Improvement of Dupilumab‐Induced Psoriasiform Eruption Following a Switch to Tralokinumab

Biologic therapies have transformed the management of atopic dermatitis (AD) and prurigo nodularis (PN), yet paradoxical adverse events such as dupilumab‐induced psoriasiform eruption (DPE) are increasingly recognized. We report a 48‐year‐old Japanese man with long‐standing AD and PN who developed scaly, erythematous plaques on the elbows, hands, and trunk 5 months after initiating dupilumab. While prurigo nodules had markedly improved, the new lesions resembled psoriasis clinically. A biopsy from the elbow revealed features consistent with psoriasiform dermatitis—regular acanthosis, thickened granular layer, and perivascular lymphocytic infiltration without neutrophils—suggesting DPE rather than true psoriasis. Topical vitamin D3 and corticosteroids were ineffective, prompting a switch to tralokinumab, an IL‐13–specific inhibitor. Following this transition, psoriasiform lesions on the trunk and hands resolved, and PN did not recur. However, plaques on both elbows persisted for over a year and remained after tralokinumab discontinuation. Histologically, these lesions lacked features of psoriasis and were more consistent with PN, suggesting a Th2‐driven relapse mimicking psoriasiform disease. This case highlights the potential of tralokinumab to manage DPE while sustaining PN control but also underscores the heterogeneity of psoriasiform eruptions during type 2 biologic therapy. Not all lesions represent Th1/Th17‐mediated processes; some may reflect residual Th2‐driven disease such as PN with atypical morphology. Histopathological evaluation is essential for distinguishing true paradoxical reactions from overlapping or relapsing dermatoses and for guiding optimal treatment selection in patients receiving targeted immunomodulators.