Clinical implications of the molecular basis of familial hypercholesterolemia and other inherited dyslipidemias.

In this issue of Circulation, van der Graaf and colleagues1 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.