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July 2016

Potentially Reversible Effect of Niacin Therapy on Edema From Retinal Vein Occlusion

Author Affiliations
  • 1Department of Ophthalmology, Palo Alto Medical Foundation, Palo Alto, California
  • 2Kellogg Eye Center, University of Michigan at Ann Arbor
  • 3Byers Eye Institute, Stanford University, Stanford, California
  • 4Department of Ophthalmology, George Washington University, Washington, DC
  • 5Department of Ophthalmology, University of Maryland, Baltimore
  • 6Virginia Retina Center, Warrenton
JAMA Ophthalmol. 2016;134(7):839-840. doi:10.1001/jamaophthalmol.2016.1028

An increasing body of evidence is supporting the role of nitric oxide (NO), a potent microcirculatory regulator, in the pathogenesis of ocular disorders. Within the posterior segment, NO is capable of dilating retinal and choroidal vessels down to the capillary level by relaxation of pericytes.1

Niacin (nicotinic acid), an established treatment for dyslipidemia, generates NO synthase, and ultimately NO, through a prostaglandin-mediated process.2 Recently, Abrishami et al3 reported the effects of niacin therapy on improving venous outflow in retinal vein occlusion (RVO) secondary to the compound’s vasodilatory properties. Herein, we present a case of macular RVO with chronic cystoid macular edema (CME) associated with resolution by use of systemic niacin therapy, including the reversibility of this effect when the patient stopped using the medication.

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