Sir,

We report the spectral domain optical coherence tomography (SD-OCT) and fundus autofluorescence (FAF) findings in a case of niacin maculopathy. To the best of our knowledge, only time domain OCT has been reported; SD-OCT yields better resolution of the affected retinal layers in this unusual disorder.

Case Report

A 57-year-old male presented with blurred vision in the right eye over the past 2 weeks. He reported taking 2000 mg of niacin daily for 5 months after suffering from myalgia related to statin therapy for hyperlipidemia. Visual acuity was 20/40 in the right eye and 20/20 in the left eye. Intraocular pressure was normal and slit lamp examination revealed no cell. Ophthalmoscopy revealed macular edema in the right eye. Fluorescein angiography demonstrated normal vasculature without petalloid leakage (Figure 1). SD-OCT found numerous large cystoid spaces involving the outer and inner nuclear layers in the right eye and to a lesser degree the inner nuclear layers in the left eye; there was a suggestion of cystoid change within the ganglion cell layer of the right eye (Figure 2). There was a normal pattern of FAF in both eyes (Figure 3). A diagnosis of niacin maculopathy was made and the patient discontinued the medication. After 1 month of cessation, visual acuity was 20/20 and the retinal architecture had returned to normal (Figure 4).

Figure 1
figure 1

Fluorescein angiography of the right (top) and left (bottom) eye showing no petalloid leakage.

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Figure 2
figure 2

Spectral domain OCT demonstrating cystoid spaces in the outer and inner nuclear layers and possibly the ganglion cell layer in the right eye and in the inner nuclear layer in the left eye.

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Figure 3
figure 3

Fundus autofluorescence of right and left eyes was normal.

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Figure 4
figure 4

One month following cessation of niacin the OCT returned to normal.

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Comment

Reversible, angiographically silent, cystoid maculopathy due to high-dose niacin was first described by Gass in 1973.1 Decades later, Spirn et al2 and then Dajani and Lauer3 demonstrated the time domain OCT findings that appeared to localize the cystoid spaces to the outer plexiform and inner nuclear layers. In contrast, SD-OCT demonstrates the spaces in the outer nuclear layer, the inner nuclear layer, and possibly the ganglion cell layer. There are two existing theories regarding the pathogenesis: Muller cell toxicity and engorgement,4 and selective vascular permeability not allowing the passage of fluorescein.3 Nicotinamide adenine dinucleotide, a metabolite of niacin, is highly active in chromatin function suggesting that derangement of nuclear metabolism might explain the appearance of cystoid spaces in the nuclear layers of the retina.