Open AccessLipid‐lowering response of the HMG‐CoA reductase inhibitor fluvastatin is influenced by polymorphisms in the low‐density lipoprotein receptor gene in Brazilian patients with primary hypercholesterolemia
Author(s) -
Salazar Luis A.,
Hirata Mario H.,
Quintão Éder C.R.,
Hirata Rosario D.C.
Publication year - 2000
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/(sici)1098-2825(2000)14:3<125::aid-jcla7>3.0.co;2-s
Subject(s) - fluvastatin , familial hypercholesterolemia , medicine , endocrinology , ldl receptor , hmg coa reductase , apolipoprotein b , hydroxymethylglutaryl coa reductase , genotype , reductase , cholesterol , biology , lipoprotein , genetics , simvastatin , gene , biochemistry , enzyme
Although the efficacy of fluvastatin (HMG‐CoA reductase inhibitor) in the treatment of primary hypercholesterolemia is well documented, a wide interindividual variation treatment response has been observed. We have studied the possible role of the Ava II (exon 13), Hinc II (exon 12), and Pvu II (intron 15) polymorphisms at the low‐density lipoprotein receptor (LDLR) gene on lipid‐lowering response in 55 patients (36 to 70 years old) with primary hypercholesterolemia treated with fluvastatin for 16 weeks. LDLR genotypes were determined by PCR‐RFLP. The results indicate that the Ava II and Pvu II polymorphisms influence the cholesterol‐lowering response of the HMG‐CoA reductase inhibitor Fluvastatin. Patients carrying A+A+ ( Ava II) or P1P1 ( Pvu II) homozygous genotypes presented lower reduction in total cholesterol, LDL‐C and apolipoprotein B levels after 16 weeks of treatment with fluvastatin, when compared to other genotypes ( P <0.05). Our data also support the previous assumption that the Ava II, Hinc II, and Pvu II polymorphisms of the LDLR gene are associated with variation of serum cholesterol levels. Therefore, the identification of the LDLR genetic profile may provide better prediction of a patient's clinical response to fluvastatin. J. Clin. Lab. Anal. 14:125–131, 2000. © 2000 Wiley‐Liss, Inc.