This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Brouwers, M. C.G.J. Articles by Cantor, R. M. Search for Related Content PubMed PubMed Citation Articles by Brouwers, M. C.G.J. Articles by Cantor, R. M.

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:e118.)
© 2006 American Heart Association, Inc.

Letters to the Editor

Longitudinal Differences in Familial Combined Hyperlipidemia Quantitative Trait Loci

Martijn C.G.J. Brouwers

Department of Medicine and Cardiovascular Research Institute Maastricht, Academic Hospital Maastricht, The Netherlands

Naoko Kono

Department of Human Genetics, David Geffen School of Medicine at UCLA, Los Angeles, Calif

Marleen M.J. van Greevenbroek

Department of Medicine and Cardiovascular Research Institute Maastricht, Academic Hospital Maastricht, The Netherlands

Carla J.H. van der Kallen

Department of Medicine and Cardiovascular Research Institute Maastricht, Academic Hospital Maastricht, The Netherlands

Aldons J. Lusis

Departments of Human Genetics and Medicine, David Geffen School of Medicine at UCLA, Los Angeles, Calif

Tjerk W.A. de Bruin

GlaxoSmithKline, Translational Medicine and Genetics, Research Triangle Park, North Carolina

Rita M. Cantor

Departments of Human Genetics and Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, Calif

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

Familial combined hyperlipidemia (FCHL), associated with premature cardiovascular disease, is the most common genetic hyperlipidemia with an estimated prevalence of 1%.¹ The complex genetic background of FCHL is slowly being dissected through genome screens and positional candidate association studies.^2–6 However, it has also been argued that although numerous studies have been conducted and reported, there are many conflicting results and a true understanding of the genetics remains largely unknown.⁷ Previously in this journal, we reported 4 quantitative trait loci (QTL) for apolipoprotein B (apoB), cholesterol, and triglycerides with P<0.001 in 22 FCHL pedigrees from Maastricht, in The Netherlands.⁸ The original QTL study was based on the premise that because FCHL is defined by increased serum levels of cholesterol, apoB, and triglycerides in families, QTL analyses of these quantitative traits in FCHL families might identify important genetic loci for this disorder. This letter reports QTL analyses of 5-year follow-up data in the same individuals.

Longitudinal studies show that the lipid phenotype within individual FCHL patients changes over time.^9,10 This expected intraindividual variability in cholesterol, triglyceride, and apoB levels may also change the heritabilities of these traits, thus affecting the locations and levels of significance of the reported QTL. However, one might expect that true QTL that are not false-positives would exhibit consistent chromosome locations, although the levels of significance might vary somewhat. To assess the impact of longitudinal lipid variability on our previous QTL, we recruited all of the Maastricht FCHL family members who participated in the . . . [Full Text of this Article]

This article has been cited by other articles:

				M. C. G. J. Brouwers, R. M. Cantor, N. Kono, J. l. Yoon, C. J. H. van der Kallen, M. A. L. Bilderbeek-Beckers, M. M. J. van Greevenbroek, A. J. Lusis, and T. W. A. de Bruin Heritability and genetic loci of fatty liver in familial combined hyperlipidemia J. Lipid Res., December 1, 2006; 47(12): 2799 - 2807. [Abstract] [Full Text] [PDF]