Authors
Arno Wahler, Sandra Guignard, Gaëlle Quéreux, Olivier Carpentier, Diane Marcé, Elise Dietrich, Matthieu Saintvoirin, Florent Amatore, Ewa Hainaut, Marine De Vicq De Cumptich, Claudia Béjar Ardiles, Olivier Dereure, Marie Beylot-Barry, Saskia Ingen-Housz-Oro
Published in
Joint bone spine. Pages 106145. Oct 10, 2026. Epub Oct 10, 2026.
Abstract
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.
To describe cases of inflammatory rheumatism (IR) induced or worsened by MOGA in MF/SS patients.
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.
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.
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.
PMID:
42858804
Bibliographic data and abstract were imported from PubMed on 11 Oct 2026.
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