Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Many patients with high levels of serum total cholesterol have a concomitant elevation of serum triglyceride levels and thus have mixed hyperlipidemia. In this study, 13 patients with mixed hyperlipidemia were treated with the cholesterol-lowering drug lovastatin to determine its effectiveness. In 9 of these patients, lovastatin therapy used alone was compared with the drug combination of lovastatin and gemfibrozil. In the 13 patients, lovastatin therapy produced a 31% reduction in total cholesterol level and a 32% decrease in triglyceride levels compared with placebo. It lowered very-low-density plus intermediate-density lipoprotein cholesterol levels by 40%, low-density lipoprotein cholesterol levels by 36%, and total apolipoprotein B levels by 28%. Concentrations of high-density lipoprotein cholesterol and apolipoprotein A-I were unchanged, but total cholesterol (and low-density lipoprotein cholesterol)/high-density lipoprotein cholesterol ratios were markedly reduced. Compared with lovastatin alone, lovastatin plus gemfibrozil produced greater decreases in very-low-density plus intermediate-density lipoprotein cholesterol levels and an increase in high-density lipoprotein cholesterol levels, but, in view of the higher risk for severe myopathy with this combination, lovastatin used alone may be adequate therapy for many patients with mixed hyperlipidemia.
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PMID:Management of primary mixed hyperlipidemia with lovastatin. 235 64

The inheritance of low density lipoprotein (LDL) subclass patterns was investigated in 234 members of seven large kindreds with familial combined hyperlipidemia (FCHL), a disorder characterized by elevated LDL cholesterol and/or triglyceride and increased coronary disease risk in families. Analysis of LDL subclasses by nondenaturing gradient gel electrophoresis showed a predominance of large, buoyant LDL particles (pattern A) in 71% of the family members and a predominance of small, dense LDL particles (pattern B) in 29% of family members. Based on complex segregation analysis, pattern B appeared to be inherited as an autosomal trait with either a dominant or an additive mode of inheritance and a small, but significant, multifactorial inheritance component. The proposed allele for pattern B was common (frequency = 0.3), and reduced penetrance was observed among men under age 20 and among women under age 50. These results in these FCHL families are consistent with those from a previously reported population-based sample of families, in which pattern B showed an apparent dominant mode of inheritance. In that study, reduced penetrance was observed for men under age 20 and for premenopausal women, but a somewhat lower allele frequency was found for pattern B (0.25). In the FCHL family members, LDL subclass pattern B was associated with significantly increased plasma levels of apolipoprotein B and triglyceride and decreased high density lipoprotein cholesterol. In comparison with a group of controls, the FCHL family members with pattern A had similar mean triglyceride levels, but higher mean apolipoprotein B. Thus, in families with FCHL, a predominance of small, dense LDL particles appears to be inherited as a common, single-gene trait, which is closely associated with the higher plasma triglyceride levels found in these families. The increased plasma apolipoprotein B levels found in FCHL cannot, however, be accounted for by this proposed locus.
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PMID:Inheritance of low density lipoprotein subclass patterns in familial combined hyperlipidemia. 236 63

The efficacy of Gemfibrozil on S. lipid levels was studied in 36 middle aged subjects with type IIA, IIB, IV hyperlipidemia. Gemfibrozil was well tolerated in the dose of 1200 mg/day and no dropouts were attributable to its use. An overall reduction in total cholesterol (39.91%), total triglycerides (71.10%), VLDL triglycerides (62.97%). LDL cholesterol (45.57%) and apolipoprotein B levels (26.83%) were observed at 24 weeks. At the same time HDL cholesterol, and apolipoprotein A levels showed increases by 26.23% and 53.67% respectively. It is concluded that Gemfibrozil is an effective lipid lowering agent. Further long term studies are necessary to determine its optimal dosage and its long term safety in Indian subjects.
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PMID:Gemfibrozil in hyperlipidaemia: an open, single blind trial. 238 Jan 32

Familial dyslipidemic hypertension (FDH) is a syndrome recently described from sibships selected for early familial hypertension and found to have one or more of three fasting lipid abnormalities [high triglycerides, low high density lipoprotein (HDL) cholesterol, high low density lipoprotein (LDL) cholesterol]. In further analyses of these same 131 hypertensive subjects, apolipoprotein A-I and B, fasting plasma insulin (adjusted for body mass index), and detailed anthropometrics were different in two subgroups of FDH. Of 63 FDH patients, 19 met the criteria for familial combined hyperlipidemia (FCHL); 44 did not, but still had high triglyceride and/or low HDL cholesterol levels. When compared to 20 normolipidemic hypertensive patients, the 19 hypertensive patients with FCHL had 196% higher very low density lipoprotein cholesterol (p = 0.0001), 33% higher apolipoprotein B (p = 0.0002), smaller LDL particles (p = 0.007), and 73% higher fasting insulin (p = 0.003), but no significant differences in body mass index or skinfold thicknesses. The other 44 FDH patients without FCHL had 33% lower HDL (p = 0.0001), with only 8% lower apolipoprotein A-I levels (p = 0.20); significantly higher subscapular skinfolds (p = 0.02), weights (p = 0.002), body mass index (p = 0.006), knee widths (p = 0.0007), and wrist circumferences (p = 0.0009); smaller, denser LDL subfractions (p = 0.001); and increased apolipoprotein B levels (p = 0.01) compared to the normolipidemic hypertensive group. Increased fasting insulin levels were similar to the normolipidemic group and significantly lower than the FCHL group after adjustment for body mass index, suggesting a relationship between obesity and fasting insulin levels only in the non-FCHL group. We conclude that FDH consists of at least two subgroups: 1) FCHL with high apolipoprotein B, small LDL particles, and increased fasting plasma insulin levels, and 2) a less well-defined residual having upper central obesity with low HDL cholesterol and high triglyceride levels. Elevated insulin levels found in both groups, but possibly originating through different physiological mechanisms, may provide the pathophysiological connections between dyslipidemia, obesity, and hypertension.
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PMID:Apolipoprotein, low density lipoprotein subfraction, and insulin associations with familial combined hyperlipidemia. Study of Utah patients with familial dyslipidemic hypertension. 249 19

Eight patients with end-stage renal failure (plasma albumin less than 35 g/l) who were established on glucose CAPD exchanges, were studied for 4-week periods before, and after 12 weeks when 1% amino-acid solution had been used for the morning exchange. Anthropometric, biochemical, clinical and dietary assessments were made every 4 weeks. Dietary intakes of protein and calories were maintained. Studies with amino-acid solutions showed a mean of 13% and 8% amino acids remaining in the dialysate after 6 and 8 h respectively. Plasma amino acids increased to a maximum after 2 h of dialysis; however, fasting concentrations were constant over the 5 months. Osmolality of amino acids decreased comparably with 1.36% glucose during 8-h exchanges although the recovery of fluid was marginally less. Plasma transferrin increased significantly after 8 weeks of amino acids but subsequently decreased in one patient due to infection. No significant changes occurred in albumin, apolipoprotein A, IgG, IgA or prealbumin. Cholesterol and apolipoprotein B decreased in seven patients but increased in one due to rising calorie intake. Increases in urea and decreases in bicarbonate were not clinically significant. Amino-acid-based fluid was well tolerated with modest nutritional benefit and reduction in hyperlipidaemia. Optimal effects of amino acids are likely at higher concentrations using two or more exchanges in patients eating less than 0.9 g protein/kg per day.
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PMID:The use of an amino-acid-based CAPD fluid over 12 weeks. 250 36

Hemodialysis (HD) patients have a high incidence of hyperlipidemia. Hypertriglyceridemia is the most frequent abnormality encountered. It results mainly from a defect in the degradation of triglycerides. The aim of this study was to evaluate the efficacy of a fish oil (Max-EPA) rich in polyunsaturated fatty acids (PUFA), such as eicosapantenoic acid (EPA), on lipid abnormalities of hemodialysis patients. Thirteen hyperlipidemic HD patients were investigated (7 males, 6 females; mean age 57 years; mean duration of HD 72 months). None were diabetic or treated with antihypertensive drugs. All patients had hypertriglyceridemia (greater than 200 mg/dl) and an increase (greater than 1) in the ratio of serum apolipoprotein B to serum apolipoprotein A1 (ApoB/ApoA1). They received for one month, 6 g/day of Max-EPA providing 1 g of EPA. After treatment, serum triglyceride levels fell by 38% from 231 +/- 40 (SD) mg/dl to 140 +/- 38 mg/dl (P less than 0.01). Total cholesterol did not change significantly (before therapy 241 +/- 33 mg/dl, after therapy 249 +/- 38 mg/dl). Apolipoprotein A1 levels (116 +/- 17 mg/dl) were not modified after therapy, 117 +/- 11 mg/dl. Apolipoprotein B decreased significantly from 182 +/- 26 mg/dl to 150 +/- 21 mg/dl after treatment (P less than 0.01). The ApoB/ApoA1 ratio showed a significant decrease from 1.56 +/- 0.26 to 1.3 +/- 0.16 after therapy (P less than 0.01). Also, the greatest reductions were found in the patients who had both the highest serum triglyceride levels and the highest ApoB/ApoA1 ratios. No side effects were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of fish oil rich in polyunsaturated fatty acids on hyperlipidemia of hemodialysis patients. 251 75

The potential role of omega-3 fatty acids in the prevention of atherosclerotic disease in the nondiabetic population currently engenders interest, enthusiasm, and controversy. Some apparently beneficial effects of omega-3 fatty acids on platelet function, eicosanoid formation, plasma triglyceride levels, and blood pressure have been described in patients with diabetes mellitus. However, enthusiasm for the use of omega-3 fatty acids in diabetes has been dampened by reports of potentially deleterious effects of these agents, including increased plasma glucose, glycosylated hemoglobin, plasma total cholesterol and LDL cholesterol, and serum apolipoprotein B levels. These adverse effects have been achieved with large, perhaps excessive, doses of omega-3 fatty acids, in the range of 4-10 g/day. The magnitude of these adverse effects has been small (typically 10-36%). It cannot be assumed that the effects of omega-3 fatty acids are the same in patients with diabetes mellitus as in nondiabetic subjects or patients with primary hyperlipidemia. First, the biosynthesis and composition of fatty acids is abnormal in diabetic animals and possibly in diabetic patients. Second, many potential mechanisms implicated in the pathogenesis of atherosclerosis are present in diabetic but not necessarily in nondiabetic subjects. Third, the mechanisms of many of the risk factors in diabetic patients differ from the mechanisms of these abnormalities in nondiabetic subjects, reflecting the effects of insulin deficiency, hyperglycemia, and their sequelae. Finally, because diabetes is a heterogeneous group of diseases, the effects of omega-3 fatty acids must be addressed separately for patients with insulin-dependent diabetes mellitus, non-insulin-dependent diabetes mellitus, and possibly other forms of diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Omega-3 fatty acids in diabetes mellitus. Gift from the sea? 265 24

The uptake and transport of beta-VLDL by the aortic endothelium was investigated in normal and hyperlipidemic rabbits fed a cholesterol-enriched diet for 1 week to 5 months. Weekly (in the first month) or every other week afterwards, animals were given one of the following probes: (a) [125I]-beta-VLDL injected in vivo and after 24 h the whole aorta or its intima and media were separately collected and examined by spectrometry and autoradiography; (b) [125I]-beta-VLDL coupled to the fluorescent probe 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate perfused in situ for 1-2 h and aorta examined by radioassay and fluorescence microscopy; (c) beta-VLDL-gold complex perfused in situ for 10-15 min and aortic fragments examined by electron microscopy. In addition, cryosections of aortic wall were processed for the immunocytochemical detection of apolipoprotein B and apolipoprotein E. The results showed that both in normal and hyperlipidemic rabbits, the aortic endothelium transports plasma beta-VLDL by a dual pathway: (i) endocytosis involving coated pits and vesicles, endosomes, multivesicular bodies and lysosomes, and (ii) transcytosis, the predominant process, carried out by plasmalemmal vesicles. Both processes, and especially transcytosis, are markedly increased in hyperlipidemia leading to progressive accumulation of beta-VLDL or/and its components in the subendothelial extracellular matrix. In prelesional stages of atherogenesis, beta-VLDL-gold complexes or deposits of apo B and apo E were detected in close association with extracellular liposomes. With the appearance of intimal macrophage-derived foam cells, the immunoperoxidase reaction product, revealing the presence of the two apolipoproteins, could also be seen in intracellular lipid inclusions.
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PMID:Transport pathways of beta-VLDL by aortic endothelium of normal and hypercholesterolemic rabbits. 271 64

There is evidence that the increase in coagulation factor VII (FVII) represents a predictive risk factor of arterial thrombosis in coronary heart disease. Its relative contribution to this multifactorial process and its relationship to other risk factors, namely cholesterol and triglycerides, is yet a matter of investigation. In this study we aimed to clarify whether FVII synthesis or activation correlated with plasma lipid concentrations. For this, we assayed the plasma levels of FVII antigen (FVII:ag) and FVII coagulant activity (FVIIc) in types IIa, IIb and IV hyperlipidemic individuals, together with the levels of cholesterol, triglycerides, high-density lipoproteins and apolipoprotein B. FVII activation state (FVIIa) was then assessed by FVIIc/FVII:ag. In order to assess the possible correlation of FVII levels with the generation of thrombin and formation of fibrin, we also assayed the plasma concentration of fibrin degradation products (D-dimers) in these patients. Considering all the patients studied, there was a fair correlation between FVIIc and FVII:ag (r = 0.704; p less than 0.01). The mean levels of FVIIc and FVII:ag were significantly higher in type IV hyperlipidemia than in controls (t = 4.260; p less than 0.001 and t = 3.015; p less than 0.01, respectively) and other types of hyperlipidemia. We also found that FVIIc and FVII:ag significantly correlated to triglyceride concentration. We could not detect an evident activation of FVII in these patients since FVIIc/FVII:ag was not elevated in comparison with controls, nor did it correlate with any of the lipid determinations in any of the types of hyperlipidemia studied.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma factor VII, triglyceride concentration and fibrin degradation products in primary hyperlipidemia: a clinical and laboratory study. 273 79

Accelerated atherosclerosis is a leading cause of death in long-term survivors of heart and renal transplantation and may be exacerbated by the frequent occurrence of posttransplant hyperlipidemia. Attempts to define the mechanism for hyperlipidemia in transplant recipients are confounded by dramatic changes in metabolism and nutritional status after transplantation, as well as by treatment with multiple immunosuppressive and antihypertensive drugs. To avoid these pitfalls and to determine if cyclosporine alone adversely affects lipid levels, we measured lipoprotein levels in a prospective, double-blind, randomized, placebo-controlled trial of cyclosporine in 36 men with amyotrophic lateral sclerosis. Plasma total cholesterol, triglyceride, high-density lipoprotein cholesterol, and apolipoprotein B levels were measured at baseline, 2 weeks, 1 month, and 2 months. Significant increases of 21% in total cholesterol, 31% in low-density lipoprotein cholesterol, and 12% in apolipoprotein B levels occurred only in the cyclosporine group. Cyclosporine therapy alone adversely affects plasma lipoprotein levels by increasing total cholesterol levels, primarily due to an increase in low-density lipoprotein cholesterol level.
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PMID:Effects of cyclosporine therapy on plasma lipoprotein levels. 273 25


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