title: Effects of niacin on glucose control in patients with dyslipidemia.
abstract: Niacin (nicotinic acid), the most effective available pharmacotherapy for increasing high-density lipoprotein cholesterol, also lowers triglycerides and hence may be useful, alone or in combination with hydroxymethylglutaryl coenzyme A reductase inhibitors (statins), to offset residual cardiovascular risk in patients with mixed or diabetic dyslipidemia. We conducted a review of published consensus guidelines since 2000 and an English-language PubMed search of prospective, randomized controlled trials and open-label studies from January 1, 1990, through December 31, 2007, concerning the effects of niacin, alone or in combination with statins, on glycemic regulation in dyslipidemic patients (with or without diabetes mellitus). For search terms, we used the title words niacin or nicotinic acid and key words including diabetes, diabetic, dyslipidemia, glucose, glycemic, HbA1c, hemoglobin, hyperglycemia, human, insulin, postprandial, and safety. Retrospective and observational studies, case reports, and case studies were excluded. On the basis of our analysis, the effects of niacin (< or =2.5 g/d), alone or in combination with statins, on fasting glucose (an increase of 4%-5%) and hemoglobin A1c levels (an increase of < or =0.3%) are modest, transient or reversible, and typically amenable to adjustments in oral hypoglycemic regimens without discontinuing niacin. Niacin therapy was infrequently associated with incident diabetes or the need for new insulin prescriptions. Studies showed important clinical benefits of niacin or niacin-statin regimens despite modest effects on glucose control. On a population basis, significant reductions in incidences of cardiovascular events and the degree of atherosclerotic progression associated with long-term niacin (or niacin-statin) therapy in patients with diabetic dyslipidemia outweigh the typically mild effects of this therapy on glycemic regulation. Consensus guidelines recommend monitoring glycemic control after initiating niacin treatment or increasing its dosage.
authors.affiliation: Lipid Disorders Clinic, Division of Endocrinology, Diabetes, and Metabolism, University of Miami Leonard M. Miller School of Medicine, 1450 NW 10th Ave, Miami, FL 33136, USA. rgoldber@med.miami.edu
authors.forename: Ronald B
authors.initials: RB
authors.lastname: Goldberg
authors.forename: Terry A
authors.initials: TA
authors.lastname: Jacobson
mesh_terms: D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism*; D050171:Dyslipidemias / Q000097:blood / Q000188:drug therapy*; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D008055:Lipids / Q000097:blood; D009525:Niacin / Q000627:therapeutic use*; D017410:Practice Guidelines as Topic; D011379:Prognosis
chemical_list: D001786:Blood Glucose; D000960:Hypolipidemic Agents; D008055:Lipids; D009525:Niacin