In summary, the occurrence of a pattern of multiple lipoprotein phenotypes within single families has been well documented. Although in some families, this pattern could represent the random occurrence of different forms of hyperlipidemia among different family members, the consensus was that in many families there is a common metabolic defect. There was a consensus amongst participants that this common defect is characterized by an overproduction of lipoproteins containing apo B. This overproduction can be manifested as increased plasma levels of VLDL, IDL, LDL, or apo B alone. While the best therapeutic regime is not known for certain, several possible approaches that can correct the abnormalities in plasma lipoprotein levels are available. Most participants agreed that nicotinic acid is the drug of choice with or without bile acid sequestrants, but difficulty with nicotinic acid by some patients prevents its use. Some participants believed that bile acid sequestrants alone or in combination with fibric acids or mevinolin can have a role in treatment of the specific forms of hyperlipidemia often present in this condition. In the absence of a primary prevention trial for FCHL, it seems likely that the best therapeutic approach will remain uncertain. Nonetheless, at the very least, an attempt to lower the elevated levels of LDL cholesterol and total apo B in FCHL seems justified.
|Original language||English (US)|
|Number of pages||5|
|State||Published - Jan 1 1987|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine