Low HDL Cholesterol (Hypoalphalipoproteinemia) Medication

  • Author: Vibhuti N Singh, MD, MPH, FACC, FSCAI; Chief Editor: George T Griffing, MD   more...
 
Updated: Dec 29, 2011
 

Medication Summary

Currently, clinical trial results suggest that raising high-density lipoprotein (HDL) levels reduces risk. However, the evidence does not support a recommendation of therapy for hypoalphalipoproteinemia (HA). Additionally, drugs available for cholesterol management do not raise HDL cholesterol levels as much as desired. However, physicians should pay reasonable attention to low HDL cholesterol levels and their management.

According to NCEP ATP III guidelines, the primary goal of therapy is to lower low-density lipoprotein (LDL) cholesterol levels.[2, 3, 4, 5] Once the LDL target has been reached, emphasize therapeutic lifestyle changes, such as weight management and increased exercise, especially if the patient has a metabolic syndrome.

If triglyceride (TG) levels are lower than 200 mg/dL (ie, isolated HA), drugs for raising HDL (eg, fibrates, nicotinic acid) can be considered. Statins have only a modest effect. Treatment for isolated low HDL cholesterol levels is reserved mostly for individuals with established coronary heart disease (CHD) and for patients with risk factors for CHD.

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Antilipemic agents

Class Summary

These medications usually lower low-density lipoprotein (LDL) cholesterol levels. In addition, they sometimes lower triglyceride (TG) levels and may modestly elevate high-density lipoprotein (HDL) cholesterol levels. Antilipemic agents may be of value to patients with hypoalphalipoproteinemia (HA).

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Niacin, nicotinic acid (Niacor, Nicobid, Nicolar, Niaspan)

 

Source of niacin used in tissue respiration, lipid metabolism, and glycogenolysis. Nicotinic acid has lipid-lowering properties, but nicotinamide and niacinamide do not.

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Gemfibrozil (Lopid)

 

Fibric acid antilipemic agent that effectively reduces serum TGs and favorably alters lipoprotein levels; the mechanism of action is unknown, but gemfibrozil may inhibit lipolysis, the secretion of VLDL, and hepatic fatty acid uptake.

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Fenofibrate (Tricor)

 

Fibric acid antilipemic agent that lowers LDL cholesterol more effectively than do older fibrates (ie, clofibrate, gemfibrozil). Fenofibrate is primarily indicated for TG reduction and for use in mixed dyslipidemia. This agent increases plasma catabolism and the clearance of TG-rich particles by lipoprotein lipase induction and the suppression of the hepatic production of apo C-III through the activation of PPARs. Fenofibrate activates acetyl-CoA and other enzymes, increasing fatty acid oxidation. TG production is also decreased via the inhibition of acetyl-CoA carboxylase and fatty acid synthase. Clinically, a marked reduction in plasma TGs and VLDL is observed, as is an increase in HDL cholesterol levels.

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HMG-CoA reductase inhibitors

Class Summary

Statins are used to lower LDL cholesterol, but they also modestly raise HDL cholesterol.

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Atorvastatin (Lipitor)

 

Selective competitive inhibition of HMG-CoA reductase decreases cholesterol synthesis and increases cholesterol metabolism. Atorvastatin may modestly elevate HDL cholesterol levels. Clinically, reduced levels of circulating total cholesterol, LDL cholesterol, and serum TGs are observed.

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Simvastatin (Zocor)

 

Inhibits HMG-CoA reductase, which, in turn, inhibits cholesterol synthesis and increases cholesterol metabolism.

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Pravastatin (Pravachol)

 

Competitively inhibits HMG-CoA reductase, which catalyzes the rate-limiting step in cholesterol synthesis. Before initiating therapy, place patients on a cholesterol-lowering diet for 3-6 mo, and continue the diet indefinitely.

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Lovastatin (Mevacor)

 

Competitively inhibits HMG-CoA reductase, which catalyzes the rate-limiting step in cholesterol synthesis. Before initiating therapy, place patients on a cholesterol-lowering diet for 3-6 mo, and continue the diet indefinitely.

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Fluvastatin (Lescol)

 

Synthetically prepared HMG-CoA reductase inhibitor with some similarities to lovastatin, simvastatin, and pravastatin. However, fluvastatin is structurally distinct and has a different biopharmaceutical profile (eg, no active metabolites, extensive protein binding, minimal CSF penetration).

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Rosuvastatin (Crestor)

 

Competitively inhibits HMG-CoA reductase, which catalyzes the rate-limiting step in cholesterol synthesis.

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Pitavastatin (Livalo)

 

HMG-CoA reductase inhibitor (statin) indicated for primary or mixed hyperlipidemia. In clinical trials, 2 mg/d reduced total cholesterol and LDL cholesterol similar to atorvastatin 10 mg/d and simvastatin 20 mg/d.

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Contributor Information and Disclosures
Author

Vibhuti N Singh, MD, MPH, FACC, FSCAI  Director, Suncoast Cardiovascular Center; Chair, Cardiology Division and Cath Labs, Department of Medicine, Bayfront Medical Center; Clinical Assistant Professor, Division of Cardiology, University of South Florida College of Medicine

Vibhuti N Singh, MD, MPH, FACC, FSCAI is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Florida Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Elena Citkowitz, MD, PhD, FACP  Clinical Professor of Medicine, Yale University School of Medicine; Director, Cholesterol Management Center, Director, Cardiac Rehabilitation, Department of Medicine, Hospital of St Raphael

Elena Citkowitz, MD, PhD, FACP is a member of the following medical societies: American College of Physicians, American Heart Association, National Lipid Association, and Sigma Xi

Disclosure: Nothing to disclose.

Specialty Editor Board

Ghassem Pourmotabbed, MD†  Former Associate Professor, Department of Internal Medicine, Division of Endocrinology and Metabolism, University of Tennessee School of Medicine and Health Science Center

Ghassem Pourmotabbed, MD† is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, and Endocrine Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Yoram Shenker, MD  Chief of Endocrinology Section, Veterans Affairs Medical Center of Madison; Interim Chief, Associate Professor, Department of Internal Medicine, Section of Endocrinology, Diabetes and Metabolism, University of Wisconsin at Madison

Yoram Shenker, MD is a member of the following medical societies: American Heart Association, Central Society for Clinical Research, and Endocrine Society

Disclosure: Nothing to disclose.

Mark Cooper, MBBS, PhD, FRACP  Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD  Professor of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

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Table. Hypoalphalipoproteinemia
VariantMolecular DefectInheritanceMetabolic DefectLipoprotein AbnormalityClinical FeaturesPremature Atherosclerosis
Familial apo A-IApo deficiencyAutosomal codominantAbsent apo A-1 biosynthesisHDL < 5 mg/dL; TGs normalPlanar xanthomas, corneal opacitiesYes
Familial apo A-I structural mutationsAbnormal apo A-IAutosomal dominantRapid apo A-1 catabolismHDL 15-30 mg/dL; TGs increasedOften none; sometimes corneal opacitiesNo
Familial LCATLCAT deficiency (complete)Autosomal



recessive



Rapid HDL catabolismHDL < 10 mg/dL; TGs increasedCorneal opacities, anemia, proteinuria, renal insufficiencyNo
Fish-eye diseaseLCAT deficiency (partial)Autosomal recessiveRapid HDL catabolismHDL < 10 mg/dL; TGs increasedCorneal opacitiesNo
Tangier diseaseUnknownAutosomal codominantVery rapid HDL catabolismHDL < 5 mg/dL; TGs usually increasedCorneal opacities, enlarged orange tonsils, hepatosplenomegaly, peripheral neuropathyNo to yes
Familial HAUnknownAutosomal dominantUsually rapid HDL catabolismHDL 15-35 mg/dL; TGs normalOften none; sometimes corneal opacitiesNo to yes
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