Presentations

Abstract

Introduction: Dupilumab, a monoclonal antibody targeting the interleukin (IL)-4 and (IL)-13 receptor subunit α, developed as an opportune therapeutic modality for moderate to severe atopic dermatitis (AD) is also approved by the Food and Drug Administration (FDA) for treatment of prurigo nodularis (PN), severe bronchial asthma, and chronic rhinosinusitis with nasal polyps. Reports have surfaced of papulosquamous psoriasiform skin changes developing in patients treated with dupilumab, including dupilumab induced cases of psoriasis, psoriasiform eruptions, and psoriasiform dermatitis. This report highlights a comparable phenomenon in a 57-year old female revealing itself after one year of treatment with dupilumab PN.

Case Information: We present the case of a 57-year-old female diagnosed with prurigo nodularis (PN) two and a half years prior, who developed erythematous, scaly, well-demarcated patches on her palms and soles after one year of successful dupilumab therapy. Despite previous treatments with clobetasol, UVA1 phototherapy, and methotrexate, among others, the patient showed marked hyperkeratosis with patchy parakeratosis and hypergranulosis consistent with psoriasiform chronic spongiotic dermatitis upon biopsy. This case highlights a dupilumab-induced palmoplantar psoriasiform dermatitis that emerged during therapy.

Discussion/Clinical Findings: Palmoplantar psoriasis (PP) is a distinct subtype of psoriasis affecting the palms and soles, often misdiagnosed due to its clinical overlap with chronic eczema and other dermatoses. Dupilumab, a monoclonal antibody targeting IL-4 and IL-13, has been associated with psoriasis, psoriasiform eruptions, and psoriasiform dermatitis as a side effect, possibly due to a shift in the immune response from a Th2 to a Th1/Th17 phenotype. The complexity of diagnosing and managing PP underscores the importance of a thorough clinical and histopathological evaluation to differentiate it from similar conditions. The balance between Th1 and Th2 pathways is crucial in the pathogenesis of both PN and psoriasis, with dupilumab potentially disrupting this balance, leading to psoriatic manifestations.

Conclusion: This case underscores the potential for dupilumab to induce psoriasiform dermatitis, highlighting the importance of comprehensive diagnostic approaches and careful management of dupilumab therapy. While dupilumab provided significant relief from PN symptoms, the emergence of psoriasiform dermatitis necessitates a balanced consideration of treatment benefits and risks. Ongoing monitoring and personalized treatment adjustments are essential to optimize patient outcomes, and further research is needed to better understand the mechanisms driving dupilumab-induced psoriatic conditions.