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Abstract
Purpose: 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. Methods: This article reviews the current developments of Vogt-Koyanagi-Harada syndrome, including epidemiology, etiology, clinical features, observational techniques, genetics, treatment, and prognosis. Results: 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. Conclusion: 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.
| ABBREVIATIONS | ||
| BAB | = | blood-aqueous barrier |
| CMV | = | cytomegalovirus |
| CNV | = | choroidal neovascularization |
| CSF | = | cerebrospinal fluid |
| CTLA-4 | = | cytotoxic T lymphocyte-associated antigen-4 |
| EB virus | = | Epstein-Barr virus |
| HLA | = | human leukocyte antigen |
| IMT | = | immunomodulatory therapy |
| IFN | = | interferon |
| IUSG | = | International Uveitis Study Group |
| LFCM | = | laser flare photometry |
| mfERG | = | multifocal electroretinography |
| PBMCs | = | peripheral blood mononuclear cells |
| PDT | = | photodynamic therapy |
| RPE | = | retinal pigment epithelium |
| VKH syndrome | = | Vogt-Koyanagi-Harada syndrome |
| ABBREVIATIONS | ||
| BAB | = | blood-aqueous barrier |
| CMV | = | cytomegalovirus |
| CNV | = | choroidal neovascularization |
| CSF | = | cerebrospinal fluid |
| CTLA-4 | = | cytotoxic T lymphocyte-associated antigen-4 |
| EB virus | = | Epstein-Barr virus |
| HLA | = | human leukocyte antigen |
| IMT | = | immunomodulatory therapy |
| IFN | = | interferon |
| IUSG | = | International Uveitis Study Group |
| LFCM | = | laser flare photometry |
| mfERG | = | multifocal electroretinography |
| PBMCs | = | peripheral blood mononuclear cells |
| PDT | = | photodynamic therapy |
| RPE | = | retinal pigment epithelium |
| VKH syndrome | = | Vogt-Koyanagi-Harada syndrome |