Case Report: Dupilumab-associated psoriasiform eruption followed by depigmentation in a patient with prurigo nodularis and Vogt-Koyanagi-Harada disease
- 1Department of Dermatology, Faculty of Medicine, Fukuoka University
Abstract
Dupilumab blocks interleukin (IL)-4 and IL-13 signaling and is effective for type 2 inflammatory diseases, including atopic dermatitis and prurigo nodularis. Paradoxical psoriasiform eruptions and, less commonly, new-onset or worsening vitiligo have been reported during treatment, suggesting that selective type 2 blockade can alter the cutaneous immune balance in susceptible individuals. We describe a 70-year-old Japanese man with long-standing atopic dermatitis that had evolved into prurigo nodularis and a medical history of Vogt-Koyanagi-Harada (VKH) disease, a melanocyte-directed autoimmune disorder. At follow-up approximately two weeks after a single 600-mg loading dose of dupilumab, the patient presented with a rapidly generalized psoriasiform eruption in a striking distribution that largely spared pre-existing pruriginous nodules. Dupilumab was discontinued, and a biopsy of a new plaque supported a treated or drug-associated psoriasiform inflammatory eruption. Oral cyclosporine was initiated, with improvement of the eruption. Approximately six months after dupilumab administration, marked depigmentation was documented at sites corresponding to the preceding psoriasiform eruption. The pigmentary change was clinically considered severe post-inflammatory hypopigmentation; however, vitiligo remained an important alternative diagnosis because of the patient’s VKH background. The temporal sequence raises the hypothesis that selective type 2 blockade may alter cutaneous immune balance in patients with pre-existing melanocyte-directed autoimmunity, but it does not establish dupilumab-induced vitiligo or systemic VKH reactivation. Broader pathway-directed approaches, including modulation of the IFN-γ–JAK–STAT axis, warrant further investigation in such patients.
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BibTeX
@article{otsuka2026case,
title = {{Case Report: Dupilumab-associated psoriasiform eruption followed by depigmentation in a patient with prurigo nodularis and Vogt-Koyanagi-Harada disease}},
author = {Miku Otsuka and Emi Sato and Shiori Katayama and Shinichi Imafuku},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1991039},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1991039/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Case Report: Dupilumab-associated psoriasiform eruption followed by depigmentation in a patient with prurigo nodularis and Vogt-Koyanagi-Harada disease
AU - Miku Otsuka
AU - Emi Sato
AU - Shiori Katayama
AU - Shinichi Imafuku
PY - 2026
DA - 2026/10/21
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1991039
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1991039/full
AB - Dupilumab blocks interleukin (IL)-4 and IL-13 signaling and is effective for type 2 inflammatory diseases, including atopic dermatitis and prurigo nodularis. Paradoxical psoriasiform eruptions and, less commonly, new-onset or worsening vitiligo have been reported during treatment, suggesting that selective type 2 blockade can alter the cutaneous immune balance in susceptible individuals. We describe a 70-year-old Japanese man with long-standing atopic dermatitis that had evolved into prurigo nodularis and a medical history of Vogt-Koyanagi-Harada (VKH) disease, a melanocyte-directed autoimmune disorder. At follow-up approximately two weeks after a single 600-mg loading dose of dupilumab, the patient presented with a rapidly generalized psoriasiform eruption in a striking distribution that largely spared pre-existing pruriginous nodules. Dupilumab was discontinued, and a biopsy of a new plaque supported a treated or drug-associated psoriasiform inflammatory eruption. Oral cyclosporine was initiated, with improvement of the eruption. Approximately six months after dupilumab administration, marked depigmentation was documented at sites corresponding to the preceding psoriasiform eruption. The pigmentary change was clinically considered severe post-inflammatory hypopigmentation; however, vitiligo remained an important alternative diagnosis because of the patient’s VKH background. The temporal sequence raises the hypothesis that selective type 2 blockade may alter cutaneous immune balance in patients with pre-existing melanocyte-directed autoimmunity, but it does not establish dupilumab-induced vitiligo or systemic VKH reactivation. Broader pathway-directed approaches, including modulation of the IFN-γ–JAK–STAT axis, warrant further investigation in such patients.
SN - 1664-3224
ER -