This Article  • Full text  • PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citing articles on ISI (2)  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Topic Collections  • Uveitis  • Alert me on articles by topic

Arch Ophthalmol. 2004;122:1878-1881.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Vogt-Koyanagi-Harada (VKH) syndrome is an autoimmune disorder against melanocytes causing inflammation of melanocyte-containing tissues, such as uvea, skin, ear, and meninges. Patients with VKH syndrome usually have bilateral granulomatous panuveitis associated with poliosis, vitiligo, alopecia, dysacousia, and signs of meningeal irritation.

The exact pathogenesis of VKH syndrome is not certain. Sugiura¹ reported that autoantibodies of VKH play a major role in melanocyte destruction via antibody-dependent, cell-mediated cytotoxicity. Melanocyte-specific antigens, such as tyrosinase proteins, can induce a VKH-like autoimmune condition in rats and have been considered to be VKH specific.² Previous viral infection might trigger immune reactions because of the homology in protein sequence between such microorganisms and ocular antigens, a process known as molecular mimicry.³ The strong associations of HLA-DR53, HLA-DR4, and HLA-DQ4 antigens with VKH syndrome further underscore an immunogenetic mechanism of the disease.⁴

Because of the variations in the clinical manifestation of VKH syndrome, early detection and accurate . . . [Full Text of this Article]

Report of a Case


Comment

AUTHOR INFORMATION
Mei-Chuan Yang, MD; Andrew J. W. Huang, MD, MPH