INTRODUCTION
Psoriasis (PsO) and atopic dermatitis (AD) immunopathogeneses are canonically driven by 2 distinct T-cell-mediated responses. In psoriasis, Th1/Th17 pathways mediated by interleukin (IL)-23/IL-17 cell-mediated signaling, while AD is marked by Th2/Th22 predominant humoral inflammatory response, eliciting IL-4, IL-13, and IL-22.1 However, certain AD subtypes (eg, intrinsic, pediatric, Asian adults) demonstrate evidence of Th2, Th17, and Th22 co-expression, resulting in a more psoriasiform phenotype.2 Several cases have also been reported of exacerbations following “unilateral” suppression of this spectrum, with cases of paradoxical reactions in which patients with psoriasis develop eczematous eruptions after initiating anti-IL-17/IL-23 biologics and psoriasiform dermatitis after AD biologics.3-5 These examples support the idea of a potential PsO-AD spectrum.
Here, we present a case of psoriasiform spongiotic dermatitis in a patient with a long-standing history of biopsy-proven psoriasis and resolution with dual biologic therapy (DBT). We also examine the PsO-AD immunopathogenic spectrum and relevant implications for long-term care, sequelae, and adverse events (AEs).
Here, we present a case of psoriasiform spongiotic dermatitis in a patient with a long-standing history of biopsy-proven psoriasis and resolution with dual biologic therapy (DBT). We also examine the PsO-AD immunopathogenic spectrum and relevant implications for long-term care, sequelae, and adverse events (AEs).
CASE REPORT
An 80-year-old black veteran with a 20-year history of severe psoriasis (body surface area [BSA] range: 10-75%+), who had failed multiple treatments (Table 1), now on secukinumab, with previously treated hepatitis B (HBV) and C (HCV) and gout was urgently referred to our clinic. He presented with 4 days of severely pruritic papulosquamous plaques on the upper back and bilateral lower extremities, with some showing significant impetiginization (Figure 1). For the past year (since 4/2021), he had been on secukinumab 300 mg every 3 weeks (increased from every 4 weeks due to frequent “exacerbations”), but reported missing his last dose. The patient also self-discontinued concurrent topical therapies (eg, clobetasol and calcipotriene) 2 days prior to presentation. A review of systems was otherwise negative, and he denied any new medications or recent illnesses.
On physical examination, there were diffuse eczematous plaques with thick scale and excoriations on the trunk, buttocks, and bilateral arms/legs (~80% BSA; Figures 1A-C). Labs were notable for peripheral eosinophilia in June 2021 (relative: 20.9%, absolute: 0.98x103 cells/μL [normal: 0-0.45x103 cells/μL]) and October 2022 (relative: 18.7%, absolute: 0.71x103 cells/μL). Biopsies from March/October 2005 and January 2011 (prior biologics) demonstrated classical psoriasis (Figures 2A-C);
On physical examination, there were diffuse eczematous plaques with thick scale and excoriations on the trunk, buttocks, and bilateral arms/legs (~80% BSA; Figures 1A-C). Labs were notable for peripheral eosinophilia in June 2021 (relative: 20.9%, absolute: 0.98x103 cells/μL [normal: 0-0.45x103 cells/μL]) and October 2022 (relative: 18.7%, absolute: 0.71x103 cells/μL). Biopsies from March/October 2005 and January 2011 (prior biologics) demonstrated classical psoriasis (Figures 2A-C);