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Published on: May 10, 2022
Vogt-koyanagi-harada syndrome
1The First Affiliated Hospital of Chongqing Medical University, Chongqing, P. R. China. peizengy@126.com
Vogt-Koyanagi-Harada syndrome, a form of uveitis, is increasingly understood to have an autoimmune basis involving Th17 cells. Early aggressive treatment with corticosteroids and immunomodulators improves visual outcomes, with new therapeutic targets emerging.
Area of Science:
- Ophthalmology
- Immunology
- Genetics
Background:
- Vogt-Koyanagi-Harada (VKH) syndrome is a chronic, diffuse granulomatous panuveitis.
- It commonly affects individuals of pigmented races and presents with neurological, auditory, and integumentary symptoms.
- VKH syndrome is a significant cause of uveitis worldwide.
Purpose of the Study:
- To review current developments in Vogt-Koyanagi-Harada syndrome.
- To cover epidemiology, etiology, clinical features, diagnostics, genetics, treatment, and prognosis.
- To highlight advancements in understanding and managing this condition.
Main Methods:
- Literature review of recent studies on Vogt-Koyanagi-Harada syndrome.
- Analysis of clinical features across diverse ethnic populations.
- Examination of immunological and genetic factors.
Main Results:
- The etiology of VKH syndrome remains incompletely understood but is strongly indicated as autoimmune.
- Th17 cells play a crucial role in the disease's initiation and progression.
- Aggressive early treatment with corticosteroids and immunomodulatory agents like cyclosporine, chlorambucil, cyclophosphamide, and azathioprine has improved visual outcomes.
Conclusions:
- Prognosis for VKH syndrome has significantly improved due to aggressive immunosuppressive therapy.
- Further multi-center studies are required to establish optimal treatment protocols.
- Targeting the IL17/23 pathway presents a promising therapeutic strategy for VKH syndrome.
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