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Letters to the Editor |
ínek4
kodova2
1 Centre for Experimental Medicine, and, 2
Department of Preventive Cardiology, Institute of Clinical, and Experimental Medicine, Prague, Czech Republic
3 Cardiovascular Research Centre, Prague, Czech Republic
4 3rd Department of Medicine, 1st School of Medicine, Charles University, Prague, Czech Republic
aAddress correspondence to this author at: IKEM-CEM-LMG, Videnska 1958/9, 140 21 Prague 4, Czech Republic. Fax 420-241-721-574; e-mail jahb@medicon.cz.
| The first 20% of the full text of this article appears below. |
To the Editor:
Schaefer et al. (1) recently reported an association between a distinct combination of variants in the apolipoprotein E (APOE) and APOAV genes and hypertriglyceridemia. Among 170 hypertriglyceridemic (HTG) patients, all carriers of APOE22 (n = 7) had at least 1 APOAV Trp19 allele, but this combination was not found in controls with triglyceride (TG) concentrations within the reference interval.
APOE is a structural component of TG-rich lipoproteins; it serves as a ligand for lipoprotein receptors and plays an important role in the catabolism of remnant particles (2)(3). Of the 3 common apoE isoforms, apoE4 (Cys112>Arg) and apoE2 (Arg158>Cys) differ from the commonest isoform, apoE3, by a single amino acid substitution. The APOE4 allele has been shown to be associated with increased plasma cholesterol and with an increased risk of coronary heart disease. In contrast, the APOE2 allele is associated with low plasma concentrations of cholesterol and is believed to be protective against coronary
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