Treatment of primary hypertriglyceridemia states - General approach and the role of extracorporeal methods

Triglycerides (TG) are mainly carried in plasma in two forms: TG-rich very low density lipoproteins (VLDL) and chylomicrons (CM). Consequently primary Hypertriglyceridemia (HTG) results from increased concentration of either or both of these lipoprotein classes. The commonest form of primary HTG involves endogenous TG, not directly derived from dietary fats. This form is described as type IV in the Fredrickson/WHO classification [1, 2]. On the other side, Hyperchylomicronemia (HCM, type I), a rare disease, is genetically, clinically and biochemically distinct. The excess TG in plasma is partly of exogenous origin but it is related to a deficiency of lipoprotein lipase (LPL) and / or its cofactor apolipoprotein CII (apoCII). In some patients with HTG an excess of both VLDL and CM is demonstrable. This is consistent with the type V pattern. When CMs are elevated in plasma, independently of the phenotype considered, biochemical and genetic disorders appear to be closely linked. Although HTG may be itself expression of a genetic disorder: Familial Hypertriglyceridemia.