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

Coronary heart disease is the leading cause of death among patients with non-insulin-dependent diabetes mellitus (NIDDM). NIDDM patients have a high frequency of dyslipidemia, which along with obesity, hypertension, and hyperglycemia may contribute significantly to accelerated coronary atherosclerosis. Because risk factors for coronary heart disease are additive and perhaps multiplicative, even mild degrees of dyslipidemia may enhance coronary heart disease risk. Therefore, therapeutic strategies for management of NIDDM should give equal emphasis to controlling hyperglycemia and dyslipidemia. The National Cholesterol Education Program recently issued guidelines for treatment of hyperlipidemia in adults including diabetic patients. Because of the unique features of diabetic dyslipidemia, however, we suggest that certain modifications in these guidelines be made to meet specific needs of diabetic patients. For example, therapeutic goals for serum cholesterol reduction should be lower in diabetic patients than in nondiabetic subjects. Particular emphasis should be given to weight reduction in NIDDM patients. In some diabetic patients, monounsaturated fatty acids may be a better replacement for saturated fatty acids than carbohydrates. The target for cholesterol lowering should include both very-low-density lipoprotein and low-density lipoprotein (LDL) (non-high-density lipoprotein) rather than LDL alone. To obtain a substantial reduction of cholesterol levels, drug therapy may be required in many patients. However, first-line drugs for nondiabetic patients (nicotinic acid and bile acid sequestrants) may be less desirable in NIDDM patients than hydroxymethylglutaryl coenzyme A (HMG CoA) reductase inhibitors and even fibric acids. In fact, HMG CoA reductase inhibitors may be the drugs of choice for NIDDM patients with elevated LDL cholesterol and borderline hypertriglyceridemia, whereas gemfibrozil appears preferable for NIDDM patients with severe hypertriglyceridemia.
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PMID:Management of dyslipidemia in NIDDM. 219 Jul 70

As hypercholesterolemia is an essential risk factor of atherosclerosis, a strategy for diagnosis and treatment of hyperlipidemia is indispensable. Differences in mortality from coronary heart disease in different cultures seem to be due to environmental, not to genetic factors. Trials in Finland and the United States have shown that cholesterol levels and smoking can be reduced by information and education with an ensuing drop in cardiovascular mortality. This experience warrants national programmes for cholesterol-lowering in high risk countries. Programmes should be directed to doctors and health officials as well as legislators and the public. Within any given population individual differences of lipid levels are due to both nutritional habits and genetic variations concerning e.g. LDL-receptors and lipase activity. At present the only means of identifying subjects at risk is to measure their lipid levels and to scrutinize their family history. Measurements should be repeated to exclude biologic and laboratory variability. Drugs currently available include HMG CoA reductase inhibitors, bile acid binding resins, clofibrate derivatives and nicotinic acid. Formerly defined age groups with regard to therapeutic measures have meanwhile been abandoned.
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PMID:Strategy for diagnosis and treatment of hyperlipidemia. 219 53

In a large percentage of cases, diabetes mellitus leads to hyperlipidemia. In addition to the diabetes-related secondary hyperlipidemias, all types of primary disturbances of lipid metabolism can also be observed in diabetics. Depending upon the degree of severity and type of metabolic disorder presenting, not only suitable dietetic treatment, but also the various lipid-lowering drugs, fibrates, nicotinic acid, probucol, cholestyramine and the HMG-CoA reductase inhibitors should be introduced into therapy. As in all groups with an elevated coronary risk, strict management of the lipid levels is mandatory in diabetics, too.
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PMID:[Treatment of hyperlipoproteinemia in patients with diabetes mellitus]. 220 98

Reasons for the current emphasis on cholesterol as coronary risk factor are multiple. On one hand current studies have shown that primary as well as secondary prevention of ischemic heart disease is a realistic possibility with lipid lowering measures. On the other hand new drugs are actually available which permit a potent and adapted therapy of hyperlipidemias. According to new guidelines of the Swiss "lipid task force" screening for hypercholesterolemia is recommended. A cholesterol value greater than 6.5 mmol/l should be investigated and treated. Because a great proportion of adult Swiss fall into this category (approximately 1/3) it is essential that all those are efficiently treated that have markedly abnormal cholesterol values or present with other risk factors such as smoking and hypertension or have a personal or familiar history of ischemic heart disease. Because progression is likely in patients with or after manifest ischemic heart disease even when hypercholesterolemia is mild (over 5.2 mmol/l) all patients presenting with an infarct should be investigated for dyslipidemia. Cholesterol, triglycerides and HDL should be determined. Dietary measures are the basis of every attempt to reduce hyperlipidemia. Most importantly intake of saturated fats prevailing in animal products should be restricted. The next important step is reduction of dietary cholesterol and in obese patients also caloric restriction. Lipid lowering agents are recommended in patients at risk who do not respond to or comply with dietary regimens. According to type of dyslipidemia bile-acid-binding resins, fibrates, nicotinic acid or HMG-CoA reductase inhibitors are available.
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PMID:[Lipid-lowering therapy in the prevention of coronary heart disease]. 221 47

Twenty-one patients with type II hyperlipidaemia were treated with the nicotinic acid analogue, acipimox (Olbetam; Farmitalia), for 6 months. Total cholesterol decreased by 10% and the high-density lipoprotein: low-density lipoprotein cholesterol ratio increased by 13%. Triglycerides were unaltered. Two patients stopped the drug after developing gastro-intestinal side-effects. Acipimox therapy warrants ongoing use and further investigation.
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PMID:Safety, tolerability and efficacy of acipimox in type II hyperlipidaemia. 234 47

Recent trials have investigated the usefulness of fenofibrate, alone and in combination with other lipid-lowering therapies, in the treatment of hyperlipidemia. Studies of fenofibrate + bile acid sequestrants demonstrate that these two therapies may have an additive effect in reducing total cholesterol, low-density lipoprotein (LDL) cholesterol, very-low-density lipoprotein (VLDL) cholesterol and triglyceride levels in patients with hyperlipoproteinemia or familial hypercholesterolemia. These lipoprotein changes have been associated with a regression of tendon xanthoma. Pharmacokinetic studies have shown that bile acid sequestrants do not alter the absorption or the plasma levels of fenofibrate. The combined use of fenofibrate with bile acid sequestrants has been found to be comparably effective with the new 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, synvinolin, with respect to the reduction of total cholesterol and LDL. Although synvinolin was more effective in lowering LDL, VLDL cholesterol and triglycerides were reduced to a greater extent with fenofibrate. Another notable difference was that fenofibrate + bile acids more markedly increased HDL levels. The combination of fenofibrate + nicotinic acid also appears to have a beneficial effect on lipoproteins. These preliminary results indicate that fenofibrate may be a useful addition to the present lipid-lowering drug armamentarium.
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PMID:Review of clinical studies of fenofibrate in combination with currently approved lipid-lowering drugs. 265 23

In the therapy of hyperlipemia nicotinic acid derivates, cholestyramine, fibrate derivates and HMG-CoA-reductase inhibitors are drugs of choice. The most important drugs of each group, the mode of action and the side effects are presented. In the therapy of hypercholesterolemia HMG-CoA-reductase inhibitors alone or in special cases in combination with low dose of cholestyramine are best qualified. For the treatment of hypercholesterolemia and hypercholesterolemia fibrate derivates are recommended.
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PMID:[Drug treatment of hyperlipidemia]. 269 28

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


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