eMedicine Specialties > Ophthalmology > Unclassified Disorders

Chloroquine/Hydroxychloroquine Toxicity

Author: Manolette R Roque, MD, MBA, DPBO, FPAO, President and CEO, Chief of Service, Ocular Immunology and Uveitis, Consulting Staff, Cornea and Refractive Surgery, Eye Republic Ophthalmology Clinic; General Manager, Ophthalmic Consultants Philippines Co; Consulting Staff, CME Liaison, Section Chief of Ocular Immunology and Uveitis, Department of Ophthalmology, Asian Hospital and Medical Center
Coauthor(s): Barbara L Roque, MD, Full Partner, Ophthalmic Consultants Philippines Co, Chief of Service, Pediatric Ophthalmology and Strabismus, Consulting Staff, Orbit and Eye Plastics, EYE REPUBLIC Ophthalmology Clinic; C Stephen Foster, MD, FACS, FACR, FAAO, Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary; Founder and President, Ocular Immunology and Uveitis Foundation, Massachusetts Eye Research and Surgery Institution
Contributor Information and Disclosures

Updated: Apr 1, 2008

Introduction

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.

Internists, rheumatologists, or dermatologists who usually give chloroquine and hydroxychloroquine may not be fully aware of the potential ophthalmic implications. Patients and primary care physicians should understand that screening helps to identify toxicity early, prior to severe damage, but cannot prevent toxicity or guarantee that no visual loss will occur.

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

United States

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.1

International

Incidence from 1-28% has been reported.

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, although older patients are believed to be at a higher risk because of the potential for diseased retinas.

Clinical

History

  • Some patients with retinopathy may be asymptomatic. When they are symptomatic, visual acuity initially remains excellent despite complaints of parafoveal metamorphopsia and difficulty in reading or performing fine visual tasks (due to central or paracentral scotomas).
  • Other reported visual symptoms include the following:
    • Dimness
    • Flickering or flashing lights of yellow
    • Green or red haloes
    • Cycloplegia
    • Amblyopia
    • Diplopia
    • Blindness
    • Photophobia
    • Oculogyric crisis
  • Systemic complaints include the following:

    • Nausea, abdominal pain, and vomiting
    • Occasionally, skin conditions, such as rashes, pruritus, and sensitivity to ultraviolet light, may be present.
    • Rarely, neurologic symptoms, such as vertigo, tinnitus, irritability, cranial nerve palsies, and myasthenialike muscle weakness, may manifest.

Physical

All patients undergoing chloroquine and/or hydroxychloroquine therapy should have a baseline ophthalmologic examination within the first year to document any complicating ocular conditions and to establish a record of the fundus appearance and the visual field.

  • Complete ophthalmologic examination
    • History (including refraction)
    • Visual acuity (uncorrected visual acuity [UCVA] and best spectacle corrected visual acuity [BSCVA])
    • Slit lamp biomicroscopy
    • Direct and indirect ophthalmoscopy
    • Dilated cornea and retina examination
  • Baseline ancillary tests (see Imaging Studies and Other Tests)  
    • Amsler grid and perimetry (Humphrey 10-2)
    • Optional color testing
    • Optional fundus photography
    • Optional specialized tests, such as fluorescein angiography or multifocal electroretinogram (ERG)
  • Corneal
    • Corneal deposits, limited to the basal epithelium, are described as tiny white dots that become yellow and then golden brown with continued use of the medication. The deposition pattern ranges from a fine diffuse punctate appearance, to radial or whorl-like lines converging just inferior to the central cornea, to coalesced and darkened lines.
    • Manifestation of these corneal deposits apparently is not related to duration or dose, and it is completely reversible once the medication is discontinued. Chloroquine has been associated with more keratopathy than has hydroxychloroquine.
    • A decrease in corneal sensation has been reported in approximately 50% of patients taking chloroquine.
  • Lenticular: Chloroquine, but not hydroxychloroquine, may cause white, flakelike posterior subcapsular lens opacity.
  • Uveal (ciliary body): Chloroquine, but not hydroxychloroquine, may decrease accommodation.
  • Retinal

    • The fundus appearance may remain entirely normal, even after scotomas have developed (see Media file 4).
    • Early changes include irregularity (mild stippling or mottling) in the macular pigmentation and blunting (reversible) of the foveal reflex. Examination with a red-free filter may enhance detection of these changes.
    • Later, the central irregular pigmentation may become surrounded by a concentric zone of hypopigmentation, usually oval and more prominent inferiorly to the fovea (see Media file 1). This condition often is bilateral, although asymmetry is not uncommon.
    • If the treatment is not halted and the toxicity progresses, the classic bull's eye maculopathy appears.
    • Further prolonged exposure to the quinolones may lead to more generalized pigmentary changes.
    • End-stage retinopathy presents with peripheral pigment irregularity and bone spicule formation, vascular attenuation, and optic disc pallor. It sometimes is mistaken for retinitis pigmentosa.
  • Systemic: The systemic complaints may be observed at consult. Poliosis has been reported.

Causes

  • Chloroquine
    • Maintenance dose greater than 3.5 mg/kg/d
    • Duration of treatment greater than 10 years
    • Evidence of renal insufficiency
  • Hydroxychloroquine
    • Maintenance dose greater than 6.5 mg/kg/d
    • Duration of treatment greater than 10 years
    • Evidence of renal insufficiency
  • In addition to the previous use of chloroquine and/or hydroxychloroquine, risk factors include the following:
    • Obesity
    • Presence of macular degeneration or retinal dystrophy
    • Advanced age
    • Hepatic and/or renal failure

More on Chloroquine/Hydroxychloroquine Toxicity

Overview: Chloroquine/Hydroxychloroquine Toxicity
Differential Diagnoses & Workup: Chloroquine/Hydroxychloroquine Toxicity
Treatment & Medication: Chloroquine/Hydroxychloroquine Toxicity
Follow-up: Chloroquine/Hydroxychloroquine Toxicity
Multimedia: Chloroquine/Hydroxychloroquine Toxicity
References
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Further Reading

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Keywords

chloroquine, hydroxychloroquine, Aralen, Plaquenil, bull's eye maculopathy, toxicity

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Contributor Information and Disclosures

Author

Manolette R Roque, MD, MBA, DPBO, FPAO, President and CEO, Chief of Service, Ocular Immunology and Uveitis, Consulting Staff, Cornea and Refractive Surgery, Eye Republic Ophthalmology Clinic; General Manager, Ophthalmic Consultants Philippines Co; Consulting Staff, CME Liaison, Section Chief of Ocular Immunology and Uveitis, Department of Ophthalmology, Asian Hospital and Medical Center
Manolette R Roque, MD, MBA, DPBO, FPAO is a member of the following medical societies: American Academy of Ophthalmic Executives, American Society of Cataract and Refractive Surgery, American Society of Ophthalmic Administrators, American Uveitis Society, International Ocular Inflammation Society, Philippine Medical Association, Philippine Ocular Inflammation Society, and Philippine Society of Cataract and Refractive Surgery
Disclosure: Nothing to disclose.

Coauthor(s)

Barbara L Roque, MD, Full Partner, Ophthalmic Consultants Philippines Co, Chief of Service, Pediatric Ophthalmology and Strabismus, Consulting Staff, Orbit and Eye Plastics, EYE REPUBLIC Ophthalmology Clinic
Disclosure: Nothing to disclose.

C Stephen Foster, MD, FACS, FACR, FAAO, Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary; Founder and President, Ocular Immunology and Uveitis Foundation, Massachusetts Eye Research and Surgery Institution
C Stephen Foster, MD, FACS, FACR, FAAO is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Association of Immunologists, American College of Rheumatology, American College of Surgeons, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, American Uveitis Society, Association for Research in Vision and Ophthalmology, Massachusetts Medical Society, Royal Society of Medicine, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor

Kilbourn Gordon III, MD, FACEP, Urgent Care Physician, Primary Medical, Huntington Walk-In and Greenwich Convenient Medical Center
Kilbourn Gordon III, MD, FACEP is a member of the following medical societies: American Academy of Ophthalmology and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

J James Rowsey, MD, Former Director of Corneal Services, St Luke's Cataract and Laser Institute, Florida
J James Rowsey, MD is a member of the following medical societies: American Academy of Ophthalmology, American Association for the Advancement of Science, American Medical Association, Association for Research in Vision and Ophthalmology, Florida Medical Association, Pan-American Association of Ophthalmology, Sigma Xi, and Southern Medical Association
Disclosure: Nothing to disclose.

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
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