Vogt-koyanagi-harada syndrome in a young patient

Abstract

Vogt-Koyanagi-Harada syndrome (VKH), initially described as uveomeningoencephalitic syndrome, is a set of signs and symptoms that involve several organs.1 It was Vogt in 1906 who reported a case of previous uveitis associated with poliosis and dysacusis and in 1926 Harada described the presence of posterior uveitis with exudative retinal detachment, associated with meningeal signs and cerebrospinal fluid pleocytosis.2 In 1929, Koyanagi described patients with bilateral iridocyclitis associated with alopecia and vitiligo, deafness and tinnitus when in the 1940s, Babel recognized VKH syndrome or uveomeningeal syndrome as a single entity.2,3 The syndrome is a bilateral chronic intraocular inflammation associated with neurological and skin changes, including headache, tinnitus, vitiligo, poliosis and alopecia. Visual impairment with headache is the most prevalent complaint and vitreous and anterior chamber cellularity are the most common signs of acute VKH. This condition represents about 2% of the cases referred to the uveitis department.4 It affects adults of both sexes, with a predilection for the female sex, between 20 and 50 years old, and for the black race, oriental and Hispanic.3 It is considered a systemic autoimmune disease characterized mainly by bilateral granulomatous panuveitis, in which antibodies are produced against tissues rich in melanocytes.5