article · SAS Journal of Medicine
Secukinumab is an interleukin-17A inhibitor commonly prescribed for moderate-to-severe plaque psoriasis. A clinical report documents a 79-year-old male with a twenty-year history of severe psoriasis who developed bullous pemphigoid associated with this medication. Following ten months of effective therapy and a three-month interruption, resuming secukinumab led to severe itching and rapid emergence of widespread, tense blistering lesions within one month. Diagnostic examinations, including histopathology and direct immunofluorescence, confirmed bullous pemphigoid characterised by subepidermal splitting and linear basement membrane deposits of IgG and C3. Although topical corticosteroids and oral doxycycline initially eased symptoms, a subsequent scheduled secukinumab injection caused a swift recurrence of blisters. Complete lesion resolution occurred only after the biologic was permanently discontinued. Clinicians are advised to maintain vigilance for rare autoimmune blistering conditions in patients taking interleukin-17A inhibitors, particularly following treatment breaks.
Biologic medications targeting interleukin-17A are widely used to manage severe autoimmune skin conditions. Recognising that these therapies can paradoxically trigger rare, severe blistering reactions such as bullous pemphigoid is vital for patient safety. Prompt recognition allows clinicians to correctly identify adverse drug effects, withdraw the implicated treatment, and manage flares effectively, particularly when patients resume therapies after a period of non-adherence.
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Background: Drug-induced bullous pemphigoid is a rare cutaneous adverse reaction linked to various systemic medications. Secukinumab, an interleukin-17A inhibitor widely used for moderate-to-severe psoriasis, has rarely been implicated in the development of bullous pemphigoid. Case Presentation: A 79-year-old male with a 20-year history of severe plaque psoriasis—previously recalcitrant to topical corticosteroids and methotrexate—was treated with secukinumab. After 10 months of successful therapy, treatment was interrupted for 3 months due to poor adherence before being resumed. One month post-reinitiation, the patient developed intense pruritus and tense bullous lesions on the upper and lower extremities, rapidly generalizing within days. Histopathological examination revealed a subepidermal split, and direct immunofluorescence demonstrated linear, homogeneous deposition of C3 and IgG along the basement membrane zone, confirming bullous pemphigoid. Treatment with topical corticosteroids and oral doxycycline led to significant clinical improvement within two weeks. However, re-challenge via his subsequent scheduled secukinumab injection triggered a rapid flare of bullous lesions. Definitive discontinuation of secukinumab resulted in lesion clearance and complete resolution. Conclusion: Clinicians should remain vigilant regarding the rare potential of interleukin-17A inhibitors, such as secukinumab, to induce autoimmune blistering conditions like bullous pemphigoid, particularly following drug reintroduction or interruption.
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DOI: 10.36347/sasjm.2026.v12i09.006
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