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Effect of apolipoprotein E polymorphism and Xbal polymorphism of apolipoprotein B on response to lovastatin treatment in familial and non‐familial hypercholesterolaemia
Author(s) -
OJALA J.P.,
HELVE E.,
EHNHOLM C.,
AALTOSETÄLÄ K.,
KONTULA K. K.,
TIKKANEN M. J.
Publication year - 1991
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.1991.tb00464.x
Subject(s) - lovastatin , apolipoprotein b , medicine , genotype , endocrinology , apolipoprotein e , cholesterol , phenotype , hydroxymethylglutaryl coa reductase , biology , hmg coa reductase , genetics , biochemistry , gene , enzyme , disease , reductase
. Despite the well‐documented efficacy of lovastatin, a wide inter‐individual variation in treatment responses has been observed. The aim of the present study was to investigate the possible roles of apolipoprotein E (apo E) phenotype and apolipoprotein B (apo B) Xbal genotype on this variation. The apo E phenotype was determined in 232 subjects (78 cases of familial hypercholesterolaemia [FH] and 154 cases of non‐familial hypercholesterolaemia [non‐FH]) and the apo B Xbal genotype was determined in 211 subjects (67 cases of FH, 144 cases of non‐FH). Depending on their baseline total serum cholesterol levels, these patients used a starting dose of lovastatin of either 20 or 40 mg nightly. After 6 weeks of therapy, slightly but significantly smaller reductions in LDL‐cholesterol were observed in patients with the E4/3 phenotype compared with those with the E3/3 phenotype in non‐FH with lovastatin 20 mg (–20 vs. –28%; P = 0.043) and in total cholesterol in FH with lovastatin 40 mg (–23 vs. –27%; P = 0.023). No significant differences were found in non‐FH patients starting with lovastatin, 40 mg. After doubling of the lovastatin doses, all treatment responses became similar among apo E phenotypes. Moreover, when all patients using lovastatin 40 mg either at 6 or 12 weeks were pooled ( n = 224), no differences in treatment responses were observed between the E3/2, E3/3, E4/3 and E4/4 phenotypes. The apo B Xbal genotype did not affect the hypocholesterolaemic efficacy of lovastatin in any of the patient groups. Thus our results indicate that inter‐individual variation in the treatment response to lovastatin in both familial and non‐familial hypercholesterolaemia is mainly due to factors other than the apo E phenotype or apo B Xbal genotype.