Of the remaining 38 children, 23 had non-hereditary abnormalities of low (LDL) or high density lipoprotein (HDL) cholesterol or apolipoprotein B. Fifteen children were suspected to have genetically determined dyslipidemias or a combination of risk factors: in four, possible familial hypercholesterolaemia (FH); in five, possible familial combined hyperlipidaemia; in three, hereditary low HDL cholesterol; and in three a combination of high LDL cholesterol and Lp(a) lipoprotein concentrations.
The association between angiotensin-converting enzyme (ACE) as well as apolipoprotein B polymorphisms and dyslipidemia and coronary artery disease (CAD) is controversial.
Hammerhead ribozyme as a therapeutic agent for hyperlipidemia: production of truncated apolipoprotein B and hypolipidemic effects in a dyslipidemia murine model.