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Purpose: To report an unusual case of incomplete Vogt-Koyanagi-Harada (VKH) in a 14-Year-Old African American female. Observations: Here we present a 14-Year-Old African American Female with incomplete VKH who presented to the emergency department with a one-month history of malaise, fever, bilateral decreased vision and temporal headaches. At the time of presentation, she was found to have bilateral anterior uveitis and disc edema. The brain and orbit MRI were unremarkable, CSF analysis showed lymphocytic pleocytosis with negative cultures and gram stain. An extensive lab workup was unrevealing. Conclusion: This is an unusual case of incomplete VKH in a young African American female presenting with anterior uveitis and disc edema without serous retinal detachments. Initiation of high dose oral prednisone promptly after diagnosis resulted in rapid improvement of symptoms and improvement in visual acuity with the resolution of the disc edema. This case highlights the importance of considering VKH in the differential diagnosis of disc edema associated with uveitis, even in the absence of serous retinal detachment.

ABSTRACT: Objective: Lenalidomide is a thalidomide analogue used to treat multiple myeloma, myelodysplastic syndromes, and solid cancers. It has been associated with thyroid abnormalities, mostly primary hypothyroidism, though rarely thyrotoxicosis. We present a case of lenalidomide-induced painless thyroiditis with initial thyrotoxicosis presentation followed by hypothyroidism requiring levothyroxine treatment in a 62-year old male with diffuse large B-cell lymphoma.Methods: The identified case is described.Results: The patient had no history of thyroid disease, with normal baseline thyroid function tests prior to lenalidomide treatment. He developed painless thyrotoxicosis after 1 week of treatment. The thyrotoxicosis resolved spontaneously, and he became euthyroid after withholding lenalidomide for 6 weeks. He was then restarted on a lower dose and developed recurrent painless thyroiditis 2 weeks later, with suppressed thyroid-stimulating hormone (TSH) of 0.05 μU/mL and elevated free thyroxine (FT4) of 2.02 ng/dL, prompting a more detailed evaluation. His thyroid-stimulating immunoglobulin, thyroperoxidase (TPO), and thyroglobulin (Tg) antibodies were not elevated. Tg was significantly elevated at 679 ng/mL. A thyroid pertechnetate scan revealed minimal uptake. There were no interim medication changes, recent iodine load, viral illness, or amiodarone or interferon treatment, suggesting he had lenalidomide-induced thyroiditis. Thyrotoxicosis again spontaneously resolved, but 3 months later, he developed hypothyroidism that required levothyroxine. Lenalidomide was later stopped, but the patient has continued to require levothyroxine therapy.Conclusion: As the medical uses for lenalidomide expand, this case stresses the importance of monitoring thyroid function in patients taking lenalidomide.Abbreviations: DLBCL = diffuse large B-cell lymphoma FT4 = free thyroxine Tg = thyroglobulin TPO = thyroperoxidase TSH = thyroid-stimulating hormone