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

Am J Cardiol. 2000 Dec 21;86(12A):35L-40L. doi: 10.1016/s0002-9149(00)01468-5.


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.

MeSH terms

  • Biological Availability
  • Cholesterol / biosynthesis*
  • Cholesterol, HDL / blood*
  • Colestipol* / pharmacology
  • Drug Interactions
  • Humans
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / metabolism
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacokinetics
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology*
  • Hypolipidemic Agents* / pharmacology
  • Liver / drug effects*
  • Liver / metabolism
  • Niacin / metabolism
  • Niacin / pharmacokinetics
  • Niacin / pharmacology*


  • Cholesterol, HDL
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors
  • Hypolipidemic Agents
  • Niacin
  • Cholesterol
  • Colestipol