Key result
This editorial discusses a study determining the proportion of 1,430 children with a dyslipidemia phenotype who possessed mutations in the LDLR, APOB, and PCSK9 genes.
Answers are grounded in this paper and cite their sources.
I n this issue of Circulation, van der Graaf and colleagues 1 studied 1430 children, aged 4 to 18 years, who were referred to an academic pediatric lipid clinic in the Netherlands because of dyslipidemia from July 1989 to January 2008.The objective was to determine what proportion of those with the phenotype of autosomal dominant hypercholesterolemia (ADH) had mutations in the genes encoding the low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB), and proprotein convertase subtilisin/kexin 9.
No takes yet. Share an insight, caveat, or question.
Peter O. Kwiterovich (2011) conducted an editorial in Autosomal dominant hypercholesterolemia (ADH) and dyslipidemia (n=1,430). Mutations in LDLR, APOB, and PCSK9 genes was evaluated on Proportion of individuals with the ADH phenotype who had mutations in LDLR, APOB, and PCSK9 genes. This editorial discusses a study determining the proportion of 1,430 children with a dyslipidemia phenotype who possessed mutations in the LDLR, APOB, and PCSK9 genes.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: