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Microsomal enzyme inducers raise plasma high‐density lipoprotein cholesterol levels in healthy control subjects but not in patients with primary hypoalphalipoproteinemia
Author(s) -
Franceschini Guido,
Werba José P.,
D'Acquarica Antonio L.,
Gianfranceschi Gemma,
Michelagnoli Silvia,
R. Sirtori Cesare
Publication year - 1995
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1016/0009-9236(95)90213-9
Subject(s) - cholesterylester transfer protein , medicine , endocrinology , apolipoprotein b , cholesterol , chemistry , high density lipoprotein , lipoprotein , reverse cholesterol transport , microsome , cholesteryl ester , inducer , enzyme , biochemistry , gene
In this study we compared the ability of phenytoin, a microsomal enzyme inducer, to raise plasma high‐density lipoprotein (HDL) levels in normolipidemic subjects and patients with primary hypoalphalipoproteinemia. In healthy control subjects, phenytoin caused a dose‐dependent increase of plasma HDL, HDL 2 , and HDL 3 cholesterol levels, up to 40% to 50%. Minor changes were recorded in the plasma concentrations of apolipoprotein (apo) A‐I and apo A‐II; the plasma level of the cholesteryl ester transfer protein (CETP) decreased by 42%. In contrast, none of the patients with hypoalphalipoproteinemia had changes in plasma HDL, HDL 2 , or HDL 3 cholesterol, apo A‐I, apo A‐II, or CETP levels. These findings indicate that microsomal enzyme inducers are unsuitable to increase plasma HDL levels in high‐risk patients with primary hypoalphalipoproteinemia, and they disclose a new mechanism, that is, decreased CETP‐mediated transfer of cholesterol out of HDL, for the HDL‐raising effect of microsomal enzyme inducers in healthy individuals. Clinical Pharmacology & Therapeutics (1995) 57 , 434–440; doi: