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

A 42-year-old woman, found to have increased blood-lipid levels, developed hand-line xanthomas 3 months later. She also had an increased erythrocyte-sedimentation rate and a type lambda monoclonal IgM abnormality. In the course of the following 4 years the IgM concentration rose (from 5.8 to 12.3 g/l) steadily and synchronously with those of the triglycerides (from 147 to 391 mg/dl) and cholesterol (from 212 to 380 mg/dl). During the entire period of observation the ratio of VLDL cholesterol and triglyceride concentrations was elevated (greater than 0.4; normal: less than 0.3). Division of the lipoprotein fractions pointed to a type III hyperlipoproteinaemia. She also had an abnormality of lipid metabolism on the basis of a genetic defect (apolipoprotein-E2 homozygotism), which only manifested itself when an additional factor, IgM paraproteinaemia, was present. Paraproteins thus apparently interfered with the breakdown of the lipoproteins. Neither bezafibrate in increasing doses (200-800 mg daily) with low-fat diet nor administration of lovastatin (20 mg twice daily) together with nicotinic acid (500 mg twice daily) were adequate treatment for this form of auto-immune hyperlipidaemia.
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PMID:[Type III hyperlipoproteinemia in monoclonal IgM gammopathy]. 193 53

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

Hyperlipidemia is usually present in patients with the nephrotic syndrome. The most common lipid abnormality is hypercholesterolemia, although as the disorder progresses, hypertriglyceridemia may develop. Elevated plasma lipids have two potential vascular consequences, namely, atherosclerosis and progression of renal failure. Neither of these complications has been proven with certainty, but there is growing evidence to indicate that both may be long-term consequences of the nephrotic syndrome. Therefore, effective therapy of hyperlipidemia, particularly elevated cholesterol levels, is needed as a protection against these complications. Since nephrotic hypercholesterolemia frequently is severe, dietary therapy, although a valuable adjunct, will not normalize cholesterol levels in most nephrotic patients. Thus, if effective serum cholesterol lowering is to be achieved, drug therapy will be required. Bile acid-binding resins have been shown to lower cholesterol levels in nephrotic patients, but the decline in cholesterol concentrations is usually insufficient to produce a marked reduction in coronary risk. Nicotinic acid theoretically should be useful for treatment of nephrotic hyperlipidemia, but it has not been adequately tested. The new drugs that inhibit cholesterol synthesis, e.g., lovastatin, appear to be highly promising for treating elevations of both serum cholesterol and triglycerides in the nephrotic syndrome. However, testing of these drugs in this condition has been limited, and the possibility of significant side effects in an appreciable portion of patients has not been ruled out. Of particular concern is the development of severe myopathy that can produce myoglobinuria and acute renal failure. This side effect is relatively rare in patients without the nephrotic syndrome, but its prevalence in the latter condition has not been determined. The fibric acids will lower triglyceride levels in nephrotic patients, but they are not effective in lowering cholesterol levels; consequently, they probably have little role in the treatment of nephrotic hypercholesterolemia. Finally, the drug probucol will lower cholesterol levels in nephrotic patients, although not to desirable levels; still, probucol could prove useful in combination with other cholesterol-lowering drugs.
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PMID:Rationale and management of hyperlipidemia of the nephrotic syndrome. 248 42

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

Approximately 15% of myocardial infarction survivors less than 60 years of age have a plasma lipid abnormality defined as combined hyperlipidaemia. Patients with this condition are at substantial risk for future cardiovascular events. Combined hyperlipidaemia involves elevations in both plasma triglycerides and low-density lipoprotein (LDL) cholesterol and may share similarities with hyperapolipoproteinaemia, LDL-pattern B and the small LDL-pattern. Treatment is directed at reduction of LDL-cholesterol and plasma triglyceride values. Nicotinic acid and the fibric acid derivatives are useful therapeutic agents. Fenofibrate is a fibric acid derivative that lowers both triglycerides and LDL-cholesterol in combined hyperlipidaemia. In combined hyperlipidaemia, fenofibrate has been shown to reduce significantly plasma triglycerides by approximately 40%, LDL-cholesterol by 6%, and to increase high-density lipoprotein cholesterol by 15%. Apoproteins are favourably altered with increases in apoprotein-A, decreases in apoprotein-E and inconsistent decreases in apoprotein-B. Fenofibrate is well tolerated with primarily dermatological side-effects.
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PMID:A review of combined hyperlipidaemia and its treatment with fenofibrate. 265 34

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


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