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Papers In Press, published online ahead of print January 1, 2004
J. Lipid Res., doi:10.1194/jlr.M300278-JLR200
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Department of Cardiology, Kanazawa Medical University, Uchinada, Uchinada 920-0293
Corresponding Author: kajinami{at}kanazawa-med.ac.jp
The mechanisms responsible for interindividual variation in response to statin therapy remain uncertain. It has been shown that hepatic cholesterol synthesis is associated with ATP binding cassette transporter G5 and G8 (ABCG5/8) activities. To test the hypothesis that genetic variation in ABCG5/8 might influence the plasma lipid response to statin therapy, we examined 5 non–synonymous polymorphisms at the ABCG5/8 loci (Q604E, D19H, Y54C, T400K, and A632V) in 338 hypercholesterolemic patients treated with atorvastatin 10mg. In carriers of the D19H variant, means of post–treatment values and adjusted % reductions in LDL cholesterol were significantly lower (p=0.028) and greater (p=0.036) (112 mg/dl, 39.7%) than those of non–carriers (119 mg/dl, 36.2%), respectively, while no significant difference was observed in % reductions in total cholesterol. Stepwise multiple regression analysis revealed significant and independent associations between D19H genotype and post–treatment LDL cholesterol levels, and with its absolute or percent reduction. The other polymorphisms were not significantly associated with treatment effects. These results suggest that, in patients with hypercholesterolemia, the ABCG8 D19H variant is associated with greater LDL cholesterol-lowering response to atorvastatin therapy.
Revised on October 14, 2003
Accepted on December 23, 2003
ATP binding cassette transporter G5 And G8 genotypes and plasma lipoprotein levels before and after treatment with atorvastatin
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