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Author Notes:

Address reprint requests and correspondence to Terry A. Jacobson, MD, Director, Office of Health Promotion and Disease Prevention, Department of Medicine, Emory University, Faculty Office Building, 49 Jessie Hill Jr Dr SE, Atlanta, GA 30303 (tjaco02@emory.edu).

Research support was provided by Abbott Laboratories (Abbott Park, IL). Dr Jacobson did not receive compensation from Abbott.

Dr Jacobson has served as a consultant for Abbott, AstraZeneca, GlaxoSmithKline, Merck, Merck/Schering-Plough, Pfizer, and Schering-Plough.


A "Hot" Topic in Dyslipidemia Management--"How to Beat a Flush": Optimizing Niacin Tolerability to Promote Long-term Treatment Adherence and Coronary Disease Prevention


Journal Title:

Mayo Clinic Proceedings


Volume 85, Number 4


, Pages 365-379

Type of Work:

Article | Post-print: After Peer Review


Niacin is the most effective lipid-modifying agent for raising high-density lipoprotein cholesterol levels, but it also causes cutaneous vasodilation with flushing. To determine the frequency of flushing in clinical trials, as well as to delineate counseling and treatment approaches to prevent or manage flushing, a MEDLINE search was conducted of English-language literature from January 1, 1985, through April 7, 2009. This search used the title keywords niacin or nicotinic acid crossed with the Medical Subject Headings adverse effects and human. Niacin flushing is a receptor-mediated, mainly prostaglandin D2–driven phenomenon, the frequency, onset, and duration of which are largely determined by the distinct pharmacological and metabolic profiles of different niacin formulations. Subjective assessments include ratings of redness, warmth, itching, and tingling. In clinical trials, most (>60%) niacin users experienced mild or moderate flushing, which tended to decrease in frequency and severity with continued niacin treatment, even with advancing doses. Approximately 5% to 20% of patients discontinued treatment because of flushing. Flushing may be minimized by taking niacin with meals (or at bedtime with a low-fat snack), avoiding exacerbating factors (alcohol or hot beverages), and taking 325 mg of aspirin 30 minutes before niacin dosing. The current review advocates an initially slow niacin dose escalation from 0.5 to 1.0 g/d during 8 weeks and then from 1.0 to 2.0 g in a single titration step (if tolerated). Through effective counseling, treatment prophylaxis with aspirin, and careful dose escalation, adherence to niacin treatment can be improved significantly. Wider implementation of these measures should enable higher proportions of patients to reach sufficient niacin doses over time to prevent cardiovascular events.

Copyright information:

© 2010 Mayo Foundation for Medical Education and Research

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