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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In Jan. 1994, The ROC Society of Internal Medicine and the International Lipid Information Bureau, Taiwan (ILIB, Taiwan) jointly announced national guidelines for the diagnosis and management of lipid disorders. This guideline review the scientific basis and strategies for coronary artery disease (CAD) prevention. This guidelines were developed by an experts panel with various scientific backgrounds. Both two recent publications, the International Task Force and European Atherosclerosis Society (EAS) in 1992 and Adult Treatment Panel II (ATP II) from the National (USA) Cholesterol Education Program (NCEP), were adopted and modified. This guideline covered basic metabolism of lipoprotein, detection method of lipoprotein analysis, coronary risk factors, managements of dyslipidemia, goal of therapy and local epidemiological data. In this guidelines, lipid disorders are classified into hypercholesterolemia (serum cholesterol > 200 mg/dL), combined hyperlipidemia (serum cholesterol > 200 mg/dL and triglyceride > 200 mg/dL) and hypertriglyceridemia (serum triglyceride > 200 mg/dL). In the absence of CAD and with less than two risk factors, target levels for LDL-cholesterol should be < 160 mg/dL; with more than two risk factors, < 130 mg/dL; in the presence of CAD, 100 mg/dL. In individuals with hypertriglyceridemia the target levels for triglyceride are 200 mg/dL. Secondary prevention of CAD is considered as one of the most important issue. Two generalized modalities are recommended to achieve the goal, i.e., non-pharmacological therapy which include weight reduction, regular exercise, smoking cessation, life style modification and pharmacological therapy. It is hoped that this guideline could help medical personnels dealing with patients with dyslipidemia and eventually, reduce the occurrence of CAD in Taiwan.
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PMID:Summary of the national guidelines for the diagnosis and management of lipid disorders in Taiwan. The experts panel. 771 90

The relationship between overweight and cardiovascular disease was a matter of debate for many years. Recent studies have demonstrated that obesity defined as body mass index of 30 kg/m2 or higher is associated with an exponential increase of cardiovascular complications. This effect is largely mediated by the induction of established risk factors such as dyslipidemia, hypertension and type 2 diabetes mellitus. Recently, there is growing evidence that the occurrence of most complications of obesity depends not only on the degree of overweight but also on the pattern of body fat distribution. Many data suggest that the anatomical localization of body fat is more important for the risk of developing complications than the adipose tissue mass per se. An abdominal, upper-body type of fat distribution, which can be easily determined by the measurement of waist and hip circumferences (waist/hip ratio = WHR), is also a confirmed risk factor for metabolic disturbances, hypertension and atherosclerosis, independent of body weight. However, the clinical appearance of these disturbances is frequently associated with the development of obesity. This network of metabolic disorders and their vascular complications is termed "metabolic syndrome" or "syndrome X" (Table 2). Abdominal obesity is now known to be closely associated with the metabolic syndrome and is regarded to represent its readily recognizable phenotypic feature. The components of the metabolic syndrome are characterized by varying forms and degrees of insulin resistance. It is assumed that insulin resistance, defined as diminished biological response to the action of insulin, represents the primary defect or at least the common pathogenetic link between these disturbances.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Abdominal obesity and coronary heart disease. Pathophysiology and clinical significance]. 771 76

Several forms of dyslipidemia are associated with premature coronary artery disease (CAD) and other vascular disease. These include elevated low-density lipoprotein cholesterol, low levels of high-density lipoprotein cholesterol, and elevated triglyceride. Because of the high incidence of CAD in many Western countries, including the United States, guidelines for managing dyslipidemia and reducing the risk of CAD have been promulgated. The National Cholesterol Education Program (NCEP) of the National Institutes of Health recently released revised guidelines for the treatment of adults with dyslipidemia, as did the European Atherosclerosis Society. Although the two reports differ in emphasis, both recommend routine screening of adults to identify specific individuals at high risk for future CAD events.
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PMID:Hyperlipidemia: perspectives in diagnosis and treatment. 771 88

Significant risk factors for premature coronary heart disease include: (1) family history, (2) elevated low density lipoprotein (LDL) cholesterol level > or = 160 mg/dl, l, (3) decreased high density lipoprotein (HDL) cholesterol level < 35 mg/dl, l, (4) cigarette smoking, (5) high blood pressure and (6) diabetes mellitus. All of these risk factors are common in patients with premature heart disease. Common familial lipid disorders associated with premature heart disease include familial lipoprotein(a) excess, familial dyslipidemia (elevated triglycerides and decreased HDL cholesterol), familial combined hyperlipidemia (elevations of LDL cholesterol and triglycerides, and often decreased HDL cholesterol), familial hypoapobetalipoproteinemia (elevated apolipoprotein B levels), familial hypoalphalipoproteinemia (low HDL cholesterol levels), and familial hypercholesterolemia (elevated LDL cholesterol levels). All these disorders have been characterized using age and gender specific 90th and 10th percentile values from the normal population. The diagnosis and potential management of these disorders is reviewed.
Atherosclerosis 1994 Aug
PMID:Familial lipoprotein disorders and premature coronary artery disease. 780 28

The early lesions of atherosclerosis in youth are strongly related to antemortem levels of total and low density lipoprotein (LDL) cholesterol, very low density lipoprotein (VLDL) cholesterol, and triglyceride, to ponderal index and to systolic and diastolic blood pressure. The major apolipoproteins of LDL and high density lipoprotein (HDL), apo B and apo A1, respectively, as well as levels of Lp(a) lipoprotein are often abnormal in children born to a parent with coronary artery disease (CAD). Other risk factors for CAD include obesity, high blood pressure, cigarette smoking, diabetes mellitus, positive family history of CAD and physical inactivity. Children from families with premature CAD, familial dyslipidemia or hypertension, and/or two other risk factors should have a lipoprotein profile determined. The first form of treatment is a diet low in total fat, saturated fat and cholesterol, combined with treatment of overnutrition and obesity, if necessary, and regular habits of aerobic physical activity. Children with inherited disorders of LDL metabolism may require the addition of lipid lowering therapy. The early detection and treatment of youth at risk for premature CAD offers the greatest promise to decrease morbidity and mortality.
Atherosclerosis 1994 Aug
PMID:Dyslipoproteinemia and other risk factors for atherosclerosis in children and adolescents. 780 29

Syndrome X is a constellation of abnormalities; it appears to be strongly linked to insulin resistance and the risk of atherosclerosis. It consists of hypertension, glucose intolerance, obesity, dyslipidemia and, observed more recently, coagulation abnormalities. It is possible that treating blood pressure levels alone while ignoring or worsening other strongly associated risk factors has resulted in minimal effects on the incidence of coronary heart disease (CHD). Syndrome X has raised the awareness of these associated risk factors and has further led to the consideration of hypertension as a metabolic disease. The epidemiologic evidence in support of the link between insulin resistance and hypertension is reviewed, and the public health implications of these data are outlined.
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PMID:Reducing the incidence of coronary heart disease by managing hypertension: implications of syndrome X. 780 51

The individual components of the metabolic syndrome such as central obesity, dyslipidemia with increased triglycerides and decreased HDL-cholesterol, hyperuricemia, hypertension and progressive glucose intolerance are markers for an increased risk of atheroma and type 2 (non-insulin-dependent) diabetes. All components, with the exception of hyperuricemia, are associated with skeletal muscle insulin resistance, leading to compensatory chronic hyperinsulinemia. Insulin resistance/hyperinsulinemia, in turn, is associated with a series of hypertensiogenic and atherogenic side effects, aggravating the individual components of the metabolic syndrome. From a more pathophysiologically orientated point of view, early identification of individuals obviously at risk for atheroma and type 2 diabetes, as well as early intervention aimed at the improvement of reduced insulin action may play a central role in an integrated life-style approach of primary prevention of atherosclerosis and type 2 diabetes.
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PMID:[The metabolic syndrome. Pathophysiologic causes, diagnosis, therapy]. 784 93

Molecular genetic approaches have added greatly to the understanding of the human hyperlipoproteinemias. Studies in mice have added interesting new information. Transgenic mice over-expressing or deficient in various individual proteins important in lipoprotein metabolism have reproduced some dyslipidemias and permitted further pinpointing of the functions of apolipoproteins, lipoprotein receptors, lipid transfer proteins and enzymes. Cross-breeding of mice with single defects has reproduced certain dyslipidemia syndromes and permits examination of the combined etiologic effects of more than one gene.
Atherosclerosis 1994 Oct
PMID:Recent concepts of lipoprotein pathophysiology. 785 81

Dietary measures, including calorie restriction and reduced fat intake, remain the mainstay of management in prevention of coronary heart disease (CHD). When this fails, drug therapy should be considered. Fibrates, a family of lipid lowering drugs, decrease plasma triglycerides and inhibit their synthesis. They are also reported to suppress cholesterol production in the liver. A disadvantage of fenofibrate is the poor solubility of the principal ingredient, with subsequent incomplete absorption after oral administration. Micronized fenofibrate, a new formulation chemically identical to the parent compound, has improved pharmacokinetic parameters which increase absorption, provide more stable plasma levels, and thus dosage can be decreased. The micronized formulation has been shown to be effective in reducing LDL cholesterol and triglycerides in patients with types IIa and IV hyperlipidemia, with increasing responsiveness to therapy in proportion to elevated baseline values of these parameters. This formulation has also been compared to simvastatin, an HMG-CoA reductase inhibitor. Results of a double-blind crossover study showed that both drugs reduced plasma cholesterol levels by similar amounts, and both produced similar increases in HDL cholesterol. The micronized formulation of fenofibrate thus provides improved efficacy in the prevention of CHD. In comparison to the standard formulation, micronised fenofibrate thus provides improved efficacy in the control of dyslipidemia and the prevention of CHD.
Atherosclerosis 1994 Oct
PMID:The fibrates in clinical practice: focus on micronised fenofibrate. 785 86

In 87 patients (studied on average 1 year after their strokes) and 26 of their first-degree relatives, our specific aim was to assess the prevalence of the following stroke risk factors: hypofibrinolysis, familial hypofibrinolysis, high lipoprotein (a) level, and dyslipidemia. At least 2 months after their strokes (primarily ischemic), 87 patients had measures of lipids and lipoprotein (a); 69 and 67 patients had measures of basal and stimulated fibrinolytic activity, respectively, four new findings were as follows. (1) Hypofibrinolysis was common, with bottom decile-stimulated tissue plasminogen activator activity (the major stimulator of fibrinolysis) in 21% of stroke probands and in 30% of their first-degree relatives, versus 7% of 29 nomolipidemic control subjects (p = 0.09 and 0.026, respectively). (2) The hypofibrinolysis was mediated by top-decile levels of basal plasminogen activator inhibitor activity (the major inhibitor of fibrinolysis), which were observed in 20% of stroke probands and in 21% of their first-degree relatives, versus 8% of 175 nomolipidemic control subjects (p = 0.007 and 0.04, respectively). Mean (SD) basal plasminogen activator inhibitor activity and antigen level were higher in stroke probands (18 +/- 18 U/ml and 35 +/- 31 ng/ml, respectively) than in the 175 normolipemic control subjects (14 +/- 10 [p = 0.002], 28 +/- 34 [p = 0.016]). (3) Levels of basal tissue plasminogen activator antigen, a probable marker for atherosclerosis, were much higher in stroke probands than in the 175 normolipemic control subjects (15 +/- 7.3 ng/ml vs 7 +/- 3.8, p = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypofibrinolytic and atherogenic risk factors for stroke. 789 94


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