Inflammatory rheumatic diseases under mogamulizumab: a multicenter series of 11 cases
Abstract
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.
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BibTeX
@article{wahler2026inflammatory,
title = {{Inflammatory rheumatic diseases under mogamulizumab: a multicenter series of 11 cases}},
author = {Arno Wahler and Sandra Guignard and Gaëlle Quéreux and Olivier Carpentier and Diane Marcé and Elise Dietrich and Matthieu Saintvoirin and Florent Amatore and Ewa Hainaut and Marine de Vicq De Cumptich and Claudia Béjar Ardiles and Olivier Dereure and Marie Beylot-Barry and Saskia Ingen-Housz-Oro},
journal = {Joint Bone Spine},
year = {2026},
month = oct,
doi = {10.1016/j.jbspin.2026.106145},
url = {https://inserm.hal.science/inserm-05793843v1},
note = {CC BY},
}
RIS
TY - JOUR
TI - Inflammatory rheumatic diseases under mogamulizumab: a multicenter series of 11 cases
AU - Arno Wahler
AU - Sandra Guignard
AU - Gaëlle Quéreux
AU - Olivier Carpentier
AU - Diane Marcé
AU - Elise Dietrich
AU - Matthieu Saintvoirin
AU - Florent Amatore
AU - Ewa Hainaut
AU - Marine de Vicq De Cumptich
AU - Claudia Béjar Ardiles
AU - Olivier Dereure
AU - Marie Beylot-Barry
AU - Saskia Ingen-Housz-Oro
PY - 2026
DA - 2026/10/12
JO - Joint Bone Spine
DO - 10.1016/j.jbspin.2026.106145
UR - https://inserm.hal.science/inserm-05793843v1
AB - 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.
SN - 1297-319X
ER -