Pharmacogenomics of Lipid-Lowering Therapies

Abstract

Statins are the most widely used group of lipid-lowering drugs and they have been shown to be effective in the prevention of cardiovascular disease, primarily by reducing plasma low-density lipoprotein cholesterol concentrations and possibly through other pleiotropic effects. However, there are large variations in lipid responses to statins and some patients have intolerable muscle adverse drug reactions, which may in part be related to genetic factors. In the last decade, pharmacogenetic studies on statins ranging from the candidate gene approach to the more recent genome-wide association studies have provided evidence that genetic variations play an important role in determining statin responses. This review summarizes the current understanding on the pharmacogenomics of statins and other lipid-lowering drugs in current use.

KEYWORDS::

• cardiovascular disease
• fibrates
• genetic polymorphisms
• low-density lipoprotein cholesterol
• pharmacogenomics
• statins

Disclaimer

This work is that of the authors and does not represent the opinions of the mentioned funding bodies.

Financial & competing interests disclosure

B Tomlinson has received research funding to perform clinical studies from Abbott Laboratories Ltd, AstraZeneca, Bristol-Myers Squibb, GlaxoSmithKline, Merck Serono, Merck Sharp and Dohme, Novartis, Roche and Takeda, and has acted as a consultant or speaker on occasions for Amgen, AstraZeneca, Boehringer Ingelheim, Genzyme, Janssen, Merck Serono, Merck Sharp and Dohme, Ranbaxy and Servier. The work described in this paper was partly supported by grants from the Research Grants Council (Project no. CUHK 4472/06M) and the Food and Health Bureau (Project no. HHSRF 09100321) of the Hong Kong Special Administrative Region, China. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

B Tomlinson has received research funding to perform clinical studies from Abbott Laboratories Ltd, AstraZeneca, Bristol-Myers Squibb, GlaxoSmithKline, Merck Serono, Merck Sharp and Dohme, Novartis, Roche and Takeda, and has acted as a consultant or speaker on occasions for Amgen, AstraZeneca, Boehringer Ingelheim, Genzyme, Janssen, Merck Serono, Merck Sharp and Dohme, Ranbaxy and Servier. The work described in this paper was partly supported by grants from the Research Grants Council (Project no. CUHK 4472/06M) and the Food and Health Bureau (Project no. HHSRF 09100321) of the Hong Kong Special Administrative Region, China. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.