Joint bone spine · 2026
Inflammatory rheumatic diseases under mogamulizumab: a multicenter series of 11 cases.
Клинический случайСтатьяНазвание и аннотация: Перевод пока не подготовлен
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Wahler Arno, Guignard Sandra, Quéreux Gaëlle, Carpentier Olivier, Marcé Diane, Dietrich Elise, Saintvoirin Matthieu, Amatore Florent, Hainaut Ewa, Cumptich Marine De Vicq De, Ardiles Claudia Béjar, Dereure Olivier, Beylot-Barry Marie, Ingen-Housz-Oro Saskia
Аннотация
BACKGROUND: Mogamulizumab (MOGA), an anti-CCR4 monoclonal antibody for mycosis fungoides (MF) and Sézary syndrome (SS), can trigger immune-mediated complications, such as rashes or endocrine disorders. Rheumatological manifestations are rare.
OBJECTIVES: To describe cases of inflammatory rheumatism (IR) induced or worsened by MOGA in MF/SS patients.
METHODS: A retrospective study collected cases of IR (polymyalgia rheumatica [PMR], rheumatoid arthritis [RA], spondylarthritis, or unclassified IR) in MF/SS patients treated with MOGA across centers of the French Cutaneous Lymphomas Group. Clinical, biological, and imaging data were analyzed.
RESULTS: Eleven patients (7 men, 4 women; median age: 72 years) developed IR during (10/11) or soon after (1/11) MOGA treatment. Symptoms included joint pain, stiffness, and functional impairment. All had biological inflammatory syndrome, synovitis on ultrasound, and no autoantibodies. PET-CT confirmed hypermetabolism consistent with intense joint inflammation (SUV=8.0). Management with systemic corticosteroids ± methotrexate led to remission in most cases. MOGA had to be discontinued in 8 patients, with lymphoma control maintained in 6.
CONCLUSIONS: MOGA may induce disabling IR, potentially via CCR4+ regulatory T-cell depletion. Early recognition and treatment with corticosteroids ± methotrexate are essential, though MOGA discontinuation may be required.
OBJECTIVES: To describe cases of inflammatory rheumatism (IR) induced or worsened by MOGA in MF/SS patients.
METHODS: A retrospective study collected cases of IR (polymyalgia rheumatica [PMR], rheumatoid arthritis [RA], spondylarthritis, or unclassified IR) in MF/SS patients treated with MOGA across centers of the French Cutaneous Lymphomas Group. Clinical, biological, and imaging data were analyzed.
RESULTS: Eleven patients (7 men, 4 women; median age: 72 years) developed IR during (10/11) or soon after (1/11) MOGA treatment. Symptoms included joint pain, stiffness, and functional impairment. All had biological inflammatory syndrome, synovitis on ultrasound, and no autoantibodies. PET-CT confirmed hypermetabolism consistent with intense joint inflammation (SUV=8.0). Management with systemic corticosteroids ± methotrexate led to remission in most cases. MOGA had to be discontinued in 8 patients, with lymphoma control maintained in 6.
CONCLUSIONS: MOGA may induce disabling IR, potentially via CCR4+ regulatory T-cell depletion. Early recognition and treatment with corticosteroids ± methotrexate are essential, though MOGA discontinuation may be required.