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 monoclonal antibody-based direct binding enzyme-linked immunosorbent assay (ELISA) for apoprotein (apo) B-100 has been developed for use as a reference method. The assay uses the two well-characterized monoclonal antibodies, MB24 and MB47. MB47, which recognizes an epitope at the low density lipoprotein (LDL) receptor-binding domain of apoB and is specific for apoB-100, is bound to the microtiter plate as the capture antibody. MB24, which binds an epitope in the amino terminal half of the apoB-100 and identifies both apoB-100 and apoB-48, is conjugated to horseradish peroxidase and is utilized as the indicating antibody. The assay was calibrated with LDL (d 1.030-1.050 g/ml) and the LDL protein was determined by a sodium dodecyl sulfate (SDS) Lowry procedure. The working range of the assay is 0.25-1.25 micrograms/ml. Optimal dilution of whole plasma was found to be 1:2000. In the assay, MB47 bound approximately 97% of the apoB in all low density lipoprotein, and greater than 90% of the apoB in the majority of very low density lipoprotein preparations. Small dense LDL from subjects with familial combined hyperlipidemia (FCHL) and large bouyant LDL from subjects with familial hypercholesterolemia (FH) exhibited binding properties similar to LDL from healthy normolipidemic subjects when tested in the reference ELISA. The intra- and interassay coefficients of variation averaged 2.5% and 6.0%, respectively. Plasma B-100 levels were not influenced by freezing and thawing or storage at 4 degrees C for up to 3 weeks or storage at -70 degrees C for up to 11 months. Excellent agreement was obtained between the reference ELISA and a polyclonal RIA which measures total apoB (r = 0.93, n = 105, mean ELISA B-100 value = 100 mg/dl, mean RIA value = 101 mg/dl, Sy = 9.6). Reference ELISA B-100 values of samples pretreated with bacterial lipase were not significantly increased in most samples with plasma triglyceride levels below 600 mg/dl. To help reduce the large among-laboratories variability of apoB measurements, we recommend that this candidate reference direct binding ELISA be used to assign apoB target values to apoB reference pools.
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PMID:Evaluation of a monoclonal antibody-based enzyme-linked immunosorbent assay as a candidate reference method for the measurement of apolipoprotein B-100. 260 May 45

Approximately 15% of myocardial infarction survivors less than 60 years of age have a plasma lipid abnormality defined as combined hyperlipidaemia. Patients with this condition are at substantial risk for future cardiovascular events. Combined hyperlipidaemia involves elevations in both plasma triglycerides and low-density lipoprotein (LDL) cholesterol and may share similarities with hyperapolipoproteinaemia, LDL-pattern B and the small LDL-pattern. Treatment is directed at reduction of LDL-cholesterol and plasma triglyceride values. Nicotinic acid and the fibric acid derivatives are useful therapeutic agents. Fenofibrate is a fibric acid derivative that lowers both triglycerides and LDL-cholesterol in combined hyperlipidaemia. In combined hyperlipidaemia, fenofibrate has been shown to reduce significantly plasma triglycerides by approximately 40%, LDL-cholesterol by 6%, and to increase high-density lipoprotein cholesterol by 15%. Apoproteins are favourably altered with increases in apoprotein-A, decreases in apoprotein-E and inconsistent decreases in apoprotein-B. Fenofibrate is well tolerated with primarily dermatological side-effects.
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PMID:A review of combined hyperlipidaemia and its treatment with fenofibrate. 265 34

In the present report we describe a patient with multiple myeloma and long-standing paraproteinemia who developed xanthoma in the absence of an elevation in plasma cholesterol or triglyceride concentrations. Studies demonstrated that our patient's monoclonal IgG antibody interacted with apoprotein B-100. The LDL-antibody complex isolated from our patient did not affect the degradation of LDL by human fibroblasts, indicating that while IgG derived from our patient interacted with LDL it did not alter the metabolism of this lipoprotein by the LDL receptor pathway. Since the LDL receptor pathway is the major route of LDL metabolism, this probably explains why our patient was not hyperlipidemic. In contrast to an absence of effect on the LDL receptor, our patient's LDL-antibody complex stimulated cholesterol esterification within macrophages indicating the uptake and degradation of the LDL-antibody complex. The LDL-antibody complex inhibited the degradation of acetyl LDL by macrophages (scavenger pathway), demonstrating that our patient's LDL-antibody complex was recognized as a modified LDL. Moreover, mixing Ig from our patient with normal LDL also resulted in the normal LDL increasing the esterification of cholesterol by macrophages. One can hypothesize that our patient's monoclonal IgG-LDL complex interacted with the macrophage scavenger receptor, thereby resulting in the occurrence of xanthoma in the absence of hyperlipidemia.
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PMID:Cutaneous xanthoma in association with paraproteinemia in the absence of hyperlipidemia. 292 22

Treatment with retinoids results in increased serum triglyceride and cholesterol and reduced HDL-cholesterol; dietary supplementation with fish oil lowers serum lipids. Therefore combining retinoids with fish oil may reduce retinoid hyperlipidaemia. Increased triglyceride due to isotretinoin was reduced by 70% (P less than 0.05) and cholesterol by 45% (P less than 0.05) after addition of fish oil; placebo oil had no effect. These decreases were not associated with changes in levels of HDL-cholesterol or reduction of increased levels of apoprotein B. Increased triglyceride due to etretinate was reversed after the addition of fish oil (P less than 0.01), but cholesterol levels did not change. Therefore fish oil inhibits hypertriglyceridaemia due to isotretinoin and etretinate and reduces increased cholesterol levels due to isotretinoin; this effect is likely to be due to altered lipoprotein composition.
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PMID:Effect of dietary fish oil on hyperlipidaemia due to isotretinoin and etretinate. 295 94

Apoprotein, lipoprotein and lipid parameters of 36 normolipidemic subjects (23 males, mean age 22.7 +/- 7.6 years; 13 females, mean age 26.2 +/- 9.8 years) receiving oral isotretinoin (mean daily dose 0.73 +/- 0.26 mg/kg body weight) for nodulocystic acne (n = 18), severe acne papulopustulosa (n = 15), gram-negative folliculitis (n = 2) and papulopustular rosacea (n = 1) were monitored before and during isotretinoin therapy at biweekly intervals over a period of 14.6 +/- 5.6 weeks. Pretreatment values of mean plasma triglycerides increased significantly (p less than 0.001) from 81.8 +/- 31.9 mg/dl to 112.4 +/- 38.7 mg/dl (47.4%) during isotretinoin treatment. With respect to the mean percent increase of plasma triglycerides from pretreatment levels, patients were classified as nonresponders (less than 10% triglyceride increase), responders (greater than 10% less than 50% triglyceride increase) and hyperresponders (greater than 50% triglyceride increase), revealing a distribution of 25.0, 36.1 and 38.9%, respectively. Isotretinoin treatment had no influence on the isoelectric focusing pattern of apoprotein E isoforms and C apoproteins. In particular, apoprotein C-II, the cofactor of lipoprotein lipase, was not affected. No correlation between apoprotein E phenotypes (2/3, 3/3, 3/4) and the mean plasma triglyceride increase could be demonstrated. Apoprotein B-48, a marker of chylomicrons and atherogenic chylomicron remnants, could not be detected by SDS-PAGE. On the other hand in 21.0% of patients with preexisting mean lipoprotein Lp(a) levels of 18.1 +/- 12.9 mg/dl a moderate increase of atherogenic Lp(a) to mean levels of 37.0 +/- 22.0 mg/dl was observed. Pretreatment values of very-low-density lipoprotein (VLDL) apoprotein (apo) B (7.5 +/- 2.0 mg/dl), low-density lipoprotein apo B (67.3 +/- 17.5 mg/dl) and total plasma apo B (76.6 +/- 19.0 mg/dl) increased significantly to levels of 10.3 +/- 2.4 mg/dl (p less than 0.001), 75.7 +/- 15.8 mg/dl (p less than 0.10) and 85.9 +/- 17.7 mg/dl (p less than 0.05), respectively. As lipoprotein lipase and hepatic lipase activities have been shown to be unaffected by isotretinoin treatment, our data support the hypothesis that isotretinoin induces hepatic oversecretion of VLDL, a condition resembling type IV hyperlipidemia in diabetics, familial hypertriglyceridemia of familial combined hyperlipidemia.
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PMID:Characterization of apoprotein metabolism and atherogenic lipoproteins during oral isotretinoin treatment. 296 29

Apolipoprotein (apo) E deficiency is a rare genetic disease characterized by palmar and tuberoeruptive xanthomas, type III hyperlipoproteinemia, and premature atherosclerotic vascular disease. The plasma level of apoE in apoE deficiency is less than 0.05 mg/dl by radioimmunoassay, and no structural variants of apoE were detected by immunoblot of plasma or VLDL separated by two-dimensional gel electrophoresis. The apoE gene is present in the apoE deficient patient, and there are no major insertions or deletions in the gene by Southern blot analysis. Blood monocyte-macrophages isolated from a patient with apoE deficiency contain 1-3% of the level of apoE mRNA present in monocyte-macrophages isolated from normal subjects. The apoE mRNA in the monocyte-macrophages of the apoE deficient patient is similar in size to normal apoE mRNA. The deficiency of plasma apoE in the patient with apoE deficiency is due to a markedly decreased level of apoE mRNA and decreased production of the E apolipoprotein. The decreased apoE mRNA may be due to a defect in transcription or processing of the primary transcript of the apoE gene or to instability of the apoE mRNA. The decreased plasma level of apoE results in delayed clearance of remnants of triglyceride rich lipoproteins, hyperlipidemia, and a type III phenotype.
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PMID:ApoE deficiency: markedly decreased levels of cellular ApoE mRNA. 300 75

This study was designed to evaluate the effects of soy fiber, a natural source of dietary fiber that consists of both cellulosic and noncellulosic dietary fiber, on human plasma lipoprotein lipids and glucose tolerance in patients with primary hyperlipidemia. Supplementing 25 g of soy fiber per day provided a significant additional reduction of plasma total-cholesterol by 13 mg/dl (P less than 0.04) and LDL cholesterol by 12 mg/dl (P less than 0.05) beyond that previously achieved by treatment with an NIH Type II-A low-fat, low-cholesterol diet for 12 weeks in Type II-A hypercholesterolemic patients. There were no effects on HDL cholesterol or apoprotein A-I and A-II levels. The hypocholesterolemic effect was greater than in the hyperlipidemic patients with impaired glucose tolerance. Soy fiber supplementation also significantly reduced insulin responses to oral glucose challenge by 20% in Type II-A hypercholesterolemic and by 16.5% in Type IV hypertriglyceridemic patients. Results from this study suggest that supplementing the diet with soy fiber may be beneficial in dietary management of hyperlipidemia in patients with hypercholesterolemia and particularly in hyperlipidemic patients with hyperinsulinemia and impaired glucose tolerance.
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PMID:Soy fiber improves lipid and carbohydrate metabolism in primary hyperlipidemic subjects. 302 11

Hyperlipaemia was induced by a high fat diet in 11 cynomolgus monkeys. Morphological study of coronary arteries was carried out in 5 coronary samples from these 11 monkeys. The degree of arterial involvement was compared with the serum and cutaneous lipoprotein levels. These experimental data confirm that cutaneous apoprotein B measurement is the best marker for evaluation of coronary atheroma.
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PMID:Coronary atheroma in the cynomolgus monkey: predictive value of serum and cutaneous lipoprotein measurement. 309 Jul 74

Apolipoproteins AIV, B, E, and the Lp(a) glycoprotein are genetically polymorphic in humans. Three common alleles epsilon 2, epsilon 3 and epsilon 4 control the polymorphism of apolipoprotein E. These code for proteins which differ in functional properties, e.g. receptor binding activity and in vivo catabolism. This explains the significant effect of the apoE gene locus on the variability of plasma lipoprotein concentrations and moreover the implication of apoE alleles in the aetiology of multifactorial forms of hyperlipidaemia e.g. familial type III hyperlipidaemia (apoE2; arg158----cys) and polygenic hypercholesterolaemia (apoE4; cys112----arg). A further gene locus controls the concentrations in plasma of the Lp(a) lipoprotein that is composed of an LDL-like particle containing apoB-100 and the disulphide-bonded Lp(a) glycoprotein. The latter exhibits a genetic size polymorphism (MW approximately 400 kD-700 kD) that is controlled by at least seven autosomal alleles. These alleles at the same time are involved in determining the plasma concentrations of the lipoprotein that range from less than 1 mg/dl to greater than 200 mg/dl. Thus there is evidence that genetic variability in apolipoproteins relates to the variability of lipoprotein concentrations in the population and is implicated in the aetiology of multifactorial hyperlipidaemias.
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PMID:Apolipoprotein polymorphism and multifactorial hyperlipidaemia. 314 88

An increase in the plasma levels of apoprotein B-containing lipoproteins is the basis of the magnetic resonance (MR) test for cancer. The narrow MR line width reported by Fossel and co-workers to be associated with the presence of malignant disease is due to a relative increase of very low density lipoprotein. In contrast, the plasma from healthy controls, which has a much broader spectrum, has a higher proportion of high density lipoprotein. However, plasma from patients with hyperlipidemia unrelated to cancer also show narrow MR line widths and are therefore a confounding variable. We used magnetic resonance spectroscopy (MRS) to assess the plasma from 253 patients with a range of lipid related diseases and cancer, and 28 controls. A significant difference (p less than or equal to 0.0005) of 10 Hz exists between the mean line width of the controls and hyperlipidemics without malignant disease. However, in patients with solid tumours a difference of 7 Hz (p less than or equal to 0.0005) in the mean values is recorded although there is an overlap of 6 Hz compared with the controls. Moreover the MRS method was not found to distinguish patients with lymphomas from the control population. The index was not found to be related to patient age or tumour burden.
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PMID:Hyperlipidemia as a biochemical basis of magnetic resonance plasma test for cancer. 327 22


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