APR 2013

EyeWorld is the official news magazine of the American Society of Cataract & Refractive Surgery.

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38 EW RETINA April 2013 Niacin-induced cystoid macular edema T he patient in this case is a 63-year-old male who happens to be an ophthalmologist and my partner of 14 years. Bob Harbin, MD, has a significant ocular history for a meridional complex in the left eye by Paul "Butch" Harton, MD that was repaired with a radial scleral sponge more than 30 years ago. He is also status post-cryopexy treatment for retinal tears OU more than three decades ago. More recently, an asymptomatic partial thickness macular hole is noticed on exam. OCT evaluation in April 2012 confirmed this finding in the left eye and showed the right eye to be normal (Figures 1a and 1b). Vision at that time was 20/20 in each eye with correction. Figure 1a: A normal retina is shown via OCT in the right eye nine months preop. Figure 1b: A longstanding partial thickness macular hole is noticed by OCT in the left eye nine months preop. Figure 2a: Retinal edema, mainly involving the outer plexiform layer of superior retina, is shown six weeks before surgery. By late 2012, Dr. Harbin began noticing blurry vision in the right eye. BSCVA was down to 20/40 OD and this was felt to be consistent with advancing lenticular nuclear sclerosis. Otherwise the ocular exam appeared normal in the right eye and the lamellar hole was noticed in the left eye. Surgery was scheduled for cataract extraction in the right eye. As part of the preoperative workup, an OCT was repeated. To our surprise it showed what appeared to be edema of the outer plexiform layer. The right eye was more dramatic where the finding was more prominent superiorly than inferiorly in the right eye (Figure 2a). However, early edema was noticed OS as well (Figure 2b). Surgery was put on hold and retinal consultation was obtained. An angiogram on the right eye showed no leakage. We were puzzled as to the etiology of the retinal findings and entertained the possibility of vitreomacular traction. However, there was no sign of traction on exam and no evidence noted on OCT so we began entertaining other possible causes of non-exudative cystoid macular edema. It occurred to us that Dr. Harbin's medical history was significant for an elevated level of lipoprotein(a), a highly atherogenic low density lipoprotein (LDL) often not responsive to medical therapy. In order to reduce the cardiovascular risk associated with elevated lipoprotein(a), medical therapy is aimed at reducing all other LDL components as aggressively as possible. Dr. Harbin had been started on Niaspan (niacin extended-release, Abbott Laboratories, Abbott Park, Ill.) in 2006. Initially he was on 2 grams per day. The dose was increased about one year ago to the current 3 grams per day. He was also taking Crestor (rosuvastatin calcium, AstraZeneca, Wilmington, Del.) 10 mg per day. With niacin being a known cause of cystoid macular edema, the decision was made to reduce the Niaspan dose down to 1500 mg per day. No other treatment was instituted. One month later, visual acuity and exam had not changed. A repeat OCT, however, showed marked improvement of the macular edema in the right eye (Figure 3). We decided to go forward with cataract surgery on the right eye,

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