Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Femoral arteriography was performed in 62 patients with significant hyperlipidemia. Sixty were asymptomatic and two had intermittent claudication. The patients participated in a study aiming to demonstrate whether serum lipid lowering by drugs could influence the development of femoral artery atheromatous disease. Half of the patients were treated with fenofibrate and nicotinic acid and the other half served as a control group. At the first arteriography atherosclerotic lesions were found in 46 of the 62 patients (74%). Arteriography was repeated up to three times without complication. Visual analysis of angiograms revealed considerable inter-observer variation. An attempt was made to assess the angiograms by a computerized method which, however, still needs improvement and a computer designed for image analysis. Most patients had small or moderate atheromatous deposits in the femoral artery at the initial examination, in most cases showing no change during the study period of 18 months. Regression was found in five patients of the treated group, but in none of the control patients as judged by visual gradation (p less than 0.001).
 ...
PMID:Repeat femoral arteriography in hyperlipidemic patients. A study of progression and regression of atherosclerosis. 296 99

Nicotinic acid (niacin) is a water-soluble vitamin widely used for the treatment of lipid disorders. In pharmacologic doses (1 g or more/day), alone or in combination with other lipid-lowering drugs, nicotinic acid lowers very low-density (VLDL) and low-density lipoprotein (LDL) levels, while concurrently increasing high-density lipoprotein (HDL) levels. It may reduce long-term mortality in patients with known coronary artery disease and may slow or reverse the progression of atherosclerosis. A major consideration against using nicotinic acid is the occurrence of frequent, bothersome, adverse reactions such as cutaneous flushing, skin rash, and gastric upset. Careful dosing titration may, however, minimize these effects. The beneficial effects, taken together with the low cost of nicotinic acid therapy and the relative freedom from serious side effects, have made nicotinic acid the agent of choice for the treatment of many patients with hyperlipidemia.
 ...
PMID:Nicotinic acid: a review of its clinical use in the treatment of lipid disorders. 267 60

The European Atherosclerosis Society has produced guidelines for the drug treatment of hyperlipidaemia. This, of necessity, is lifelong and therefore should be prescribed only after exclusion of secondary causes for the disorder, after dietary advice has failed to produce desirable plasma lipid levels and after careful consideration of the individual case. A plasma lipid-lowering drug should be efficacious on a long term basis on plasma lipid levels, should fulfil conditions for long term compliance regarding simplicity of administration and lack of subjective side effects, have a documented effect on the clinical endpoint (e.g. myocardial infarction) and be safe on a long term basis. Based on these conditions, plasma lipid-lowering drugs can be classed as first- or second-line treatments. At present, examples of first-line drugs are cholestyramine, nicotinic acid and gemfibrozil, while second-line drugs are lovastatin, simvastatin, probucol and 'third generation' fibrates. With increasing experience with the newer drugs regarding clinical efficacy and long term safety, one hopes that lovastatin, simvastatin and probucol will fulfil all criteria and become first-line drugs. These have advantages over cholestyramine and nicotinic acid in terms of better patient compliance.
 ...
PMID:The future of pharmacological therapy for risk factor reduction. Hyperlipidaemia. 307 15

The long term use of lipid-lowering drugs in the treatment of patients with hyperlipoproteinaemia is aimed at reducing plasma concentrations of known atherogenic lipoproteins with a favourable effect on lipid deposition in the arterial wall. A less common aim is to prevent the adverse sequelae of hyperchylomicronaemia in patients with severe hypertriglyceridaemia. The decision to begin drug therapy should be made only after the exclusion of secondary factors and after an adequate trial of diet has failed to produce acceptable concentrations of plasma lipids and lipoproteins. The bile acid sequestrants (cholestyramine and colestipol), nicotinic acid, fenofibrate and inhibitors of hydroxymethylglutaryl coenzyme A (HMG CoA) reductase (e.g. lovastatin or simvastatin) are the most effective drugs for use in patients with primary hypercholesterolaemia; these agents reduce plasma concentrations of total and LDL-cholesterol by 15 to 45%. For those patients with concurrent hypertriglyceridaemia, nicotinic acid, lovastatin or simvastatin, or fenofibrate are the preferred drugs for initial use; bile acid sequestrants frequently exacerbate hypertriglyceridaemia in these patients. Fibric acid derivatives (e.g. clofibrate, gemfibrozil, bezafibrate or fenofibrate) are all effective in the therapy of patients with type III hyperlipoproteinaemia, as is nicotinic acid and I have found lovastatin to be effective also. Gemfibrozil or nicotinic acid are the most effective agents to use in the treatment of patients with severe hypertriglyceridaemia who are at increased risk of abdominal pain and pancreatitis. Combined therapy with drugs which have different mechanisms of action can be effectively used in the treatment of patients with severe hypercholesterolaemia or combined hyperlipidaemia; for the former group, combinations which use bile acid sequestrants, HMG CoA reductase inhibitors and nicotinic acid are the most effective.
 ...
PMID:An overview of lipid-lowering drugs. 307 24

Consecutive survivors of a myocardial infarction from the Southern Hospital, below 70 years of age, were randomized into a Control group (n = 276) and a Treatment group (n = 279). The latter was openly prescribed the combination of clofibrate and nicotinic acid for serum lipid lowering. Each patient should remain in the study for 5 years and be seen regularly every 4 months at a special IHD outpatient clinic within the hospital. The concentration of serum cholesterol and triglyceride was lowered by 13% and 19%, respectively, in the Treatment group compared to the Control group. Total mortality was 82 cases in the Control group and 61 in the Treatment group, a 26% reduction (p less than 0.05). For patients above 60 years of age in the Treatment group the reduction in mortality was 28% (p less than 0.05). IHD mortality was reduced by 36% (p less than 0.01) in the Treatment group compared to the Control group. The beneficial effect of the serum lipid lowering treatment was related to the serum triglyceride concentration in two ways. First, it only occurred in patients with a triglyceride level greater than 1.5 mmol/l (n = 216). Secondly, it was most pronounced in the 44% of the treated patients who had a lowering of the serum triglyceride by 30% or more, and in this subgroup the reduction of IHD mortality was 60% (p less than 0.01). For serum cholesterol there were no such relations. The difference between serum triglycerides and cholesterol concerning these relations to the treatment outcome may be due to the fact that hypertriglyceridaemia was the most common hyperlipidaemia among our patients, occurring in 50%, while hypercholesterolaemia only occurred in 13%. Caution should be exercised in the interpretation of the results as the trial was not blind. However, the fact that the decrease in IHD deaths was directly related to the degree of serum triglyceride lowering indicates that it was the drug effect on serum lipids that was responsible for the beneficial effect of the treatment.
 ...
PMID:Reduction of mortality in the Stockholm Ischaemic Heart Disease Secondary Prevention Study by combined treatment with clofibrate and nicotinic acid. 328 37

Experimental hyperlipidemia was induced in ddY, C57BL, BALB and ICR strain mice and in Wistar rats. By feeding the animals a high cholesterol diet (HCD) for 2 weeks or by administering a high fat emulsion for a week, plasma level of total cholesterol (TC) increased in these animals. The increment of TC in mice was less than that of TC in rats. In rats, plasma level of triglyceride (TG) increased, but it decreased in mice of all these strains. Plasma level of high density lipoprotein cholesterol (HDL-C) decreased in rats and mice except BALB mice. By feeding these animals a HCD, the relative liver weight increased in rats and mice. In rats, clofibrate (CF), 100 mg/kg/day, decreased TC and TG and increased HDL-C, and nicotinic acid (NA), 100 mg/kg/day, decreased and increased HDL-C. However, in mice, CF decreased TC only in ICR mice fed a HCD. The hypolipidemic effects of gemfibrozil, LK-903 and pirozadil were also studied in rats and ICR mice.
 ...
PMID:[Strains and species differences in experimental hyperlipidemia]. 345 57

Recent experimental and epidemiologic evidence has dispelled all doubts about the need to treat patients with hyperlipidemia. Therapy should focus on 3 areas: control of concomitant risk factors for atherosclerosis, reduction of lipid levels through diet and, if response to diet proves inadequate, administration of lipid-lowering agents. There are 4 categories of first-line drugs: resins, fibrates, nicotinic acid and probucol. Probucol has a sustained effect, additive to that of a lipid-lowering diet; it can reduce total serum cholesterol and cause xanthoma regression even in patients with receptor-defective homozygous familial hypercholesterolemia. It is effective when used alone and has an additive effect when combined with resins or nicotinic acid. Compared with many other lipid-lowering medications, it is well tolerated. Although the combination of probucol and clofibrate may cause a significant decrease in high density lipoproteins, there is no evidence that this decrease carries any adverse consequences for the underlying disease process.
 ...
PMID:Medical management of hyperlipidemia and the role of probucol. 346 Mar 20

Xenalipin (4'-trifluoromethyl-2-biphenylcarboxylic acid) is a chemically novel compound which has been found to be an effective hypolipidemic agent in two animal species. Significant reductions in serum cholesterol and triglycerides were observed in cholesterol-cholic acid-fed rats following oral doses of 10-30 mg/kg/day. Xenalipin was considerably more potent than clofibrate, nicotinic acid, and cholestyramine in the same model. Lipoprotein analysis showed that xenalipin reduced cholesterol and protein content in very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), and low density lipoprotein (LDL). Triglycerides were reduced in VLDL and IDL. Xenalipin was also effective in reducing serum cholesterol and triglyceride concentrations in normocholesterolemic rats. In diet-induced hypercholesterolemic African green monkeys, xenalipin at oral doses of 15-60 mg/kg b.i.d. reduced serum LDL-cholesterol concentrations. These results suggest that xenalipin has a profile of activity which would be beneficial in therapy for hyperlipidemia.
 ...
PMID:Evaluation of the hypolipidemic activity of xenalipin in experimental animals. 368 93

The hypolipidemic activity of the tetraester of pantethine with 3-(3-pyridinemethoxycarbonyl)propionic acid (MG 28362) was assessed in various experimental conditions versus the corresponding activities of nicotinyl alcohol (NA), nicotinyl alcohol hemisuccinate (NAH), nicotinic acid (NAC), and pantethine tetranicotinate (PTN). In the normolipidemic rat, MG 28362 causes a more durable reduction of non-esterified fatty acids (NEFA) and serum triglycerides than the reference products. NEFA values return slowly to pretreatment levels without causing the rebound effect typical of most nicotinic acid derivatives. Likewise in the test of ethanol-induced hypertriglyceridemia, MG 28362 shows more pronounced and sustained activity compared to the reference products. It is also more effective on Triton hyperlipidemia and on diet-induced hypercholesterolemia; in the latter test, MG 28362 caused no triglyceride accumulation in the liver. Even at high dosage levels, MG 28362 did not cause the characteristic flushing of nicotinic acid congeners. Last, the new substance displays a fairly marked antiaggregating activity on blood platelets, some anti-hypoxic activity, and a generally low order of toxicity.
 ...
PMID:Pharmacological study of a new hypolipidemic drug of prolonged activity, the tetraester of pantethine with 3-(3-pyridinemethoxycarbonyl)propionic acid. 384 36

The available preclinical literature on the antihyperlipidemic properties of beta-pyridylcarbinol is reviewed. Similarities between the pharmacological profiles for beta-pyridylcarbinol and nicotinic acid, and evidence for the metabolic conversion of beta-pyridylcarbinol to nicotinic acid are discussed. Several reviews discussing the antihyperlipidemic effects of beta-pyridylcarbinol (beta-PC, nicotinyl alcohol, Roniacol) and nicotinic acid (NA) have appeared during the last 15 years (1-6). However, continuing clinical interest in the ability of nicotinic acid analogs to reduce plasma lipids indicated that an update and critical evaluation of the preclinical literature on this subject would be of value in order to permit a more complete assessment of the relevance of several animal models to effects in human subjects. The literature reviewed included (a) preclinical studies of beta-PC where it was the sole compound examined; (b) comparative studies of beta-PC and NA; and (c) studies relating to the metabolism of beta-PC. The literature chosen included experiments involving fasted animals, satiated animals, and effects of Triton-induced hyperlipidemia. Data on other pharmacological properties of beta-PC and/or NA that might contribute to antihyperlipidemic efficacy (e.g., fibrinolysis, inhibition of platelet aggregation, erythrocyte membrane changes) were also included where available.
 ...
PMID:Antihyperlipidemic properties of beta-pyridylcarbinol. A review of preclinical studies. 390 30


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>