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Multiple evidence shows that nicotinic acid can prevent myocardial infarction.1 The mechanisms underlying the antiatherogenic effects of nicotinic acid have been disputed during the past decades, and there is evidence for beneficial effects on plasma lipid levels, as well as for anti-inflammatory effects.1–4 Nicotinic acid has been suggested as an add-on therapy to the well-established statins for prevention of cardiovascular disease. However, recent clinical data indicate no additional benefit of nicotinic acid treatment in high-risk patients under optimal statin therapy,5,6 and it is currently only recommended in patients in whom statins cannot be given or do not lead to sufficient changes in plasma lipid levels. The most important unwanted effect of nicotinic acid is a transient skin irritation called flushing.7,8 Although harmless, it causes many patients to discontinue nicotinic acid therapy. Flushing has a vascular component consisting of a cutaneous vasodilation resulting in a reddening and warming of the skin. This is accompanied by a sensory component that includes tingling and burning sensations in the skin. Past research has shown that, in particular, the vascular component of flushing is mediated by the hydroxycarboxylic acid receptor 2 (HCA2), also known as G-protein–coupled receptor 109A (GPR109A), expressed in epidermal Langerhans cells and in keratinocytes and directly activated by nicotinic acid.9 This is based on studies in HCA …

Heating Up the Cutaneous Flushing Response