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

There are indications that treatment of hypercholesterolemia by means of drugs reduce risk of atherosclerosis in patients with increased concentrations of atherogenic lipoproteins. Such therapy should be initiated only after satisfactory exclusion of secondary causes of hyperlipoproteinemia, and should be regarded as an adjunct to appropriate dietary therapy. Drug therapy should be strongly considered in patients with total cholesterol above 8-9 mmol/l on diet therapy only. Drug therapy should be considered at even lower concentrations of cholesterol when coronary heart disease is present and in familial forms of hyperlipidemia when increased risk of atherosclerosis has been documented. In patients with increased plasma concentrations of total cholesterol the drugs of choice are agents which enhance the rate of LDL catabolism (resins) or reduce the rate of LDL synthesis (nicotinic acid). Fibrates should be used when triglycerides and cholesterol are both increased. HMG CoA reductase inhibitors offer considerable promise in the therapy of patients with primary hypercholesterolemia. Probucol may be used in combination with other drugs, particularly when xanthomas are present in patients with familial hypercholesterolemia.
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PMID:[Drug therapy of hypercholesterolemia. Treatment of hypercholesterolemia in adults--a Norwegian therapeutic program 1988]. 270 70

We evaluated the changes in frequency of pharmacologic treatment of hyperlipidemia in 345 hyperlipidemic patients with symptomatic cardiovascular disease requiring cardiac catheterization between 1982 and 1987. The frequency of pharmacologic treatment increased from 13% (1982) to 59% (1987), with the major increase occurring in 1984. Increases in the frequency of treatment were paralleled by increases in prescriptions for lipid-lowering drugs nationwide. During this period the percentage of hyperlipidemic patients we evaluated who were treated with various agents changed, and at the end of the study the use of gemfibrozil, bile acid-binding resins, and nicotinic acid had increased, whereas clofibrate and probucol use decreased. Although the data showed an increase in prevalence of treatment, almost half the patients remained untreated, and of those treated over half remained hypercholesterolemic despite treatment. The results suggest increasing but incomplete physician awareness of hyperlipidemia as a cardiovascular disease risk factor and the need for further physician education in the pharmacologic management of hyperlipidemia.
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PMID:Changes in pharmacologic treatment of hyperlipidemia. 273 Jul 96

All types of hyperlipoproteinaemia must be corrected to prevent or delay the atheroma they produce, or even bring about its regression. A dietetic regimen is prescribed first to be completed, if necessary, by a medicinal treatment. Once instituted, these treatments must be pursued indefinitely, the return to normal lipid levels being a sign of their effectiveness and not a reason for their discontinuation. Conversely, failure to obtain normal lipid levels indicates that the treatment should be modified, especially the dietetic regimen which, when not regularly adhered to, often is the cause of resistance of hyperlipoproteinaemia. One must watch for iatrogenic complications in order to detect and prevent them. The drugs most frequently prescribed for hypercholesterolaemia are resins that absorb biliary acids, fibrates, probucol and, very soon, HMG coareductase inhibitors, and for mixed hyperlipidaemia and hypertriglyceridaemia, fibrates and, accessorily, nicotinic acid.
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PMID:[Hypolipidemic treatments]. 295 88

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).
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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.
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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.
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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.
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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.
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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.
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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.
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PMID:Medical management of hyperlipidemia and the role of probucol. 346 Mar 20


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