Gene/Protein Disease Symptom Drug Enzyme Compound
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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 purpose of this study was to investigate the prevalence of hypercholesterolemia among subjects having diabetes and glucose intolerance, according to the guidelines of the National Cholesterol Education Program (Adult Treatment Panel II, ATP II). This survey consisted of 2090 subjects (856 men, 1234 women) aged 30 years or more from the Sun-Ming district of Kaohsiung city. Glucose tolerance status was ascertained for both medical history and a 75-g oral glucose tolerance test according to World Health Organization criteria. Frequency of elevated total cholesterol in female subjects with abnormal glucose tolerance is significantly greater than in those with normal glucose tolerance (NGT). However, only male subjects with undiagnosed NIDDM (UDDM) had a statistically higher rate of hypercholesterolemia than those with NGT. Of UDDM individuals, 68% have total cholesterol level between 200 and 239 mg/dl and two or more risk factors for heart disease or evidence of coronary heart disease or total cholesterol > or = 240 mg/dl or high-density lipoprotein (HDL) cholesterol < or = 35 mg/dl. Such individuals should have their low-density lipoprotein (LDL) cholesterol measured. Using the ATP II, LDL cholesterol levels warranting dietary treatment for hypercholesterolemia would be expected in 76% of UDDM. Due to the high prevalence of coronary heart disease in diabetic patients, investigation of blood lipid levels and coronary heart disease risk factors should be routine in these patients, and treatment strategies should include management of lipid disorders and the many other risk factors. A high frequency of dyslipidemia was found among UDDM group in our study. Early detection of undiagnosed diabetic patients is also very important in decreasing the prevalence of coronary heart disease.
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PMID:Hypercholesterolemia in undiagnosed non-insulin-dependent diabetes in southern Taiwan. 868 43

The ATP cassette-binding (ABC) gene superfamily contains more than 40 members, many of which are involved in cellular lipid transport. The most prominent example is ABCA1, mutations in which affect plasma high-density lipoprotein (HDL) cholesterol concentration. ABCC6 is another member of the ABC gene family, and mutations in ABCC6 were recently shown to cause pseudoxanthoma elasticum (PXE). A Canadian patient with PXE was referred for assessment of moderately severe type IV hyperlipoproteinemia with hypoalphalipoproteinemia, which was refractory to pharmacological treatment. We identified intron-exon boundaries of ABCC6 to sequence genomic DNA from this patient to find the disease mutation. We report (1) identification of a set of amplification primers for the 31 exons of ABCC6; (2) identification of the ABCC6 R>X1164 nonsense mutation in the PXE subject with dyslipidemia; (3) identification of common amino acid variants and silent nucleotide variants in ABCC6, with a range of allele frequencies across ethnic groups; (4) evidence consistent with a possible pseudogene encoding 9 exons with sequence homology to ABCC6; and (5) association of the ABCC6 R>Q1268 variant with plasma triglyceride and HDL cholesterol. The results suggest that ABCC6 may be a determinant of plasma lipoproteins.
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PMID:ABCC6 gene polymorphism associated with variation in plasma lipoproteins. 1177 82

Reducing high levels of plasma low-density lipoprotein cholesterol (LDL-C) is still the primary focus of the Adult Treatment Panel III (ATP III) guidelines developed by the National Cholesterol Education Program. The LDL-C goal of less than 100 mg/dL for those with coronary heart disease (CHD) is now extended to patients with diabetes and those with a Framingham risk score of greater than 20% in 10 years, both of which are now considered "CHD risk equivalents." Consequently, many more people will be considered candidates for aggressive lipid-lowering therapy under the new ATP III guidelines. Other prominent features in the new guidelines include determining an individual's absolute risk category by using a nine-step process, instituting therapeutic lifestyle changes to reduce LDL-C levels, and strategies for treating patients with other forms of dyslipidemia such as metabolic syndrome.
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PMID:Adult Treatment Panel III: do we really need another set of cholesterol guidelines? 1204 81

Here we propose that glucose metabolism can be understood on the basis of three concept-derived axioms: (I) A hierarchy exists among the glucose-utilizing organs with the brain served first, followed by muscle and fat. (II) Tissue-specific glucose transporters allocate glucose among organs in order to maintain brain glucose concentrations. (III) Exogenous carbohydrate supply compensates for glucose alterations that can temporarily occur in muscle and fat. Derived from the control theory, the simplest solution of allocating supply to 2 organs, e.g. brain and muscle, is a "fishbone"-structured model. We reviewed the literature, searching for neuroendocrine and metabolic mechanisms that can fulfill control functions in such a model: The tissue-specific glucose transporters are differentially regulated. GLUT 1, carrying glucose across the blood-brain-barrier, is independent of insulin. Instead, this trans-endothelial glucose transporter is rather dependent on potent regulators of blood vessel function like vascular endothelial growth factor - a pituitary counterregulatory hormone. GLUT 4, carrying glucose across the membranes of muscle and fat cells, depends on insulin. Thereby, insulin allocates glucose to muscle and fat. The hypothalamus-pituitary-adrenal (HPA) axis, the sympathetic nervous system (SNS), and vascular endothelial growth factor allocate glucose to the brain. Multiple "sensors" (some of which have only recently been identified as ATP sensitive potassium channels) measure glucose or glucose equivalents at various sites of the body: the ventromedial hypothalamus, the lateral hypothalamus, portal vein, pancreatic beta cell, renal tubule, muscle and adipose tissue. Feedback pathways both from the brain and from muscle and fat are involved in regulating glucose allocation and exogenous glucose supply. The main feedback signal from the brain is found to be glucose, that from muscle and fat appears to be leptin. In fact, the literature search revealed two or more biological mechanisms for the function of each component in the model, finding glucose regulation highly redundant. This review focuses on "brain glucose" control. The concept of glucose allocation presented here challenges the common opinion of "blood glucose" being the main parameter controlled. According to the latter opinion, hyperglycemia in the metabolic syndrome is due to a putative defect located within the closed loop including the beta cell, muscle and fat cells. That traditional view leaves some peculiarities of e.g. the metabolic syndrome unexplained. The concept of glucose allocation, however, would predict that weight gain - with abundance of glucose in muscle and fat - increases feedback to the brain (via hyperleptinemia) which in turn results in HPA-axis and SNS overdrive, impaired insulin secretion, and insulin resistance. HPA-axis overdrive would account for metabolic abnormalities such as central adiposity, hyperglycemia, dyslipidemia, and hypertension, that are well known clinical aspects the metabolic syndrome. This novel viewpoint of "brain glucose" control may shed new light on the pathogenesis of the metabolic syndrome and type 2 diabetes.
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PMID:The neuroendocrine control of glucose allocation. 1214 83

The third edition of guidelines from the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III [ATP III]) is discussed. The most recent classifications for low-density-lipoprotein (LDL) cholesterol, high-density-lipoprotein (HDL), total cholesterol, and triglycerides are provided. LDL cholesterol goals, cardiovascular risk assessment, therapeutic goals, and pharmacologic treatment options are discussed for both primary and secondary prevention of cardiovascular disease. In addition, the management of dyslipidemia in patients with diabetes and metobolic syndrome is addressed, and the differences between the old and new guidelines are highlighted. The ATP III guidelines may help health care professionals to better screen and categorize patients on the basis of their coronary heart disease (CHD) risk. The updated guidelines recommend more intensive lipid-lowering treatments for primary prevention in patients with two or more risk factors.
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PMID:Update on the management of dyslipidemia. 1222 42

Coronary heart disease (CHD) is a common, costly, and undertreated disorder in the United States, and dyslipidemia is one of its most important modifiable risk factors. Recently, the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) published updated guidelines for the treatment of lipid disorders, greatly expanding the number of patients eligible for therapy. In the new recommendations, several significant changes have been made in the identification and management of patients at risk for CHD. Although ATP III maintains that low-density lipoprotein (LDL) cholesterol should be the primary target of lipid-lowering therapy, it identifies non-high-density lipoprotein (HDL) cholesterol (total cholesterol minus HDL cholesterol) as a secondary target in patients with elevated triglycerides. Patients with > or = 2 CHD risk factors should now be assessed for 10-year absolute CHD risk based on the Framingham Point Scale to identify those who require more aggressive treatment. The guidelines also designate a new category, CHD risk equivalent, which recognizes that certain patients have the same high risk as those with established CHD. Diabetes is now identified as a CHD risk equivalent, as are other forms of atherosclerotic disease and multiple risk factors comprising a CHD 10-year risk of > 20%. New lipoprotein classifications are given, and increased emphasis is placed on the metabolic syndrome, a constellation of metabolic risk factors, as a marker for CHD risk. Since adherence poses a major challenge in the management of patients with or at risk for CHD, the new guidelines provide physicians with several strategies for increasing patient compliance. The new guidelines should help physicians better identify and manage patients at risk for CHD, help more patients reach their lipid goals, and thereby decrease cardiovascular morbidity and mortality.
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PMID:New therapeutic options in the National Cholesterol Education Program Adult Treatment Panel III. 1224 Jul 1

Patients with combined dyslipidemia are at high risk for coronary artery disease and often require combination drug therapy to achieve lipid levels recommended by the US National Cholesterol Education Program's third Adult Treatment Panel (ATP III). In addition to recommendations for low-density lipoprotein (LDL) cholesterol and triglyceride levels, ATP III established non-high-density lipoprotein (HDL) cholesterol goals for individuals with triglycerides >or=2.26 mmol/L (>or=200 mg/dL). It also introduced certain criteria for the diagnosis of the metabolic syndrome, a clustering of risk factors (abdominal obesity, elevated triglycerides, low HDL cholesterol, elevated blood pressure, impaired fasting glucose) that increases cardiovascular risk and is common in patients with combined dyslipidemia. Statin monotherapy has been shown to benefit these patients, and additional benefit may be obtained by combination therapy that provides greater reductions in both LDL cholesterol and triglycerides as well as greater increases in HDL cholesterol. However, combining a statin with either niacin or a fibrate may increase the risk for myopathy and therefore requires careful monitoring and evaluation of the risk-benefit ratio for each patient. Moreover, combination therapy may be associated with increased drug costs and decreased patient compliance. Recently developed agents that may improve the effectiveness of combination therapy include ezetimibe-a cholesterol absorption inhibitor-and a formulation that combines extended-release niacin and lovastatin in a single pill. Clinical trials are needed to determine the optimal treatment in patients with combined dyslipidemia.
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PMID:Combination therapy for combined dyslipidemia. 1246 37

Lipid-lowering agents have been shown to reduce morbidity and mortality associated with coronary heart disease (CHD), particularly in high-risk patients. The identification and treatment of these patients should therefore be a high priority for clinicians. Guidelines from medical organizations, such as the National Cholesterol Education Program Adult Treatment Panel (NCEP ATP) and the American Diabetes Association (ADA), suggest that patients with low-density lipoprotein cholesterol (LDL-C) levels > or =130 mg/dL, and perhaps even those with levels > or =100 mg/dL, should receive drug therapy. Optimal LDL-C levels have been set at <100 mg/dL and <115 mg/dL for high-risk patients by US and European guidelines, respectively. However, a recent survey shows that only about 20% of high-risk patients currently meet these goals. In order to achieve therapeutic targets for LDL-C, the statins are the foundation of treatment, as they are the most effective and best-tolerated form of lipid-lowering therapy. Other therapeutic options include bile acid sequestrants, niacin, and plant stanols, although seldom as monotherapy. Combination therapy with a statin and one of these other lipid-lowering agents can be useful in patients who are unable to achieve target lipid levels through monotherapy. There remains, however, a need for additional agents. Some of the new options for reducing LDL-C levels that may be available in the near future include 2 new statins, pitavastatin and rosuvastatin. In patients with heterozygous familial hypercholesterolemia, rosuvastatin, which is currently under review by the Food and Drug Administration (FDA), has been shown to produce significantly greater reductions in LDL-C than atorvastatin over its full dose range. In comparative clinical trials, it has also enabled more patients with primary hypercholesterolemia to meet lipid goals than atorvastatin, simvastatin, and pravastatin. Inhibitors of bile acid transport or cholesterol absorption may also have therapeutic value. The first cholesterol absorption inhibitor, ezetimibe, which has just been approved by the FDA, appears to be most effective when combined with a statin. It is anticipated that such new options will allow clinicians to optimize the management of dyslipidemia in high-risk patients, thereby reducing the morbidity and mortality of CHD.
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PMID:Management of dyslipidemia in the high-risk patient. 1248 15

Coronary heart disease (CHD) remains the leading cause of death in the United States with more than 40% of all deaths each year directly attributed to the disease. Current evidence suggests that early identification and aggressive modification of risk factors offer the most promising approach to reducing the burden of CHD. Dyslipidemia has been identified as the primary risk factor leading to the development of CHD. It is estimated that nearly 65 million Americans require some form of lipid-modification therapy. The National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) set of guidelines released in May 2001 provides physicians with evidence-based recommendations on the classification, diagnosis, and treatment of lipid disorders. New features of the guidelines include a scoring system for calculating CHD risk, as well as the identification of CHD risk equivalents, lower treatment target goals, and an emphasis on conditions conferring a higher risk for CHD, such as the metabolic syndrome. The ATP III emphasis on risk assessment substantially increases the number of patients considered at risk for CHD and will expand the number eligible for lifestyle and drug interventions. This article highlights the new recommendations and reviews the impact of ATP III on osteopathic physicians.
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PMID:The national cholesterol education program adult treatment panel ill guidelines. 1257 22


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