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)

Muscle weakness and tenderness together with a rise in serum creatine kinase (C.K.) were noted in five uraemic patients treated with 1-2 g of clofibrate ('Atromid-S') daily. Excessive accumulation of both total and free serum chlorophenoxyisobutyric acid (C.P.I.B.), the active circulating metabolite after clofibrate therapy, was found in three patients in whom it was sought. It is suggested that chronic renal failure should be regarded as a contraindication to the use of clofibrate for the treatment of any coexisting hyperlipidaemia. If such therapy is contemplated it must be cautiously instituted at low dosage and the patient monitored by regular assessment of serum C.K. and levels of both total and free C.P.I.B.
Lancet 1975 Dec 27
PMID:Clofibrate-induced muscle damage in patients with chronic renal failure. 5

High-density lipoprotein (H.D.L.) cholesterol has been measured by the 'Autoanalyzer', and apolipoproteins A-I, A-II, and B by an immunochemical method, in 100 patients with peripheral vascular disease (P.V.D.) and in 93 age and sex matched controls with an approximately similar prevalence of hyperlipidaemia. The patients with P.V.D. had significantly lower levels of the H.D.L. apolipoproteins (especially of apo A-I) than the controls. Further analysis of the data showed low H.D.L. levels to be related to the presence (but not to the severity) of the arterial disease and to be independent of concurrent hyperlipidaemia and smoking habits. The changes in H.D.L. apoproteins were not so clearly reflected by H.D.L.-cholesterol measurements in the same patients, possibly because of methodological reasons. It is therefore suggested that studies relating serum-H.D.L. to arterial disease may be more informative if both the lipid and protein portions of these lipoproteins are measured.
Lancet 1978 Dec 16
PMID:Serum high-density lipoproteins in peripheral vascular disease. 8 79

We investigated the possibility of a drug interaction between the antilipemic agent halofenate and sulfonylureas. Twelve young, healthy men were given 1 g of tolbutamide by mouth before and after 12 days of double-blind treatment with 1 g per day of halofenate, or placebo. There was a significant increase in serum tolbutamide at eight, 10 and 12 hours (P less than 0.01) and a significant (P less than 0.01) decrease in serum glucose at one, four and six hours after halofenate treatment, but not after placebo. In a long-term, double-blind study of halofenate or clofibrate treatment of patients with Type IV hyperlipoproteinemia, diabetic patients receiving a sulfonylurea and halofenate either required a reduction in the dose of the sulfonylurea or demonstrated significantly improved control of hyperglycemia (P less than 0.05) or both. No appreciable decrease in serum glucose levels was noted in diabetic patients receiving sulfonylurea and clofibrate. This interaction between halofenate and sulfonylureas is clinically important, especially in view of the association of hyperlipemia and diabetes.
N Engl J Med 1975 Dec 18
PMID:Potentiation of hypoglycemic effect of sulfonylureas by halofenate. 17 74

Methods for quantitation of the major apoproteins of human serum very low density lipoprotein have been developed employing tetramethylurea, which delipidates the lipoprotein and selectively precipitates apolipoprotein B. Six soluble apoproteins are separated by electrophoresis in polyacrylamide gel. One of these is a previously unrecognized species of R-alanine (R4-alanine), more anionic than the R3-alanine polypeptide. Conditions of staining have been found which yield reproducibly linear chromogenic response with native lipoprotein and with each purified apoprotein. Recovery of protein in the seven species measured accounts for over 97% of the total in the very low density lipoprotein of normolipidemic individuals and in most samples from individuals with endogenous hyperlipemia. The mean content of apolipoprotein B in 43 samples from normolipidemic subjects was 36.9(+/-1.2 SEM)% of total protein, The distribution of the major soluble apoproteins as mean (+/-SEM) percentage of the soluble fraction was : R-serine, 5.3+/-o.5; arginine-rich, 20.6+/-1.0; R-glutamic, 10.6+/-0.4; R2-alanine, 28.3+/-0.7; R3-alanine, 26.9+/-0.5; and R4-alanine, 8.0+/-0.5. Distribution of the apoproteins was a function of particle diameter of very low density lipoprotein in fractions separated by gel permeation chromatography and by density gradient ultracentrifugation. In fractions below 700-800 A, apolipoprotein B comprised an increasing percentage of the total protein with decreasing particle diameter. Among the soluble proteins the percentage of the arginine-rich and R-serine polypeptides increased and that of the R-glutamic polypeptide declined progressively with decreasing particle size. Apoprotein distribution was similar in fractions of similar particle size from normolipidemic and hyperlipemic subjects with the exception that all fractions from the hyperlipemic subjects contained more R-serine and some, more arginine rich polypeptide. Even in the absence of chylomicrons, the distribution of soluble apoproteins in particles of diameters greater than 700-800 A was usually similar to that of the smallest particles. This suggests that the largest particles may include products of the partial catabolism of chylomicrons.
J Clin Invest 1975 Dec
PMID:Apoprotein composition of very low density lipoproteins of human serum. 17 34

The authors report 4 cases of hyperlipemia and show the great benefit which results from ileal exclusion when there is an atherogenic risk. The considerable reduction in total lipid, cholesterol, triglycerides, and prebeta-lipoproteins is constant together with clarification of the serum. In one case, angina pectoris regressed considerably, as did arteritis of the lower limbs (unlimited walking became possible, oscillometry in the leg improved from 2 to 7). Surgery is indicated whenever by lack of will power, the diet and medical treatment cannot be followed, when social and economic conditions make proper medical treatment impossible, or when the latter has failed. The existence of arterial lesions, cardiac or cerebral complications makes surgery even more urgent. Gall-stones were observed in gall bladder. The authors raise the problem of oxalate stones. Only type II familial hyperlipemia in homozygotes should be excluded: and end-to-side portacaval anastomosis seems to be preferable.
Sem Hop 1977 Dec 23
PMID:[Surgical treatment of primary hyperlipoproteinemia]. 20 70

To determine whether human small intestine synthesizes apoA-I, the major apoprotein of plasma high-density lipoproteins, we used immunofluorescence technics and monospecific antiserums to visualize apoA-I within intestinal epithelial cells from four normal subjects and one patient with Tangier disease. Biopsies from all subjects during fasting showed limited fluorescence. After lipid feeding intracellular apoA-I markedly increased in both normal subjects and the patient. During alimentary lipemia, mean plasma apoA-I levels (milligrams per deciliter) increased in four normal subjects from 161 +/- 12 (+/- S.E.M.) to 180 +/- 15 (P less than 0.05) and in the patient from 1.9 to 6.8. Normal plasma chylomicrons contained apoB, apoE and the C peptides but not apoA-I. The patient's chylomicrons contained ap0A-I. Normal and Tangier-disease intestinal-mucosa cells increase their content of apoA-I during chylomicron formation and subsequently contribute to plasma apoA-I levels. The low levels of apoA-I in Tangier disease are not due to a failure of intestinal synthesis but might be due to abnormal metabolism of chylomicron apoproteins.
N Engl J Med 1978 Dec 28
PMID:Apoprotein A-I synthesis in normal intestinal mucosa and in Tangier disease. 21 20

Some of the component moieties of high density lipoproteins (HDL) were analyzed in normal subjects and in patients with hyperlipidemia. Apoproteins A-I and A-II were quantified by radioimmunoassay, HDL cholesterol and triglycerides were assessed on heparin-MnCl2 supernates of fasting plasmas. We found that HDL is enriched in triglycerides in all forms of hyperlipidemia, while the proportion of ApoA-II is unaltered and the proportion of ApoA-I is decreased. Thus, the composition of HDL is altered in hupertirglyceridemia. The molecular associations of ApoA-I and ApoA-II in plasma were also examined by assaying the apoprotein contents of plasma fractions prepared by ultracentrifugation and by gel filtration column chromatograpy. The ApoA-I contents of d smaller than 1.063 fraction increased in hyperlipidemia from smaller than 0.5% to approximately 2%, but the ApoA-I contents of the d greater than 1.21 fraction remained at less than 12% of total plasmas with triglyceride levels smaller than 1500 mg/dl. d greater than 1.21 ApoA-I rose to 23% in one plasma with a triglyceride level of greater than 1700 mg/dl. On column chromatography, ApoA-I eluted with the lipoproteins and also in a fraction whose molecular weight (MW) appeared to be approximately 50,000 daltons. The proportion of plasma ApoA-I which eluted in the 50,000 MW peak was positively correlated with plasma triglyceride levels, but at triglyceride levels of less than 1500 mg/dl, less than 20% of ApoA-I was in the 50,000 MW peak. Between levels of approximately 2000 and 12,000 mg/dl, the percentage "50,000 M.W. ApoA-1" was 20-25%. The ApoA-II contents of d smaller than 1.063 fractions were also increased in hyperlipidemia, but greater than 95% of ApoA-II was found in the HDL fractions in both normal and hyperlipidemic plasma both by column chromatography and ultracentrifugation. Thus, the molecular association of ApoA-I appears to be altered in hyperlipidemia.
Lipids 1978 Dec
PMID:Plasma, apolipoprotein, A-I and A-II levels in hyperlipidemia. 22 Apr 91

15 outpatients with type II hyperlipoproteinemia (7 with type IIa and 8 with type IIb) were treated with soybean. This diet induced a significant decrease of plasma cholesterol levels from 314 +/- 24 to 267 +/- 30 mg/100 ml. Triglycerides levels remained unchanged. LDL-cholesterol decreased significantly from 241 +/- 26 to 194 +/- 32 mg/100 ml, whereas HDL-cholesterol increased only slightly and not significantly from 38 +/- 7 to 40 +/- 8 mg/100 ml. In our efforts to reduce hyperlipidemia the very low cost of these vegetable proteins is a further advantage. The hypocholesterolemic mechanism of soybean diet is unknown.
Schweiz Med Wochenschr 1979 Dec 08
PMID:[Treatment of hyperlipidemia type II with soybeans]. 23 4

The mechanism of hyperlipidaemia in the nephrotic syndrome has not been fully established. We propose that it results from hypoalbuminaemia due to inhibition of the reaction catalysed by lecithin cholesterol acyltransferase converting cholesterol of high density lipoproteins to cholesterol esters and to an inhibition of high density lipoprotein particle formation from very low density lipoproteins due to reduced activity of lipoprotein lipase.
Med Hypotheses 1979 Dec
PMID:The mechanism of hyperlipidaemia in the nephrotic syndrome. 23 35

Dietary Cr deficiency may cause the aging-related Cr depletion observed in humans. Such depletion, when it occurs with excessive consumption of sugar and other carbohydrates, may result in glucose intolerance, glycosuria, hyperinsulinemia, and hyperlipidemia. These metabolic disorders could explain why athero-sclerotic diseases are endemic to most Western industrial societies. This review detailed significant current research and findings on the manifestations of Cr deficiency in humans and animal models.
South Med J 1977 Dec
PMID:Chromium depletion in the pathogenesis of diabetes and atherosclerosis. 33 61


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