Like dapsone, the antimalarial drugs chloroquine, hy-droxychloroquine, and quinacrine are useful in some noninfectious skin diseases, although the mechanism of their therapeutic effect is unknown.
Antimalarial drugs have many effects, including im-pairment of lysosomal phagosomal activity, inhibition of neutrophilic iodination and locomotion, and diminu-tion of macrophage and T-cell responsiveness in vitro. Chloroquine (Aralen) and hydroxychloroquine (Plaquenil) also form complexes with hepatic por-phyrins and can chelate iron, thereby enhancing their urinary excretion. Both drugs have an affinity for melanin, which may at least partially explain their oph-thalmological toxicities (retinopathy).
Hydroxychloroquine is approved for the treatment of both systemic and cutaneous lupus erythematosus. Both chloroquine and quinacrine (Atabrine) are also ef-fective in this skin disease. Low-dose chloroquine is used for the therapy of porphyria cutanea tarda in pa-tients in whom phlebotomy has failed or is contraindi-cated. Other skin diseases in which the drugs are useful (after sunscreens and avoidance of sun exposure) in-clude polymorphous light eruption and solar urticaria.
The duration of treatment for skin diseases is often longer than it is for malaria, and therefore, dose-related toxicities are important. The most serious toxicities are ophthalmological. Reversible alterations include ciliary body dysfunction and corneal changes with edema and deposits. Irreversible retinopathy also occurs; however, it is less common with quinacrine than with the other two drugs. Toxicity may be asymptomatic, but the earliest symptoms are night blindness, scotoma, or tunnel vision.
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