Low HDL Cholesterol (Hypoalphalipoproteinemia) Medication

Updated: Nov 03, 2016
  • Author: Vibhuti N Singh, MD, MPH, FACC, FSCAI; Chief Editor: George T Griffing, MD  more...
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Medication

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. [3, 4, 5, 6] 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).

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.

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.

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.

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.

Simvastatin (Zocor)

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

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.

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.

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).

Rosuvastatin (Crestor)

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

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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