Anti-TNF-Alpha Associated Central Nervous System Demyelination. Drug-Induced Demyelination or Multiple Sclerosis Trigger? A Case Series.

Adalimumab is a monoclonal antibody that targets TNF-α and is effective in treating several autoimmune disorders, including non-infectious uveitis; however, it has been associated with demyelinating lesions. This study presents two cases of CNS demyelination in patients who consumed adalimumab. First, an 18-year-old man presented with subacute lower-limb paresis over the past month. He had an 8-year history of uveitis, which was treated with adalimumab. The patient was initially treated with intravenous methylprednisolone, which resulted in improvement of the symptoms; however, the patient subsequently presented with new symptoms of left lower limb paresis and right homonymous hemianopia. MRI showed periventricular lesions, including two ill-defined tumefactive demyelinating lesions (TDLs) and a cervical cord lesion. Second, a 35-year-old woman with a six-year history of recurrent inflammatory uveitis, who had been treated with adalimumab every 2 weeks for the last 6 months, developed right-sided paresthesia and mild weakness. MRI showed classic periventricular "Dawson's fingers" and a short-segment lesion in the cervical spinal cord. This study demonstrates the diagnostic challenges of demyelination following administration of anti-TNF-α agents. Persistence or recurrence of disease activity after discontinuation of adalimumab, along with fulfillment of MS diagnostic criteria, may favor an underlying demyelinating disease rather than a monophasic drug-induced process. This study emphasizes the importance of careful consideration before prescribing anti-TNF-α agents, particularly in patients with risk factors for demyelinating disease.