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Baricitinib triggering a central nervous system inflammatory-demyelinating disease: A case report
Rozita Khalili1,2, Ahmad A Toubasi2, Meryim Poursheykhi3
1Neuroimmunology Division, Department of Neurology, University of Tennessee Health Science Center (UTHSC), Memphis, TN, USA.
Janus kinase inhibitors (JAKis), such as baricitinib, target the Janus kinase/signal transducers and activators of transcription pathway to regulate proinflammatory cytokines and T-helper cell activity, thereby reducing inflammation. Despite their therapeutic benefits, inflammatory demyelinating diseases of the central nervous system (CNS) have been reported in association with JAKi treatment, most previously involving tofacitinib in patients with rheumatoid arthritis. We report the first case of a CNS inflammatory demyelinating disease that was possibly exacerbated by baricitinib, underscoring the need for heightened clinical vigilance and close monitoring of patients receiving JAKi therapy.
Janus kinase inhibitors (JAKis), such as baricitinib, target the Janus kinase/signal transducers and activators of transcription pathway to regulate proinflammatory cytokines and T-helper cell activity, thereby reducing inflammation. Despite their therapeutic benefits, inflammatory demyelinating diseases of the central nervous system (CNS) have been reported in association with JAKi treatment, most previously involving tofacitinib in patients with rheumatoid arthritis. We report the first case of a CNS inflammatory demyelinating disease that was possibly exacerbated by baricitinib, underscoring the need for heightened clinical vigilance and close monitoring of patients receiving JAKi therapy.
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