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September 15, 2004

Genetic Polymorphisms and Statin Therapy

Author Affiliations

Letters Section Editor: Robert M. Golub, MD, Senior Editor.

JAMA. 2004;292(11):1302-1303. doi:10.1001/jama.292.11.1302-b

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.