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CETP Genes, Metabolic Effects, and Coronary Disease Risk
Peter W. F. Wilson, MD
JAMA. 2008;299(23):2795-2796.
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The burden of atherosclerotic coronary heart disease (CHD) is tremendous—both genes and environment contribute to this problem. From a clinical perspective, physicians are well aware of the importance of genetic lipid abnormalities in the causation of CHD.1 The best studied genetic lipid abnormality is familial hypercholesterolemia (FH), which can cause clinical findings such as xanthomas, early atherosclerosis, and premature CHD. Approximately 1 out of 500 of the population are FH heterozygotes and 1 out of 1 000 000 are homozgotes.2 It has been estimated that FH accounts for approximately 6% of CHD on a population basis.3
The availability of widespread gene testing in population studies has turned the tables, and now it is possible to investigate the role of gene variants that initially do not manifest with clinical signs and symptoms.4 For example, apolipoprotein E4 variants are common and affect more than 20% of the population, and . . . [Full Text of this Article]
Author Affiliation: Emory University School of Medicine, Atlanta VAMC Epidemiology and Genetics Section, Atlanta, Georgia.
RELATED ARTICLE
Association of Cholesteryl Ester Transfer Protein Genotypes With CETP Mass and Activity, Lipid Levels, and Coronary Risk
Alexander Thompson, Emanuele Di Angelantonio, Nadeem Sarwar, Sebhat Erqou, Danish Saleheen, Robin P. F. Dullaart, Bernard Keavney, Zheng Ye, and John Danesh
JAMA. 2008;299(23):2777-2788.
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