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Relentless Placoid Chorioretinitis in a Patient with Atopic Dermatitis Treated with Dupilumab
Raul E Ruiz-Lozano1, Jessica E Kuhn2, Jonathan Malka2,3
1Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, Florida, USA.
Purpose:
Dupilumab is an injectable human IgG4 monoclonal antibody targeting the IL-4 receptor indicated for moderate to severe atopic dermatitis (AD) refractory to standard topical treatments. We report an association of dupilumab with non-infectious posterior uveitis in a 10-year-old boy.
Methods:
Case report.
Results:
A 10-year-old boy was referred for specialty eye examination due to bilateral blurry vision, redness, and light sensitivity unresponsive to topical ocular corticosteroids in the setting of using dupilumab for severe AD. There was iritis and vitreitis and numerous yellow-white moderate-sized retinochoroidal lesions in both eyes, with evidence of retinal vasculitis in one eye. Optical coherence tomography showed sublesional choroidal swelling with sub-retinal pigment epithelial deposits, full thickness retinal hyperreflectivity, and overlying vitreous cells. Fluorescein angiography revealed early blockage and late staining of lesions. Indocyanine green angiography showed hypofluorescent lesions throughout the course. An extensive immunological and infectious workup was negative. Dupilumab was stopped with some improvement noted. He was started on oral corticosteroids with additional improvement and rapidly transitioned to steroid-sparing therapy with mycophenolate, methotrexate and adalimumab. New retinal hemorrhages and inflammatory signs resolved after starting adalimumab. Visual acuity was maintained at 20/20. He was diagnosed with relentless placoid chorioretinopathy - possible associated with dupilumab use, which was permanently discontinued.
Conclusion:
Relentless placoid chorioretinopathy is a rare sight-threatening posterior uveitis that is ordinarily classified as undifferentiated but, in this case, could be an immunologic reaction to dupilumab. The immunopathogenic mechanism is presumably related to dupilumab-mediated Th2 IL-4/IL-13 dual blockade which polarizes Th17 (IL-23/IL-17) responses.
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