Acquired Dyschromatopsia and Its Link to Drug Toxicity
Abstract
Colour vision defects (CVDs) can be both congenital and acquired, with acquired dyschromatopsia often associated with medication toxicity. This review explores various standardised colour vision tests used to detect these defects, including the Ishihara plate test, Farnsworth-Munsell 100 hue test, and anomaloscopes. These methods are evaluated for their effectiveness in diagnosing CVDs, particularly in acquired conditions. Specific focus is given to medications known to induce dyschromatopsia, including chloroquine and hydroxychloroquine (CQ/HCQ), digoxin, ethambutol (EMB), and phosphodiesterase-5 (PDE-5) inhibitors. CQ/HCQ primarily causes tritan defects at early stages of retinal toxicity and progresses to red-green defects with more advanced retinopathy. Digoxin-induced CVDs are typically temporary red-green defects linked to the inhibition of Na+/K+ ATPase in retinal cells. EMB, used to treat tuberculosis, is associated with blue-yellow (tritan) dyschromatopsia, likely due to optic neuropathy. PDE-5 inhibitors, such as sildenafil, cause transient blue-tinted vision due to their effect on the phototransduction cascade in cones. Although most drug-induced CVDs are reversible upon discontinuation, CQ/HCQ toxicity often leads to irreversible damage. This review underscores the importance of colour vision monitoring in patients on long-term medication therapy to detect early toxicity and prevent irreversible damage.
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