title: Pleiotropic effects of nicotinic acid: beyond high density lipoprotein cholesterol elevation.
abstract: OBJECTIVE
  Treatment with statins has significantly reduced cardiovascular morbidity and mortality, an effect attributed to both the low-density lipoprotein cholesterol (LDL-C) lowering capacity and the pleiotropic actions of these drugs. However, residual risk remains even after intense LDL-C lowering. Therefore, additional treatment with lipid-lowering drugs which improve other lipid parameters and have favourable non-lipid effects may be of clinical value. The aim of the present article is to review the actions of nicotinic acid and comment on the limitations and possible benefits of this drug in clinical practice.
  
  
  METHODS
  Relevant articles were identified through a Pubmed search up to July 2010.
  
  
  RESULTS
  Nicotinic acid (niacin) improves the lipid profile and has been associated with reduction in morbidity and mortality from cardiovascular disease. This favourable outcome may be due to several beneficial actions of this drug, such as antithrombotic, anti-inflammatory and antioxidant. However, its use has been limited due to side effects, especially flushing. A novel formulation with a prostaglandin D2 receptor antagonist (laropiprant) appears to substantially decrease the frequency and intensity of flushing, without affecting the other properties of niacin. Some concerns regarding treatment with nicotinic acid include impaired glucose metabolism and elevations in uric acid and homocysteine levels.
  
  
  CONCLUSIONS
  Nicotinic acid is a safe supplementary (to statins) lipid lowering agent which may also improve cardiovascular outcomes. Whether its combination with laropiprant will be proved equally effective and more favourable in terms of adverse effects remains to be established by large clinical trials.
authors.affiliation: Department of Clinical Biochemistry (Vascular Disease Prevention Clinics), Royal Free Campus, University College London Medical School, University College London (UCL), UK.
authors.forename: Matilda
authors.initials: M
authors.lastname: Florentin
authors.forename: Evangelos N
authors.initials: EN
authors.lastname: Liberopoulos
authors.forename: Anastazia
authors.initials: A
authors.lastname: Kei
authors.forename: Dimitri P
authors.initials: DP
authors.lastname: Mikhailidis
authors.forename: Moses S
authors.initials: MS
authors.lastname: Elisaf
mesh_terms: D000818:Animals; D008076:Cholesterol, HDL / Q000097:blood / Q000187:drug effects*; D004359:Drug Therapy, Combination; D005483:Flushing / Q000139:chemically induced / Q000517:prevention & control; D005947:Glucose / Q000378:metabolism; D006710:Homocysteine / Q000378:metabolism; D006801:Humans; D000960:Hypolipidemic Agents / Q000009:adverse effects / Q000494:pharmacology*; D007211:Indoles / Q000008:administration & dosage / Q000494:pharmacology; D009525:Niacin / Q000009:adverse effects / Q000494:pharmacology*; D011971:Receptors, Immunologic / Q000037:antagonists & inhibitors; D011982:Receptors, Prostaglandin / Q000037:antagonists & inhibitors; D014527:Uric Acid / Q000378:metabolism
chemical_list: D008076:Cholesterol, HDL; D000960:Hypolipidemic Agents; D007211:Indoles; C518174:MK-0524; D011971:Receptors, Immunologic; D011982:Receptors, Prostaglandin; D006710:Homocysteine; D009525:Niacin; D014527:Uric Acid; D005947:Glucose; C036293:prostaglandin D2 receptor