Rechtman Ehud, Harris Alon, Garzozi Hanna J, Ciulla Thomas A
Goldschleger Eye Institute, Sheba Medical Center, Tel-Hashomer, Israel.
Clin Ophthalmol. 2007 Dec;1(4):383-91.
Diabetic retinopathy (DR) and diabetic macular edema (DME) are leading causes of blindness in the working-aged population of most developed countries. The increasing number of persons with diabetes worldwide suggests that DR/DME will continue to be major contributors to vision loss and associated functional impairment for years to come. Early detection of retinopathy in persons with diabetes is critical in preventing visual loss, but current methods of screening fail to identify a sizable number of high-risk patients. The control of diabetes-associated metabolic abnormalities (ie, hyperglycemia, hyperlipidemia, and hypertension) is also important in preserving visual function, as these conditions have been identified as risk factors for both the development and progression of DR/DME. The non-pharmacologic interventions for DR/DME, laser photocoagulation and vitrectomy, only target advanced stages of disease. Several biochemical mechanisms, including increased vascular endothelial growth factor production, protein kinase C beta activation, oxidative stress, and accumulation of intracellular sorbitol and advanced glycosylation end products, may contribute to the vascular disruptions that characterize DR/DME. The inhibition of these pathways holds the promise of the intervention for diabetic retinopathy with higher success rate and also at earlier, non-sight-threatening stages.
糖尿病视网膜病变(DR)和糖尿病性黄斑水肿(DME)是大多数发达国家劳动年龄人口失明的主要原因。全球糖尿病患者数量不断增加,这表明在未来几年,DR/DME仍将是导致视力丧失和相关功能障碍的主要因素。糖尿病患者视网膜病变的早期检测对于预防视力丧失至关重要,但目前的筛查方法未能识别出相当数量的高危患者。控制与糖尿病相关的代谢异常(即高血糖、高血脂和高血压)对于保护视觉功能也很重要,因为这些情况已被确定为DR/DME发生和发展的危险因素。DR/DME的非药物干预措施,如激光光凝和玻璃体切除术,仅针对疾病的晚期阶段。包括血管内皮生长因子产生增加、蛋白激酶Cβ激活、氧化应激以及细胞内山梨醇和晚期糖基化终产物的积累在内的几种生化机制,可能导致DR/DME所特有的血管破坏。抑制这些途径有望在糖尿病视网膜病变的干预中取得更高的成功率,并且在早期、不威胁视力的阶段进行干预。