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At least 397 records · Page 22Linked to original sources
PubMed1990

Management of primary mixed hyperlipidemia with lovastatin.

Many patients with high levels of serum total cholesterol have a concomitant elevation of serum triglyceride levels and thus have mixed hyperlipidemia. In this study, 13 patients with mixed hyperlipidemia were treated with the cholesterol-lowering drug lovastatin to determine its effectiveness. In 9 of these patients, lovastatin therapy used alone was compared with the drug combination of lovastatin and gemfibrozil. In the 13 patients, lovastatin therapy produced a 31% reduction in total cholesterol level and a 32% decrease in triglyceride levels compared with placebo. It lowered very-low-density plus intermediate-density lipoprotein cholesterol levels by 40%, low-density lipoprotein cholesterol levels by 36%, and total apolipoprotein B levels by 28%. Concentrations of high-density lipoprotein cholesterol and apolipoprotein A-I were unchanged, but total cholesterol (and low-density lipoprotein cholesterol)/high-density lipoprotein cholesterol ratios were markedly reduced. Compared with lovastatin alone, lovastatin plus gemfibrozil produced greater decreases in very-low-density plus intermediate-density lipoprotein cholesterol levels and an increase in high-density lipoprotein cholesterol levels, but, in view of the higher risk for severe myopathy with this combination, lovastatin used alone may be adequate therapy for many patients with mixed hyperlipidemia.

Adult↗
PubMed1989

Hyperlipidemia of nephrosis: pathophysiologic role in progressive glomerular disease.

During the past few years, the increasing speculation that the hyperlipidemia of nephrosis may be one of several pathogenic mechanisms involved in the progression of initial glomerular injury to glomerulosclerosis has generated many clinical and experimental investigations. This discussion reviews pertinent studies that address two major issues. First, the underlying pathophysiologic mechanisms involved in the development of the hyperlipidemia of nephrosis are explored. Second, this article examines recent studies that investigate how this secondary hyperlipidemia may further aggravate initial glomerular injury and contribute to a progressive glomerulopathy, primarily mediated through alterations in monocyte/macrophage function.

Animals↗
PubMed1989

Rationale and management of hyperlipidemia of the nephrotic syndrome.

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.

Humans↗
PubMed1989

[Mechanism of inner ear damage due to hyperlipidemia].

Some clinical data concerning the relationship between hyperlipidemia and sensorineural hearing loss have been reported, however, definite mechanism causing pathological changes in the cochlea and hearing loss has not yet been clarified. We studied the mechanism of hearing loss due to hyperlipidemia in rabbits by ABR hearing examination, biochemical study of the sera, observation of the inner ear morphology by Sem and Tem. We suggest that the decreased blood supply in the inner ear during hyperlipidemia because of increased platelet aggregation and blood viscosity may be responsible for the inner ear damage. At the same time, a high lipid peroxide level in the serum and the inner ear, as well as the metabolic disorder of lipids in the inner ear may also contribute to the development of hearing loss.

Animals↗
PubMedDate not supplied

Changes in pharmacologic treatment of hyperlipidemia.

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.

Cholesterol↗
PubMed1989

Lack of awareness and treatment of hyperlipidemia in type II diabetes in a community survey.

Cardiovascular disease is the leading cause of morbidity, disability, and death among patients with type II (non-insulin-dependent) diabetes mellitus. Moreover, hyperlipidemia is also common among these patients. Despite this, there are virtually no data regarding the level of awareness and treatment of hyperlipidemia among diabetic subjects at the community level. We therefore examined 374 Mexican-Americans and 86 non-Hispanic whites with type II diabetes identified in an epidemiologic survey that involved 3279 Mexican-Americans and 1847 non-Hispanic whites who resided in San Antonio, Tex. More than 40% of the diabetic subjects were hyperlipidemic according to the criteria of the National Cholesterol Education Program, and an additional 23% had hypertriglyceridemia and/or low levels of high-density lipoprotein cholesterol. By contrast, less than one fourth of the nondiabetic subjects were hyperlipidemic. Only approximately 25% of non-Hispanic whites with diabetes were aware of their hyperlipidemia, and less than 10% were receiving treatment. Awareness and treatment were even less frequent among Mexican-Americans with diabetes. Community physicians should be encouraged to give early attention to the management of lipid disorders in their diabetic patients.

Adult↗
PubMed1978

Hyperlipidemia in a Lebanese community: difficulties in definition, diagnosis and decision on when to treat.

Fasting serum cholesterol and triglyceride levels were measured in 131 randomly selected adult members of a Lebanese Community of Western New York. Mean cholesterol levels (males, 217 mg%; females 234 mg%) were higher than those reported from the Lebanon but similar to those reported in most other populations. Mean triglyceride levels (males, 153 mg%; females, 115 mg%) were higher than those reported in most other populations. Twenty-three subjects were hyperlipidemic on the basis of age and frequency distribution adjusted serum lipid levels above the 90th percentile. Clinical and family studies carried out on 13 of these 23 hyperlipidemic subjects suggested that 77% had monogenic hyperlipidemia and 23% primary non-monogenic hyperlipidemia. A high frequency of familial hypercholesterolemia (minimum estimate 0.7%) was found, in keeping with the high frequency of the disorder in Lebanon. The study serves to emphasize the difficulties in defining hyperlipidemia, in establishing a specific diagnosis in the individual patient, and in distinguishing between optimum and normal serum lipid levels.

Adult↗
PubMed1987

[A case of superior sagittal thrombosis secondary to hyperlipidemia].

A 42-year-old man was admitted to the Saiseikai Fukuoka General Hospital on March 22, 1985 with complaints of nausea, vomiting and headache which had continued for twelve days. On physical examinations, multiple subcutaneous nodules were noted in the chest, abdomen and extremities with dilated veins in the chest wall. Furthermore, the discoloration of the skin attributable to the venous occlusion was noted in the left foot. Neurological examinations failed to reveal any abnormalities except for moderate choked disc in bilateral ocular fundi. Spinal puncture revealed CSF pressure as high as 350 mmH2O with slight increase in cell numbers. CT demonstrated small intracerebral hematomas bilaterally in occipital lobes with evidence of "empty delta" sign in the superior sagittal sinus. On angiographical findings, the superior sagittal sinus was not demonstrated in venous phase and the blood was drained mainly through the paravertebral plexus and the pterygoid plexus without any abnormalities in arterial and capillary phases. Serological examination revealed a hypercoagulability and hyperlipidemia especially in LDL (Low Density Lipoprotein) and VLDL (Very Low Density Lipoprotein). On etiological considerations, all of these abnormalities seemed to be derived from the hyperlipidemia. Furthermore, multiple symmetrical lipomatosis was defined as a "lipoprotein storage disease" in which laboratory examinations revealed hyperlipidemia especially in LDL and in some subfraction of HDL. Although not a typical case, there must be some possibilities that the lipomatosis of this case is secondary to disorder of lipid metabolisms. In conclusion, all of various pathological conditions observed in this case were considered to be due to the disorder of lipid metabolism.

Adult↗
PubMed1985

Comparative pharmacokinetics of doxycycline and oxytetracycline in patients with hyperlipidemia.

This study examines the pharmacokinetics of lipophilic drug doxycycline (Vibramycin) and water-soluble antibiotic oxytetracycline hydrochloride (Oxyterracyna) in patients with hyperlipidemia type IIa and type IV according to Fredrickson. Antibiotics were administered orally as a single dose and determined in plasma by a fluorimetric method. The calculations were performed by aid of a computer. Increased concentrations of doxycycline were found; they were higher in type IIa, as compared with type IV. Area under the curve (AUC) and peak concentrations as well as rate constant for elimination in subjects with type IV were significantly elevated; volumes of distribution and total body clearance were markedly diminished. Decreased concentrations of oxytetracycline, area under the curve, peak concentration and rate constant for elimination were observed in patients with type IV. In both types of hyperlipidemia volume of distribution was increased and half-life in patients with type IV was significantly prolonged. The findings show that hyperlipidemia can be an important factor of drug action. Alterations of pharmacokinetics of lipophilic doxycycline and hydrophilic oxytetracycline were contrasting.

Adult↗
PubMed1980

Effect of blood viscosity decrease on exercise ST segment depressions in hyperlipidemia.

In order to study the possible relation between blood viscosity and exercise ST segment depressions in hyperlipidemia the former was lowered by infusion of dextran and by treatment with clofibrate 1 g twice daily. Acute decrease of blood viscosity with dextran infusion in two cases increased the ST segment depressions during work. Nine subjects with asymptomatic hyperlipidemia, hyperfibrinogenemia and exercise ST segment depressions were treated with clofibrate in order to lower plasma fibrinogen and serum lipids. This did not influence the area of ST segment depression with either Frank leads or CH leads as determined by computer estimation. As the plasma fibrinogen level is of major importance for the blood viscosity it is concluded that the ischaemic ST segment depression seen in hyperlipidemia is not due to increased blood viscosity but more likely to a premature subclinical coronary atherosclerosis.

Blood Viscosity↗
PubMed1982

Prevalence of hyperlipidemia in a large sample population.

In recent times, increasing attention has been focused on serum lipid levels as a risk factor for coronary heart disease. With an extremely large data base available at Metpath clinical laboratory--more than 3 million cholesterol and triglyceride determinations, and over 500,000 high-density lipoprotein (HDL) cholesterol analyses performed yearly on ambulatory asymptomatic and symptomatic individuals seen by primary care office-based physicians in the United States--an investigation was undertaken to provide a clear indication of the actual prevalence of hyperlipidemia in this country. All lipid measurements were performed routinely by standard automated procedures at one laboratory site, and the test results were analyzed statistically. Computer analysis clearly shows that hyperlipidemia is the most prevalent disorder detected in samples sent to this laboratory. According to the American Heart Association's criterion for elevated cholesterol levels (260 mg/dl and above), our figures show that 41.6 percent of females and 34.2 percent of males tested in the United States are hypercholesterolemic. Cholesterol levels were observed to rise steadily after the age of 20 and to decline after age 60 in men and age 70 in women. Similar analysis for HDL cholesterol shows that 12.2 percent of men and 4.2 percent of women over 49 years of age have HDL cholesterol levels below 35 mg/dl, which, according to the guidelines from the Framingham Heart Study, would be classified as being at high risk for coronary heart disease. The mean HDL cholesterol level was about 10 mg/dl higher in women of all ages than in men of all ages. Diagnostic approaches to hyperlipidemia and clinical implications are discussed, and a guide for predicting the risk of coronary heart disease is provided.

Adolescent↗
PubMedDate not supplied

[Association of hyperlipidemia, acute pancreatitis and diabetic keto-acidosis. A case report (author's transl)].

A 32-year-old man was admitted semi-comatose with digestive troubles to the hospital. A diabetic keto-acidosis was discovered. The diabetes was known by the patient for one year and a half, but it was not treated. Furthermore the laboratory studies showed a hyperlipidemia (type V) and an increase in pancreatic enzymes. The hyperlipidemia disappeared with insulin therapy. The chronology of the facts was probably: a hyperlipidemia associated with the diabetes, responsible of an acute pancreatitis, which induced a keto-acidosis.

Acute Disease↗
PubMed1984

Lipoprotein genes and hyperlipidemia.

The hyperlipidemias, with hypertension, diabetes mellitus and cigarette smoking, are amongst the major risk factors for the development of atheroma. The inter-relationships of hyperlipidemia and atheroma are complex but both appear to have a strong inherited component. Amongst the multiple genetic factors determining the common forms of hyperlipidemia, the apolipoprotein genes coding for the major peptides of the plasma lipoproteins (chylomicrons, VLDL, LDL and HDL) may be of particular relevance since the latter form a system of inter-converting particles for the delivery of lipid (triglyceride and cholesterol) to peripheral tissues (including the arterial wall). Recently several apolipoprotein genes have been isolated. Particularly interesting results have been obtained with the apolipoprotein AI and CIII genes. The DNA sequence of both genes and their immediate flanking region was determined. The two genes are physically linked and convergently transcribed. The cloning of the apolipoprotein genes made possible a detailed genetic study of patients with defects in lipid metabolism. An altered apo AI gene was shown to be inherited as a Mendelian trait linked to premature atherosclerosis in an affected family. Furthermore, the alteration of the apo AI gene seems to affect the expression of the apo CIII gene. Another DNA polymorphism that generates a new SstI site was shown to be present at low frequency (8%) in a random sample of the population. However, its frequency increased dramatically (42%) in a group of hypertriglyceridemic patients. It is thus not inconceivable that further studies of the genes involved in lipid metabolism will eventually help to replace the present phenotype based classification of lipid metabolism disorders by a genotype based system.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoproteins↗
PubMedDate not supplied

Hyperlipidemia in acute lymphoblastic leukemia.

Studies were conducted on lipemic serum obtained from a 26 month old male to determine possible mechanisms for the association of a Type V hyperlipidemic phenotype with advanced lymphoblastic leukemia (ALL). Antibodies to apolipoproteins and endogenous heparin were not detected as previously reported. Fatty acid analysis of the triglyceride esters revealed a high proportion of stearic-acid (18:0) which was associated with a slower in vitro degradation of very low density lipoproteins (VLDL) by human milk lipoprotein lipase (LPL). This suggests that a cause of the hyperlipidemia could be abnormal composition of triglycerides which render the VLDL a poor substrate for lipoprotein lipase. Hyperlipidemia in leukemia may be more prevalent than previously realized since nine other cases of newly diagnosed ALL have been studied who had moderate hypertriglyceridemia associated with elevated ApoB and low ApoA-I levels, but normal triglyceride composition. These findings suggest that the abnormal triglyceride composition is a late feature of the hyperlipidemia in leukemia, as observed in the case studied.

Adult↗
PubMed1978

Value and safety of diet modification to control hyperlipidemia in childhood and adolescence. A statement for physicians. Ad Hoc Committee of the Steering Committee for Medical and Community Program of the American Heart Association.

Hyperlipidemia clearly is a risk factor for atherosclerotic disease in adults and very likely contributes to atherogenesis in children. The American Heart Association recommends that children with elevated plasma cholesterol or triglyceride be placed on an appropriate diet in order to reduce their risk of hyperlipidemia and possibly to reduce their risk of atherosclerotic disease when they become adults. Although the evidence does not yet support the recommendation that cholesterol and saturated fat should be reduced in the diet of all children, the public should be advised that such modification appears safe and very likely to be beneficial. Measuring plasma lipids of all children in order to prevent atherosclerotic disease probably is not cost effective. However, children of high risk families should be examined for hyperlipidemia.

Adolescent↗
PubMed1995

Hyperlipidemia, hyperlipemia, and hepatic lipidosis in American miniature horses: 23 cases (1990-1994).

The medical records of 23 American Miniature Horses with hyperlipidemia, hyperlipemia, or hepatic lipidosis were reviewed. The most common clinical signs were anorexia and lethargy. The mean duration of clinical signs was 2.4 days. A primary disease was identified in 19 cases. Enterocolitis was the most common primary disease (n = 10). Intentional feed restriction, as part of treatment for colic, resulted in hyperlipemia in 2 horses and hyperlipidemia in 1. Four horses had primary hyperlipemia, 3 of which had signs of hepatoencephalopathy secondary to hepatic lipidosis. Dextrose, heparin, and insulin were the most common treatments. The overall survival was 61% (14/23). All horses with peak serum triglyceride concentrations > 1,200 mg/dl died or were euthanatized, whereas all but 1 with peak serum triglyceride concentrations < 1,200 mg/dl survived. These findings suggest that when American Miniature Horses, like other ponies and donkeys, are in a negative energy balance, they can rapidly develop hyperlipidemia or hyperlipemia. Early detection and treatment may improve survival.

Animal Feed↗
PubMed1993

The effect of parenteral lipid emulsion-induced hyperlipidemia on prostaglandin E1 modulation of platelet function.

The purpose of this study is to better understand how hyperlipidemia alters the modulating action of prostaglandin E1 (PGE1) on platelet function. Using our previously characterized rat model of atherogenesis, we demonstrate that the parenteral lipid emulsions, Lipofundin-S and Liposyn, significantly (p < or = 0.05) enhance baseline platelet aggregation. In addition, dose response curves show that in all animals, PGE1 substantially inhibits platelet aggregation at 10(-7) to 10(-6) M, while significantly stimulating platelet function at lower doses. However, at all PGE1 concentrations, aggregation values are higher in platelets from lipid-treated vs. control rats, showing that hyperlipidemia significantly reduces the ability of high concentrations of PGE1 to inhibit platelet activity, based on the absolute values of the controls. Also, dose response curves for PGE1 on platelet aggregation show a marked similarity in shape for control ratsvs. normal humans. Thus, this study demonstrates that hyperlipidemia significantly alters the platelet modulating action of prostaglandin E1, and it shows that PGE1 can either inhibit or stimulate platelet activity in both rat and human platelets.

Adenosine Diphosphate↗