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Vogt-Koyanagi-Harada Disease Medication

  • Author: R Christopher Walton, MD; Chief Editor: Hampton Roy, Sr, MD  more...
 
Updated: Apr 15, 2016
 

Medication Summary

As previously mentioned, early, aggressive treatment with systemic corticosteroids—including prednisone and possibly, in the most severe cases, intravenous methylprednisolone—is key to the effective treatment of VKH disease (although intravenous therapy has not been found to improve visual outcomes).

Immunomodulatory treatment can be used in patients who are not responsive to high-dose systemic corticosteroids or who suffer from intolerable adverse effects. Immunomodulatory agents include cyclosporine, tacrolimus, mycophenolate mofetil, azathioprine, cyclophosphamide, and chlorambucil.[1, 62, 63, 64, 65, 66]

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Corticosteroids

Class Summary

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

Prednisone

 

Prednisone is a synthetic adrenocortical steroid with predominantly glucocorticoid properties. An immunosuppressant, it is used for the treatment of autoimmune disorders. Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear (PMN) leukocyte activity. It stabilizes lysosomal membranes and suppresses lymphocytes and antibody production.

Prednisolone acetate (Millipred, Orapred)

 

This agent is useful for the treatment of associated anterior uveitis. It decreases inflammation by suppressing the migration of PMN 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 is causing deep, aching pain and photophobia.

Homatropine (Isopto Homatropine)

 

Homatropine blocks responses of the sphincter muscle of the iris and the muscle of the ciliary body to cholinergic stimulation, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia). This agent induces mydriasis in 10-30 minutes and cycloplegia in 30-90 minutes. These effects last up to 48 hours. Individuals with heavily pigmented irides may require larger doses.

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Immunosuppressants

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.

Cyclosporine (Sandimmune, Neoral, Gengraf)

 

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

Mycophenolate mofetil (CellCept, Myfortic)

 

This agent is a prodrug that, once hydrolyzed in vivo, releases the active moiety mycophenolic acid. The active compound inhibits inosine monophosphate dehydrogenase (IMPDH) and suppresses de novo purine synthesis by lymphocytes, thereby inhibiting their proliferation. It inhibits antibody production.

Azathioprine

 

Azathioprine may be used alone or as a steroid-sparing agent. It antagonizes purine metabolism and inhibits the synthesis of deoxyribonucleic acid (DNA), ribonucleic acid (RNA), and proteins. Azathioprine may decrease the proliferation of immune cells, in this way lowering autoimmune activity.

Tacrolimus (Prograf, Hecoria)

 

Tacrolimus is a macrolide immunosuppressive agent that inhibits the activation of T cells.

Cyclophosphamide

 

Cyclophosphamide may be used as monotherapy or as a steroid-sparing agent. It is a cyclic polypeptide that is chemically related to nitrogen mustards and that suppresses some humoral activity. It is 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 the growth of normal and neoplastic cells.

Cyclophosphamide is biotransformed by the cytochrome P-450 system to hydroxylated intermediates that break down to active phosphoramide mustard and acrolein. The interaction of phosphoramide mustard with DNA is considered to be cytotoxic.

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

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

Chlorambucil (Leukeran)

 

Chlorambucil is a bifunctional, slow-acting, aromatic nitrogen mustard derivative that interferes with DNA replication, transcription, and nucleic acid function by alkylation. Known chemically as 4-[bis(2chlorethyl)amino]benzene butanoic acid, the drug alkylates and cross-links strands of DNA.

Alkylation takes place through formation of the highly reactive ethylenimonium radical. Chlorambucil's probable mode of action involves cross-linkage of the ethylenimonium derivative between 2 strands of helical DNA and subsequent interference with replication.

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.

Methotrexate (Trexall, Rheumatrex)

 

Methotrexate ameliorates the symptoms of inflammation (eg, pain, swelling, stiffness). Its mechanism of action in the treatment of inflammatory reactions is unknown, but immune function may be affected. Gradually adjust the dose to achieve a satisfactory response.

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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, Association for Research in Vision and Ophthalmology, Retina Society, American College of Healthcare Executives, American Uveitis Society

Disclosure: Nothing to disclose.

Coauthor(s)

Camila K Janniger, MD Clinical Professor of Dermatology, Clinical Associate Professor of Pediatrics, Chief of Pediatric Dermatology, Rutgers New Jersey Medical School

Camila K Janniger, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Anna Choczaj-Kukula, MD, PhD Locum Consultant Dermatologist, Barnet and Chase Farm NHS Trust; Honorary Clinical Research Fellow, Royal Free Hospital, UK

Anna Choczaj-Kukula, MD, PhD is a member of the following medical societies: American Academy of Dermatology, Royal Society of Medicine, European Academy of Dermatology and Venereology, British Association of Dermatologists

Disclosure: Partner received salary from Johnson & Johnson for management position.

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, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Acknowledgements

David F Butler, MD Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

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

Anna Choczaj-Kukula, MD, PhD Locum Consultant Dermatologist, St John's Institute of Dermatology, St Thomas' Hospital, UK

Anna Choczaj-Kukula, MD, PhD is a member of the following medical societies: American Academy of Dermatology, British Association of Dermatologists, European Academy of Dermatology and Venereology, and Royal Society of Medicine

Disclosure: Johnson & Johnson Salary Management position

Dirk M Elston, MD Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Janet Fairley, MD Professor and Head, Department of Dermatology, University of Iowa, Roy J and Lucille A Carver College of Medicine

Janet Fairley, MD is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, American Federation for Medical Research, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Camila K Janniger, MD Clinical Professor of Dermatology, Clinical Associate Professor of Pediatrics, Chief of Pediatric Dermatology, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Camila K Janniger, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

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

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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. Midphase is shown on the left, with multiple areas of hyperfluorescence at the level of the retinal pigment epithelium (RPE). Late phase on the same angiogram (right) reveals multiple placoid areas of hyperfluorescence at the level of the RPE 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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