Rubarth, Kerstin

Abstract Background: Optic neuritis (ON) is a frequent presentation of multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and myelin oligodendrocyte glycoprotein-antibody disease (MOGAD) at onset. The pathophysiology underlying these diseases, especially MOGAD, is still being elucidated. While obesity has been reported to potentially be a risk factor for MS, this has not been explored in NMOSD or MOGAD. We aimed to investigate a possible association between obesity (body mass index [BMI] >30 kg/m²) and patients with MOGAD, NMOSD or MS. Methods: Multicenter non-interventional retrospective data collection from a first ever demyelinating attack of ON in patients subsequently diagnosed with MOGAD, NMOSD or MS between 2005-2020. The following data was collected: age, gender, ethnicity, BMI at disease onset and the etiology of ON after diagnostic work-up. A mixed model analysis was performed to assess the ability of obesity or BMI to predict MOGAD-ON and distinguish MOGAD-ON from NMOSD- and MS-ON. Main outcome measures included BMI in patients with acute ON and subsequent diagnosis of MOGAD, NMOSD or MS. Results: One-hundred and eighty-three patients were included: 44 with MOGAD, 49 with NMOSD, and 90 with MS. A higher BMI was significantly associated with a diagnosis of MOGAD-ON (p<0.001); in MOGAD patients the mean BMI was 31.6 kg/m² (standard deviation (SD) 7.2), while the mean BMI was 24.7 kg/m² (SD 5.3) in NMOSD patients and 26.9 kg/m² (SD 6.2) in MS patients. Mixed effects multionimal logistic regression, adjusted for age and gender with obesity as a binary variable revealed that obesity was associated with a higher odds ratio (OR) of a subsequent MOGAD diagnosis (OR 5.466, 95% CI: [2.039, 14.650], p = 0.001) in contradistinction with NMOSD. Conclusion: This study suggests an association between obesity and MOGAD. Our finding requires further exploration, but could have significant pathophysiologic implications if confirmed in larger prospective studies.

Abstract Background: Optic neuritis (ON) is a frequent presentation of multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and myelin oligodendrocyte glycoprotein-antibody disease (MOGAD) at onset. The pathophysiology underlying these diseases, especially MOGAD, is still being elucidated. While obesity has been reported to potentially be a risk factor for MS, this has not been explored in NMOSD or MOGAD. We aimed to investigate a possible association between obesity (body mass index [BMI] >30 kg/m²) and patients with MOGAD, NMOSD or MS. Methods: Multicenter non-interventional retrospective data collection from a first ever demyelinating attack of ON in patients subsequently diagnosed with MOGAD, NMOSD or MS between 2005-2020. The following data was collected: age, gender, ethnicity, BMI at disease onset and the etiology of ON after diagnostic work-up. A mixed model analysis was performed to assess the ability of obesity or BMI to predict MOGAD-ON and distinguish MOGAD-ON from NMOSD- and MS-ON. Main outcome measures included BMI in patients with acute ON and subsequent diagnosis of MOGAD, NMOSD or MS. Results: One-hundred and eighty-three patients were included: 44 with MOGAD, 49 with NMOSD, and 90 with MS. A higher BMI was significantly associated with a diagnosis of MOGAD-ON (p<0.001); in MOGAD patients the mean BMI was 31.6 kg/m² (standard deviation (SD) 7.2), while the mean BMI was 24.7 kg/m² (SD 5.3) in NMOSD patients and 26.9 kg/m² (SD 6.2) in MS patients. Mixed effects multionimal logistic regression, adjusted for age and gender with obesity as a binary variable revealed that obesity was associated with a higher odds ratio (OR) of a subsequent MOGAD diagnosis (OR 5.466, 95% CI: [2.039, 14.650], p = 0.001) in contradistinction with NMOSD. Conclusion: This study suggests an association between obesity and MOGAD. Our finding requires further exploration, but could have significant pathophysiologic implications if confirmed in larger prospective studies.