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Retina.com.ph >
Age-related macular degeneration | Chloroquine
and hydroxychloroquine toxicity | Cystoid macular
edema | Color blindness |
Central serous chorioretinopathy |
Diabetic eye diseases |
Diabetic retinopathy |
Macular hole |
Posterior vitreous detachment |
Retinal detachment | Retinopathy of prematurity
Chloroquine and Hydoxychloroquine Toxicity
Background:
Chloroquine and hydroxychloroquine belong to the quinolone
family. They are related drugs with different therapeutic and toxic doses
with similar clinical indications for use and manifestations of retinal
toxicity.
Initially, chloroquine was given for
malaria prophylaxis and treatment, and, later, it was used by
rheumatologists for treating rheumatoid arthritis, systemic/discoid lupus
erythematosus, and other connective tissue disorders. Dermatologists use
these drugs for cutaneous lupus. Since it is far less toxic to the retina,
hydroxychloroquine has replaced chloroquine, except for individuals who
travel in areas endemic with malaria.
Expanded use of these drugs for
nonmalarial disease entities has resulted in prolonged duration of therapy
and higher daily dosages leading to cumulative doses greater than those used
in antimalarial therapy. The first reports of retinal toxicity attributed to
chloroquine appeared during the late 1950s. In 1958, Cambiaggi first
described the classic retinal pigment changes in a patient receiving
chloroquine for systemic lupus erythematous (SLE) treatment. In 1959, Hobbs
established a definite link between long-term use of chloroquine and
subsequent development of retinal pathology. In 1962, J Lawton Smith coined
the term bull's eye maculopathy, regarded as the classic finding of macular
toxicity. Many reports on chloroquine retinopathy exist. In contrast, only a
few cases of hydroxychloroquine toxicity have been reported.
Pathophysiology:
Chloroquine has an affinity for pigmented
(melanin-containing) structures, which may explain its toxic properties in
the eye. Melanin serves as a free-radical stabilizer and as an agent that
can bind toxins. Although it binds potentially retinotoxic drugs, it is
unclear whether the effect is beneficial or harmful. Chloroquine and its
principal metabolite have been found in the pigmented ocular structures at
concentrations much greater than in any other tissue in the body. With more
prolonged exposure, the drug accumulates in the retina. The drug is retained
in the pigmented structures long after its use is stopped. The kinetics of
chloroquine metabolism are complicated, with the half-life increasing as the
dosage is increased. In patients with retinopathy, 5 years or more after
discontinuation, traces of chloroquine have been found in plasma,
erythrocytes, and urine.
Frequency:
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In the US:
Two trends are consistent in literature, despite the
variability of the statistics; the incidence of retinopathy increased with
both the dose and the duration of treatment.
Bernstein estimated an incidence of 10%
in unmonitored patients taking 250 mg/d of chloroquine and 3-4% in
unmonitored patients taking 400 mg/d of hydroxychloroquine.
Mortality/Morbidity:
See
Clinical for detailed information.
Race:
No known racial predilection exists.
Sex:
No known sexual predilection exists.
Age:
No known age predisposition exists.
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