Mogamulizumab‐Induced Linear IgA Bullous Dermatosis in a Patient With Sézary Syndrome

A 67-year-old woman with Sézary syndrome, diagnosed in May 2024, commenced treatment with mogamulizumab in February 2025 after failure of methotrexate and doxorubicin. One week following the first infusion, she developed an intensely pruritic bullous eruption of 24-h duration involving the forearms and thighs. Examination revealed multiple tense bullae on an erythematous base affecting the limbs, with additional erythematous–oedematous plaques on the trunk and scalp (Figure 1). Nikolsky sign was negative and there was no mucosal involvement. Laboratory investigations were unremarkable except for elevated serum IgA. Indirect immunofluorescence for circulating antibodies to intercellular substance and basement membrane zone was negative. Histopathology demonstrated a subepidermal blister with a predominantly neutrophilic infiltrate and scattered eosinophils (Figure 2A). Direct immunofluorescence showed strong, continuous linear IgA deposition along the basement membrane zone, with accompanying C3 (Figure 2B), consistent with Linear IgA bullous dermatosis (LABD). LABD is an uncommon autoimmune subepidermal blistering disorder characterised clinically by tense vesicles or bullae, sometimes arranged in annular or polycyclic configurations. Diagnosis relies on demonstration of linear IgA deposition at the dermoepidermal junction on direct immunofluorescence. Drug-induced cases are well recognised, most commonly associated with vancomycin 1. Mogamulizumab is a humanised monoclonal antibody targeting CCR4, approved for relapsed or refractory cutaneous T cell lymphomas, including Sézary syndrome 2. Increasing evidence suggests it may trigger immune-related adverse events, including severe cutaneous reactions and autoimmune phenomena 3. The proposed mechanism involves depletion of regulatory T cells, promoting immune dysregulation and autoantibody production 4. In this case, the differential diagnosis included bullous pemphigoid and severe cutaneous adverse reactions. However, the absence of mucosal involvement, neutrophil-predominant subepidermal blistering, and characteristic linear IgA deposition established the diagnosis of LABD. The close temporal relationship with drug initiation supports a drug-induced mechanism. Rechallenge was not performed. The patient was treated with intravenous methylprednisolone (250 mg daily for 3 days), followed by an oral prednisone taper and topical clobetasol propionate, with rapid clinical improvement. To our knowledge, mogamulizumab-induced LABD has not been previously reported. Recognition of this potential adverse effect is important for early diagnosis and management in patients receiving CCR4-targeted therapy. The authors have nothing to report. Use of generative artificial intelligence: No generative artificial intelligence tools were used in the preparation of this manuscript. The authors have nothing to report. Written informed consent was obtained for publication of all patient photographs and relevant medical information. The authors declare no conflicts of interest. Data sharing is not applicable to this article as no datasets were generated or analysed during the current study.