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To the Editor: Dr Chasman and colleagues¹ recently reported the impact of genetic polymorphisms on variability in response to pravastatin using a candidate gene approach. While these findings are of considerable interest, their impact may be limited from a public policy perspective. For example, while AT heterozygotes at single-nucleotide polymorphism 12 (3-hydroxy-3-methylglutaryl-coenzyme A [HMG-CoA] reductase gene) had an attenuated response to pravastatin in lowering low-density lipoprotein (LDL) cholesterol, variant carriers represented only 6.7% of the population. Whether it is cost-effective to genotype 15 patients initiated on statin therapy to identify 1 patient who will have an attenuated LDL cholesterol response must be decided from a societal perspective. The fact that even those with an attenuated response had a 28-mg/dL (0.73-mmol/L) reduction in LDL cholesterol further challenges the usefulness of genotype-guided therapy in this scenario.

Pharmacogenomics of lipid-lowering therapy is further complicated in that the appropriate response phenotype is unclear. For . . . [Full Text of this Article]

Issam Zineh, PharmD
zineh@cop.ufl.edu
College of Pharmacy
Center for Pharmacogenomics
University of Florida
Gainesville

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Pharmacogenetic Study of Statin Therapy and Cholesterol Reduction
Daniel I. Chasman, David Posada, Lakshman Subrahmanyan, Nancy R. Cook, Vincent P. Stanton, Jr, and Paul M Ridker
JAMA. 2004;291(23):2821-2827.
ABSTRACT | FULL TEXT