Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Fibric Acids”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed2006

The role of high-density lipoprotein cholesterol in the prevention and possible treatment of cardiovascular diseases.

Despite significant progress in the management of atherosclerosis and its resultant complications, cardiovascular disease remains the principal cause of death in the world. The National Cholesterol Education Project Adult Treatment Panel III (NCEP ATP III) recognizes low levels of high-density lipoprotein cholesterol (HDL) as a risk factor for coronary heart disease (CHD) and high levels of HDL as a risk-reducing factor; however, the elevation of HDL as a specific therapeutic target for the prevention and treatment of CHD has yet to be accepted on the same level as low-density lipoprotein (LDL)-reducing therapies. Current HDL elevators including nicotinic acid, fibric acid derivatives, peroxisome proliferator activated receptor (PPAR) agonists and statins also affect other lipid constituents which make interpretation of the clinical trials of these drugs difficult in teasing out the independent effect of HDL elevation. Ample laboratory investigation suggests that HDL elevation would reduce atherosclerotic burden through multiple independent mechanisms. In this review, we explore HDL biology, its potential mechanisms in the treatment of atherosclerotic disease, and promising new drugs with HDL-raising activity.

Animals↗
PubMed2006

The role of high-density lipoprotein cholesterol in atherothrombosis.

Despite considerable progress in the development of new therapies to control atherosclerosis and its complications, coronary heart disease (CHD) remains the number one cause of death in the Western world. While low high-density lipoprotein (HDL) has been associated with increased risk for CHD, raising HDL to reduce risk of disease has yet to be accepted as a standard therapeutic strategy. Currently available drugs that raise HDL (e.g., nicotinic acid, fibric acid derivatives, peroxisome proliferator-activated receptor agonists, and statins) also affect low-density lipoprotein (LDL) and other lipid constituents, making independent interpretation of their HDL-raising effect difficult to tease apart. Nevertheless, basic science studies suggest that HDL has multiple beneficial effects, and current efforts to develop new pharmacologic products with potent HDL-elevating effects may herald a day when HDL elevation becomes part of standard management of atherosclerotic diseases.

Cholesterol, HDL↗
PubMed1996

Drug therapy of severe hypercholesterolemia in patients with coronary artery disease.

The beneficial effect of cholesterol-lowering therapy for secondary prevention in patients with coronary artery disease (CAD) is well established. The therapeutic goal in this situation is a low-density lipoprotein (LDL) cholesterol level of 100 mg/dl. Cholesterol-lowering therapy will not only lead to a reduction in the progression of lesions but also and probably more importantly will reduce lesion activation and rupture and improve endothelial vasomotor function. Depending on the underlying hyperlipoproteinemia, the first choice for single drug therapy is a bile acid-binding resin or a hepatic hydroxymethyl glutaryl coenzyme A (HMG-CoA) reductase inhibitor in isolated LDL hypercholesterolemia, and nicotinic acid, a fibric acid, or a HMG-CoA reductase inhibitor in combined hyperlipidemia. Combination therapy usually consists of a bile acid-binding resin with either an HMG-CoA reductase inhibitor, a fibric acid, or nicotinic acid in LDL hypercholesterolemia and nicotinic acid with a fibric acid in combined hyperlipidemia.

Acyl Coenzyme A↗
PubMed2004

Hypolipidemic therapy and cholesterol absorption.

The advent of safe and effective hypolipidemic therapy has revolutionized the ability of the clinician to optimize abnormalities in the lipid profile. The advent of statin therapy has provided a potent option to decrease low-density lipoprotein and frequently allows achievement of National Cholesterol Education Program target lipid levels with monotherapy. However, lipid goals are frequently not achieved due to inadequate response to therapy or side effects. The role of combination therapy in the optimization of the lipid profile provides a means by which the implementation of pharmacologic agents with synergistic mechanisms of action allows further improvement in circulating levels of low-density lipoprotein cholesterol. Statins have been combined with bile acid resins, fibric acid derivatives, and nicotinic acid. However, bile acid resins, although not systemically absorbed, have significant problems with patient compliance and drug interactions. The implementation of therapy with fibric acid derivatives or nicotinic acid increases the risk of significant side effects such as rhabdomyolysis or liver toxicity. Ezetimibe is a prototype of a new class of agents that specifically block the absorption of cholesterol from the gastrointestinal tract. Ezetimibe has minimal systemic absorption and a metabolic pathway involving enterohepatic circulation that allows for once a day administration due to a prolonged half-life. Ezetimibe lacks the drug interactions that are common with the bile acid resins and it may be utilized as either monotherapy or in combination with other pharmacologic agents. Ezetimibe has a relatively flat dose-response curve and titration is not required. This review centers on the role of pharmacologic agents that act predominantly by the reduction of cholesterol absorption, including colesevelam and ezetimibe.

Allylamine↗
PubMed1999

PPARalpha activators inhibit cytokine-induced vascular cell adhesion molecule-1 expression in human endothelial cells.

BACKGROUND: Adhesion molecule expression on the endothelial cell (EC) surface is critical for leukocyte recruitment to atherosclerotic lesions. Better understanding of transcriptional regulation of adhesion molecules in ECs may provide important insight into plaque formation. Peroxisome proliferator-activated receptor-alpha (PPARalpha), a member of the nuclear receptor family, regulates gene expression in response to certain fatty acids and fibric acid derivatives. The present study investigated PPARalpha expression in human ECs and their regulation of vascular cell adhesion molecule-1 (VCAM-1). METHODS AND RESULTS: Immunohistochemistry revealed that human carotid artery ECs express PPARalpha. Pretreatment of cultured human ECs with the PPARalpha activators fenofibrate or WY14643 inhibited TNF-alpha-induced VCAM-1 in a time- and concentration-dependent manner, an effect not seen with PPARgamma activators. Both PPARalpha activators decreased cytokine-induced VCAM-1 mRNA expression without altering its mRNA half-life. Transient transfection of deletional VCAM-1 promoter constructs and electrophoretic mobility shift assays suggest that fenofibrate inhibits VCAM-1 transcription in part by inhibiting NF-kappaB. Finally, PPARalpha activators significantly reduced adhesion of U937 cells to cultured human ECs. CONCLUSIONS: Human ECs express PPARalpha, a potentially important regulator of atherogenesis through its transcriptional control of VCAM-1 gene expression. Such findings also have implications regarding the clinical use of lipid-lowering agents, like fibric acids, which can activate PPARalpha.

Anticholesteremic Agents↗
PubMed2001

PPARalpha activators inhibit tissue factor expression and activity in human monocytes.

BACKGROUND: Tissue factor (TF), expressed on the surface of monocytes and macrophages in human atherosclerotic lesions, acts as the major procoagulant initiating thrombus formation in acute coronary syndromes. Peroxisome proliferator-activated receptor-alpha (PPARalpha), a nuclear receptor family member, regulates gene expression in response to certain fatty acids and fibric acid derivatives. Given that some of these substances reduce TF activity in patients, we tested whether PPARalpha activators limit TF responses in human monocytic cells. METHODS AND RESULTS: Pretreatment of freshly isolated human monocytes or monocyte-derived macrophages with PPARalpha activators WY14643 and eicosatetraynoic acid (ETYA) led to reduced lipopolysaccharide (LPS)-induced TF activity in a concentration-dependent manner (maximal reduction to 43+/-8% with 250 micromol/L WY14643 [P:<0.05, n=5] and to 42+/-12% with 30 micromol/L ETYA [P:>0.05, n=3]). Two different PPARgamma activators (15-deoxy(_Delta12,14)-prostaglandin J(2) and BRL49653) lacked similar effects. WY14643 also decreased tumor necrosis factor-alpha protein expression in supernatants of LPS-stimulated human monocytes. Pretreatment of monocytes with WY14643 inhibited LPS-induced TF protein and mRNA expression without altering mRNA half-life. Transient transfection assays of a human TF promoter construct in THP-1 cells revealed WY14643 inhibition of LPS-induced promoter activity, which appeared to be mediated through the inhibition of nuclear factor-kappaB but not to be due to reduced nuclear factor-kappaB binding. CONCLUSIONS: PPARalpha activators can reduce TF expression and activity in human monocytes/macrophages and thus potentially reduce the thrombogenicity of atherosclerotic lesions. These data provide new insight into how PPARalpha-activating fibric acid derivatives and certain fatty acids might influence atherothrombosis in patients with vascular disease.

5,8,11,14-Eicosatetraynoic Acid↗
PubMedDate not supplied

A review of combined hyperlipidaemia and its treatment with fenofibrate.

Approximately 15% of myocardial infarction survivors less than 60 years of age have a plasma lipid abnormality defined as combined hyperlipidaemia. Patients with this condition are at substantial risk for future cardiovascular events. Combined hyperlipidaemia involves elevations in both plasma triglycerides and low-density lipoprotein (LDL) cholesterol and may share similarities with hyperapolipoproteinaemia, LDL-pattern B and the small LDL-pattern. Treatment is directed at reduction of LDL-cholesterol and plasma triglyceride values. Nicotinic acid and the fibric acid derivatives are useful therapeutic agents. Fenofibrate is a fibric acid derivative that lowers both triglycerides and LDL-cholesterol in combined hyperlipidaemia. In combined hyperlipidaemia, fenofibrate has been shown to reduce significantly plasma triglycerides by approximately 40%, LDL-cholesterol by 6%, and to increase high-density lipoprotein cholesterol by 15%. Apoproteins are favourably altered with increases in apoprotein-A, decreases in apoprotein-E and inconsistent decreases in apoprotein-B. Fenofibrate is well tolerated with primarily dermatological side-effects.

Fenofibrate↗
PubMed2003

What future for combination therapies?

For most patients who require lipid-lowering treatment, statin monotherapy is the appropriate treatment. However, in those patients where statin monotherapy does not produce optimal lipid levels, the combination of a statin with niacin, a bile acid sequestrant, a fibric acid derivative, a cholesterol absorption inhibitor or a fish oil preparation may provide improved control. The choice of combination therapy depends upon the patient's lipid profile and tolerability of the medication. Combination of a statin with niacin, a bile acid sequestrant or ezetimibe, a cholesterol absorption inhibitor, should be considered for patients with very high low-density lipoprotein cholesterol (LDL-C) levels, while combination with either a fibric acid derivative or a fish oil should be considered for patients with high LDL-C and high triglyceride levels. A number of new lipid-lowering agents are currently in development, including cholesteryl ester transfer protein (CETP) inhibitors, acyl coenzyme A: cholesterol acyltransferase (ACAT) inhibitors, ileal bile acid transport (IBAT) inhibitors, microsomal triglyceride transfer protein (MTP) inhibitors and dual peroxisome proliferator-activated receptor (PPAR) alpha and gamma agonists. Introduction of these novel therapies will provide opportunities for developing different combination strategies that may help to optimise lipid profiles in patients who are currently difficult to treat. The introduction of new combinations will require careful study to ensure that the risks of drug interactions and adverse events are minimised.

Bile Acids and Salts↗
PubMedDate not supplied

Peroxisome proliferator-activated receptor-alpha and atherosclerosis: from basic mechanisms to clinical implications.

Atherosclerosis is an inflammatory process, triggered by the presence of lipids in the vascular wall, and encompasses a complex interaction among inflammatory cells, vascular elements, and lipoproteins through expression of several adhesion molecules and cytokines. Activation of the nuclear receptor, peroxisome proliferator-activated receptor-alpha (PPAR-alpha), has been demonstrated to modulate many aspects of lipoprotein metabolism and inflammation in vitro as well as in animal and human studies. The tissue distribution of PPAR-alpha is extensive, and it is abundantly present in the vascular wall where it may mediate many of antiinflammatory and antiatherogenic effects. Major clinical trials such as the Veterans Affairs High-Density Lipoprotein Intervention Trial (VA-HIT), the Helsinki Heart Study, and the Diabetes Atherosclerosis Intervention Study (DAIS) have demonstrated the beneficial effects of synthetic agonists of PPAR-alpha, specifically fibric acid derivatives, on cardiovascular disease outcome. Although fibric acid trials have reported cardiovascular risk reduction in patients with dyslipidemia, the favorable alterations in plasma lipids can only partially explain the reduction in cardiovascular events in these studies. One common link among these trials was a cohort with a high prevalence of insulin resistance or diabetes, conditions associated with heightened systemic inflammation and increased risk for development and progression of atherosclerosis. We review the many antiatherogenic effects of PPAR-alpha ligands and evidence from fibric acid trials that individuals with insulin resistance or diabetes benefit the most from these drugs, consistent with their antiinflammatory and antithrombotic properties.

Acute-Phase Proteins↗
PubMed2004

Peroxisome proliferator-activated receptor-alpha and atherosclerosis: from basic mechanisms to clinical implications.

Atherosclerosis is an inflammatory process triggered by the presence of lipids in the vascular wall and encompasses a complex interaction between inflammatory cells, vascular elements and lipoproteins through the expression of several adhesion molecules and cytokines. Activation of the nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR-alpha) has been demonstrated to modulate many aspects of lipoprotein metabolism and inflammation in vitro as well as in animal and human studies. The tissue distribution of PPAR-alpha is extensive and it is abundantly present in the vascular wall where it may mediate many of anti-inflammatory and antiatherogenic effects. Major clinical trials, such as the Veterans Affairs High-Density Lipoprotein Intervention Trial, the Helsinki Heart Study and the Diabetes Atherosclerosis Intervention Study, have demonstrated the beneficial effects of synthetic agonists of PPAR-alpha, specifically fibric acid derivatives, on cardiovascular disease outcome. Although fibric acid trials have reported cardiovascular risk reduction in patients with dyslipidemia, the favorable alterations in plasma lipids can only partially explain the reduction in cardiovascular events in these studies. One common link among these trials was a cohort with a high prevalence of insulin resistance or diabetes, conditions associated with heightened systemic inflammation and increased risk for development and progression of atherosclerosis. In this paper, we will review the many antiatherogenic effects of PPAR-alpha ligands and evidence from fibric acid trials that individuals with insulin resistance or diabetes benefit the most from these drugs, consistent with their anti-inflammatory and antithrombotic properties.

Acute-Phase Proteins↗
PubMed1999

Should hyperlipidemia in children with the nephrotic syndrome be treated?

The pathogenesis, clinical significance, and treatment options of the disturbances in lipid metabolism in children with persistent nephrotic syndrome are reviewed. The lipoprotein profile is characterized by elevations of total plasma cholesterol and often triglycerides, elevated very low-density lipoprotein and low-density lipoprotein cholesterol, whereas high-density lipoprotein-cholesterol levels are variable; plasma levels of the atherogenic and thrombogenic lipoprotein(a) are also elevated. The pathophysiology of nephrotic dyslipoproteinemia is multifactorial, including both an increased hepatic synthesis and a diminished plasma catabolism of lipoproteins. There is a rationale for treatment, since dyslipidemia may contribute to the development of atherosclerosis and the progression of chronic renal failure. However, the benefits of treatment with lipid-lowering drugs have not been proven. Short-term studies in adults with nephrotic syndrome have documented safety and efficacy of lipid-lowering drugs, including hydroxymethylglutaryl-CoA reductase inhibitors ("statins"), bile acid sequestrants, fibric acids, fish oil, and probucol. Statins are the most-effective mediation, resulting in a decrease of total cholesterol levels by about 30%-40%. Prospective controlled studies in children evaluating efficacy and safety of lipid-lowering drugs are needed.

Child↗
PubMed1992

Therapeutic management of triglycerides: an international perspective.

Current recommendations from various international expert committees generally concur in their definitions of borderline and high triglyceride levels, with small but important differences between recommendations in the definition of normal levels. However, population-based data on triglyceride levels are poorly developed in most countries, making difficult any international comparisons of prevalences of hypertriglyceridemia using the new definitions. However, it is probable that there should be considerable differences in the prevalence of hypertriglyceridemia, probably due to a mixture of genetic and environmental influences. The management of hypertriglyceridemia must continue to emphasize the detection and correction of secondary causes, even though the specific secondary causes may vary between countries. Dietary and exercise interventions must deal with local customs and resources, including striking international differences in alcohol consumption. Pharmacologic therapies will likely increase in use if they follow the trends in countries with available data. Although various drugs are available, nicotinic acid and fibric acid derivatives remain the drugs of choice. Considerably more research is needed to describe these international differences in etiology, prevalence and management practices of hypertriglyceridemia.

Humans↗
PubMed2000

The pharmacokinetics and pharmacodynamics of agents proven to raise high-density lipoprotein cholesterol.

Bile acid sequestrants, fibric acid derivatives (fibrates), hydroxy-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors ("statins"), and niacin are able to increase HDL-C serum concentrations to varying degrees. Bile acid sequestrants are the least effective, whereas niacin is the most powerful agent for increasing HDL-C levels. Because of 2 alternate metabolic pathways of niacin breakdown, flushing or hepatotoxicity can occur in patients taking niacin. These effects can be mediated in a carefully designed formulation of niacin that releases the drug at a predictable rate. Niacin has few drug interactions and is a relatively inexpensive means of increasing HDL-C. A combination formulation that combines niacin plus a statin has shown promise in ongoing clinical trials.

Biological Availability↗
PubMed2003

Treating dyslipidemia with statins: the risk-benefit profile.

BACKGROUND: Coronary heart disease (CHD), the result of coronary atherosclerosis, is the largest single killer of Americans. Central to the pathogenesis of atherosclerosis are the deposition and retention of cholesterol in the arterial walls. Lipid modification, therefore, is key to CHD prevention. METHODS: Data from trials evaluating the safety and efficacy of several pharmacologic agents for dyslipidemia were thoroughly reviewed. RESULTS: Agents such as bile acid sequestrants, fibric acids, and nicotinic acid have a role in treating dyslipidemia. However, statins are the safest and most effective of the lipid-modifying drugs, reducing the incidence of CHD by as much as 21% to 43%. Despite the overall safety and efficacy of these agents, many patients undergoing statin therapy fail to achieve the treatment goals specified in the National Cholesterol Education Program Adult Treatment Panel III guidelines, often because of suboptimal use, tolerability problems, or lack of compliance. Although adverse effects of statins are generally mild and transient, more serious adverse effects, including myotoxicity, liver toxicity, and rhabdomyolysis, are still possible with statin monotherapy and are more common in patients receiving concomitant therapy with other drugs metabolized by the cytochrome P-450 enzyme system. CONCLUSIONS: Because of the overall safety and efficacy of the statins, more patients with or at risk for CHD should be receiving aggressive therapy to lower low-density lipoprotein cholesterol levels and reduce CHD risk.

Atorvastatin↗
PubMed2002

Micronised fenofibrate: an updated review of its clinical efficacy in the management of dyslipidaemia.

Micronised fenofibrate is a synthetic phenoxy-isobutyric acid derivative (fibric acid derivative) indicated for the treatment of dyslipidaemia. Recently, a new tablet formulation of micronised fenofibrate has become available with greater bioavailability than the older capsule formulation. The micronised fenofibrate 160mg tablet is bioequivalent to the 200mg capsule. The lipid-modifying profile of micronised fenofibrate 160mg (tablet) or 200mg (capsule) once daily is characterised by a decrease in low-density lipoprotein cholesterol (LDL-C) and total cholesterol (TC) levels, a marked reduction in plasma triglyceride (TG) levels and an increase in high-density lipoprotein cholesterol (HDL-C) levels. Micronised fenofibrate 200mg (capsule) once daily produced greater improvements in TG and, generally, in HDL-C levels than the hydroxymethylglutaryl coenzyme A reductase inhibitors simvastatin 10 or 20 mg/day, pravastatin 20 mg/day or atorvastatin 10 or 40 mg/day. Combination therapy with micronised fenofibrate 200mg (capsule) once daily plus fluvastatin 20 or 40 mg/day or atorvastatin 40 mg/day was associated with greater reductions from baseline than micronised fenofibrate alone in TC and LDL-C levels. Similar or greater changes in HDL-C and TG levels were seen in combination therapy, compared with monotherapy, recipients. Micronised fenofibrate 200mg (capsule) once daily was associated with significantly greater improvements from baseline in TC, LDL-C, HDL-C and TG levels than placebo in patients with type 2 diabetes mellitus enrolled in the double-blind, randomised Diabetes Atherosclerosis Intervention Study (DAIS) [> or =3 years follow-up]. Moreover, angiography showed micronised fenofibrate was associated with significantly less progression of coronary atherosclerosis than placebo. Micronised fenofibrate has also shown efficacy in patients with metabolic syndrome, patients with HIV infection and protease inhibitor-induced hypertriglyceridaemia and patients with dyslipidaemia secondary to heart transplantation. Micronised fenofibrate was generally well tolerated in clinical trials. The results of a large (n = 9884) 12-week study indicated that gastrointestinal disorders are the most frequent adverse events associated with micronised fenofibrate therapy. Elevations in serum transaminase and creatine phosphokinase levels have been reported rarely with micronised fenofibrate. In conclusion, micronised fenofibrate improves lipid levels in patients with primary dyslipidaemia; the drug has particular efficacy with regards to reducing TG levels and raising HDL-C levels. Micronised fenofibrate is also effective in diabetic dyslipidaemia; as well as improving lipid levels, the drug reduced progression of coronary atherosclerosis in patients with type 2 diabetes mellitus. The results of large ongoing studies (e.g. FIELD with approximately 10 000 patients) will clarify whether the beneficial lipid-modifying effects of micronised fenofibrate result in a reduction in cardiovascular morbidity and mortality.

Cardiovascular Diseases↗
PubMed2006

Familial dyslipidaemias: an overview of genetics, pathophysiology and management.

Plasma lipid disorders can occur either as a primary event or secondary to an underlying disease or use of medications. Familial dyslipidaemias are traditionally classified according to the electrophoretic profile of lipoproteins. In more recent texts, this phenotypic classification has been replaced with an aetiological classification. Familial dyslipidaemias are generally grouped into disorders leading to hypercholesterolaemia, hypertriglyceridaemia, a combination of hyper-cholesterolaemia and hypertriglyceridaemia, or abnormal high-density lipoprotein-cholesterol (HDL-C) levels. The management of these disorders requires an understanding of plasma lipid and lipoprotein metabolism. Lipid transport and metabolism involves three general pathways: (i) the exogenous pathway, whereby chylomicrons are synthesised by the small intestine, and dietary triglycerides (TGs) and cholesterol are transported to various cells of the body; (ii) the endogenous pathway, whereby very low-density lipoprotein-cholesterol (VLDL-C) and TGs are synthesised by the liver for transport to various tissues; and (iii) the reverse cholesterol transport, whereby HDL cholesteryl ester is exchanged for TGs in low-density lipoptrotein (LDL) and VLDL particles through cholesteryl ester transfer protein in a series of steps to remove cholesterol from the peripheral tissues for delivery to the liver and steroidogenic organs. The plasma lipid profile can provide a framework to guide the selection of appropriate diet and drug treatment. Many patients with hyperlipoproteinaemia can be treated effectively with diet. However, dietary regimens are often insufficient to bring lipoprotein levels to within acceptable limits. In this article, we review lipid transport and metabolism, discuss the more common lipid disorders and suggest some management guidelines. The choice of a particular agent depends on the baseline lipid profile achieved after 6-12 weeks of intense lifestyle changes and possible use of dietry supplements such as stanols and plant sterols. If the predominant lipid abnormality is hypertriglyceridaemia, omega-3 fatty acids, a fibric acid derivative (fibrate) or nicotinic acid would be considered as the first choice of therapy. In subsequent follow-up, when LDL-C is >130 mg/dL (3.36 mmol/L) then an HMG-CoA reductase inhibitor (statin) should be added as a combination therapy. If the serum TG levels are <500 mg/dL (2.26 mmol/L) and the LDL-C values are over 130 mg/dL (3.36 mmol/L) then a statin would be the first drug of choice. The statin dose can be titrated up to achieve the therapeutic goal or, alternatively, ezetimibe can be added. A bile acid binding agent is an option if the serum TG levels do not exceed 200 mg/dL (5.65 mmol/L), otherwise a fibrate or nicotinic acid should be considered. The decision to treat a particular person has to be individualised.

Biological Transport↗
PubMed2000

Attenuating cardiovascular risk factors in patients with type 2 diabetes.

Patients with type 2 diabetes (formerly known as non-insulin-resistant diabetes) have a significantly increased risk of developing cardiovascular disease. Once clinical cardiovascular disease develops, these patients have a poorer prognosis than normoglycemic patients. By inducing endothelial changes, hyperglycemia contributes directly to atherosclerosis. Type 2 diabetes is also associated with atherogenic dyslipidemias. This form of diabetes, or the precursor state of insulin resistance, commonly occurs as a metabolic syndrome (formerly known as syndrome X) consisting of hypertension, atherogenic dyslipidemia and a procoagulant state, in addition to the disorder of glucose metabolism. All cardiovascular risk factors except smoking are more prevalent in patients with type 2 diabetes. In addition to exercise, weight control, aspirin therapy and blood pressure control, therapy to modify lipid profiles is usually necessary. The choice of agent or combination of statin, bile acid sequestrant, fibric acid derivative and nicotinic acid depends on the lipid profile and characteristics of the individual patient.

Anticholesteremic Agents↗
PubMed1994

Rational treatment for dyslipidemias.

High blood cholesterol is one of the three most common risk factors for cardiovascular disease. Several antihyperlipidemic agents are available to the prescriber; however, first line therapy is a diet low in cholesterol and saturated fats. The choice of therapy must be based on the type of abnormality present, concurrent disease states, side effect profiles, ease of use and cost. Several differences exist among the various dyslipidemic agents such as mechanism of action, effectiveness, pharmacokinetics, side effects, drug interactions and cost. For these reasons, this review focuses on the most commonly used dyslipidemic agents, e.g. the bile-acid sequestrants, nicotinic acid, fibric-acid derivatives and HMG-CoA reductase inhibitors.

Humans↗