Exposure to TNF Inhibitors is Rare at MOGAD Diagnosis

Objective To assess the potential association between TNF-inhibitors and MOGAD Background The association of tumor necrosis factor-a (TNF)-inhibitors with MS has previously been suggested, whereas little is known about MOG-IgG-associated disease (MOGAD) in the context of these drugs. We recently encountered two patients who developed MOGAD while receiving TNF-inhibitors, prompting a search for similar cases in the literature and clinical practice. Design/Methods The two cases were seen at Mayo Clinic, Rochester (bilateral optic neuritis) and the University-Hospital of Sassari (brainstem syndrome). Three additional cases of MOGAD presenting during treatment with TNF-inhibitors were identified through Pubmed. We searched the medical records of 336 MOGAD patients seen at the Mayo Clinic, to assess if they had been treated with TNF-inhibitors. Results A total of 5 patients were identified. The median age at MOGAD presentation was 40 years (range, 36-49); 4/5 were male (80%). The median time from TNF-inhibitor initiation to MOGAD presentation was 6.5 years (range, 2-18). Of 4 patients who discontinued the TNF-inhibitor due to MOGAD onset, two subsequently had a MOGAD relapse. While in another patient, neurological symptoms subsided with corticosteroids despite TNF-inhibitor being maintained. The frequency of MOGAD presenting during TNF-inhibitors treatment at Mayo Clinic was 0.3% (1/336 cases). Conclusions We found that MOGAD is unlikely to present during treatment with TNF-inhibitors. The outcomes in these patients seemed not to be influenced by TNF-inhibitor treatment duration or discontinuation. These findings suggest the benefit of TNF-inhibitor withdrawal is not obvious, and the choice of discontinuing vs maintaining treatment with TNF-inhibitors should be weighted based on symptoms severity and activity status of the underlying systemic disorder. When withdrawal is considered, immunosuppression with agents potentially effective for both MOGAD and the immune-mediated disease originally managed by the TNF-inhibitor, could serve as dual purpose treatment.