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Curr Eye Res. 2008 Jul;33(7):517-23. doi: 10.1080/02713680802233968.

Vogt-koyanagi-harada syndrome.

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The First Affiliated Hospital of Chongqing Medical University, Chongqing, P. R. China.

Erratum in

  • Curr Eye Res. 2008 Sep;33(9):812..



Vogt-Koyanagi-Harada syndrome is a bilateral, chronic, diffuse granulomatous panuveitis frequently associated with neurological, auditory, and integumentary manifestations. It is also one of the most common forms of uveitis among pigmented races including Chinese patients.


This article reviews the current developments of Vogt-Koyanagi-Harada syndrome, including epidemiology, etiology, clinical features, observational techniques, genetics, treatment, and prognosis.


Increasing reports have been published to describe the clinical features of Vogt-Koyanagi-Harada syndrome in various ethnic populations from different parts of the world. In spite of tremendous progress in laboratory and clinical research, the etiology of Vogt-Koyanagi-Harada syndrome is still not completely known. Numerous studies indicate an autoimmune nature for this disease. A recent study has shown that Th17, a new subset of T cell, plays an important role in the initiation and maintenance of this disease. Early and aggressive systemic corticosteroids are still the mainstay of initial therapy for Vogt-Koyanagi-Harada syndrome. However, nonsteroid immunomodulatory therapy, including cyclosporine, chlorambucil, cyclophosphamide, and azathioprine have brought out encouraging results. Improved visual outcomes in patients with Vogt-Koyanagi-Harada syndrome in recent years have been reported when compared with decades ago, presumably due to the more aggressive use of immunosuppressive agents.


Although the prognosis for VKH syndrome was greatly improved, future prospective, controlled, multi-center studies are needed to determine the optimal treatment regime for this disease. The IL17/23 pathway may provide a novel therapeutic target to control inflammation in VKH syndrome.

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