Birdshot chorioretinopathy is a chronic posterior uveitis that often requires systemic immunomodulatory therapy, yet biologic agents, particularly tumor necrosis factor alpha (TNF-α) inhibitors, may trigger paradoxical cutaneous inflammation and complicate multidisciplinary management. A 32-year-old man was evaluated for progressive right eye (RE) visual decline and long-standing floaters. Examination showed bilateral posterior uveitis with chorioretinitis and retinal vasculitis, more severe in the RE, with significant cystoid macular edema (CME) and leakage on fluorescein angiography (FA). Infectious and systemic causes were excluded, and human leukocyte antigen A29 (HLA-A29) was not detected. Systemic methylprednisolone induced partial anatomic improvement but was limited by recurrence during tapering and by intraocular pressure (IOP) elevation, prompting escalation with mycophenolate mofetil and later adalimumab therapy for persistent, refractory CME. After an insufficient response, an intravitreal dexamethasone implant achieved edema regression but was followed by ocular hypertension requiring sustained IOP-lowering therapy. During the same treatment course, new-onset palmoplantar pustular and scalp lesions developed, with steroid-dependent fluctuations, and histopathology showed mild spongiotic dermatitis with Langerhans cell microabscesses; the overall presentation was considered consistent with adalimumab-associated paradoxical psoriasis. Cutaneous disease showed only transient benefit from topical therapy and phototherapy, and an interleukin-17 (IL-17) inhibitor was recommended but declined by the patient. This case illustrates how anti-TNF-α therapy may be insufficient for ocular inflammatory control while precipitating paradoxical psoriasis. Optimal outcomes rely on coordinated ophthalmology-dermatovenereology care when ocular disease activity and treatment-emergent skin complications evolve in parallel.
Naumkinaite et al. (Wed,) studied this question.