There are roughly two forms of this lipid disorder:
Familiar combined hyperlipidemia (FCH) is the familiar occurrence of this disorder, probably caused by polymorphisms in molecules and enzymes that participate in lipoprotein metabolism, such as ApoCII and ApoCIII and CETP (cholesterylester transferring protein).
Acquired combined hyperlipidemia is extremely common in patients who suffer from other diseases from the metabolic syndrome ("syndrome X", incorporating diabetes mellitus type II, hypertension, central obesity and CH). Excessive free fatty acid production by various tissues leads to increased VLDL synthesis by the liver. Initially, most VLDL is converted into LDL until this mechanism is saturated, after which VLDL levels elevate.
Both conditions are treated with fibrate drugs, which act on the peroxisome proliferator-activated receptors (PPARs), specifically PPARα, to decrease free fatty acid production. Statin drugs, especially the synthetic statins (atorvastatin and rosuvastatin) can decrease LDL levels by increasing hepatic reuptake of LDL due to increased LDL-receptor expression.
Familialcombinedhyperlipidemia is sometimes confused with familialhypercholesterolemia.
Familial defective apolipoprotein B (apo B) is a very uncommon condition caused by mutations in the gene for apo B (the protein moiety of LDL), rendering the protein poorly recognized or unrecognized by the LDL receptor.
Depending on the lipoprotein excess present, familialcombinedhyperlipidemia responds well to weight reduction and restriction of saturated fat and cholesterol, followed when necessary by niacin 3 g/day, a statin (see below), or a combination of cholestyramine with niacin or gemfibrozil.