October 1, 2000Arteriosclerosis Thrombosis and Vascular BiologyOpen Access

Replication of Linkage of Familial Combined Hyperlipidemia to Chromosome 1q With Additional Heterogeneous Effect of Apolipoprotein A-I/C-III/A-IV Locus

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Population

71 Familial combined hyperlipidemia families from the Family Heart Study, comprising 170 cases and 137…

Design

Other

Authors

HCHilary CoonUniversity of Utah RMRichard H. MyersBoston University IBIngrid B. BoreckiPennington Biomedical Research Center

Discussion

Member takes

Implication

Reinforces 1q as FCHL susceptibility locus; leaves open causal variant identification before any clinical translation.

Structured PICO

Population

71 Familial combined hyperlipidemia (FCHL) families from the Family Heart Study (FHS), comprising 170 cases and 137 possible affected sibling pairs. Diagnostic criteria required elevation in serum low density lipoprotein cholesterol and triglyceride levels within the family, with at least 2 affected first-degree relatives.

Intervention

Genotyping and linkage analysis of chromosome 1q markers (D1S104 and D1S1677), apolipoprotein A-I/C-III/A-IV marker (D11S4127), and markers near the lipoprotein lipase gene region.

Outcome

Genetic linkage (allele sharing) to chromosome 1q markers D1S104 and D1S1677.surrogate

This study replicates the genetic linkage of familial combined hyperlipidemia to chromosome 1q and suggests an additional heterogeneous effect of the apolipoprotein A-I/C-III/A-IV locus.

Cite This Study

Coon et al. (2000) studied this question.

synapsesocial.com/papers/6a793347e9a465269f0d9dca https://doi.org/10.1161/01.atv.20.10.2275

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