Case Report: bullous pemphigoid during secukinumab treatment for plaque psoriasis: therapeutic challenges and long-term follow-up
- 1Department of Dermatology, Zhongnan Hospital of Wuhan University
Abstract
Background: Bullous pemphigoid (BP) may occur during interleukin-17A inhibitor therapy in patients with psoriasis. Most reported cases have focused on BP onset and short-term management, with limited information on long-term outcomes and subsequent targeted treatment.
Case presentation: A 68-year-old man with a history of severe plaque psoriasis for more than 20 years developed generalized pruritic tense bullae after 10 injections of secukinumab, despite improvement of his psoriatic lesions. Laboratory testing showed peripheral eosinophilia, elevated total immunoglobulin E, anti-BP180 antibody levels above 400 RU/mL, and an anti-BP230 antibody level of 344.06 RU/mL. Histopathology demonstrated a subepidermal blister with eosinophil-rich inflammation, and direct immunofluorescence showed linear IgG and C3 deposition along the basement membrane zone, confirming BP. Secukinumab was discontinued, and treatment with prednisone, cyclosporine, minocycline, nicotinamide, and topical corticosteroids rapidly controlled blister formation. Psoriasis subsequently remained inadequately controlled despite sequential treatment with tildrakizumab and ustekinumab. In June 2025, BP remained clinically quiescent, although anti-BP180 antibodies exceeded 400 RU/mL, total immunoglobulin E exceeded 1,100 kU/L, and C3 deposition persisted along the basement membrane zone. Deucravacitinib was subsequently administered for approximately 6 months, during which psoriasis improved from moderate to mild severity without clinical recurrence of BP. At the latest structured telephone follow-up, approximately 6 months after deucravacitinib discontinuation, the patient reported that psoriasis remained mild and stable and that no BP manifestations had recurred.
Conclusion: This case provides more than two years of longitudinal follow-up after BP developed during secukinumab treatment. It illustrates the challenges of sequential targeted therapy for coexisting psoriasis and BP and shows that clinical quiescence may coexist with persistent BP-associated serological and immunopathological abnormalities. Continued clinical and immunological monitoring is advisable when switching therapeutic targets in these patients.
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BibTeX
@article{deng2026case,
title = {{Case Report: bullous pemphigoid during secukinumab treatment for plaque psoriasis: therapeutic challenges and long-term follow-up}},
author = {Han Deng and Hongli Rao and Si Jiang and Jun Xie},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1964020},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1964020/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Case Report: bullous pemphigoid during secukinumab treatment for plaque psoriasis: therapeutic challenges and long-term follow-up
AU - Han Deng
AU - Hongli Rao
AU - Si Jiang
AU - Jun Xie
PY - 2026
DA - 2026/10/20
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1964020
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1964020/full
AB - Background: Bullous pemphigoid (BP) may occur during interleukin-17A inhibitor therapy in patients with psoriasis. Most reported cases have focused on BP onset and short-term management, with limited information on long-term outcomes and subsequent targeted treatment. Case presentation: A 68-year-old man with a history of severe plaque psoriasis for more than 20 years developed generalized pruritic tense bullae after 10 injections of secukinumab, despite improvement of his psoriatic lesions. Laboratory testing showed peripheral eosinophilia, elevated total immunoglobulin E, anti-BP180 antibody levels above 400 RU/mL, and an anti-BP230 antibody level of 344.06 RU/mL. Histopathology demonstrated a subepidermal blister with eosinophil-rich inflammation, and direct immunofluorescence showed linear IgG and C3 deposition along the basement membrane zone, confirming BP. Secukinumab was discontinued, and treatment with prednisone, cyclosporine, minocycline, nicotinamide, and topical corticosteroids rapidly controlled blister formation. Psoriasis subsequently remained inadequately controlled despite sequential treatment with tildrakizumab and ustekinumab. In June 2025, BP remained clinically quiescent, although anti-BP180 antibodies exceeded 400 RU/mL, total immunoglobulin E exceeded 1,100 kU/L, and C3 deposition persisted along the basement membrane zone. Deucravacitinib was subsequently administered for approximately 6 months, during which psoriasis improved from moderate to mild severity without clinical recurrence of BP. At the latest structured telephone follow-up, approximately 6 months after deucravacitinib discontinuation, the patient reported that psoriasis remained mild and stable and that no BP manifestations had recurred. Conclusion: This case provides more than two years of longitudinal follow-up after BP developed during secukinumab treatment. It illustrates the challenges of sequential targeted therapy for coexisting psoriasis and BP and shows that clinical quiescence may coexist with persistent BP-associated serological and immunopathological abnormalities. Continued clinical and immunological monitoring is advisable when switching therapeutic targets in these patients.
SN - 1664-3224
ER -