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A promoter polymorphism in cholesterol 7alpha-hydroxylase interacts with apolipoprotein E genotype in the LDL-lowering response to atorvastatin. | LitMetric

AI Article Synopsis

  • Bile-acid biosynthesis affects cholesterol levels in liver cells, suggesting that variations in the CYP7A1 gene may impact how patients respond to the cholesterol-lowering drug atorvastatin.* -
  • A study involving 324 patients found that those with the C allele of the CYP7A1 A-204C variant had poorer reductions in LDL cholesterol levels, with more pronounced effects in men.* -
  • The presence of the CYP7A1 variant combined with certain alleles of the APOE gene led to even lower cholesterol reductions, highlighting the importance of considering both genetic factors for predicting statin response.*

Article Abstract

Bile-acid biosynthesis is a key determinant of intracellular cholesterol and, in turn, cholesterol synthesis rate in hepatocytes. This suggests that variation in the cholesterol 7alpha-hydroxylase gene (CYP7A1), a key enzyme in bile-acid biosynthesis, may influence the statin response. To test this hypothesis, a promoter polymorphism (A-204C) in CYP7A1 was examined in 324 hypercholesterolemic patients treated with atorvastatin 10mg. The variant C allele was significantly and independently associated with poor LDL cholesterol reductions; -39% in wild type allele homozygotes, -37% in variant allele heterozygotes, and -34% in variant allele homozygotes (p<0.0001 for trend). Differences were more striking in men, and were enhanced by the coexistence of common variants of apolipoprotein E gene (APOE), epsilon2 or epsilon4. In subjects having wild type alleles at both loci, the mean reduction in LDL cholesterol was -40%, while the value in subjects having two CYP7A1 variant alleles and at least one variant APOE allele was -31% (p<0.0001). Combination analysis of these two loci more accurately predicted the achievement of goal LDL cholesterol, than did both single locus analysis. We concluded that the CYP7A1 A-204C promoter variant was associated with poor response to atorvastatin, which were additively enhanced by common variants in another locus, APOE.

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Source
http://dx.doi.org/10.1016/j.atherosclerosis.2004.12.019DOI Listing

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