CASE REPORTS - Severe chloroquine and hydroxychloroquine-induced retinopathy

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J Fr Ophtalmol. 2006 Jun;29(6):642-50.

[severe chloroquine- and hydroxychloroquine-induced retinopathy].

[Article in French]

Ingster-Moati I, Bui Quoc E, Crochet M, Orssaud C, Dufier JL, Roche O.

Hôpital Lariboisière, Assistance Publique-Hôpitaux de Paris, Paris, France.

Abstract

INTRODUCTION: Antimalarial drug-induced retinopathy was first

described in the 1950s. Irreversible retinal damage still occurs 50

years later, despite knowledge of the phenomenon. This raises several

questions: How aware are physicians of this problem and do they inform

their patients? What efficient prevention strategies should be

advocated and what are the legal aspects? We present four cases of

severe chloroquine- and hydroxychloroquine-induced retinopathy to try

to understand what led to these situations.

CASE REPORTS: The fist case, a male patient born in 1956, had

chloroquine therapy for lupus initiated in 1987, at a dose ranging

from 3 to 6 mg/kg per day. In 1992, no toxicity was clinically or

electrophysiologically noted. In 1997, macular abnormalities were

diagnosed; chloroquine treatment was nevertheless continued. In 2002,

the electroretinogram and central visual field examinations were

abnormal. Chloroquine treatment was discontinued. In 2005,

abnormalities of full-field and multifocal electroretinograms,

electro-oculogram, color vision, and visual field confirmed the

maculopathy. The second case, a female patient, born in 1956, had

chloroquine therapy for rheumatoid arthritis beginning in 1993, at a

dose of 5 mg/kg per day. In 1999, 2000, and 2001, electroretinograms

were reported as normal. Clinical maculopathy occurred in 2003 and

treatment was continued. In January 2004, the central visual field was

found abnormal; treatment was discontinued in July 2004. The third

case, a female patient born in 1931, had chloroquine therapy for

malaria prevention initiated in 1975, at a dose of 1.7 mg/kg per day.

No exams were performed after 1983. In 2001, she complained of a left

unilateral vision loss. Bilateral maculopathy was clinically found,

and confirmed by full-field and multifocal electroretinograms. The

fourth case, a female patient born in 1944, had hydroxychloroquine

therapy for lupus initiated in 1982 at a dose of 6.9 mg/kg per day. In

2000 and 2002, full-field electroretinograms were reported as normal

despite low amplitudes. In 2004, clinical examination was normal,

whereas electroretinogram, electro-oculogram, color vision, and

central visual field examinations proved severe damage; the treatment

was discontinued.

DISCUSSION: Retinal damage in these cases was caused by several

factors. Treatment was not stopped despite clinically obvious

maculopathy in cases 1 and 2. In case 3, no ophthalmologic

examinations were performed between 1983 and 2001. In case 4, despite

a high cumulative dose, therapy was not discontinued, as also seen in

cases 1 and 2, in which ophthalmologic monitoring was not increased.

Higher doses than the maximal recommended daily dose occurred in cases

1, 2, and 4.

CONCLUSION: Antimalarial drug therapy still requires intensive

monitoring to avoid severe retinal damage that can lead to legal

blindness. Appropriate examinations should be performed regularly in

order to decide whether to taper or stop when damage is still mild,

preclinical, or reversible.

PMID: 16885894

http://www.ncbi.nlm.nih.gov/pubmed/16885894

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