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
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.