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Abstract Details

Vogt-Koyanagi-Harada Syndrome: A COVID Sequela?
Autoimmune Neurology
P2 - Poster Session 2 (2:45 PM-3:45 PM)
039

We report a case of Vogt-Koyanagi-Harada disease (VKH) in a young male patient in the setting of COVID-19 infection.

VKH is a T-cell mediated multi-systemic autoimmune inflammatory disorder presenting with skin, ocular, auditory and neurologic involvement. T-cells target melanocytes, resulting in four distinct disease phases: prodromal, uveitis, convalescent, and recurrent. Intraocular inflammation is T-cell mediated and granulomatous in nature, leading to vitritis, disk edema, serous retinal detachments, sunset glow fundus, cataracts, glaucoma, subretinal fibrosis, and choroidal neovascularization. Symptoms include headache, meningismus, hearing loss, poliosis, alopecia, and vitiligo. It is most prevalent in Asians, Native Americans, Hispanics, and Middle Easterners.

All procedures performed in this de-identified, retrospective case report adhered to the Declaration of Helsinki.

A 27-year-old man with no past medical history presented with a two-week history of intermittent unilateral headache, bilateral eye pain with photophobia, and phonophobia, followed by tinnitus and blurry vision, which ultimately progressed to total bilateral vision loss. VDRL, FTA, QuantiFERON gold, flow cytometry, cytology, and cultures were all negative, except for moderate pleocytosis with lymphocytic predominance and elevated CSF protein. COVID-19 PCR was positive. CT, B-scan, and MRI showed bilateral retinal detachment with no optic nerve involvement. Fundus fluorescein angiography of the bilateral retinal vessels revealed mottled hyperfluorescence and hypofluerescence and bilateral fundus autofluorescence associated with retinal pigment epithelium detachment consistent with VKH.

VKH is a rare and potentially debilitating disorder in which severe complications can be avoided by early diagnosis and adequate treatment. Mainstay treatment includes corticosteroids and immunosuppressants. Viral infections such as cytomegalovirus (CMV) have been reported to trigger the development of VKH, possibly due to underlying molecular mimicry. COVID-19 was a potential immunological trigger of VKH in our patient, given infection onset was prior to the 2-week history of VKH onset. Although rare, COVID-19 may be considered a precipitant of VKH.

Authors/Disclosures
Tiffany A. Eatz, MD (University of Miami Miller School of Medicine)
PRESENTER
Dr. Eatz has nothing to disclose.
Jude H. Charles, MD Dr. Charles has nothing to disclose.