SAT-573 Should We Be Keeping a Closer Eye? A Case of Non-arteritic Anterior Ischemic Optic Neuropathy (Naion) After Semaglutide Initiation

Abstract Disclosure: A. Shah: None. R. Wardeh: None. F. Alawadi: None. F. Rashid: None. F. Ahamed: None. Introduction: Semaglutide changed the landscape of modern medicine with its cardiovascular, renal and metabolic benefits. Semaglutide garnered adverse attention when researchers in Massachusetts reported an increased incidence of non-arteritic anterior ischemic optic neuropathy (NAION) in patients treated with Semaglutide. Clinical Case: We present the case of a 68-year-old South-asian gentleman, with long-standing Type 2 Diabetes Mellitus, hypertension, dyslipidaemia and obesity. He was seen for poorly controlled Diabetes (HbA1C 11.9%) complicated by nephropathy and neuropathy. In view of his cardiometabolic risk, we initiated him on guideline-directed therapy, and GLP1 agonist therapy was switched from Dulaglutide 1.5mg weekly to Semaglutide 0.5 mg weekly. Ophthalmological evaluation prior to initiation of Semaglutide showed no evidence of diabetic retinopathy. He completed four doses of Semaglutide 0.5mg after which he did not collect his medication refill. Within two weeks of Semaglutide discontinuation, he developed sudden onset deteriorating vision in the inferior field of his right eye. Nonarteritic anterior ischemic optic neuropathy was diagnosed with significant edema of the optic disc and corresponding visual field defects. A comprehensive evaluation ruled out any underlying neurologic, systemic, or optic disorders. A repeat assessment of A1C showed a drop of 3% (11.9% to 8.9%) over a period of 3 months. Interestingly, he did not show any evidence of new-onset diabetic retinopathy. Clinical Lessons: The most widely accepted pathophysiological basis of NAION describes hypoperfusion of the short posterior ciliary arteries supplying the optic nerve, which results in ischemia and resultant NAION. A host of systemic conditions have been implicated in increasing the risk of NAION, including hypertension, diabetes, dyslipidaemia, obstructive sleep apnoea and use of phosphodiesterase-5 inhibitors. GLP-1 has been demonstrated to exert a vasodilatory effect on coronary microvasculature and bronchial arteries. While there are no studies on the direct effect of GLP-1 on the optic vasculature, the effect of GLP-1 in reducing blood pressure is well-established. We may then hypothesize that if the addition of Semaglutide could have a vasodilatory effect on the posterior ciliary arteries, along with the reduction in blood pressure can potentially result in hypoperfusion and NAION. While we acknowledge that this patient had multiple risk factors for NAION, these have been long-standing with no new changes in these parameters. Physicians must keep an eye open for the potential risk Semaglutide poses, demanding more studies in this field. Presentation: Saturday, July 12, 2025