Lixi Filippo, Calabresi Valerio, Cukurova Feyza, Giannaccare Giuseppe
Eye Clinic, Department of Surgical Sciences, University of Cagliari, Cagliari, 09124, Italy.
Department of Ophthalmology, Mardin Training and Research Hospital, Mardin, 47100, Turkey.
Int Med Case Rep J. 2025 Aug 7;18:991-995. doi: 10.2147/IMCRJ.S531930. eCollection 2025.
To report a case of non-arteritic ischemic optic neuropathy (NAION) in an otherwise healthy patient treated with Glucagon-Like Peptide-1 (GLP-1) receptor agonists (RAs) liraglutide and semaglutide.
A 47-year-old Caucasian female with a Body Mass Index (BMI) of 27.92, and no known history of diabetes, hypertension, or ischemic heart disease, developed a progressive decline in visual acuity in the right eye one month after initiating liraglutide therapy for weight loss. Upon symptom presentation, ophthalmic examination performed elsewhere revealed a best-corrected visual acuity (BCVA) of 20/40, optic nerve head (ONH) swelling, and inferior hemifield scotoma on Humphrey Visual Field testing. Oral corticosteroids were prescribed and discontinued because of poor glycemic control. Liraglutide therapy was continued for further three months and then switched to semaglutide owing to poor clinical results. Eight months later, the patient discontinued weight loss therapy because of progressive visual deterioration and presented to our clinic for a second opinion. Upon examination, BCVA was limited to 20/400, ONH edema was evident and confirmed on optical coherence tomography (OCT), and further worsening of the visual field defects was detected. Given the absence of anatomical and/or systemic risk factors, NAION secondary to GLP-1 RAs was diagnosed.
In our patient, liraglutide likely served as the initial trigger for the NAION, with semaglutide acting as an additional contributing factor in the progression of the disease. This case adds to the complex puzzle regarding the association between GLP-1 RAs therapy and NAION. Given the increasing use of these drugs for both obesity and diabetes and the close temporal correlations between GLP-1 RAs use and NAION, healthcare providers should be aware of the possible risk of serious ocular complications. Upon onset of visual symptoms, early ophthalmologic diagnosis and treatment interruption are essential to prevent or limit severe visual morbidities.
报告一例在使用胰高血糖素样肽-1（GLP-1）受体激动剂（RA）利拉鲁肽和司美格鲁肽治疗的健康患者中发生非动脉炎性缺血性视神经病变（NAION）的病例。
一名47岁的白种女性，体重指数（BMI）为27.92，无糖尿病、高血压或缺血性心脏病病史，在开始使用利拉鲁肽减肥治疗一个月后，右眼视力逐渐下降。出现症状后，在其他地方进行的眼科检查显示最佳矫正视力（BCVA）为20/40，视神经乳头（ONH）肿胀，在Humphrey视野测试中存在下方半视野暗点。因血糖控制不佳，口服皮质类固醇药物被开具并停用。利拉鲁肽治疗持续了三个月，之后由于临床效果不佳改为司美格鲁肽治疗。八个月后，由于视力逐渐恶化，患者停止了减肥治疗，并到我们诊所寻求第二种意见。检查时，BCVA降至20/400，ONH水肿明显，并经光学相干断层扫描（OCT）证实，且视野缺损进一步恶化。鉴于不存在解剖学和/或全身性危险因素，诊断为继发于GLP-1 RA的NAION。
在我们的患者中，利拉鲁肽可能是NAION的初始触发因素，司美格鲁肽在疾病进展中起到了额外的促成因素作用。该病例为GLP-1 RA治疗与NAION之间的关联这一复杂难题增添了内容。鉴于这些药物在肥胖症和糖尿病治疗中的使用日益增加，以及GLP-1 RA使用与NAION之间密切的时间相关性，医疗保健提供者应意识到严重眼部并发症的潜在风险。一旦出现视觉症状，早期眼科诊断和中断治疗对于预防或限制严重视觉疾病至关重要。
