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

Mean plasma cholesterol and triglyceride concentrations were measured in White female users and non-users of oral contraceptives and oestrogens in 10 diverse, demographically defined North American populations. About 50% of the younger women (20-24 years old) were taking oral contraceptives. In these women mean triglyceride concentrations were up to 48% higher and mean cholesterol concentrations were about 5% higher than in non-users. The 95% percentile of the total lipid distribution among non-users was used to define hyperlipidaemia. In young women on oral contraceptives hypercholesterolaemia was up to three times more common and hypertriglyceridaemia was up to five times more common than in non-users. 37% of older women (50-54 years) (presumably intramenopausal and postmenopausal) were hormone users, and in this group there were small, inconsistent alterations in plasma-triglyceride and a modest but consistent reduction in mean cholesterol concentration.
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PMID:Altered plasma-lipids associated with oral contraceptive or oestrogen consumption. The Lipid Research Clinic Program. 6 1

Detected using a method involving gradient electrophoresis on polyacrylamide gel, the presence of a high level of an Lp(a) was demonstrated in 17% of control subjects and 39% oh hyperlipidaemic subjects explored. The difference appeared to be particularly significant in subjects with a pure hypercholesterolaemia (type IIA) or dominant hypercholesterolaemia (type IIB), which may be accounted for by the antigenic communities and related substances in the lipid composition uniting Lp(a) to LDL. The association of frank atherosclerosis with the hyperlipidaemia substantially increased the frequency of high levels of circulating Lp(a). A combined elevation of levels of Lp(a) and LDL would seem to be associated with a particular atherogenic power.
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PMID:[Detection of a new lipoprotein: Lp(a). Its occurrence in atherosclerosis with or without hyperlipemia]. 7 59

Alcohol promotes accumulation of fat in the liver mainly by substitution of ethanol for fatty acids as the major hepatic fuel. The degree of lipid accumulation depends on the supply of dietary fat. Progressive alteration of the mitochondria, which occurs during chronic alcohol consumption, decreases fatty acid oxidation by interfering with citric acid cycle activity. This block is partially compensated for by increased ketone body production, which results in ketonemia. Thus, mitochondrial damage perpetuates fatty acid accumulation even in the absence of ethanol oxidation. Alcohol facilitates esterification of the accumulated fatty acids to triglycerides, phospholipids, and cholesterol esters, all of which accumulate in the liver. The accumulated lipids are disposed of in part as serum lipoprotein, resulting in moderate hyperlipemia. In some individuals with pre-existing alterations of lipid metabolism, small ethanol dose may provoke marked hyperlipemia which responds to alcohol withdrawal. Inhibition of the catabolism of cholesterol to bile salt may contribute to the hepatic accumulation and hypercholesterolemia. The capacity of lipoprotein production and hyperlipemia development increases during chronic alcohol consumption, probably as a result of the concomitant hypertrophy of the endoplasmic reticulum and Golgi apparatus. However, this compensation is relatively inefficient in ridding the liver of fat. This inefficiency may be linked to alterations of hepatic microtubules induced by ethanol or its metabolites, which interfere with the export of protein from liver to serum, promoting hepatic accumulation of proteins as well as fat. As liver injury aggravates, hyperlipemia wanes and liver steatosis is exaggerated. Derangements of serum lipids similar to those found in other types of liver disease also become apparent. The changes in serum lipids may be a sensitive indicator of the progression of liver damage in the alcoholic.
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PMID:Effects of ethanol on lipid metabolism. 8 83

The clinical and biochemical features of type III hyperlipoproteinemia are described in 49 patients from 23 to 70 years of age. An increase in very low-density lipoproteins (VLDL) of abnormal chemical composition was the basis for diagnosis. The untreated patients all had hypercholesterolemia and hyperglyceridemia, and, on the average, decreased concentrations of both low- and high-density lipoproteins. Seventy-four percent had xanthomas, and classic "xanthoma striata palmaris" was found in more than half. Twenty-seven percent had ischemic heart disease, detected earlier in men than in women. Twenty-seven percent had peripheral vascular disease (compared to 4% of subjects with type II hyperlipoproteinemia). Twenty-five of 35 subjects achieved normal lipid levels with dietary therapy alone. Analysis of 29 kindred showed hyperlipidemia in half of adult blood relatives; half of these had type III, the remainder usually had sample endogenous hyperglyceridemia (type IV). Only 2 of 55 children less than 20 years of age were affected, both with type IV.
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PMID:The biochemical, clinical, and genetic features of type III hyperlipoproteinemia. 16 8

Hyperlipidaemia in children is most commonly expressed as hypercholesterolaemia. "Normal values" for serum cholesterol, if defined statistically, vary between communities, and levels of cholesterol in childhood above which an increased risk of coronary heart disease in adult life may be expected have not been firmly established. It is suggested that serum cholesterol concentration over 250 mg/dl (6.47 mmol/l) in a child over 1 year of age merits detailed investigation, including full lipoprotein analysis, and levels of serum cholesterol between230 and 250 mg/dl (5.95-6.47 mmol/l) should be repeated with further studies if indicated. Secondary hyperlipoproteinaemia rarely presents diagnostic problems but must always be excluded. The only primary hyperlipoproteinaemia likely to be encountered in childhood is familial hyperbetalipoproteinaemia in its common heterozygous form. The most effective means to date of lowering serum cholesterol in this condition is cholestyramine, but the long-term consequences of therapy are not known and treatment should at present be limited to children from high-risk families. Long-term follow-up is essential and until results of such studies are available population screening is unjustified.
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PMID:Hyperlipidaemia in children. 16 1

Starting from previous observations emphasizing an increased pseudocholinesterase (PCE) activity in obese and hyperlipemic subjects, the behaviour of this enzyme and of ceruloplasmin was studied in connection with changes of serum lipids and lipoproteins in various types of hyperlipoproteinemia. When compared to values detected in 67 middle-aged normal weight normolipemic subjects, PCE activity was found to be significantly greater (smaller than 0.001) in the 49 overweight subjects without obvious hyperlipemia but presenting a moderate increase of the prebeta electrophoretic fraction. PCE activity was much higher in lean or overweight subjects with endogenous hypertriglyceridemia (68 patients with type IV and 86 patients with mixed hyperlipemia). The slight increase of mean values of PCE activity in the 53 subjects with type II-a was due mainly to overweight subjects, while this enzyme's activity was not significantly changed in lean subjects with pure hypercholesterolemia. PCE activity was positively correlated with serum triglyceride (r equals 0.540; p smaller than 0.001) and the prebeta electrophoretic fraction (r equals 610; p smaller than 0.001). The correlation with beta-lipoproteins was not significant. Ceruloplasmin levels were not significantly changed. It is suggested that elevation of PCE activity could be connected to mechanisms leading to an increased secretion rate of lipoproteins.
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PMID:Serum pseudocholinesterase and ceruloplasmin in various types of hyperlipoproteinemia. 16 6

Univariate and bivariate analyses of cholesterol and triglycerides are performed after appropriate age adjustment on 247 individuals in 33 families where the probands have elevations of cholesterol, low density lipoprotein and triglycerides, and type IIb lipoprotein phenotype. Mixture of lognormal distributions are fitted by maximum likelihood to the data. Best fitting single and mixtures of lognormal distributions are compared with empirical cumulative plots, and the likelihood-ratio criterion is used to test for significance. A mixture of two lognormal distributions fits significantly better than one lognormal distribution for cholesterol but not for triglycerides. When a mixture of bivariate lognormals is fitted to the data, only one local maximum is found, suggesting action of a single genetic determinant in this sample. The best cutoff line is almost parallel to the triglyceride axis, indicating the relatively high involvement of cholesterol compared to triglycerides in separating the normal and abnormal groups. Using the best linear function, the difference in the two bivariate means is found to account for 61% of the total variation in log cholesterol and log triglycerides. To determine if the results are due to enrichment of the sample with familial hypercholesterolemia syndrome, seven families where the proband and/or any relative has tendon xanthomas are removed and the analyses repeated on the remaining 26 kindreds. The results of these analyses are virtually the same as those of the total sample. Also, a subsample of 21 families in which the proband and at least one additional kindred member are affected is analyzed in the same manner with similar results. For comparison, data from a study of families with combined hyperlipidemia [1] are analyzed in an analogous manner, bearing in mind that the populations sampled are probably different. Fitting a mixture of two bivariate distributions and finding the best cutoff to these data indicate that triglycerides are more involved in separating the two groups. Probably because of major differences in ascertainment, the distribution of lipid levels in oour patient group is practically indistinguishable from that of hypercholesterolemia, and the Seattle data [1] are more nearly similar to hypertriglyceridemia. It may be premature to consider familial combined hyperlipidemia as an entity distinct from both hypercholesterolemia and hypertriglyceridemia. We hope it will eventually be possible to analyze these data using a refined genetic model that includes both major gene and polygenic effects and to combine this form of analysis with quantitative tissue culture methods.
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PMID:Bivariate analyses of cholesterol and triglyceride levels in families in which probands have type IIb lipoprotein phenotype. 16 68

We have studied the effects of diet-induced hypercholesterolemia on the rates of secretion of triglycerides into the plasma of fasted squirrel monkeys. Two groups of monkeys were studied: control animals which were fed a semipurified diet not associated with hyperlipemia (plasma cholesterol 127 +/- 8 mg/100 ml), and animals made hypercholesterolemic (plasma cholesterol 307 +/- 31 mg/100 ml) by being fed a diet containing 25% butter and 0.5% cholesterol. After intravenous infusion of Triton WR 1339 (300 mg/kg body wt), plasma triglycerides increased almost linearly for 9-12 hours. Analysis of individual lipoproteins separated by ultracentrifugation showed that newly secreted triglycerides were present almost exclusively in the very low density lipoprotein fraction. The rates of triglyceride secretion in the hypercholesterolemic group of monkeys (5.15 +/- 0.86 mg/kg/hr) were less than half those of the control animals (10.96 +/- 2.15 mg/kg/hr). We suggest that in monkeys with diet-induced hypercholesterolemia high concentrations of plasma low density lipoproteins may inhibit the synthesis and/or secretion of their parent very low density lipoprotein molecules into the circulation.
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PMID:Metabolism of lipoproteins in nonhuman primates. Reduced secretion of very low density lipoproteins in squirrel monkeys with diet-induced hypercholesterolemia. 17 53

The demonstration in certain sera by electrophoresis an Agar gel, according to Noble's technique, of a further band of intermediate pre-betalipoprotein, between the betalipoproteins and the usual rapid pre-betalipoproteins, led to the designation of this fraction under the name of slow pre-betalipoprotein or pre-beta-lipoprotein. To the rare studies so far published on this subject, we bring here our contribution in the form of a routine analysis of the variations, and not only the presence, but also the relative concentration of the slow pre-beta-lipoproteins with regard to the rapid prebetalipoproteins. On the fasting serum, after 12 hours fasting, comparative studies of normal control subjects (104 cases) of essential hypercholesterolemia, with or without tendinous xanthomas, corresponding to type IIa (110 cases), mixed hyperlipidemia of type II + IV or III, on paper electrophoresis, corresponds usually to type IIb (204 cases) and, finally, massive endogenous hypertriglyceridemia, corresponding to type IV (95 cases). These indicate clearly the elective concentration of the band of slow pre-betalipoproteins persisting after 12 hours fasting in cases of mixed hyperlipidemia (73% of cases), whilst it is rare in the other groups (no more than 5% of cases). A more complete study of 204 cases of mixed hyperlipidemia showed that the high frequency of slow pre-betalipoproteins is situated in a fairly narrow range of relatively moderate hypertriglyceridemia, between the lower limit of 1.50 and the upper limit of 6 to 7 g/l: the maximum frequency and intensity is situated within the area of 2.50 to 4 g/l. The cases who have already had cardiovascular accidents are more often found to have this band than the cases without complications in a fairly similar age group. However, longitudinal studies, both midterm in relation to therapeutic correction, and short term throughout the day or between the 8th and 12th hour of fasting, have clearly revealed the potential labile nature of this fraction, and show the pathological nature of its sometimes massive persistence beyond the 8th hour and even beyond the 12th hour of fasting. This is a sign of pathological blocking of its transformation rather than of a constitutional lipoprotein abnormality.
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PMID:[Detection and distriburion of slow pre-betalipoprotein in agar gel electrophoresis of total serum in 204 cases of mixed hyperlipidemia]. 18 Aug 62

A subnormal activity of postheparin plasma hepatic lipase was demonstrated in nine of 16 patients with familial type II hypercholesterolemia. On the other hand, in patients with combined hyperlipidemia (type II b) the hepatic lipase activity was mostly in upper normal range. The postheparin plasma lipoprotein lipase activity was normal in both patient groups. It is suggested that the low hepatic lipase activity may have a role in the patholgenesis of one form of familial hypercholesterolemia.
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PMID:Low postheparin plasma hepatic lipase activity in familial type IIa hyperlipoproteinemia. 18 Aug 67


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