Niacin is one of the oldest yet also most diverse lipid lowering agents. As it not only lowers low-density-lipoprotein (LDL) cholesterol, triglycerides (TG) and lipoprotein(a) [Lp(a)] but also increases high-density-lipoprotein (HDL) cholesterol, it is useful for treating a wide variety of lipid disorders including mixed hyperlipidaemia, hypertriglyceridaemia and isolated low HDL cholesterol, as well as elevated Lp(a). Niacin, which exists in several different formulations, such as immediate release (IR), extended release (ER) and slow release (SR) niacin, has several modes of action: it modulates liver TG synthesis, which leads to increased intracellular apolipoprotein (apo) B degradation and increases TG lipolysis in adipose tissue. Recently, a specific niacin receptor has also been discovered. Several clinical outcome trials have demonstrated that niacin reduces coronary artery disease risk in combination with statins and two large mortality trials are currently underway looking at hard end-point reduction with niacin and statin compared to statin alone. Niacin's major adverse event (AE) is flushing, and this prevents many patients from either taking it or reaching target doses of this drug. Flushing incidence and intensity is reduced with ER-niacin and by co-administration of aspirin and a selective or non-selective prostaglandin inhibitor.
Kostner K, Gupta S. Niacin: a lipid polypill? Expert Opin Pharmacother. 2008 November University of Queensland, Department of Cardiology, Mater Hospital, Raymond Terrace, South Brisbane 4101, Australia.