UMLS:C0242339 - FACTA Search

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

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

Cholesterol management to reduce the burden of cardiovascular disease is a major public health concern. Despite widespread recognition of lipid abnormalities as cardiovascular risk factors, significant cardiovascular event reductions with cholesterol-lowering therapies, and dissemination of treatment guidelines, most high-risk patients are not at target lipid levels. In addition to lifestyle changes, four major drug classes are available to modify lipid levels: fibrates, niacin, resins, and statins. High efficacy and tolerability in clinical trials make statins the most widely prescribed of these agents. Newer, more potent members of this class and novel formulations of niacin and resins may provide more effective therapy for dyslipidemia with fewer side effects. Several agents in development (cholesterol-absorption inhibitors and ACAT inhibitors) exploit mechanisms of action complementary to those of current treatments and combined with statins may produce greater improvements in lipid profiles than are now possible. These innovations should enable a greater number of patients to achieve more aggressive cholesterol goals, thereby reducing the risk of cardiovascular events.
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PMID:Future directions in lipid therapies. 1206 69

Hyperhomocysteinemia is now recognized as an independent risk factor for atherosclerotic cardiovascular disease in patients with normal renal function. Hyperhomocysteinemia is common in patients with chronic renal failure. Kidney transplant recipients have a high risk of cardiovascular death. Recently, attention has been paid to the association between homocysteine and cardiovascular disease. Dyslipidemia is also common in kidney transplant recipients. The purpose of this study was to assess whether fluvastatin in a dose of 20 mg affects homocysteine concentration in 10 stable renal transplant recipients. We evaluated Hcy, lipoprotein (a) by the use of commercially available kits as well as plasma fibrinogen and cholesterol, triglycerides and albumin levels. All the parameters were studied before and after 1, 2 and 3 months of fluvastatin treatment. Cholesterol and LDL decreased significantly as early as after 1 month and remained lowered during the therapy. No significant changes in Hcy, lipoprotein (a) and fibrinogen were found during therapy with fluvastatin. Fluvastatin is an effective hypolipemic agent and has no effect on Hcy and fibrinogen concentration in kidney transplant recipients.
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PMID:Effects of fluvastatin on homocysteine and serum lipids in kidney allograft recipients. 1222 4

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

Updated guidelines published recently by the National Cholesterol Education Program place greater emphasis on atherogenic dyslipidemia, characterized by low high-density lipoprotein (HDL) cholesterol; elevated triglycerides; and small, dense, low-density lipoprotein (LDL) particles, as well as the drugs that can alter the condition. Both low HDL cholesterol and elevated triglycerides are independent risk factors for coronary artery disease. Low-density lipoprotein particles can be divided into subclasses with differing atherogenicity. Phenotype A is characterized by large buoyant LDL particles, and phenotype B by small, dense particles associated with increased atherogenicity. The frequency of phenotype B in patients increases as triglyceride levels increase and HDL cholesterol levels decrease. Fibrates and niacin have been shown to improve atherogenic dyslipidemia in clinical trials. Niacin effectively lowers triglycerides, raises HDL cholesterol, and shifts LDL particles to a less atherogenic phenotype (phenotype A). The various niacin formulations available differ in terms of safety and efficacy. When administered alone or in combination with other lipid-modifying agents, niacin prevents progression and promotes regression of coronary atherogenic lesions and reduces coronary risk. Combination therapy is also an effective option for improving multiple lipoprotein abnormalities. In studies, a once-daily, single-tablet combination of niacin extended-release/lovastatin showed additive LDL cholesterol lowering and was more effective than would be anticipated from doubling the component lovastatin dose. Combination products provide a viable strategy for treating the full spectrum of lipid abnormalities seen in some patients, including those with atherogenic dyslipidemia, and will be increasingly used in the treatment of dyslipidemia. Other combination products are currently undergoing clinical testing.
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PMID:Niacin-based therapy for dyslipidemia: past evidence and future advances. 1224 Jul 3

Peritoneally dialyzed subjects (CAPD) are prone to dyslipidemia and have a high risk of cardiovascular death. Statins (hydroxy-methylglutaryloCoA reductase inhibitors) show beneficial effects on serum lipids and hemostasis in kidney diseases. The purpose of this study was to assess platelet functions, some hemostatic parameters-extrinsic coagulation pathway-total, truncated, free TFPI (tissue factor pathway inhibitor), TF (tissue factor), TFPI/Xa and TF/VIIa complexes, as well as a marker of endothelial cell injury--von Willebrand factor--vWF and serum lipids in 10 hyperlipidemic CAPD patients treated with simvastatin (Zocor, MSD, at a dose of 10 mg at bedtime) for 3 months. Cholesterol and LDL fell significantly as early as after 1 month and remained lowered during further months of the therapy. No significant changes in von Willebrand factor, free TFPI, TF, TFPI/Xa and TF/VIIa complexes were found during therapy with simvastatin. Truncated TFPI decreased significantly as early as after 1 month and total TFPI decreased after 3 months of the therapy with simvastatin. Simvastatin is an effective hypolipemic agent. It seems that simvastatin have no or only little effect on endothelial function and extrinsic coagulation pathway in peritoneally dialyzed patients.
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PMID:[Simvastatin and extrinsic coagulation pathway in peritoneally dialyzed patients]. 1237 84

Traditional risk factors for coronary artery disease (CAD) predict about 50% of the risk of developing CAD. The Adult Treatment Panel (ATP) III has defined emerging risk factors for CAD, including small, dense low-density lipoprotein (LDL). Small, dense LDL is often accompanied by increased triglycerides (TGs) and low high-density lipoprotein (HDL). An increased number of small, dense LDL particles is often missed when the LDL cholesterol level is normal or borderline elevated. Small, dense LDL particles are present in families with premature CAD and hyperapobetalipoproteinemia, familial combined hyperlipidemia, LDL subclass pattern B, familial dyslipidemic hypertension, and syndrome X. The metabolic syndrome, as defined by ATP III, incorporates a number of the components of these syndromes, including insulin resistance and intra-abdominal fat. Subclinical inflammation and elevated procoagulants also appear to be part of this atherogenic syndrome. Overproduction of very low-density lipoproteins (VLDLs) by the liver and increased secretion of large, apolipoprotein (apo) B-100-containing VLDL is the primary metabolic characteristic of most of these patients. The TG in VLDL is hydrolyzed by lipoprotein lipase (LPL) which produces intermediate-density lipoprotein. The TG in intermediate-density lipoprotein is hydrolyzed further, resulting in the generation of LDL. The cholesterol esters in LDL are exchanged for TG in VLDL by the cholesterol ester tranfer proteins, followed by hydrolysis of TG in LDL by hepatic lipase which produces small, dense LDL. Cholesterol ester transfer protein mediates a similar lipid exchange between VLDL and HDL, producing a cholesterol ester-poor HDL. In adipocytes, reduced fatty acid trapping and retention by adipose tissue may result from a primary defect in the incorporation of free fatty acids into TGs. Alternatively, insulin resistance may promote reduced retention of free fatty acids by adipocytes. Both these abnormalities lead to increased levels of free fatty acids in plasma, increased flux of free fatty acids back to the liver, enhanced production of TGs, decreased proteolysis of apo B-100, and increased VLDL production. Decreased removal of postprandial TGs often accompanies these metabolic abnormalities. Genes regulating the expression of the major players in this metabolic cascade, such as LPL, cholesterol ester transfer protein, and hepatic lipase, can modulate the expression of small, dense LDL but these are not the major defects. New candidates for major gene effects have been identified on chromosome 1. Regardless of their fundamental causes, small, dense LDL (compared with normal LDL) particles have a prolonged residence time in plasma, are more susceptible to oxidation because of decreased interaction with the LDL receptor, and enter the arterial wall more easily, where they are retained more readily. Small, dense LDL promotes endothelial dysfunction and enhanced production of procoagulants by endothelial cells. Both in animal models of atherosclerosis and in most human epidemiologic studies and clinical trials, small, dense LDL (particularly when present in increased numbers) appears more atherogenic than normal LDL. Treatment of patients with small, dense LDL particles (particularly when accompanied by low HDL and hypertriglyceridemia) often requires the use of combined lipid-altering drugs to decrease the number of particles and to convert them to larger, more buoyant LDL. The next critical step in further reduction of CAD will be the correct diagnosis and treatment of patients with small, dense LDL and the dyslipidemia that accompanies it.
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PMID:Clinical relevance of the biochemical, metabolic, and genetic factors that influence low-density lipoprotein heterogeneity. 1241 79

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

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