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)

High performance gel chromatography (HPGC) was used to separate lipoproteins on the basis of their size and to generate lipoprotein profiles for plasma collected from patients with different lipoprotein phenotypes. These profiles provided a direct measurement of low density lipoprotein (LDL)-cholesterol which was more precise than LDL-cholesterol values calculated by the Friedewald equation. In addition, LDL-cholesterol concentrations were obtained in patients with combined hyperlipidemia in whom LDL-cholesterol could not be accurately calculated by the Friedewald equation. The response of LDL-cholesterol to the drug gemfibrozil was reliably monitored and in addition changes in LDL particle size could be assessed from the LDL apolipoprotein B/cholesterol ratio. HPGC also assisted in the diagnosis of type III hyperlipidemia by revealing a characteristic lipoprotein profile. HPGC-derived lipoprotein profiles provided additional useful clinical information for combined hyperlipidemia (Fredrickson lipoprotein phenotypes IIb, III).
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PMID:Lipoprotein profiling by high performance gel chromatography. 798 33

Elevated serum levels of the atherogenic and thrombogenic lipoprotein (a) (Lp(a)) have been recognized as a feature of the nephrotic syndrome associated hyperlipidaemia. To examine a possible relationship between serum Lp(a) concentration and proteinuria, serum albumin, or blood pressure, we studied nine patients with nephrotic-range proteinuria both at baseline and after various forms of antihypertensive and antiproteinuric treatment. In fixed order, patients received conventional antihypertensive treatment (either alpha-methyldopa or clonidine), subsequently ACE-inhibition therapy (lisinopril), ACE inhibition combined with an NSAID (indomethacin), and finally NSAID plus conventional antihypertensive therapy. Measurements were performed at the end of each 2-month study period. When compared to controls (n = 29), proteinuric patients before treatment showed increased levels of total cholesterol, very-low and low-density lipoprotein (VLDL+LDL) cholesterol, triglycerides and apolipoprotein B (apoB), while high-density lipoprotein (HDL) HDL cholesterol was lower. Lp(a) was significantly higher in patients (107 (95% CI: 55-208) mg/l) as compared to controls (25 (13-49) mg/l, P < 0.01). Conventional antihypertensive treatment did not reduce proteinuria, while Lp(a) remained unaffected. ACE-inhibitor treatment lowered proteinuria, raised serum albumin, while La(a) tended to fall (-11 +/- 8%). Addition of an NSAID induced a further fall in proteinuria and a rise in serum albumin. Lp(a) now fell by 40 +/- 5% from baseline values (P < 0.01). Both serum total, HDL and VLDL+LDL cholesterol fell significantly. Finally, during subsequent single therapy with NSAID most parameters, including proteinuria and Lp(a), returned towards values obtained during single therapy with ACE inhibiton.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Symptomatic antiproteinuric treatment decreases serum lipoprotein (a) concentration in patients with glomerular proteinuria. 805 29

The prevalence of hyperlipidemia in adolescents and young adults who are long-term survivors of pediatric renal transplantation with stable graft function has not previously been examined. We studied 33 renal transplant recipients aged 5 to 23 years, who were an average of 7.4 years (range 3 to 11 years) post-transplant. We found hypercholesterolemia in 17 (total cholesterol (TC) > 5.18 mmol/l). Both low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) levels were increased, such that the mean TC/HDL-C and apolipoprotein B/apolipoprotein A1 (Apo B/Apo A1) ratios were below levels associated with increased coronary artery disease risk. Subjects with hypercholesterolemia did not differ from those with normal cholesterol values in current age or age at transplant, serum creatinine, serum albumin, serum triglycerides, HDL-C, TC/HDL-C ratio, Apo B/Apo A1 ratio, prednisone dose, body mass index, gender, use of thiazides or beta blockers, or family history of premature atherosclerosis. Coronary risk factors appear to cluster in these patients, with hypertension in 53% of those with hypercholesterolemia. Lipid profiles were not different in patients treated with prednisone-azathioprine vs. prednisone-azathioprine-cyclosporine A immunosuppression. A significant correlation was found between prednisone dose (mg/m2) and TC, LDL-C and TC/HDL-C. According to National Cholesterol Education Program guidelines, 32% of these long-term survivors of pediatric renal transplantation warrant at least dietary intervention and 10% are candidates for treatment with lipid-lowering drugs. This proportion is likely to increase as the safety of lipid-lowering agents is established in younger children.
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PMID:Hyperlipidemia in long-term survivors of pediatric renal transplantation. 806 64

Hyperlipidemia arises from a disturbance in the balance between production and degradation of lipoprotein particles. Variation in the secretion of human apolipoprotein B (apoB), the major protein component of triglyceride-rich lipoproteins, directly affects this homeostasis. Naturally occurring apoB signal peptide variants (associated with hypertriglyceridemia, altered postprandial lipid metabolism, or atherosclerosis) were investigated for their ability to direct transit through the secretion pathway. Three apoB signal peptide isoforms were fused to the secretory protein, invertase, and expressed in yeast. A deletion or insertion in the hydrophobic core of the signal peptide mediated inefficient translocation into the endoplasmic reticulum and was secretion-defective, relative to the common 27-residue isoform. Additionally, the insertion apoB isoform was observed in yeast to confer a defect in export from the endoplasmic reticulum. Secretion of the apoB signal peptide-invertase fusions responded positively to an inhibitor of calpain type I proteases. These observations suggest that the apoB signal peptide plays a role in determining the levels of apoB degradation and secretion and, thus, hyperlipidemia.
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PMID:Human apolipoprotein B signal sequence variants confer a secretion-defective phenotype when expressed in yeast. 806 10

In 34 cases of ischaemic cerebral vascular disease (24 patients with completed stroke and 10 with RIND or TIA) complex studies of serum lipids were performed. The level of total cholesterol, cholesterol HDL, phospholipids, triglycerides and apolipoprotein B was evaluated. The obtained results revealed in RIND and TIA syndrome higher values of phospholipids, apolipoprotein B and cholesterol HDL than in completed ischaemic stroke. However the differences were not great enough, draw conclusions about the dynamics of changes in course of progress of the ischaemic cerebral vascular disease. In allmost all cases of completed stroke and in RIND or TIA syndrome a drop of cholesterol HDL was found. Other deviations of lipid level were noticed only in few cases. Notwithstanding the significance of other than hyperlipidemia risk factors, especially of elevated blood pressure, it seems reasonable to start adequate treatment when in patient with RIND or TIA abnormal values of serum lipids are found.
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PMID:[Patterns of lipid change in serum as a risk factor for ischemic brain disease]. 811 88

Many factors influence carbohydrate absorption. Slower rates of absorption may have advantages in reducing postprandial glycemia and insulinemia and, in time, reduce serum low-density-lipoprotein (LDL) cholesterol and apolipoprotein B concentrations. Foods high in viscous fiber or antinutrients, or foods that are resistant to gelatinization, show slower rates of digestion and absorption and may be called low glycemic index or lente carbohydrate foods. Specific enzyme inhibitors may also cause lente effects. Certain small-intestinal effects of lente carbohydrate may be mimicked by altering feeding frequency (eg, nibbling vs gorging). Increased meal frequency reduces post-prandial insulin and glucose responses in people with non-insulin-dependent diabetes and in nondiabetic volunteers and lowers serum concentrations of LDL cholesterol and apolipoprotein B. Reduced hepatic cholesterol synthesis has been reported. Increased meal frequency may also slow small-intestinal absorption in the treatment of conditions such as diabetes, hyperlipidemia, and possibly obesity.
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PMID:Low glycemic index: lente carbohydrates and physiological effects of altered food frequency. 811 54

The influence of simvastatin, a competitive inhibitor of 3-hydroxy-3-methyl glutaryl coenzyme A reductase, on quantitative and qualitative changes in lipoprotein metabolism was investigated in 18 patients (group I, 10 with primary kidney disease and group II, 8 with diabetic nephropathy) with nephrotic syndrome. Nephrotic patients exhibited severe hyperlipidemia (serum cholesterol 390 +/- 17 mg/dl and triglyceride 335 +/- 42 mg/dl; mean +/- SEM) and had significantly higher lipoprotein (a) [Lp(a)] levels (54 +/- 12 mg/dl; median 31 mg/dl, p < 0.01) compared with 20 healthy subjects (mean 12 +/- 1.8 mg/dl; median 7 mg/dl). Fifty-six percent of the patients and 15% of the controls had values greater than 30 mg/dl. Treatment with simvastatin in increasing doses over a period of three months (13 patients received 40 mg/day and 5 patients 20 mg/day at the end of the third month) reduced LDL-cholesterol in both groups of patients (35% and 54%) as well as apolipoprotein B (apoB) (31% and 46%) significantly, but Lp(a) levels were not influenced (57 +/- 21 vs 59 +/- 20 and 50 +/- 14 vs 53 +/- 16 mg/dl, respectively). On the other hand a complex change in lipoprotein composition occurred. The ratio of LDL apoB/LDL cholesterol-ester increased significantly (0.75 +/- 0.03 to 0.84 +/- 0.03 and 0.80 +/- 0.03 to 1.02 +/- 0.1, respectively) and cholesterol concentration in VLDL (64 +/- 16 to 39 +/- 7 and 74 +/- 18 to 55 +/- 74 mg/dl, respectively) was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of simvastatin on lipoprotein (a) and lipoprotein composition in patients with nephrotic syndrome. 818 55

Fifty nine cases with hyperlipidemia were divided randomly into two groups. In group I, each patient took simvastatin 10-40mg/day (mean 17.9mg/day). In group 2, each patient took gemfibrozil 1200mg/day. After treatment with simvastatin, in comparing with baseline values, serum level of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) triglyceride (TG), apolipoprotein B (ApoB), and TC/HDL-C (high-density lipoprotein cholesterol) reduced by 34.6% (P < 0.001), 45.4% (P < 0.001), 22.1% (P < 0.01), 21.1% (P < 0.001), and 39.4% (P < 0.001) respectively, and HDL-C, apolipoprotein A-I(Apo A-I) and Apo A-I/Apo B elevated by 14.2%, 21.9% and 64.5% respectively. For lowering TC, LDL-C, Apo B and elevating Apo A-I/Apo B, Simvastatin was better than gemfibrozil (P < 0.01-0.001). However, for lowering TG, gemfibrozil was better than simvastatin (P < 0.001). As for increasing HDL-C and Apo A-I, no significant differences were found between the two groups. No significant side effects were found in all patients but one who developed hypersensitive eruption after gemfibrozil taken, and he was excluded from the trial.
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PMID:[Clinical evaluation of simvastatin in the treatment of hyperlipidemia]. 819 33

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

A sample enriched for familial combined hyperlipidemia (FCHL) was examined for evidence of an association between genotype at an apolipoprotein B (apoB) elevating locus defined by complex segregation analysis and FCHL. Complex segregation analysis detected a locus with a large effect on plasma apoB levels and was used to compute the most probable genotype of family members. None of the 35 normolipidemic adults carried a copy of the allele associated with elevated apoB levels, yet 58% of the 109 adults with FCHL carried 1 (29%) or 2 (28%) copies. Two of 28 (7%) normal children had 1 copy of this allele and none had 2 copies, while 88 of 182 (48%) children with FCHL had 1 (26%) or 2 (22%) copies. Further, 41 of 48 (85%) individuals classified as having hyperapobetalipoproteinemia did not carry a copy of this "elevated apoB" allele. Therefore, the presence of the allele associated with elevation of apoB level is highly predictive of FCHL and this association cannot be explained solely by the presence of elevated apoB levels in FCHL, suggesting that the locus controlling apoB levels may play an etiologic role in FCHL.
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PMID:Genotype at a major locus with large effects on apolipoprotein B levels predicts familial combined hyperlipidemia. 822 6


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