Diabetic retinopathy causes up to 24 000 new cases of blindness each year in the United States (CDC，2003). According to CDC statistics, 3 million people in the US over 18 years of age had uncorrectable visual impairments related to diabetes (CDC，2003). Epidemiological studies have established that good metabolic control (i. e. preventing abnormally elevated blood glucose) significantly reduces the risk of development and progression of ocular and visual complications of both Type 1 and Type 2 diabetes[Stratton et al. .2001; The Diabetes Control and Complications (DCCT). Rescarch Group, 1995: UKPDS.1998]However, good metabolic control is difficult to achieve and maintain. In addition, sight-threatening diabetic retinopathy occurs at a substantial rate even among those who manage their diabetes well [The Diabetes Control and Complications (DCCT) Research Group,1995].

Diabetic retinopathy has classically been defined as pathology of the microvasculature, primarily of the inner retina (Gardner et al, 2000). The earliest form is nonproliferative diabetic retinopathy (NPDR), also referred to as background or simple diabetic retinopathy. In this form, there is abnormal dilation of blood vessels,leakage and blceding of the blood-vessels, and fluid accumulation within the retina. A more advanced form, proliferative diabetic retinopathy, is more sight-threatening. It is characterized by neovascularization. the formation of abnormal new blood vessels that are fragile and leaky. Proliferative diabetic retinopathy is the primary cause of severe vision loss in Type 1 diabetes (Aiello et al. , 1998; Cunha-Vaz and Bernardes, 2005). The retinas of both types of diabetics are also at risk for the development of ederna. Edema results from the breakdown of the blood-retinal barrier and leakage of plasma constituents into the middle retinal layers, and can be focal (cystoid) and/or diffuse. Diabetic retinopathy and clinically significant macular ederna (CSME) are largely responsible for the irreversible, debilitating visual consequences of diabetes[Early Treatment Diabetic Retinopathy Study Research Group (ETDRS),1985,1991]. In addition, there is a large body of evidence suggesting that some of the diabetesrelated visual abnormalities are due to neurodegeneration that may occur independent of microvasculature pathology (Barber, 2003). One example of neuropathy affecting ocular function is the inability of the pupil to dilate normally (Cahill et al., 2001; Pittasch et al. ,2002; Sharma et al. , 1997). In addition to the vascular and neural abnormalities, there are other changes to the eye that are associated with diabetes. These include increased risk of glaucoma, reductions in the clarity and spectral transmission curve of the crystalline lens (cataract), and changes in refraction (Fledelius, 1987; Sparrow, 1990). However, the retinal complications of diabetes are the most devastating.

                                                     [Progress in Retinal and Eye Research, 2006;(25)425-448]

参考译文

在美国，每年糖尿病视网膜病变使24000人致盲。据疾病控制中心统计，美国18岁以上人群中有3百万人因糖尿病导致无法矫正的视力缺损。流行病学研究表明良好控制代谢能够明显减少1型和2型糖尿病眼部并发症的发生和发展的风险，但是良好的代谢控制很难达到和维持。此外。即使是那些控制糖尿病效果良好的人群，仍有可能发生威胁视力的糖尿病视网膜病变。

传统的观点认为糖尿病视网膜病变的病理基础是微血管病变，主要侵犯内层视网膜。早期形式是非增殖型糖尿病性视网膜病变，也叫做背景型或单纯型糖尿病视网膜病变。这种形式表现为血管异常的扩张、渗漏和出血，视网膜内积液。进一步发展为对视力损害更大的增殖型糖尿病性视网膜病变。其特征性改变为新生血管的形成，这些异常的新生血管很脆弱，容易渗漏。增殖型糖尿病性视网膜病变是导致1型糖尿病严重视力损害的主要原因。两种类型的糖尿病，其视网膜都有发生水肿的风险。因血-视网膜屏障的破坏和血浆成分渗漏到视网膜中层而导致的水肿，可以被局限化(囊样)或弥散。糖尿病性视网膜病变和临床上显著的视盘水肿是导致糖尿病不可逆性视力损害的主要原因。另外，有大量的证据表明某些与糖尿病相关的视觉异常可能由与微血管病变发生无关的神经病变引起。随着糖尿病的发生，除了血管和神经的异常之外，眼部也出现了一些其他变化。包括青光眼、晶状体透明度和光线传播曲线的下降(白内障)和屈光改变的发生率的增加。但是，糖尿病视网膜并发症是最具破坏性的。

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