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]

參考譯文

在美國，每年糖尿病視網(wǎng)膜病變使24000人致盲。據(jù)疾病控制中心統(tǒng)計，美國18歲以上人群中有3百萬人因糖尿病導(dǎo)致無法矯正的視力缺損。流行病學(xué)研究表明良好控制代謝能夠明顯減少1型和2型糖尿病眼部并發(fā)癥的發(fā)生和發(fā)展的風(fēng)險，但是良好的代謝控制很難達(dá)到和維持。此外。即使是那些控制糖尿病效果良好的人群，仍有可能發(fā)生威脅視力的糖尿病視網(wǎng)膜病變。

傳統(tǒng)的觀點認(rèn)為糖尿病視網(wǎng)膜病變的病理基礎(chǔ)是微血管病變，主要侵犯內(nèi)層視網(wǎng)膜。早期形式是非增殖型糖尿病性視網(wǎng)膜病變，也叫做背景型或單純型糖尿病視網(wǎng)膜病變。這種形式表現(xiàn)為血管異常的擴(kuò)張、滲漏和出血，視網(wǎng)膜內(nèi)積液。進(jìn)一步發(fā)展為對視力損害更大的增殖型糖尿病性視網(wǎng)膜病變。其特征性改變?yōu)樾律艿男纬?，這些異常的新生血管很脆弱，容易滲漏。增殖型糖尿病性視網(wǎng)膜病變是導(dǎo)致1型糖尿病嚴(yán)重視力損害的主要原因。兩種類型的糖尿病，其視網(wǎng)膜都有發(fā)生水腫的風(fēng)險。因血-視網(wǎng)膜屏障的破壞和血漿成分滲漏到視網(wǎng)膜中層而導(dǎo)致的水腫，可以被局限化(囊樣)或彌散。糖尿病性視網(wǎng)膜病變和臨床上顯著的視盤水腫是導(dǎo)致糖尿病不可逆性視力損害的主要原因。另外，有大量的證據(jù)表明某些與糖尿病相關(guān)的視覺異?？赡苡膳c微血管病變發(fā)生無關(guān)的神經(jīng)病變引起。隨著糖尿病的發(fā)生，除了血管和神經(jīng)的異常之外，眼部也出現(xiàn)了一些其他變化。包括青光眼、晶狀體透明度和光線傳播曲線的下降(白內(nèi)障)和屈光改變的發(fā)生率的增加。但是，糖尿病視網(wǎng)膜并發(fā)癥是最具破壞性的。

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