Adalimumab induced CNS demyelination in a patient with multiple pre-existing autoimmune diseases; treatment contemplation.

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Anti-TNF agents like Adalimumab are safe and effective for rheumatologic disorders, but they have been reported to cause demyelinating diseases like Multiple Sclerosis (MS). A 47-year-old woman with left hand weakness was evaluated. She had a previous medical history of Intermediate Uveitis (IU) and Rheumatoid arthritis (RA). anti-TNF-α treatment was initiated with adalimumab two years before this visit. MRI 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 MS, and Adalimumab was discontinued. IV glucocorticoids (GCs) 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 MRI showed no new lesions. The link between MS 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 personalized medicine advances, understanding genetic risk is crucial for selecting appropriate therapeutic targets. A thorough evaluation of a patient's family background is recommended before 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.