Vogt-Koyanagi-Harada Disease: Extensive Vitiligo with Prodromal Generalized Erythroderma

Abstract

The occurrence of vitiligo with prodromal erythema in Vogt-Koyanagi-Harada (VKH) disease is rarely observed. We describe a 68-year-old Chinese woman who developed extensive vitiligo 6 months after the onset of a generalized erythroderma and 12 months after the onset of acute bilateral uveitis. She also had a 4-year history of psoriatic plaques on the trunk which resolved completely without recurrence 15 months after the onset of erythroderma. The extensive cutaneous inflammation prior to the onset of vitiligo in our patient with VKH disease has not been reported before and strongly suggests an immunologic etiology for VKH disease.

Vitiligo: A comprehensive overview

“…97 Vogt-Koyanagi-Harada disease is a rare systemic T-cell mediated disorder characterized by uveitis, aseptic meningitis, dysacusis, alopecia, poliosis, tinnitus, and vitiligo (8-100%). [98][99][100][101][102][103][104] Kabuki syndrome is a rare multiple malformation disorder that is characterized by developmental delay, distinct facial anomalies, congenital heart defects, limb and skeletal anomalies, and short 110 Vitiligo lesions typically appear unremarkable with only scant cellular infiltrates and few or no melanocytes. 72 Melanocytes on the pigmented edge of vitiliginous skin are larger, often vacuolated, and with long dendritic processes filled with melanin granules.…”

Disorders of pigmentation

“…222 It may be less expensive than the widely used cosmetic camouflages, such as Dermablend ® and Covermark ® . 132 A rare variant of this syndrome with inflammatory vitiligo has been described. 128 The best known of these is the Vogt-Koyanagi-Harada syndrome, which includes uveitis, poliosis, dysacusis, alopecia, 129 vitiligo, and signs of meningeal irritation.…”

Primary Cutaneous Cryptococcosis Presenting as a Whitlow

“…The onset of vitiligo after prodromal erythroderma has been reported previously (3,9). However, to our knowledge, widespread vitiligo following erythrodenna caused by nevirapine has not been reported previously.…”

“…Thus, the development of vitiligo in HIV-infected patients may be due to an autoimmune inflammatory reaction in a genetically predisposed host (5). In accordance with these theories, the role of cell-mediated immunity for melanocytic destruction in classical vitiligo has been postulated based on the increased number of CD8^ cytotoxic T cells in lesional skin as well as in peripheral blood (9), together with a decrease in CD4* T cells (10,II), leading together to an increased CD8VCD4'ratio. Thus, in accordance with these data, the decreased number of CD4" peripheral T cells usually observed in patients with AIDS, which is closely correlated with disease stage, could also favour the development of vitiligo in these patients.…”