 g/l for apolipoprotein B. Among 3,565 children routinely evaluated at 4 years of age, 525 (16.2%) had a positive family history; of these, 72 underwent lipid investigations. Eight children (11%) had hypercholesterolemia type IIA, eight had a variety of lipid disorders, and 14 (20.6%) had increased Lp(a) levels as an isolated anomaly or concomitantly with an atherogenic dyslipidemia. Because Lp(a) is a cardiovascular risk factor independent from total cholesterol levels, we believe this parameter should be determined in high risk children.
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PMID:[Screening in the school milieu, at 4 years old, for hypercholesterolemia]. 823 96

We examined the effects of a fibric acid, clinofibrate, on lipoprotein metabolism in 12 hyperlipidemic patients with uremia treated on continuous ambulatory peritoneal dialysis during a 24 week treatment. Daily dose of clinofibrate was 200 mg for the initial four weeks, 400 mg for the second four weeks, and 600 mg for the subsequent 16 weeks. Serum and very-low density lipoprotein (VLDL) triglyceride were decreased by 36% and 48%, respectively. Neither total cholesterol nor apolipoprotein B changed significantly, whereas cholesterol was decreased in VLDL and increased in low (LDL) and high density lipoprotein (HDL) fractions. Post-heparin plasma lipoprotein lipase (LPL) before treatment was not lower than the normal value, and we found no change in LPL activity following clinofibrate. Hepatic triglyceride lipase also did not change. Apolipoprotein (apo) C-II/C-III ratio was low as compared to the normal value before treatment, and the ratio was increased by 38% after the treatment. Decrease in VLDL triglyceride was associated with increase in apo C-II/C-III ratio in all the cases. Abnormal enrichment with triglyceride of LDL and HDL fractions was improved by clinofibrate. Although one patient had a transient and asymptomatic elevation of serum creatine phosphokinase, no patient had muscle pain. There was no accumulation of the drug in the 24 week trial. These results suggest that clinofibrate is an effective and safe approach to the management of dyslipidemia in CAPD patients.
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PMID:Hypertriglyceridemia and lowered apolipoprotein C-II/C-III ratio in uremia: effect of a fibric acid, clinofibrate. 830 36

To determine whether the offspring of hypertensive patients (OHP) might have a higher serum insulin level than offspring of normotensive parents, we studied 152 girls in junior high school, 21 of whom had at least one hypertensive parent. The remaining 131 girls had normotensive parents and served as the controls. After an overnight fast, we measured the subjects' height, body weight, blood pressure and body fat mass, and collected blood for assay of serum immunoreactive insulin (IRI), lipids and apolipoproteins. Despite a similar body mass index, the OHP had a significantly greater body fat mass (P < 0.05) and % fat mass (P < 0.05) than the controls. The OHP exhibited a significantly higher serum IRI level than the controls (P < 0.05), but no differences in blood pressure or serum lipids. In the OHP, % body fat mass was significantly correlated with systolic blood pressure (P < 0.05), triglyceride (P < 0.01) and apolipoprotein B (P < 0.01), not observed in controls. The serum IRI of the OHP, but not that of controls, was significantly correlated with systolic blood pressure (P < 0.05), serum triglyceride (P < 0.02) and apolipoprotein B (P < 0.05). Thus, a higher serum IRI level due to an increase in total body fat mass appears to be an inherited trait that contributes to the development of hypertension and dyslipidemia.
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PMID:Higher serum insulin level due to greater total body fat mass in offspring of patients with essential hypertension. 834 31


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