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)

A procedure to measure total and direct bilirubin using the Abbott Bichromatic Analyser is described. The method is an adaptation of a sodium dodecyl sulfate method. Reaction products are measured at an acid pH in a buffered matrix using a 600-650 filter wheel. The method has very little spectral interference from either hemolysis or lipemia and correlates well with the manual Jendrassik-Grof method.
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PMID:A total and direct bilirubin determination using an SDS procedure on the Abbott Bichromatic Analyser. 661 11

Turbidimetry of inorganic sulfate, after precipitation with barium sulfate, can be done simply in a Cobas Bio centrifugal analyzer. Polyethylene glycol is used as the precipitate-stabilizing agent. Reproducibility of precipitation is enhanced by the presence of BaSO4 particles, which function as seed nuclei. There is no interference by normal or above-normal concentrations of phosphate, heparin, bilirubin, hemoglobin, or erythrocyte contents, or by lipemia (triglyceride concentrations up to 6.5 mmol/L). Analytical recovery of added inorganic sulfate was found to be quantitative. Precision is similar to that for other methods for inorganic sulfate in plasma. This method is suitable for the rapid, routine analysis of plasma inorganic sulfate, and it is simple and less expensive to perform than alternative methods.
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PMID:Determination of inorganic sulfate in plasma with a centrifugal analyzer. 669 33

Effects of L-ascorbate 2-sulfate (AAS) on fatty liver and hyperlipidemia induced by various treatments were studied in rats and guinea pigs. L-Ascorbic acid (AA) (50 or 175 mg/kg), a reference compound, lowered the lipid levels in the serum and/or liver in guinea pigs, while AA had little effect in rats. On the other hand, AAS (300 mg/kg) was effective in both animals. In rats, AAS lowered cholesterol and triglycerides in the serum from ethionine-treated animals and in the liver from orotic acid-supplemented animals. In guinea pigs, this compound lowered cholesterol and triglycerides in the serum from ethionine-treated animals, lipids in the liver from cholesterol-supplemented animals, and lipids in the serum and liver from scorbutic animals. AA markedly increased the content of AA in the organs in all experiments, while AAS had a slight effect. Thus, it is suggested that AAS exerts its hypolipidemic and lipotropic effects by the specific actions of AAS.
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PMID:Effect of l-ascorbate 2-sulfate on fatty liver and hyperlipidemia induced by various treatments in rats and guinea pigs. 724 Dec 35

The atherogenic low density lipoproteins were evaluated using two turbidimetric methods: one based on the precipitation of LDL and VLDL by heparin-CaCl2 and the other on the precipitation of the VLDL by sodium dodecyl sulfate. In search of hyperlipoproteinemia, both tests were applied to a population of blood donors aged from 18 to 60 years. when both tests were negative, hyperlipoproteinemia can be excluded without quantitative evaluation of cholesterol and triglycerides levels. If the heparin-CaCl2 test is high and the SDS normal it can be concluded that it is a case of type IIa hyperlipidemia. When both test are high, further investigations are required. In the present study, corresponding to the screening of the sera from 2656 blood donors (including 1280 males and 1376 females), the high level of atherogenic lipoproteins is most frequently observed in the males (10 per cent for men and 2,5 per cent for women). This frequency increases with age.
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PMID:[Systematic detection of elevated low density lipoproteins (LDL and VLDL) in a population of 2656 blood donors]. 729 63

We have developed a procedure to quantify apolipoprotein (apo) B-100, apoB-48, and apoE in human triglyceride-rich lipoproteins. This procedure permits delipidation of small amounts of triglyceride-rich lipoproteins without appreciable losses, and quantification of these apolipoproteins in samples containing as little as 10 micrograms of protein. Delipidated triglyceride-rich lipoproteins are subjected to sodium dodecyl sulfate polyacrylamide slab gel electrophoresis, and the mass of apolipoproteins is estimated after densitometric scanning and volume integration of Coomassie blue-stained bands. The chromogenicities of apoB-100 and apoB-48 are virtually identical, and twofold lower than that of apoE. The standard curve for each apolipoprotein follows a power function over a wide protein range, permitting quantification of as little as 0.2 microgram of apoB-48 and as much as 30 micrograms of apoB-100 from a single application of triglyceride-rich lipoproteins to the gels. This method is suitable for routine use in studies of the intestinal and hepatic contributions to triglyceride-rich lipoproteins and their responses to postprandial lipemia.
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PMID:Quantification of apolipoproteins B-100, B-48, and E in human triglyceride-rich lipoproteins. 761 30

The pregnancy and delivery of a subject with homozygous familial hypercholesterolemia (FH) and coronary artery disease (CAD) were monitored closely for signs of maternal and fetal distress. Biweekly treatment with low-density lipoprotein (LDL) apheresis using dextran-sulfate cellulose columns was continued throughout the pregnancy, and lipid and lipoprotein levels were evaluated. During the course of the pregnancy and delivery, no signs of maternal coronary insufficiency developed. Serial ultrasonographic measurements of fetal growth indices and the blood flow velocity waveforms (FVWs) of the uterine and umbilical artery did not reveal any sign of fetal growth retardation or insufficiency of the uteroplacental circulation, respectively. During pregnancy, time-averaged concentrations of serum total cholesterol (TC), LDL cholesterol (LDL-C), apolipoprotein (apo) B, and lipoprotein(a) [Lp(a)] showed a gradual decline. Notwithstanding LDL apheresis, a gradual twofold increase of serum triglyceride (TG) levels was found. In the second and third trimester, high-density lipoprotein cholesterol (HDL-C) levels showed a 55% increase that coincided with a 75% reduction in hepatic lipase activity in postheparin plasma, normalizing after parturition. After delivery, lp(a) levels showed an almost twofold increase, which could not be explained by the interruption of LDL apheresis alone, and may be caused by changes in gonadal steroids. Histologic examination of the placenta and the umbilical arteries revealed no atherosclerotic changes, infarctions, or lipid deposits. In general, long-term LDL apheresis in homozygous FH can delay the onset and complications of severe CAD. In case of a pregnancy, LDL apheresis seems feasible and should be continued during the pregnancy to prevent superimposed hyperlipidemia and placental insufficiency.
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PMID:Pregnancy in a patient with homozygous familial hypercholesterolemia treated with long-term low-density lipoprotein apheresis. 808 91

The plasma concentration, particle size, and chemical composition of high density lipoproteins (HDLs) are associated with the metabolism of triglyceride-rich lipoproteins (TGRLs). During alimentary lipemia there is active exchange of lipids and apolipoproteins between HDL and apolipoprotein B-containing lipoproteins. Whereas HDL has been assigned a protective role against the development of atherosclerosis, alimentary lipemia has been proposed to represent a potentially atherogenic state. We examined plasma HDL concentration, particle size, and composition and their relations to postprandial TGRLs in 32 postinfarction patients and 10 healthy control subjects after intake of a standardized oral fat load of a mixed-meal type. All patients had undergone coronary angiographies in connection with the myocardial infarction and around 5 years thereafter. The plasma HDL cholesterol concentration decreased significantly in response to the oral fat load, particularly in hypertriglyceridemic patients, with a concomitant increase of HDL triglycerides. A limited and reversible yet consistent increase of HDL particle size (1-2%) was seen 6 hours after intake of the oral fat load on nondenaturing gradient gel electrophoresis (GGE) in both patients and control subjects. Virtually no changes in the plasma concentration of HDL GGE subclasses, lipoproteins containing apolipoprotein A-I but no apolipoprotein A-II (LpA-I), or lipoproteins containing both apolipoproteins A-I and A-II (LpA-I:A-II) were induced in the postprandial state despite massive increases of large very low density lipoprotein (VLDL) and large chylomicron remnant levels (determined as apolipoproteins B-100 and B-48 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis). Strong inverse correlations with fasting plasma HDL cholesterol and the larger HDL GGE subspecies were found for large postprandial VLDL and large chylomicron remnants, whereas the corresponding relations for small VLDL and small chylomicron remnants were weaker. The relations of both large and small VLDL and chylomicron remnants to HDL cholesterol were confined to subjects in the lower fasting plasma HDL cholesterol range (< 1.2 mmol/l). None of the HDL parameters measured, either in the fasting or in the postprandial state (HDL cholesterol, HDL triglycerides, HDL GGE subclasses, LpA-I, and LpA-I:A-II), were related to the development of coronary atherosclerosis, whereas the postprandial plasma levels of small chylomicron remnants, which showed weak negative correlations with HDL, related positively to the progression of coronary atherosclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:HDLs and alimentary lipemia. Studies in men with previous myocardial infarction at a young age. 842 32

Low-density lipoprotein (LDL) is widely recognized as one of the major risk factors for developing coronary heart diseases. Despite intensive development of LDL-lowering drugs, there still exist those patients with refractory hyperlipidemia whose plasma LDL levels are not sufficiently lowered by drugs. LDL apheresis, direct removal of plasma LDL from circulating blood, is thought to be the most promising treatment for such refractory patients. Various techniques, such as the use of an immunoadsorbent utilizing an anti-LDL antibody, have been used in an attempt to achieve the selective removal of LDL. However, none were widely used because of complications, poor selectivity, and so forth. To establish a safe and effective LDL apheresis system, we chose a synthetic affinity adsorbent as the LDL-removing device. Synthetic polyanion compounds were used as the affinity ligands for LDL adsorbent to simulate the anion-rich sequence of LDL binding sites in the human LDL receptor. Among various polyanion compounds, those polyanions with sulfate or sulfonate groups and hydrophilic backbone were found to have strong affinity for LDL. In contrast, polyanions with carboxyl groups showed poor affinity. Dextran sulfate (DS) was selected as the affinity ligand of LDL adsorbent for its high affinity and low toxicity. The influence of its charge density and molecular weight on its affinity for LDL was suitable. The affinity rapidly increased as the charge density increased, then, reached a constant value. Little affinity was found for either the DS monomer (glucose sulfate) or DS with a molecular weight higher than 10(4) daltons whereas DS with molecular weights in the midrange showed strong affinity. DS with a midrange molecular weight was immobilized on cellulose hard gel to give LDL adsorbent clinical application. The adsorbent demonstrated an excellent selectivity for LDL and very low density lipoprotein (VLDL) in vitro. Adsorption of high-density lipoprotein and major plasma proteins was almost negligible. Additional study of the LDL-binding mechanism revealed that DS directly interacts with positively charged sites on LDL, which demonstrates that the nature of the interaction is the same as that of LDL receptor. An LDL adsorption column (Liposorber) packed with an LDL adsorbent and polysulfone hollow-fiber plasma separator (Sulflux) was developed as an efficient LDL apheresis system. Clinical investigation proved that this system is capable of intensively lowering the plasma LDL level without affecting major plasma components.
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PMID:Development of selective low-density lipoprotein (LDL) apheresis system: immobilized polyanion as LDL-specific adsorption for LDL apheresis system. 885 8

Low-density lipoproteins (LDL)-apheresis is a well established treatment of severe hypercholesterolemia resulting in fast clinical improvement and angiographically proven regression after 6 months of therapy. The underlying mechanisms, beside lipoprotein removal, are still under debate. Recently, oxidized LDL were shown to be of key importance in foam cell formation and atherosclerotic lesion development. We examined the influence of dextran-sulfate LDL-apheresis on the susceptibility of LDL to oxidation in 6 patients (5 males, 1 female, age: 41-60 years) suffering from severe heterozygous hypercholesterolemia or combined hyperlipidemia. LDL-apheresis influenced the oxidizability of LDL by a significant (P < 0.01) prolongation of the median of lag time (min) for LDL samples (before treatment 75, range: 31-176 versus after treatment 129.5, range 45-286). A significant (P < 0.01) difference could be also observed in the amount of conjugated dienes as expressed by the maximum rate in absorbance (before treatment 15.39, range: 5.29-21.22 versus after treatment 20.20, range 12.88-72.33). Thiobarbituric acid reactive substances (TBARS) formation was significantly decreased in LDL obtained after apheresis treatment as compared to pretreatment LDL. Electrophoretic mobility (EM) of LDL obtained before and after LDL-apheresis revealed a significant increase (P < 0.05) from a mean of 8.8 +/- 0.5 to a mean of 10.5 +/- 0.5 mm. The titers of plasma autoantibodies against oxLDL (oLAb) which varied considerably interindividually, were not influenced by LDL-apheresis treatment. Levels of F2-isoprostanes, as measured by plasma levels of 8-iso-prostaglandin-F2 alpha (8-iso-PGF2 alpha), reflecting oxidative stress, did not change, either. In summary, our findings provide evidence that even one single dextran sulfate LDL-apheresis treatment decreases LDL-oxidizability, which is an additional beneficial effect to that of lipid lowering.
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PMID:Decreased susceptibility of low-density lipoproteins to in-vitro oxidation after dextran-sulfate LDL-apheresis treatment. 890 56

A wide variety of treatments is now available for arteriosclerosis obliterans (ASO) patients, not very successful in some cases. Low-density lipoprotein (LDL) apheresis using an extracorporeal adsorption column containing dextran sulfate cellulose beads was applied to control lipid levels intensively in ASO patients with accompanying drug-resistant hyperlipidemia. A series of the apheresis procedures had a remarkable impact on clinical symptoms and physiological findings with improvement in intermittent claudication observed in more than 80% of the patients. Improvements in plethysmogram and thermogram readings suggested an increased circulation in lower extremities in more than 80% of patients. In addition, the treatment improved blood rheology, as evidenced by a reduction in blood viscosity. In a follow-up study made by sending a questionnaire to previously treated patients it was revealed that improvements in clinical symptoms were well maintained even after cessation of the treatment. In conclusion, LDL apheresis proved to be a useful therapeutic tool in ASO patients having elevated lipid levels.
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PMID:Low-density lipoprotein adsorption for arteriosclerotic patients. 913 17


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