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. 2000 Apr 19;14(3):125–131. doi: 10.1002/(SICI)1098-2825(2000)14:3<125::AID-JCLA7>3.0.CO;2-S

Lipid‐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

Luis A Salazar 1,✉, Mario H Hirata 1, Éder CR Quintão 2, Rosario DC Hirata 1
PMCID: PMC6807834  PMID: 10797611

Abstract

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 AvaII (exon 13), HincII (exon 12), and PvuII (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 AvaII and PvuII polymorphisms influence the cholesterol‐lowering response of the HMG‐CoA reductase inhibitor Fluvastatin. Patients carrying A+A+ (AvaII) or P1P1 (PvuII) 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 AvaII, HincII, and PvuII 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.

Keywords: low‐density lipoprotein receptor gene, genetic polymorphisms, primary hypercholesterolemia, fluvastatin, treatment response

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