Adalimumab-Induced Cns Demyelination in a Patient With Multiple Pre-Existing Autoimmune Diseases:Treatment Contemplation Publisher Pubmed



Khosravi S^{1, 2} ; Zamani B¹ ; Motamed MR¹ ; Akhoundi FH¹ Show Affiliations
Source: Modern Rheumatology Case Reports Published:2025

Abstract

Anti-tumour necrosis factor (TNF) agents like adalimumab are safe and effective for rheumatologic disorders, but they have been reported to cause demyelinating diseases like multiple sclerosis. A 47-year-old woman with weakness in the left hand was evaluated. She had a previous medical history of intermediate uveitis and rheumatoid arthritis. Anti-TNF-α treatment was initiated with adalimumab 2 years before this visit. Magenetic resonance imaging showed numerous T2-hyperintense lesions in bilateral periventricular, juxtacortical, and subcortical areas, which were absent in her scan before anti-TNF therapy. She was diagnosed with multiple sclerosis, and adalimumab was discontinued. IV glucocorticoids were administered with marked improvement. She was then started on anti-CD20 therapy with rituximab. A year later, she was symptom-free, and her follow-up brain magnetic resonance imaging showed no new lesions. The link between multiple sclerosis and TNF-α inhibitors is poorly understood, but several hypotheses have been proposed. Discontinuing anti-TNF therapy alone may not be enough to prevent further demyelinating disease activity, and it is essential to consider the necessity of starting a disease-modifying treatment. Autoimmunity plays a significant role in rheumatologic and neurological diseases, and as personalised medicine advances, understanding genetic risk is crucial for selecting appropriate therapeutic targets. A thorough evaluation of a patient’s family background is recommended before a therapeutic decision-making, especially in patients with multiple autoimmune disorders, and the question of whether TNF-α is a suitable therapeutic target in patients with multiple autoimmune disorders is raised. © Japan College of Rheumatology 2024.