Vogt-Koyanagi-Harada Disease Medication

  • Author: R Christopher Walton, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Apr 30, 2012
 

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

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Corticosteroids

Class Summary

Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

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Prednisone (Deltasone, Meticorten, Orasone, Sterapred)

 

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

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Prednisolone acetate (Pred Forte)

 

Useful for the treatment of associated anterior uveitis. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

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Cycloplegics

Class Summary

Instillation of a long-acting cycloplegic agent can relax any ciliary muscle spasm that can cause a deep aching pain and photophobia.

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Homatropine (Isopto Homatropine, AK-Homatropine)

 

Blocks responses of sphincter muscle of iris and muscle of ciliary body to cholinergic stimulation, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia). Induces mydriasis in 10-30 min and cycloplegia in 30-90 min. These effects last up to 48 h. Individuals with heavily pigmented irides may require larger doses.

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Immunosuppressive therapy

Class Summary

Agents in this category inhibit key factors involved in the immune response. May be used when inflammation is not controlled adequately by systemic corticosteroids and/or in patients who develop intolerable adverse effects. Ophthalmologists should seek the assistance of a clinician experienced in the use of these drugs when treating patients with ocular inflammatory diseases.

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Cyclosporine (Sandimmune, Neoral)

 

A cyclic polypeptide that suppresses humoral immunity and, to a greater extent, cell-mediated immunity.

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Mycophenolate mofetil (CellCept, Myfortic)

 

Prodrug that once hydrolyzed in vivo releases the active moiety mycophenolic acid. Inhibits inosine monophosphate dehydrogenase (IMPDH) and suppresses denovo purine synthesis by lymphocytes, thereby inhibiting their proliferation. Inhibits antibody production.

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Azathioprine (Imuran)

 

Antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. May decrease proliferation of immune cells, which results in lower autoimmune activity.

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Tacrolimus (Prograf)

 

A macrolide immunosuppressive agent that inhibits the activation of T cells.

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Cyclophosphamide (Cytoxan, Neosar)

 

Cyclic polypeptide that suppresses some humoral activity. Chemically related to nitrogen mustards. Activated in the liver to its active metabolite, 4-hydroxycyclophosphamide, which alkylates the target sites in susceptible cells in an all-or-none type reaction. As an alkylating agent, the mechanism of action of the active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and neoplastic cells.

Biotransformed by cytochrome P-450 system to hydroxylated intermediates that break down to active phosphoramide mustard and acrolein. Interaction of phosphoramide mustard with DNA considered cytotoxic.

When used in autoimmune diseases, mechanism of action is thought to involve immunosuppression due to destruction of immune cells via DNA cross-linking.

In high doses, affects B cells by inhibiting clonal expansion and suppression of production of immunoglobulins. With long-term low-dose therapy, affects T cell functions.

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Chlorambucil (Leukeran)

 

Bifunctional slow-acting aromatic nitrogen mustard derivative, which interferes with DNA replication, transcription, and nucleic acid function by alkylation. Alkylates and cross-links strands of DNA. Alkylation takes place through formation of highly reactive ethylenimonium radical. Probable mode of action involves cross-linkage of the ethylenimonium derivative between 2 strands of helical DNA and subsequent interference with replication. Known chemically as 4-[bis(2chlorethyl)amino]benzene butanoic acid.

Dosage must be carefully adjusted according to the response of the patient and must be reduced as soon as an abrupt fall in the white blood cell count occurs.

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Contributor Information and Disclosures
Author

R Christopher Walton, MD  Professor, Director of Uveitis and Ocular Inflammatory Disease Service, Department of Ophthalmology, University of Tennessee College of Medicine

R Christopher Walton, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Healthcare Executives, American Uveitis Society, Association for Research in Vision and Ophthalmology, and Retina Society

Disclosure: Nothing to disclose.

Specialty Editor Board

John D Sheppard Jr, MD, MMSc  Professor of Ophthalmology, Microbiology and Molecular Biology, Clinical Director, Thomas R Lee Center for Ocular Pharmacology, Ophthalmology Residency Research Program Director, Eastern Virginia Medical School; President, Virginia Eye Consultants

John D Sheppard Jr, MD, MMSc is a member of the following medical societies: American Academy of Ophthalmology, American Society for Microbiology, American Society of Cataract and Refractive Surgery, American Uveitis Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Steve Charles, MD  Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine; Adjunct Professor of Ophthalmology, Columbia College of Physicians and Surgeons; Clinical Professor Ophthalmology, Chinese University of Hong Kong

Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Club Jules Gonin, Macula Society, and Retina Society

Disclosure: Alcon Laboratories Consulting fee Consulting; OptiMedica Ownership interest Other; Topcon Medical Lasers Consulting fee Consulting

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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Bilateral multifocal serous detachments in a patient with Vogt-Koyanagi-Harada disease. Disc hyperemia is evident in the right eye.
Fluorescein angiography of the left eye in a patient with Vogt-Koyanagi-Harada disease. Mid phase is shown on the left with multiple areas of hyperfluorescence at the level of the retinal pigment epithelium. Late phase of the same angiogram (right) reveals multiple placoid areas of hyperfluorescence at the level of the retinal pigment epithelium and pooling of dye in the areas of serous detachment.
Patient with progressive dysacusis and recent onset of visual loss. Fundus photo shows a large multifocal serous detachment of the right eye. B-scan ultrasonography reveals posterior choroidal thickening with an overlying retinal detachment.
Patient with progressive dysacusis and recent onset of visual loss is shown here following 6 weeks of systemic corticosteroid therapy. Diffuse depigmentation of the choroid with retinal pigment epithelium migration is seen. Residual retinal striae are present in the peripapillary region. B-scan ultrasonography shows resolution of retinal detachment and choroidal thickening.
 
 
 
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