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

From 30 cases of mixed hyperlipidemia which were resistant to apparently correctly managed treatment, combining an adapted diet and Clofibrate, the authors confirmed that there is no specific clinical or laboratory picture in these cases: except for the constant presence of two beta-lipoproteins, with a high percentage of slow pre-beta, on electrophoresis on agarose, persisting throughout the length of inactive treatment. Analysis of the factors of resistance, whether exogenous and/or endogenous show that: bad adhesion to the "anticholesterol" diet (persistance of the supply of alcohol and/or sugar, insufficiency of unsaturated fats) and the incomplete reduction of a residual plethoric overload however minimal, constitute the two factors of resistance which are most easily picked out and overcome, but such factors are fat to be constantly causal. And in other cases, the contribution of drug interference or of considerable glycoregulation disorder remains to be excluded or discussed. In the absence of such factors or of their decisive role, a more specific cause of metabolic resistance had to be looked for. A disorder in Clofibrate mechanism, detected by gaseous chromatography in the form of an abnormal peak at C15 (clofibric acid) is found 12 hours or more after the last ingestion of the drug in certain cases. Binding of this molecule with VLDL, and perhaps with slow pre-betalipoprotens and nolonger with albumin, could explain the fault in metabolic clearance and in good metabolic utilization of this drug.
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PMID:[Mixed hyperlipidemia resistant to ordinary dietetic and medical treatment. 30 cases]. 17 69

Type V hyperlipemia is not very common. The series of 54 cases descrubed here is the largest reported to date. Our observations were recorded when lipidograms showed the presence of chylomicrons and a large pre-beta-lipoprotein spot in the serum of fasting subjects. Type V hyperlipemia was often combined with other metabolic syndromes such as diabetes, hyperuricemia or gout, or obesity. Chronic alcoholism was also noted in half our subjects, in whom hyperlipemia quickly regressed after alcohol consumption ceased. Ischemic arterial complications, chiefly coronary, were found in one third of our cases, and the vascular risks accompanying this type of hyperlipemia rose considerably in patients with high blood pressure. Various type of treatment were administered, but all subjects were put on a special diet, comprising either the elimination of alcoholic drinks only, or, in addition to this, reduced carbohydrate or calorie intake. As a rule, these measures resulted in a distinct regression of lipid anomalies. Clofibrate or derivatives proved effective in cases where hyperlipemia failed to respond to dietary measures.
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PMID:[Type V hyperlipemia. 54 cases (author's transl)]. 22 80

Implantation of MtT-F4 tumor, a mammotropic tumor that secretes large quantities of ACTH, GH and prolactin, into male Fisher rats induced the development of hyperlipidemia. Free fatty acid, triglyceride and cholesterol levels in the plasma were significantly increased at 31 days after tumor implantation. Blood glucose and glycerol levels remained normal, while uric acid concentration in the blood was significantly decreased. The concentrations of the serum lipoproteins were significantly increased, while, only small changes in the distribution of the serum lipids and the composition of the lipoproteins were observed. Following stimulation of isolated adipose tissue cells with ACTH, the lipolytic response and the accumulation of cyclic AMP was higher in cells derived from the rats with the tumor, although the accumulation of cyclic GMP was not different from control adipocytes. Further, when the isolated adipose tissue cells were stimulated with dibutyryl cyclic AMP no difference was observed between the control and tumor bearing groups. Clofibrate administered in the diet resulted in a complete elimination of the tumor effect on serum triglycerides and to a great extent prevented the rise in serum cholesterol. The tumor-induced increase in the concentration of the high density lipoproteins was not affected, but the elevation of the d less than 1.063 lipoproteins was not affected, but the elevation of the d less than 1.063 lipoproteins was partially reversed. The increased lipolytic response and accumulation of cyclic AMP following stimulation by ACTH was not altered in adipocytes derived from tumor bearing rats. However, clofibrate treatment resulted in a significantly greater accumulation of cyclic GMP in fat cells stimulated with ACTH from both control and tumor bearing rats. Clofibrate in the diet did not alter the levels of GH or prolactin or serum lipids in the control rats nor were the elevated hormone levels of the tumor bearing rats changed.
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PMID:Experimental hyperlipidemia in rats. 22 51

Sixteen patients with different kinds of hyperlipidemia were treated with Atroplex (Mg-Chlorphenoxyisobutyrate 350 mg, Mesoinositol-Hexanicotinate 250 mg), a new serum lipid decreasing drug. Within an interval of 60 days' standard treatment of 3 tablets of Atroplex, the serum level of cholesterol was reduced by 16-20% and that of triglycerides by 36-49%. This significant effect was obvious over the whole period of treatment. According to the compound of Clofibrate, Atroplex interfered with the anticoagulant treatment with phenprocoumon. In spite of this an AC-therapy is possible during the Atroplex medication, if the AC doses are reduced by 30-50%.
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PMID:[New drug combination for medical management of hyperlipemia: clinical study]. 34 Mar 91

The MtT-F4 tumor, a transplantable pituitary tumor of rats, induces significant hyperlipidemia in male Fisher 344 rats. The increasive hypercholesterolemia was accompanied by hypertriglyceridemia only in the first month of tumor implantation. Clofibrate feeding inhibited the development of hypercholesterolemia and maintained normal serum triglyceride levels. In contrast to the changes in lipoprotein cholesterol distribution and profile found in experimental hyperlipidemia induced by high fat and cholesterol feeding, the hypercholesterolemic tumor-bearing rats showed no accumulation of cholesterol in the very low density and intermediate density lipoproteins, and no appearance of a new class of lipoprotein, B-VLDL. An HDLc-like lipoprotein appeared as hypercholesterolemia developed. Increased amounts of cholesterol were deposited in the aorta. The effects are attributed to the lipolytic hormones secreted by the tumor and antagonism to their action by clofibrate.
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PMID:Hyperlipoproteinemia induced by a transplantable pituitary tumor in the rat. 46 11

Repeatedly-bred, male and female Sprague-Dawley rats which develop hyperglycemia, hyperlipidemia, hypertension, and arteriosclerosis spontaneously were killed at sequential time intervals, i.e., when the females had completed 1, 2, 3 and 4 pregnancies. The control breeders received no treatment; the experimental animals were given 113 mg of clofibrate/100 g of b.w., subcutaneously, daily, 5 times per week. Clofibrate-treated breeders manifested reduction in blood pressure and in the incidence and severity of arterial disease characteristic of repeatedly-bred rats. The aortic lesions of the clofibrate-treated breeders showed attenuation of the usual severe ground substance alterations, the degenerative changes in connective tissue elements, e.g., fibrosis and elastosis, and absence of calcification and cartilaginous metaplasia. Clofibrate-treated breeders did not show any unusual elevation in serum enzymes, e.g., CPK, SGOT, SGPT and LDH, or significant reduction of their hyperlipidemia. They manifested a definite reduction in adrenocortical and medullary histopathology and their circulating corticosterone levels were subnormal compared to non-treated breeders. It is suggested that the protective effect of clofibrate was mediated through its ability to block normal adrenal steroidogenic pathways rather than through its antilipemic action.
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PMID:Clofibrate retardation of naturally-occurring arteriosclerosis in repeatedly-bred male and female rats. 66 83

The effect of Etofibrate, a chemical compound of the two antihyperlipidemic agents Clofibrate and nicotinic acid, on elevated plasma fibrinogen and plasminogen concentrations was investigated in a 6 months' survey in 25 patients with different types of primary hyperlipidemia. A consistent reduction of fibrinogen levels to normal occurred after 6 months' therapy, whereas the effect on plasminogen concentrations was weaker and not significant. The fibrinogen-lowering effect of Etofibrate was not related to the pretreatment levels but nearly equal in all cases. The possible consequences on the hemostatic system are discussed. On account of the low daily dosage, apart from a slight flush, no side-effects were noted.
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PMID:Influence of Etofibrate on plasma fibrinogen and plasminogen concentrations in patients with different forms of primary hyperlipoproteinemia. 100 13

Nephrotic mixed hyperlipidemia may be associated with accelerated coronary artery disease. To investigate the response of experimental nephrotic hyperlipidemia to therapy, a 2(4) factorial study of sodium clofibrate and beta-benzalbutyrate, halofenate and oxandrolone (250, 150, 100 and 10 mg/kg/day, respectively) was carried out. Nephrotic syndrome was induced by a single i.p. injection of puromycin aminonucleoside (90 mg/kg) in 80 female white rats of average weight 160 g. Oxandrolone proved to be significantly hypotriglyceridemic in combined therapy (average fall, 38%; P less than .05), and also lowered serum total cholesterol and phospholipid concentrations (23% and 21% falls, P less than .01) and less than .05), due largely to synergistic interactions with clofibrate-like drugs. Hypocholesteremic effects (23 and 22% average falls) were also significant for halofenate (P less than .01) and clofibrate (P less than .05) . Serum triglyceride levels actually rose significantly (P less than .05) with drug combinations containing beta-benzalbutyrate. Clofibrate and its analogs (halofenate and beta-benzalbutyrate) produced significant hepatomegaly (mean responses of +18, +18 and +10%, respectively) whereas oxandrolone produced significant hepatic shrinkage (-10%)(P less than .05). Secondary effects (drug interactions) were also found; hypotriglyceridemic synergism (effects more than additive) occurred between oxandrolone and clofibrate or its analogs (P less than .05), whereas antagonism (effects less than additive) was observed within the clofibrate-like group (P less than .01 or less .05).
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PMID:Efficacy and interactions of oxandrolone, halo-fenate and clofibrate in a factorial study on experimental acute nephrotic hyperlipidemia. 117 Dec 21

We examined the effect of ethyl all-cis-5,8,11,14,17-eicosapentaenoate (EPA-E) with high purity on circulating lipids in rats under several experimental conditions. In normolipidemic rats, EPA-E decreased the lipids in a dose-dependent manner. Clofibrate (100 mg/kg/day) was more potent in lowering the lipids than EPA-E (1000 mg/kg/day). In high cholesterol diet-fed rats, EPA-E (300 mg/kg/day) decreased the total cholesterol. However, clofibrate (300 mg/kg/day) had little effect on the total cholesterol. In hypertriglycemic rats induced by corn oil, EPA-E (300 mg/kg/day) or clofibrate (100 mg/kg/day) reduced the rise of triglycerides. EPA-E (300 mg/kg/day), clinofibrate (100 mg/kg/day) or clofibrate (300 mg/kg/day) caused a significant reduction in the lipids induced by the injection of Triton WR-1339. Furthermore, EPA-E (300 mg/kg/day) or clinofibrate (100 mg/kg/day) decreased the elevation of lipids produced by feeding the rats a casein-rich diet. These results show that EPA-E possesses potent inhibitory activity on experimental hyperlipidemia induced either exogenously or endogenously.
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PMID:Hypolipidemic effect of ethyl all-cis-5,8,11,14,17-eicosapentaenoate (EPA-E) in rats. 143 27

Gemfibrozil, like clofibrate, is effective in lowering both serum cholesterol and triglycerides and in increasing high-density lipoproteins. The information available about its effects on biliary lipids is still limited, and conflicting results have been reported. In this study we evaluated the effect of gemfibrozil (1.2 g/day) and clofibrate (2.0 g/day), in a single-blind crossover design for 6 weeks with a 4-week washout period, on the biliary cholesterol saturation index (SI) in stimulated hepatic bile and on the hepatic secretion rate of biliary lipids in patients with hyperlipidemia. Clofibrate increased cholesterol SI (from 1.70 +/- 0.14 to 2.05 +/- 0.24), whereas gemfibrozil decreased it (from 1.70 +/- 0.14 to 1.54 +/- 0.16). The results were not statistically significant. The hepatic secretion rate of cholesterol was significantly (p less than 0.04) increased by clofibrate therapy, whereas it was significantly (p less than 0.04) decreased after gemfibrozil; a significant (p less than 0.04) decrease in the hepatic secretion rate of bile acids, bile acid pool size, and bile acid fecal excretion (p less than 0.04) was also found after gemfibrozil administration. Gemfibrozil interferes extensively with bile acid metabolism, but it does not increase biliary cholesterol secretion, as clofibrate does. These results suggest that gemfibrozil does not seem to increase the risk of gallstone formation in patients with hyperlipidemia.
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PMID:Effect of gemfibrozil administration on biliary lipid secretion in hyperlipidemic patients. A crossover study with clofibrate. 227 44


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