Acquired and genetic forms of hyperlipidaemia can occur as a result of disturbances at four main sites in the endogenous pathway: increased input of VLDL and impaired LPL-mediated triglyceride removal can cause hypertriglyceridaemia; impaired remnant removal results in a combined elevation of cholesterol and triglyceride levels of approximately equal extent; and accumulation of LDL due to impaired LDL receptor-mediated clearance leads to hypercholesterolaemia.
