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Dermatology > PEDIATRIC DISEASES
Vogt-Koyanagi-Harada Syndrome
Article Last Updated: Dec 6, 2006
AUTHOR AND EDITOR INFORMATION
Section 1 of 10  
Author: Anna Choczaj-Kukula, MD, PhD, Lecturer, Department of Dermatology, Medical University of Lodz, Poland
Coauthor(s):
Camila K Janniger, MD, Clinical Professor of Dermatology, Clinical Associate Professor of Pediatrics, Chief of Pediatric Dermatology, New Jersey Medical School
Editors: Janet Fairley, MD, Professor, Program Director, Section Chief, Department of Dermatology, Medical College of Wisconsin; David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Director, Division of Dermatology, Scott and White Clinic; Director Dermatology Residency Training Program, Scott and White Clinic; Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School; Glen H Crawford, MD, Assistant Clinical Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Chief, Division of Dermatology, The Pennsylvania Hospital; Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Author and Editor Disclosure
Synonyms and related keywords:
VKH syndrome, oculocutaneous syndrome, uveocutaneous syndrome, uveoencephalitis, posterior uveitis, bilateral iridocyclitis, iritis, glaucoma, alopecia, vitiligo, dysacusia, CSF pleocytosis, Harada syndrome, poliosis, vitiligo, halo nevi, alopecia, HLA-DR4 antigen
Background
Vogt-Koyanagi-Harada (VKH) syndrome is a rare systemic disease involving various melanocyte-containing organs. Bilateral uveitis associated with cutaneous, neurologic, and auditory abnormalities characterizes this syndrome. As first described by Vogt in 1906 and Koyanagi in 1929, predominantly anterior uveitis associated with poliosis, vitiligo, and auditory disturbances characterizes Vogt-Koyanagi syndrome. In 1926, Harada reported a patient with idiopathic uveitis affecting the posterior segment with retinal detachment and meningeal irritation. At present, these 2 disorders are considered variations of a single entity referred to as Vogt-Koyanagi-Harada syndrome or uveoencephalitis.
Pathophysiology
The etiologic and pathogenic factors in VKH syndrome remain unclear. The clinical course of VKH syndrome with an influenzalike episode suggests a viral or postinfectious origin. Some studies invoke a possible role of Epstein-Barr virus reactivation in this disease (Sunakawa, 1985). Although a viral cause has been proposed, no virus has been isolated or cultured from patients with VKH syndrome. Morris and Schlaegel found viruslike inclusion bodies in the subretinal fluid of a patient with VKH syndrome.
Clinical and experimental data continue to support an immunologic etiology. An autoimmune reaction seems to be directed against an antigenic component shared by uveal, dermal, and meningeal melanocytes, possibly tyrosinase or a tyrosinase-related protein.
Single reports of patients developing VKH syndrome after cutaneous injury have been noted, as well as 2 cases of this condition occurring after BCG therapy for melanoma and 1 case following surgery of metastatic malignant melanoma. Recently, a case of this syndrome was reported to be linked to malignant lymphoma.
Immunologic analysis of cerebrospinal fluid (CSF) lymphocytes in VKH syndrome and studies of human uveal melanocytes show that uveal pigment can stimulate lymphocyte cultures from patients with VKH syndrome. Lymphocytes of peripheral blood and CSF from these patients may reveal in vitro cytotoxicity against allogenic melanoma cells.
Circulating antibodies against a retinal photoreceptor region have been detected in patients with this disorder.
The possibility that VKH syndrome has an autoimmune pathogenesis is supported by the statistically significant frequency of HLA-DR4, an antigen commonly associated with other autoimmune diseases. VKH syndrome has been closely associated with HLA-B54, HLA-DR4, and HLA-DR53 in Japanese patients; with HLA-DR4, HLA-DRw53, and HLA-DQw3 in subjects of Native American ancestry; with HLA-DR1 and HLA-DR4 in Hispanic patients living in southern California; and with HLA-DR4 and HLA-DQw7 in Chinese patients. HLA-DR4 also was found to be significantly related to VKH syndrome in white Europeans, specifically in Italian patients. These findings confirm the possibility of immunogenic predisposition and the decisive role of HLA-DR4 antigen in the development of the disease.
Recent data indicate that patients with VKH syndrome are sensitized to melanocyte epitopes and display a peptide-specific Th1 cytokine response. Patients bearing HLA-DRB1*0405 recognize a broader melanocyte-derived peptide repertoire, so the presence of this allele increases susceptibility to the development of VKH disease.
Frequency
United States
VKH syndrome is rare. No precise data are available regarding frequency of the disease.
International
VKH syndrome is rare but widely distributed.
Mortality/Morbidity
VKH syndrome is not associated with mortality. Acute disturbances in hearing and vision may occur, and the cutaneous changes may be permanent.
Race
VKH syndrome occurs more frequently in individuals with darker pigmentation (eg, persons of Asian, Native American, Latin American, or black heritage). The manifestations of VKH syndrome in whites resembles those in the Japanese population. However, cutaneous signs are much more rare.
Sex
Women appear to be affected more frequently than men.
Age
The onset of VKH syndrome has been reported to range from 10-52 years, with a maximum frequency in the thirties. Although often unrecognized, VKH syndrome may affect children.
History
VKH syndrome is usually preceded by a prodromal stage of nonspecific symptoms including headache, vertigo, nausea, nuchal rigidity, vomiting, and low-grade fever that may last a few days. Patients usually initially present to an ophthalmologist for ocular problems, including sudden loss of vision, ocular pain, and photophobia. Hearing disturbances and dizziness may be present. After weeks or months, most patients notice cutaneous signs (eg, hair loss, poliosis, vitiligo).
Physical
- The American Uveitis Society has recommended that, in addition to an absence of prior trauma or surgery, at least 3 of the following 4 criteria be met to confirm the diagnosis of VKH syndrome:
- Bilateral iridocyclitis
- Posterior uveitis, which may include exudative retinal detachment, optic nerve swelling, or atrophy of the retinal pigment epithelium
- CSF pleocytosis or evidence of tinnitus, dysacusis, headache or meningismus, or cranial nerve involvement
- Cutaneous findings of vitiligo, alopecia, or poliosis
- The classic course of VKH syndrome consists of the following 3 phases:
- In the meningoencephalitis phase, the degree of neurologic symptoms may vary. Generalized muscle weakness, hemiparesis, hemiplegia, dysarthria, and aphasia have been reported. Most of the neurologic symptoms have been directly attributed to changes in CSF (eg, pleocytosis, increased pressure, protein levels), inflammatory arachnoiditis, or resulting subarachnoidal adhesions. Mental changes ranging from mild confusion to psychosis may occur.
- The ophthalmic-auditory phase is characterized by common features such as decreased visual acuity, eye pain, eye irritation, and loss of vision. Dysacusis (usually bilateral) and tinnitus develop in 50% of patients.
- The convalescent phase is characterized by cutaneous signs developing after uveitis begins to subside, usually within 3 months from the onset of the disease. Although cutaneous signs typically occur several weeks to months after the onset of ocular inflammation, skin changes have sometimes been observed many years before uveitis appeared. Pigmentary changes tend to be permanent.
- Poliosis, which occurs in 90% of patients, involves the eyebrows and eyelashes and, occasionally, the scalp and body hair. Poliosis affects 50% of patients and usually appears after the onset of alopecia, which may be patchy or diffuse.
- Vitiligo manifests in 63% of patients and is often symmetric. Most patients have perilimbal vitiligo (Sugiura sign). Atypical variants of vitiligo with inflammatory raised borders and plaque-type inflammatory erythema have also been reported.
- Halo nevi may be present.
Causes
The cause of VKH syndrome is unknown, but a viral factor has been suggested in the pathogenesis. An autoimmune reaction to melanocytes with the involvement of T-cell–mediated cytotoxicity and apoptosis is postulated. Although almost all instances of VKH syndrome are sporadic, and familial cases are rare, some authors suggest that the condition may be inherited, probably as an autosomal recessive trait. Numerous data demonstrate the association of HLA-DR4 antigen and VKH syndrome in different racial groups. According to recent studies, the major factor contributing to susceptibility for the disease is presence of the DRB*0405 allele (Goldberg, 1998).
Alezzandrini Syndrome
Alopecia Areata
Piebaldism
Vitiligo
Other Problems to be Considered
Vitiligo with poliosis
Lab Studies
- For quick diagnosis and early treatment, VKH syndrome requires a multidisciplinary management strategy involving dermatologists and ophthalmologists.
- Perform neurologic examination with lumbar puncture to detect associated abnormalities.
- Detailed CSF cell analysis is necessary. Changes in the CSF include pleocytosis with the presence of melanin-laden macrophages (specific for the syndrome and helpful in confirming the diagnosis), increased protein levels, and increased pressure.
Imaging Studies
- Standardized A-scan and contact B-scan echography, performed by ophthalmologist
Procedures
- Perform fluorescein angiography, which shows multiple hypofluorescent areas in the retina at the level of the retinal pigment epithelium.
- Perform indocyanine green choroidal angiography.
- Audiometry may reveal sensorineural hearing loss.
Histologic Findings
A skin biopsy specimen taken a month after the onset of ocular symptoms will likely reveal a mononuclear infiltrate concentrated in the area of hair follicles and sweat glands, consisting mostly of T lymphocytes with a small number of B cells. In depigmented skin, the absence of melanin, as anticipated in vitiligo, can be noted. Vasodilatation in the dermis, pigment-laden macrophages, and a lymphocytic infiltrate have also been described.
Medical Care
- For pigmentary changes, treatment options mirror those for vitiligo.
- For eye inflammatory changes, treatment includes systemic corticosteroids, with an average initial dose of 80-100 mg of oral prednisone per day. Early, aggressive use of systemic corticosteroids and a gradual tapering of drug dosage for 6 months after presentation are recommended to prevent progression and development of complications. Some authors recommend pulse corticosteroid therapy.
- In patients whose conditions fail to respond to high-dose corticosteroid (oral or intravenous) therapy or who develop significant adverse effects, immunosuppression with cyclosporine or other antimetabolites (eg, azathioprine, cyclophosphamide, methotrexate [MTX]) may be required.
- Topical and periocular corticosteroids are used. Cycloplegic-mydriatic eye drops are used symptomatically.
Surgical Care
- Surgical therapy for glaucoma is necessary in some patients. Surgical intervention includes laser iridotomy, surgical iridectomy, and trabeculectomy.
Consultations
Ophthalmologists and neurologists must be consulted.
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Drug Category: Corticosteroids
Have anti-inflammatory properties and cause profound and varied metabolic effects. Modify the body's immune response to diverse stimuli.
| Drug Name | Prednisone (Deltasone, Orasone) |
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| Description | Synthetic adrenocortical steroid with predominantly glucocorticoid properties. Immunosuppressant for treatment of autoimmune disorders; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and suppresses lymphocytes and antibody production. |
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| Adult Dose | 60-100 mg PO every am or more often prn |
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| Pediatric Dose | Initial: 0.14-2 mg/kg/d PO divided tid/qid (4-60 mg/m2/d) |
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| Contraindications | Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective-tissue infections; fungal or tubercular skin infections; GI tract disease |
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| Interactions | Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics |
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| Pregnancy | C - Safety for use during pregnancy has not been established.
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| Precautions | Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use |
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Drug Category: Immunosuppressive agents
Have antiproliferative and immunosuppressive effects.
| Drug Name | Azathioprine (Imuran) |
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| Description | May be used alone or as steroid-sparing agent. Antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. May decrease proliferation of immune cells, resulting in lower autoimmune activity. |
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| Adult Dose | 100-200 mg PO qd in combination with prednisone |
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| Pediatric Dose | Not established |
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| Contraindications | Documented hypersensitivity; deficiency of thiopurine methyltransferase |
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| Interactions | Toxicity increases with allopurinol; concurrent use with ACE inhibitors may induce severe leukopenia; may increase levels of MTX metabolites and decrease effects of anticoagulants, neuromuscular blockers, and cyclosporine |
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| Pregnancy | D - Unsafe in pregnancy
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| Precautions | Adverse effects include teratogenicity, hepatitis, bone marrow suppression, and increased risk of cancer; before initiating therapy and regularly thereafter, monitor urinalysis, CBC count, renal and LFTs, and serum electrolyte levels; increases risk of neoplasia; caution with liver disease and renal impairment; hematologic toxicities may occur, check thiopurine methyltransferase prior to treatment |
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| Drug Name | Cyclophosphamide (Cytoxan, Neosar) |
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| Description | May be used as monotherapy or as a steroid-sparing agent. Chemically related to nitrogen mustards. 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. |
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| Adult Dose | 50-100 mg IV qd in combination with prednisone |
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| Pediatric Dose | Not established |
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| Contraindications | Documented hypersensitivity; severely depressed bone marrow function; renal insufficiency; cystitis |
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| Interactions | Allopurinol may increase risk of bleeding or infection and enhance myelosuppressive effects; may potentiate doxorubicin-induced cardiotoxicity; may reduce digoxin serum levels and antimicrobial effects of quinolones; chloramphenicol may increase half-life while decreasing metabolite concentrations; may increase effect of anticoagulants; coadministration with high doses of phenobarbital may increase rate of metabolism and leukopenic activity; thiazide diuretics may prolong cyclophosphamide-induced leukopenia and neuromuscular blockade by inhibiting cholinesterase activity |
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| Pregnancy | D - Unsafe in pregnancy
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| Precautions | Regularly examine hematologic profile (particularly neutrophils and platelets) to monitor for hematopoietic suppression; regularly examine urine for RBCs, which may precede hemorrhagic cystitis; agent is teratogenic and may cause nausea, vomiting, alopecia, sterility, hemorrhagic cystitis, bone marrow suppression, and increased risk of cancer |
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| Drug Name | Methotrexate (Folex PFS, Rheumatrex) |
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| Description | Unknown mechanism of action in treatment of inflammatory reactions; may affect immune function. Ameliorates symptoms of inflammation (eg, pain, swelling, stiffness). Gradually adjust dose to attain satisfactory response. |
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| Adult Dose | 7.5 mg/wk or 2.5 mg PO/IM bid for 3 doses qwk |
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| Pediatric Dose | 5-15 mg/m2/wk PO/IM as single dose or 3 divided doses administered 12 h apart |
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| Contraindications | Documented hypersensitivity; alcoholism; hepatic insufficiency; documented immunodeficiency syndromes; preexisting blood dyscrasias (eg, bone marrow hypoplasia, leukopenia, thrombocytopenia, significant anemia); renal insufficiency |
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| Interactions | Oral aminoglycosides may decrease absorption and blood levels of concurrent oral MTX; charcoal lowers levels; coadministration with etretinate may increase hepatotoxicity; folic acid or its derivatives contained in some vitamins may decrease response; coadministration with NSAIDs may cause death; indomethacin and phenylbutazone can increase plasma levels; may decrease phenytoin serum levels; probenecid, salicylates, procarbazine, and sulfonamides, including TMP-SMZ, may increase effects and toxicity; may increase plasma levels of thiopurines |
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| Pregnancy | D - Unsafe in pregnancy
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| Precautions | Initially monitor CBC count weekly for 1 month and liver function pretreatment; then, monitor CBC counts monthly, and liver and renal function q1-3mo during therapy (monitor more frequently during initial dosing, dose adjustments, or when risk of elevated MTX levels, eg, dehydration); has toxic effects on hematologic, renal, GI, pulmonary, and neurologic systems; discontinue if significant drop in blood cell counts; aspirin, NSAIDs, or low-dose steroids may be administered concomitantly (possibility of increased toxicity with NSAIDs, including salicylates, has not been tested) |
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Further Outpatient Care
- Follow routine outpatient care guidelines.
Complications
- Long-term complications include reversible and irreversible vision loss, intraocular pressure elevation, glaucoma, and cataracts.
- Ocular complications are more severe in children than in adults, leading to rapid deterioration in vision.
Prognosis
- Pigmentary changes are usually permanent.
- Final visual outcome depends on the rapidity and appropriateness of treatment.
- Hearing is restored completely in most patients.
Medical/Legal Pitfalls
- Delayed or missed diagnosis
- Failure to provide rapid and appropriate treatment for the best visual outcome
- Failure to monitor patients on systemic therapy for adverse effects, toxicity, and response
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Vogt-Koyanagi-Harada Syndrome excerpt Article Last Updated: Dec 6, 2006
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