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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.
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PMID:Clofibrate-induced muscle damage in patients with chronic renal failure. 5

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

BR-931 [4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio-(N-beta-hydroxyethyl)-acetamide], a new hypolipidemic agent of low toxicity, was evaluated in several tests of lipolysis and hyperlipidemia in rats, and in the cholesterol-induced atherosclerosis in rabbits. Significant hypolipidemic activity was observed in rats with doses of the agent at 12.5--50 mg/kg. In the Triton-induced hyperlipidemia, 50 mg BR-931 per kg was equieffective as 200 mg of clofibrate (CPIB) per kg. In contrast with CPIB, BR-931 exerted a powerful antilipolytic activity against epinephrine, ACTH, nicotine and cold exposure. BR-931 was particularly effective in diet-induced hyperlipidemias. Ethanol lipemia was totally prevented by the agent at 100 mg/kg. With Nath's diet, doses as low as 25 mg/kg significantly reduced hypercholesterolemia and hypertriglyceridemia. In these last two tests, the distribution of lipoprotein cholesterol was also determined. CPIB did not affect HDL cholesterol levels that had been decreased by the diets; in contrast, BR-931, already at doses of 50 mg/kg, brought the HDL/total cholesterol ratio back toward normal. A significant HDL cholesterol increase, together with some reduction of atheromatosis, was also observed in cholesterol-fed rabbits. BR-931, a potent inducer of liver peroxisones and of mitochondrial carmitine acetyltransferase, appears to be a hypolipidemic agent of high efficacy and low toxicity for the clinical treatment of hyperlipidemias and atherosclerosis.
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PMID:Pharmacological profile of BR-931, a new hypolipidemic agent that increases high-density lipoproteins. 20 96

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

Since dietary calcium had been reported to reduce plasma lipids, the effects of calcium carbonate (CaCO3, 2 g/day) and the calcium salt of p-chlorphenozyisobutyrate (Ca-CPIB, 2 g/day), both singly and in combination, were studied in outpatients with primary hyperlipidaemia. Three groups of five patients were followed in a double-blind cross-over study, in which placebo and the drugs were given alternately during four-week periods. The main results were: 1) CaCO3 alone did not produce any significant changes in plasma lipids. 2) Ca-CPIB reduced LDL-cholesterol in patients with type IIa and IIb by an average of 29 and 21%, respectively. It also lowered VLDL-triglyceride by 50% in type IIb and by 48% in four out of five patients with type IV. 3) The combination of CaCO3 and Ca-CPIB reduced LDL-cholesterol by 31 and 25% in types IIa and IIb, respectively. It also lowered VLDL-triglyceride by 48-52% in types IIa and by 46% in four out of five patients with type IIb. 4) Three out of five patients with type IV had a rise of LDL-cholesterol while on Ca-CPIB alone; two of the patients had the rise while on the combination. 5) After treatment with Ca-CPIB, either singly or in combination, there was a statistically significant lowering of ESR and of plasma inorganic phosphate and alkaline phosphatase. No clinical side effects were noted.
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PMID:Effect of calcium p-chlorphenoxyisobutyrate and calcium carbonate on plasma lipids and lipoproteins of patients with hyperlipoproteinaemia. 35 20

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


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