Hyperlipoproteinemia Medication

Drugs are used to lower cholesterol and triglyceride levels. Because of the possibility of adverse effects and the question of whether the triglyceride level is an independent risk factor for atherosclerosis, many physicians use drugs to reduce the triglyceride level only when the level exceeds 500 mg/100 mL.^{[3, 4, 5]}

Class Summary

These agents are competitive inhibitors of 3-hydroxy-3-methyl Co-A reductase, an enzyme that catalyzes the rate-limiting step in cholesterol biosynthesis, resulting in up-regulation of LDL receptors in response to the decrease in intracellular cholesterol. The HMG-CoA reductase inhibitors are indicated for the secondary prevention of cardiovascular events and for the treatment of hypercholesterolemia and mixed dyslipidemia.

A number of HMG-CoA reductase inhibitors are indicated for patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatments. However, these agents may be less effective in patients with rare homozygous familial hypercholesterolemia, possibly because these patients are lacking functional LDL receptors, making it more likely to raise serum transaminases.

Pravastatin (Pravachol)

Lipid-lowering compound; HMG-CoA reductase inhibitor; reduces cholesterol biosynthesis; orally administered in active form; rapidly absorbed (peak plasma 1-1.5 h). Therapeutic response is usually 1 wk. Highly effective in reducing total-C, LDL-C, and triglycerides in patients with heterozygous familial, presumed familiar forms of primary hypercholesterolemia, and mixed dyslipidemia.

Lovastatin (Mevacor, Altocor)

This is a cholesterol-lowering agent, isolated from a strain of Aspergillus terreus. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, which is an early and rate-limiting step in the biosynthesis of cholesterol. Available in immediate-release (Mevacor) and sustained-release (Altocor) dosage forms.

Simvastatin (Zocor)

Inhibits 3-hydroxy-3-methylglutaryl-coenzyme A reductase, an enzyme in an early and rate-limiting step in the synthetic pathway of cholesterol. Peak plasma 1.3-2.4 h; peak antilipemic effects 3-4 mo.

Rosuvastatin (Crestor)

HMG-CoA reductase inhibitor, which, in turn, decreases cholesterol synthesis and increases cholesterol metabolism. Reduces total-C, LDL-C, and TG levels and increases HDL-C level. Used adjunctively with diet and exercise to treat hypercholesterolemia.

Class Summary

Niacin (vitamin B-3) inhibits the hepatic secretion of VLDL cholesterol. Niacin is effective in most categories of hyperlipidemia. Niacin has been demonstrated to lower LDL cholesterol by 32%, lower triglycerides by 20-50%, and raise HDL cholesterol by 43%. Niacin lowers lipoprotein (a) levels, which may be of some clinical importance because lipoprotein (a) levels have been associated with coronary heart disease in numerous epidemiological studies. The clinical benefit of lowering lipoprotein (a) levels has not been determined.

Niacin (Nicobid, Niaspan, Nicotinex)

Niacin functions in the body after conversion to nicotinamide adenine dinucleotide (NAD) in the NAD coenzyme system. Niacin in gram doses reduces total cholesterol, LDL-C, and triglycerides and increases high-density lipoprotein cholesterol. The magnitude of individual lipid and lipoprotein responses may be influenced by the severity and type of underlying lipid abnormality. Niacin should be taken at bedtime after a low-fat snack and individualized according to patient response.