Semaglutide dose escalation linked to atypical retrobulbar optic neuropathy in young man

The global use of glucagon-like peptide-1 receptor agonists (GLP-1RAs), particularly semaglutide, has expanded significantly for managing type 2 diabetes and obesity. While generally safe, pharmacovigilance signals have indicated a low but increased incidence of nonarteritic anterior ischemic optic neuropathy (NAION) among users. However, the spectrum of potential ocular adverse events remains under investigation, with atypical presentations challenging existing diagnostic frameworks and necessitating further clinical vigilance beyond typical NAION concerns.

This case report details a man in his early 30s with class III obesity, obstructive sleep apnea, and prediabetes who developed acute, painless, asymmetric bilateral visual dysfunction. Symptoms emerged four weeks after semaglutide dose escalation to 1 mg per week. The diagnostic workup included comprehensive ophthalmological evaluation, visual field testing, optical coherence tomography (OCT), visual evoked potentials (VEP), and neuroimaging to characterize the optic neuropathy and rule out other etiologies.

The patient presented with acute, painless, asymmetric bilateral visual dysfunction. Evaluation revealed retrobulbar optic neuropathy, characterized by distinct visual field defects: a central scotoma in the left eye and an altitudinal defect in the right eye. Notably, optic disc appearance was preserved, and OCT and neuroimaging results were unremarkable, distinguishing this case from typical NAION. Visual evoked potentials (VEP) showed markedly delayed responses, confirming optic nerve dysfunction. The clinical picture was atypical for NAION and did not fully align with classical demyelinating optic neuritis, presenting a mixed diagnostic challenge. > Semaglutide was immediately discontinued, and visual function remained stable over serial follow-up, with adaptation to a persistent left central scotoma but no further deterioration.