Neuromyelitis Optica Spectrum Disorder in a 29-Year-Old Woman on Semaglutide: A Case of Acute Myelopathy Following Weight Loss Treatment.
Moneera Aldraihem1, Ghadah Shareefi1, Walaa Alyami1, Othman Aldraihem2, Rana AlDosary1, Ahmad Almutlaq1
1Neurology, King Fahad Medical City, 2College of Medicine, King Saud University
Objective:
This case report aims to investigate the potential link between the glucagon-like peptide-1 receptor agonist (GLP-1RA) semaglutide for weight loss and the development of seronegative neuromyelitis optica spectrum disorder (NMOSD), broadening our understanding of possible NMOSD triggers.
Background:
NMOSD is a rare yet debilitating autoimmune disorder that targets the central nervous system, often resulting in significant neurological impairment. While anti-aquaporin-4 (AQP4) antibodies are frequently associated with NMOSD, a notable subset of patients presents seronegative, complicating the understanding of its pathophysiology. GLP-1RAs, such as semaglutide, are increasingly utilized for weight management and diabetes control. Despite extensive research on their metabolic benefits, the potential relationship between GLP-1RA usage and the onset of NMOSD remains largely unexplored and poorly understood.
Design/Methods:
During the preparation of this work, the authors used OpenAI GPT-04 for language improvement. They reviewed and edited the content as needed and take full responsibility for the publication's content.
Results:
A 29-year-old woman developed seronegative NMOSD after two months of semaglutide use for weight loss. She initially presented with severe gastrointestinal symptoms, including abdominal pain, nausea, vomiting, and diarrhea, which progressed to acute, asymmetric flaccid quadriparesis. Comprehensive testing, including lumbar puncture, revealed negative results for albuminocytologic dissociation, oligoclonal bands, anti-AQP4, and MOG antibodies, ruling out other potential causes. MRI of the brain and spine revealed hyperintensities and a long central intramedullary signal abnormality typical of NMOSD. The patient was treated with plasma exchange and high-dose intravenous methylprednisolone, resulting in significant improvement. Semaglutide was discontinued, and rituximab initiated for long-term prevention.
Conclusions:
This case report highlights a potential link between semaglutide use and seronegative NMOSD, raising concerns about GLP-1 receptor agonists in patients predisposed to autoimmune conditions. It emphasizes the need for research into the neurological effects of semaglutide and other GLP-1RAs, particularly their role in triggering immune disorders.
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