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

Vitamin E, cholesterol and triglycerides were measured in blood sera of 167 patients (40-59 years old) with angina pectoris. An increase in concentration of vitamin E was observed only in patients with hyperlipidemia, whereas the vitamin content was similar to the control values in patients with hypertension, in smokers and in the persons free of risk factor. Distinct correlation was found only between vitamin E and the triglycerides contents (r = 0.42). These data corresponded to the results of a previous examination of 224 men and 435 women without ischemic heart disease: in men the content of vitamin E correlated with triglycerides (r = 0.50) and in women--with cholesterol (r = 0.34). The ratio of vitamin E/triglycerides appears to be a more adequate index of the vitamin content in men.
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PMID:[Vitamin E and serum lipids in ischemic heart disease]. 647 33

A randomized prospective study of LBW infants was undertaken to evaluate the effect of parenteral lipid infusions upon their antioxidant systems. Ten babies received a parenteral nutrition regimen with lipid emulsion, and ten received a regimen without lipid. Although the addition of lipid emulsion to the total parenteral nutrition regimen led to a rise in vitamin E levels, the selenium levels fell in both groups. Neither group showed evidence of deficient antioxidant systems by the peroxide hemolysis test or thiobarbituric acid test. There did not seem to be any adverse effect of the lipid infusion upon the clinical course of the infants except for hyperlipidemia. There was a better weight gain in infants receiving lipid.
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PMID:Selenium and vitamin E sufficiency in premature infants requiring total parenteral nutrition. 682 76

Lipid peroxides act harmfully on cell membranes to result in cellular dysfunction. On the other hand, vitamin E (VE) having antioxidant effect is considered to protect the generation of lipid peroxides. In this study, the changes in the levels of lipid peroxides and VE of pregnant sera were followed clinically and biochemically in relation to lipoprotein metabolism. The results obtained were as follows. 1) Lipoprotein metabolism in pregnancy was characterized by an increase in very low density lipoprotein (VLDL) which is a major carrier of triglyceride. The amount of VLDL in pre-eclamptic subjects increased more than that of normal gravidas. The ratios of HDL cholesterol/LDL cholesterol of pre-eclamptic subjects were significantly (p less than 0.01) low levels compared with those of non-gravidas. 2) The contents of lipid peroxides and alpha-tocopherol (alpha-toc) in each serum lipoprotein fraction were also elevated in pregnant subjects. Lipid peroxide levels in HDL fraction of pre-eclamptic subjects were significantly (p less than 0.005) higher than those of normal gravidas. On the contrary, the levels of alpha-toc in HDL fraction of pre-eclamptic subjects were significantly (p less than 0.005) lower than those of normal gravidas. 3) As a result of examining the correlationship between the levels of lipid components and those of lipid peroxides and alpha-toc in each lipoprotein fraction of pregnant sera, both levels of lipid peroxides and alpha-toc were positively correlated with those of major lipid components in VLDL and LDL fractions, while no significant correlation was found in HDL fraction. Also in VLDL fraction, the level of lipid peroxides was positively correlated with that of alpha-toc whereas in HDL fraction the former tends to correlate reversely with the latter. From the above observation, it is worthwhile to study on HDL fraction which is associated with cell membrane lipids and received less influence of the amounts of serum lipids, when the damage with lipid peroxides under pregnancy accompanied of hyperlipemia is examined in relation to alpha-toc.
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PMID:[Changes in lipid peroxide and alpha-tocopherol levels of pregnant serum lipoproteins (author's transl)]. 727 45

The symptomatic postmenopausal woman with breast cancer presents the clinician with a difficult task with respect to hormone replacement therapy (HRT). All of the published meta-analyses have been consistent in showing that there is a slightly increased risk of developing breast cancer in those patients using postmenopausal estrogens for greater than 10 years. However, there have been no published placebo-controlled clinical trials on the effects of HRT in women with a history of breast cancer. Quality of life must be balanced against the theoretical risk of tumor promotion. Assessment of osteoporotic and cardiac risk factors (i.e., smoking, hypertension, family history, hyperlipidemia) should influence the decision. Valid alternatives to estrogen replacement include low-dose progesterones such as Bellergal or vitamin E for hot flashes, and biphosphonates, calcium, anabolic steroids, and calcitonin for osteoporosis.
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PMID:The management of menopausal symptoms in women with breast cancer. 761 Jun 43

The effect of orlistat, a nonabsorbed inhibitor of gastric and pancreatic lipases, was examined in patients with primary hyperlipidaemia (serum cholesterol > or = 6.2 mmol.l-1 and triglycerides < or = 5.0 mmol.l-1) not responsive to dietary change alone. In a multicentre, randomised, double-blind study, 103 men and 70 women received 30, 90, 180, or 360 mg or orlistat or placebo for 8 weeks. Total and low-density lipoprotein cholesterol levels were reduced by 4% and 5% with 30 mg orlistat, by 7% and 8% with 90 mg orlistat, by 7% and 7% with 180 mg orlistat and by 11% and 10% with 360 mg orlistat compared to placebo. High density lipoprotein cholesterol levels significantly decreased in the 360 mg orlistat group. Triglyceride levels significantly increased in the placebo group but not in the drug groups. Body weight decreased by 1.2 kg with 360 mg orlistat, despite a weight maintenance diet. Decreases in vitamin E and D levels occurred, although both vitamins remained within the normal range. Adverse effects from the gastrointestinal tract were frequent, but led to discontinuation of therapy in only seven patients. Orlistat is a new therapeutic drug for the treatment of hyperlipidaemia that may be particularly useful among overweight patients. Its potential place in therapy will await long-term studies. Vitamin supplementation should be considered during treatment.
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PMID:The effect of the gastrointestinal lipase inhibitor, orlistat, on serum lipids and lipoproteins in patients with primary hyperlipidaemia. 795 33

The RRR-alpha-tocopherol (vitamin E) content in plasma from 46 patients with liver diseases and 23 healthy controls was determined by high performance liquid chromatography and electrochemical detection. Patients were divided into three groups: alcoholic liver diseases (n = 17; group A), hemochromatosis (n = 17; group B) and Wilson's disease (n = 12; group C). Lipid-standardized alpha-tocopherol levels were determined to neutralize differences due to hyperlipemia. The ratio of serum vitamin E to serum lipids (cholesterol, triglycerides, phospholipids) was highest in healthy controls and in patients in group A with cirrhosis and normal transaminases and bilirubin. Patients in group A with acute or chronic ethanol intoxication and high bilirubin levels had a 37% lower lipid-standardized vitamin E level than controls. Patients in group B with hemochromatosis, showing high serum iron (> 180 micrograms/dl), a low free iron binding capacity (< 8 mumol/l) and high ferritin-levels (< 450 micrograms/l), had a 34% lower vitamin E/lipid ratio than healthy controls. No significant lowering of the vitamin E/lipid ratio was observed in the other patients in group B. A significant decrease (37%) in the vitamin E/lipid ratio was only detectable in patients with Wilson's disease (group C) showing high free serum copper (> 10 micrograms/dl). The data support a role for free radicals in the pathogenesis of active liver diseases.
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PMID:Low vitamin E content in plasma of patients with alcoholic liver disease, hemochromatosis and Wilson's disease. 781 21

In a group of 18 patients with essential hyperlipidaemia the influence was studied of multivitamin CRP preparation given for 12 weeks, on lipid peroxides, cholesterol and triglycerides in the serum. The level of lipid peroxides was decreased significantly. This effect was associated with the increase of the serum level of vitamin E. A decrease was also found of the levels of total cholesterol and LDL-cholesterol.
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PMID:[Effect of CRP preparation on serum lipids in patients with hyperlipidemia]. 823 91

The effect of Vitamin E treatment was studied in experimental hyperlipidaemia. The male Wistar rats got control diet and parallel fat rich diet contained 2% cholesterol, 0.5% cholic acid and 20% sunflower oil added into LATI food during 9 days. The treated hyperlipidemic animals got vitamin E for 9 days in daily 8.56 mg/b.w.kg dose mixed in food. The effect of antioxidant treatment on changes of lipid peroxidation, content of diene conjugates, thiobarbituric acid reactive products and natural scavenger capacity of rat liver homogenates and microsome fractions were measured by spectrophotometric and luminometric methods. Fatty acid composition of lipid fraction of samples was determined by capillary gas chromatography. Vitamin E in hyperlipidemia increased the natural scavenger capacity of liver and decreased the level of thiobarbituric acid reactive products and dien conjugates. There was no change in fatty acid composition of samples on effect of vitamin E antioxidant treatment.
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PMID:[Antioxidant effect of vitamin E in experimental hyperlipidemia]. 835 Nov 40

Patients presenting combined hyperlipidemia (CHL) display an elevated risk of coronary heart disease. The atherogenic lipoprotein particles implicated in this disorder remain ill defined. We determined the qualitative and quantitative characteristics of the density distribution of low density lipoprotein (LDL) particle subspecies in nine subjects defined phenotypically as presenting CHL, and under strict dietary control. Seven CHL patients possessed familial antecedents of premature coronary heart disease; none were E2E2 homozygotes. Five LDL subspecies were isolated by density gradient ultracentrifugation in the density range 1.019-1.063 g/ml. In all patients, the LDL profile was skewed towards the dense subspecies (LDL-4, d 1.039-1.050 g/ml and LDL-5, d 1.050-1.063 g/ml), representing 47% of total LDL mass; by contrast, these subspecies accounted for only 30% of LDL mass in five normolipidemic subjects (P < 0.01). In addition, plasma LDL mass concentrations were some twofold higher in CHL patients as compared to normolipidemic subjects. The % mass of LDL-4 was positively correlated with plasma triglyceride and apoB levels. LDL-2 and LDL-3 in CHL patients were triglyceride-enriched (11.9 and 7.2%, respectively) as compared to the corresponding subspecies in normolipidemic subjects (6.6 and 3.7%, respectively; P < 0.05 in each case). LDL particle size decreased with increase in density in both groups; however, significant differences were found between corresponding LDL subspecies (LDL-1, -3, -4, and -5) in CHL patients and normolipidemic subjects, a finding suggestive of dissimilar molecular organization, despite correspondence in hydrated density. The copper-induced oxidative modification of LDL subspecies was assessed by determination of conjugated diene formation. In both groups, LDL-5 was distinct in exhibiting a marked diminution in oxidative resistance as indicated by a significant reduction (P < 0.01) in mean lag time. The oxidative susceptibility of LDL subspecies in both groups was independent of vitamin E content when expressed as the ratio vitamin E/LDL mass, although dense LDL in CHL patients tended to be deficient in this antioxidant. The diminished oxidative resistance of dense LDL subspecies could not be accounted for by enrichment in polyunsaturated fatty acids in either group. These studies suggest that in consequence of their elevated circulating concentration and diminished oxidative resistance, dense LDL subspecies represent putative atherogenic subspecies in combined hyperlipidemia.
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PMID:Dense low density lipoprotein subspecies with diminished oxidative resistance predominate in combined hyperlipidemia. 842 63

Given the current interest in the cardiovascular complications of Mg deficiency, the aim of the present experiment was to investigate the effect of Mg deficiency on the time-course of lipoprotein oxidation and to assess whether short-term Mg deficiency results in vitamin E depletion that predisposes lipoproteins and tissues to subsequent oxidation. Weanling rats were pair-fed for 8 d with control and Mg-deficient diets respectively. Plasma triacylglycerol and alpha-tocopherol levels were significantly greater in Mg-deficient rats compared with control animals. The increase in plasma apolipoprotein B concentration indicated that a corresponding increase in plasma triacylglycerol-rich lipoproteins (TGRLP) occurred in Mg-deficient animals. Hyperlipaemia was associated with modifications in the composition of TGRLP. The proportion of triacylglycerols was elevated whereas that of cholesterol and protein was reduced, and Mg deficiency resulted in a slight significant reduction in alpha-tocopherol content. When the TGRLP fractions were subjected to in vitro Cu-induced oxidation the lipoprotein fractions from Mg-deficient rats were more susceptible to oxidative damage than lipoprotein fractions from control rats. Mg deficiency did not modify the alpha-tocopherol content of liver, heart and skeletal muscle. However, after exposure of tissue homogenates to Fe-induced lipid peroxidation, thiobarbituric acid-reactive substances were significantly higher in tissues from Mg-deficient rats compared with those from control rats. These results complement previous findings, showing that Mg deficiency increases the susceptibility of TGRLP and tissues to peroxidation and suggest that oxidative damage is not the result of a decrease in vitamin E antioxidant status.
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PMID:Effect of magnesium deficiency on triacylglycerol-rich lipoprotein and tissue susceptibility to peroxidation in relation to vitamin E content. 856 71


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