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

A 34-year-old male with a history of angina pectoris suddenly developed weakness in the right upper and lower limbs, and consulted our hospital. Computed tomography (CT) and magnetic resonance imaging (MRI) suggested cerebral infarction. Cerebral angiography revealed stenosis at the M1 portion of the left middle cerebral artery. Hypertension, diabetes, tobacco or hyperlipidemia were not considered as risk factors for cerebral infarction. The lipoprotein (a) [Lp(a)] level was high. In the present case, medication with a nicotinic acid agent, niceritrol, for hyperlipoproteinemia and low density lipoprotein (LDL) apheresis were performed. Concerning family history, the patient's mother and younger sister had hyperlipoproteinemia. Recent studies have reported that increased Lp(a) levels are an independent risk factor even in cerebral infarction and coronary artery disease. Measurement of Lp(a) levels and treatment for increased Lp (a) levels may be important.
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PMID:[Juvenile cerebral infarction with familial hyperlipoproteinemia (a)--case report]. 916 61

Pravastatin treatment of combined hyperlipidemia lowers low-density lipoprotein effectively; nicotinic acid lowers remnant cholesterol and raises high-density lipoprotein. A combination of these 2 drugs may be indicated for optimal treatment of lipoprotein abnormalities in combined hyperlipidemia.
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PMID:Comparison of pravastatin with crystalline nicotinic acid monotherapy in treatment of combined hyperlipidemia. 916 13

The aim of the treatment of dyslipidaemia is the primary and secondary prevention of coronary heart disease (CHD). Dietary therapy is the first line in the management of hyperlipidaemia. Lipid-lowering drugs should be used in patients with an inadequate dietary response, with CHD and/or multiple CHD risk factors. The choice of drug depends on the lipid disorder type, the desired plasma lipids reduction and presence of contraindications. Lipid-lowering drugs-anion-exchange resins, nicotinic acid and acipimox, fibrates, statins, probucol and two new classes used in experimental studies (ansamycins and ACAT inhibitors) are presented. Antiatherosclerotic properties of statins are characterized.
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PMID:[Pharmacologic treatment of lipid metabolism disorders]. 921 49

In all patients with coronary heart disease a fasting lipid profile (total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides) should be obtained. Hyperlipidemias can then be classified as hypercholesterolemia (LDL cholesterol elevated), mixed hyperlipidemia (LDL cholesterol elevated, triglycerides elevated) and hypertriglyceridemia (triglycerides elevated). Primary goal of lipid intervention is a LDL cholesterol < 100 mg/dl, secondary goals are HDL cholesterol > 35 mg/dl and triglycerides < 200 mg/dl. These goals can be reached by dietary intervention alone (reduction in fat and modification of fat intake) or in combination with lipid lowering drugs. Monotherapy with HMG-CoA reductase inhibitors or combined therapy with bile acid sequestrants will allow a reduction in LDL cholesterol by more than 50%; in predominant hypertriglyceridemia fibrates or nicotinic acid will lower triglycerides and elevate HDL cholesterol.
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PMID:[Goals and practical implementation of lipid therapy in coronary heart disease]. 930 97

Subjects with diabetes have a greatly increased risk of CHD, which is only partially related to their elevated glucose. Other factors such as insulin resistance and dyslipidemia are likely to be important. The type of dyslipidemia that is most characteristic of type 2 diabetic subjects is elevated triglycerides and decreased HDL cholesterol levels, although all lipoproteins have compositional abnormalities. Surprisingly few good prospective studies of lipoprotein levels in relation to CHD have been done in diabetic subjects. Available studies suggest that low HDL cholesterol may be the most important risk factor for CHD in observational studies. In studies in which total cholesterol and triglyceride were done, cholesterol and triglycerides were risk factors for CHD, although triglycerides were often a stronger predictor. However, the strength of triglyceride as a risk factor for CHD may depend partially on its association with other variables (e.g., hypertension, plasminogen activator inhibitor 1 [PAI-1], etc.). In clinical trials in diabetic subjects, LDL reduction with statins has led to significant reductions in CHD incidence. In addition, overall mortality was reduced with statin therapy, although the results were not statistically significant. Gemfibrozil has led to reductions in CHD incidence in diabetic subjects, although the results were not statistically significant perhaps because of low sample size. Regarding lipoproteins and CHD risk in diabetic patients, the very positive results of statin trials point to LDL cholesterol being more important than previous realized. Apparently, having a borderline high LDL cholesterol (between 130 and 160 mg/dl) in a diabetic patient is equivalent to a much higher LDL cholesterol in terms of CHD risk for a nondiabetic subject. Therefore, the primary target of therapy in diabetic patients is lowering LDL cholesterol (or possibly, non-HDL cholesterol). Statins are the preferred pharmacological agent in this situation. Once LDL cholesterol levels have been lowered, attention can be given to treatment of residual hypertriglyceridemia and low HDL. The goal here is weight reduction and increased exercise. However, for selected patients, combining a fibric acid (or low-dose nicotinic acid) with a statin also can be considered. Reduction of LDL levels should take priority over reduction of triglycerides in combined hyperlipidemia because of the proven safety of the statin class of drugs as well as greater reduction in CHD incidence.
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PMID:Management of dyslipidemia in adults with diabetes. 953 88

The aim of the study was to compare efficacy and safety of one-year therapy with slow-release nicotinic acid (KN-SR) and with ordinary form of the acid (KN). The examination was performed in the group of 136 patients with hyperlipidemia-type II. KN-SR had satisfactory effectiveness and was much better tolerated than KN. During one-year treatment with KN-SR there were observed the decrease of total cholesterol (TC) by 18%, LDL-C by 22%, triglycerides by 36%, Lp(a) by 56%, and the increase of HDL-C by 12%. The percentage of skin unwanted signs differed significantly between KN-group (90.2%) and KN-SR group (24%). Hepatotoxic effects were not observed and antipyrine kinetics did not change during one-year treatment with slow-release nicotinic acid.
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PMID:[Prolonged treatment with slow release nicotinic acid in patients with type II hyperlipidemia]. 959 56

The importance of treating dyslipidemias based on cardiovascular risk factors is highlighted by the National Cholesterol Education Program guidelines. The first step in evaluation is to exclude secondary causes of hyperlipidemia. Assessment of the patient's risk for coronary heart disease helps determine which treatment should be initiated and how often lipid analysis should be performed. For primary prevention of coronary heart disease, the treatment goal is to achieve a low-density lipoprotein (LDL) cholesterol level of less than 160 mg per dL (4.15 mmol per L) in patients with only one risk factor. The target LDL level in patients with two or more risk factors is 130 mg per dL (3.35 mmol per L) or less. For patients with documented coronary heart disease, the LDL cholesterol level should be reduced to less than 100 mg per dL (2.60 mmol per L). A step II diet, in which the total fat content is less than 30 percent of total calories and saturated fat is 8 to 10 percent of total calories, may help reduce LDL cholesterol levels to the target range in some patients. A high-fiber diet is also therapeutic. The most commonly used options for pharmacologic treatment of dyslipidemia include bile acid-binding resins, HMG-CoA reductase inhibitors, nicotinic acid and fibric acid derivatives. Other possibilities in selected cases are estrogen replacement therapy, plasmapheresis and even surgery in severe, refractory cases.
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PMID:Management of dyslipidemia in adults. 960 9

The paper is aimed at evaluation of the efficacy and safety of one-year therapy with slow-release nicotinic acid (NA-SR). The study involved a group of 30 patients with hyperlipidemia of type II. The concentration of nicotinic acid in serum was determined using capillary electrophoresis. After the placebo period (2 months), NA-SR was applied at the dose of 1.5 g/d (2 months), and subsequently 2-3 g/d (10 months), on average 2.13 g/d. During the treatment with 2.0 g/d dose, the steady-state concentration of NA in serum was within a range of 2.7-4.9 microg/ml and with 3.0 g/d of 6.17-7.75 microg/ml. These doses of the drug were tolerated well and advantageously modified the serum lipids.
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PMID:Efficacy and safety of one-year treatment with slow-release nicotinic acid. Monitoring of drug concentration in serum. 966 40

According to the NCEP resins and nicotinic acid were selected as drugs of choice to treat hypercholesterolemia. Gemfibrozil and nicotinic acid were recommended for patients with HDL cholesterol below 35 mg/dl. Current concepts of efficacy and side effects lead to the following recommendations. a) type IIa severe hypercholesterolemia (LDL > 220 mg/dl): HGMC inhibitors or combined therapy with resins and nicotinic acid, fenofibrate, or bezafibrate. b) Moderate hypercholesterolemia (LDL < 220 mg/dl): bezafibrate and/or acipimox if HDL is < 35 mg/dl; fenofibrate, bezafibrate and/or acipimox if HDL > 35 mg/dl. As second line drugs, the HGMC inhibitors. c) Type IIb hyperlipidemia: first line, acipimox; second line, fibrates associated to acipimox. d) Type III hyperlipidemia: first line, fibrates; second line, an association of HGMC inhibitors and fibrates or acipimox. e) Type IV moderate hyperlipidemia (TG < 500 mg/dl): first line, acipimox, second line, fibrates alone or in association with acipimox. As general remarks, lovastatin has been effective and well tolerated in 98% of cases. Pravastatin seems to have very little side effects. Acipimox, a nicotinic acid derivative is especially effective in elevating HDL2b levels and decreasing LDL III. Given its adequate tolerance, acipimox has replaced nicotinic acid.
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PMID:[Pharmacologic treatment of dyslipidemias: Analysis of initiation recommendations and drug selection]. 972 1

Hyperlipidemia (HP) was induced in quails by feeding high lipid food. Effect of tea polyphenol (TP) on development of HP was observed by feeding various dosage of TP simultaneously and was compared with that of nicotinic acid (NA). The results showed: (1) TP could prevent the increase of serum total cholesterol (TC), triglycerides (TG) and low-density lipoprotein cholesterol (LDL-C). Effect of the group treated with large dose of TP was more significant than that treated with NA (P < 0.05). But no statistically significant difference was observed on the changes of TG and LDL-C between TP and NA treated group. (2) No significant change of HDL-C level was observed in both TP groups and NA group, but both of them could inhibit the elevation of atherogenic index (TC/HDL-C), their effects were similar. It suggested that TP might be a regulator of blood lipid.
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PMID:[Experimental study on tea polyphenols in prevention of hyperlipidemia]. 977 5


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