| Serious ophthalmologic toxicity occurs rarely if the patient is periodically monitored, but remains the most feared adverse effect of antimalarial drugs since it can result in loss of vision. The most common ocular toxicity of antimalarials relates to the cornea (always reversible) and retinopathy.
Corneal deposits: Corneal deposits are found rarely with hydroxychloroquine (HCQ) at a dose of 400 mg/day. The deposits do not affect vision, but can create transient halos or heightened light sensitivity, and they are reversible upon discontinuation of the medication.
Retinopathy: Retinopathy is the most important ophthalmologic complication of antimalarial therapy. Antimalarials bind to melanin in the pigmented epithelial layer of the retina, which may damage rods and cones and may lead to permanent vision loss. The exact incidence of retinopathy is uncertain; with at least 10 years of use, it may occur in up to 3–4% of patients taking HCQ, in up to 10% of those taking chloroquine, and never in those taking quinacrine.1–3
The earliest retinal abnormalities are asymptomatic and can only be detected by ophthalmologic examination. These ‘premaculopathy’ changes consist of macular edema, increased pigmentation, increased granularity, and loss of the foveal reflex. Subtle functional loss in the paracentral retina can occur before biomicroscopic changes in the retinal pigment epithelium.4–6 Detection of changes at this stage, using techniques such as multifocal electroretinography, is desirable since they may be completely reversible upon discontinuation of the medication.7
More advanced macular disease, a true retinopathy, is characterized by a central patchy area of depigmentation of the macula surrounded by a concentric ring of pigmentation, a ‘bull’s eye’ lesion. Symptoms at this stage are generally not reversible and may include dropout of letters from words when reading, photophobia, blurred distance vision, visual field defects and flashing lights.1,8 In such patients, continuing depigmentation and functional loss may continue for a year or more after the drug has been stopped.9
References
- Wallace DJ. Antimalarial therapies. In: Dubois’ Lupus Erythematosus, 7th edn. Wallace DJ, Hahn BH (eds). Baltimore: Williams & Wilkins, 2007.
- Rynes RI. Ophthalmologic considerations in using antimalarials in the United States. Lupus 1996;5(Suppl 1):S73.
- Wolfe F, Marmor MF. Rates and predictors of hydroxychloroquine retinal toxicity in patients with rheumatoid arthritis and systemic lupus erythematosus. Arthritis Care Res (Hoboken) 2010;62:775.
- Maturi RK, Yu M, Weleber RG. Multifocal electroretinographic evaluation of long-term hydroxychloroquine users. Arch Ophthalmol. 2004;122:973.
- >Kellner U, Renner AB, Tillack H. Fundus autofluorescence and mfERG for early detection of retinal alterations in patients using chloroquine/hydroxychloroquine. Invest Ophthalmol Vis Sci. 2006;47:3531.
- Lai TY, Chan WM, Li H, et al. Multifocal electroretinographic changes in patients receiving hydroxychloroquine therapy. Am J Ophthalmol. 2005;140:794.
- Lyons JS, Severns ML. Using multifocal ERG ring ratios to detect and follow Plaquenil retinal toxicity: A review: Review of mfERG ring ratios in Plaquenil toxicity. Doc Ophthalmol. 2009;118:29.
- Shinjo SK, Maia OO Jr, Tizziani VA, et al. Chloroquine-induced bull's eye maculopathy in rheumatoid arthritis: Related to disease duration? Clin Rheumatol. 2007;26:1248.
- Marmor MF, Kellner U, Lai TY, et al. Revised recommendations on screening for chloroquine and hydroxychloroquine retinopathy. Ophthalmology 2011;118:415.
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