Salvetat Maria Letizia, Pellegrini Francesco, Spadea Leopoldo, Salati Carlo, Musa Mutali, Gagliano Caterina, Zeppieri Marco
Department of Ophthalmology, Azienda Sanitaria Friuli Occidentale, 33170 Pordenone, Italy.
Eye Clinic, Policlinico Umberto I, "Sapienza" University of Rome, 00142 Rome, Italy.
J Clin Med. 2024 Feb 26;13(5):1327. doi: 10.3390/jcm13051327.
Diabetic macular edema (DME) is a common complication of diabetes mellitus and a leading cause of visual impairment worldwide. It is defined as the diabetes-related accumulation of fluid, proteins, and lipids, with retinal thickening, within the macular area. DME affects a significant proportion of individuals with diabetes, with the prevalence increasing with disease duration and severity. It is estimated that approximately 25-30% of diabetic patients will develop DME during their lifetime. Poor glycemic control, hypertension, hyperlipidemia, diabetes duration, and genetic predisposition are recognized as risk factors for the development and progression of DME. Although the exact pathophysiology is still not completely understood, it has been demonstrated that chronic hyperglycemia triggers a cascade of biochemical processes, including increased oxidative stress, inflammation, activation of vascular endothelial growth factor (VEGF), cellular dysfunction, and apoptosis, with breakdown of the blood-retinal barriers and fluid accumulation within the macular area. Early diagnosis and appropriate management of DME are crucial for improving visual outcomes. Although the control of systemic risk factors still remains the most important strategy in DME treatment, intravitreal pharmacotherapy with anti-VEGF molecules or steroids is currently considered the first-line approach in DME patients, whereas macular laser photocoagulation and pars plana vitrectomy may be useful in selected cases. Available intravitreal steroids, including triamcinolone acetonide injections and dexamethasone and fluocinolone acetonide implants, exert their therapeutic effect by reducing inflammation, inhibiting VEGF expression, stabilizing the blood-retinal barrier and thus reducing vascular permeability. They have been demonstrated to be effective in reducing macular edema and improving visual outcomes in DME patients but are associated with a high risk of intraocular pressure elevation and cataract development, so their use requires an accurate patient selection. This manuscript aims to provide a comprehensive overview of the pathology, epidemiology, risk factors, physiopathology, clinical features, treatment mechanisms of actions, treatment options, prognosis, and ongoing clinical studies related to the treatment of DME, with particular consideration of intravitreal steroids therapy.
糖尿病性黄斑水肿(DME)是糖尿病的常见并发症,也是全球视力损害的主要原因。它被定义为黄斑区域内与糖尿病相关的液体、蛋白质和脂质积聚以及视网膜增厚。DME影响相当一部分糖尿病患者,其患病率随疾病持续时间和严重程度增加。据估计,约25%-30%的糖尿病患者在其一生中会发生DME。血糖控制不佳、高血压、高脂血症、糖尿病病程和遗传易感性被认为是DME发生和发展的危险因素。尽管确切的病理生理学仍未完全了解,但已证明慢性高血糖会引发一系列生化过程,包括氧化应激增加、炎症、血管内皮生长因子(VEGF)激活、细胞功能障碍和细胞凋亡,同时血视网膜屏障破坏,黄斑区域内液体积聚。DME的早期诊断和适当管理对于改善视力结果至关重要。尽管控制全身危险因素仍然是DME治疗中最重要的策略,但玻璃体内注射抗VEGF分子或类固醇药物治疗目前被认为是DME患者的一线治疗方法,而黄斑激光光凝和玻璃体切割术在特定情况下可能有用。现有的玻璃体内类固醇药物,包括曲安奈德注射液、地塞米松和氟轻松醋酸酯植入物,通过减轻炎症、抑制VEGF表达、稳定血视网膜屏障从而降低血管通透性发挥治疗作用。它们已被证明可有效减轻DME患者的黄斑水肿并改善视力结果,但与眼压升高和白内障形成的高风险相关,因此其使用需要准确选择患者。本手稿旨在全面概述与DME治疗相关的病理学、流行病学、危险因素、病理生理学、临床特征、治疗作用机制、治疗选择、预后及正在进行的临床研究,尤其考虑玻璃体内类固醇药物治疗。