【作者】 朴勇虎；

【导师】 李亚萍；

【作者基本信息】 吉林大学 ， 临床医学， 2012， 硕士

【摘要】 目的：研究糖尿病性黄斑病变视网膜内外屏障的损伤特点。方法：选取2011年1月-2012年3月期间在我院门诊就诊的Ⅱ型糖尿病患者67例（119眼）的临床资料，根据眼底表现及荧光素眼底血管造影(Fundus fluoresceinangiography，FFA)检查结果将病例资料分为正常对照组19例（33眼）和病例组，病例组资料又分为：糖尿病FFA眼底正常组10例（20眼）、糖尿病性视网膜病变（Diabeticretinopathy，DR）微血管瘤拱环未破坏组8例（16眼）、DR拱环破坏组20例（34眼）、DR拱环破坏伴黄斑区硬性渗出组20例（37眼）、DR黄斑水肿组9例（12眼）。所有病例均进行眼底照像、FFA、视网膜电图（Electroretinogram，ERG）及光学相干断层扫描（Optical coherence tomograph，OCT）检查，检查结果经统计学分析。结果：(1)OCT结果：糖尿病黄斑病变组在视网膜内丛状层、内核层、外核层、外丛状层出现颗粒状的高反光，随着黄斑病变发展而加重；黄斑病变继续发展而出现视网膜光感受器层的断裂及视网膜色素上皮层的厚薄不均；在DR拱环破坏组、拱环破坏伴硬性渗出组及黄斑水肿组中有不完全玻璃体后脱离。(2)ERG结果：糖尿病FFA正常组出现最大混合反应a波振幅下降、峰时延迟，随着黄斑病变发展而加重（P＜0.05）;DR拱环破坏组开始出现明视视锥细胞a波振幅下降、峰时延迟,随着黄斑病变发展而加重（P＜0.05）；糖尿病FFA眼底正常组出现暗视视杆细胞b波峰时延迟、最大混合反应b波峰时延迟、明视视锥细胞b波的振幅下降，随着黄斑病变发展而加重（P＜0.05），并在DR拱环破坏组开始出现暗视视杆细胞b波振幅下降、最大混合反应b波振幅下降、明视视锥细胞b波的波峰时延迟，随着黄斑病变发展而加重（P＜0.05）；OPS振幅下降、峰时延迟，随着黄斑病变发展而加重（P＜0.05）。结论：（1)糖尿病FFA正常组黄斑区视杆、视锥细胞出现功能性改变，并随着黄斑病变发展而加重，并在OCT出现外核层、外丛状层高颗粒状的高反光，随着黄斑病变的发展出现光感受器层的断裂及视网膜色素上皮层的厚薄不均。(2)糖尿病性黄斑病变视网膜内屏障破坏的同时伴有外屏障的损伤。更多还原

【Abstract】 Objective: Study the damage of blood-retinal barrier and tight junction of retinalpigment epithelium cells in diabetic maculopathy.Methods: The clinical datum of119eyes of67outpatient with type Ⅱdiabetes werecollected in department of ocular fundus of the Second Hospital of Jilin Universityfrom Jan.2011to Mar.2012. The clinical datum were classed to6group as photo ocularfundus and FFA (Fundus fluoresce in angiography): age-matched normal control group (33eyes of19case), the group of normal ocular fundus in FFA with diabetes (20eyes of10patients), the group of only microaneurysm in macula lutea with diabetic retinopathy (DR)(16eyes of8patients), the group of capillary vessel zone enlarge in macula lutea with DR(34eyes of20patients), the group of capillary vessel zone enlarge and hard exudate inmacula lutea with DR (37eyes of20patients), and the group of diabetic macular edema(DME)（12eyes of9patients）. FFA, ERG, OCT were performed in all cases.Results:(1) OCT results: There were granular reflective signal in inner plexiform layer,inner nuclear layer, outer nuclear layer and outer plexiform layer of retina in diabeticmaculopathy, and granular reflective signal increased with the development of diabeticmaculopathy; and there were rupture in the photoreceptor layer and uneven in retinalpigment epithelium; There was posterior vitreouse detachment (PVD) in the group ofcapillary vessel zone enlarge in macula lutea with DR, the group of capillary vessel zoneenlarge and hard exudate in macula lutea with DR, and DME.(2) ERG results: Amplitudevalue of a-wave was decreased and latency of a-wave delayed in maximal mixed responsein the group of normal ocular fundus in FFA with diabetes, and aggravated with thedevelopment of diabetic maculopathy (P <0.05); amplitude value of a-wave was decreasedand latency of a-wave delayed in photopic ERG of cone cells in the group of no capillaryvessel zone enlarge in macula lutea with DR, and aggravated with the development ofdiabetic maculopathy (P <0.05); latency of b-wave was delayed in scotopic ERG of rodcells, maximal mixed response, and amplitude value of b-wave in photopic ERG of conecells was decreased in the group of normal ocular fundus in FFA with diabetes, aggravatedwith the development of macular degeneration; and amplitude value of b-wave was decreased in scotopic ERG of rod cells, in maximal mixed respons and latency of b-wavewas delayed in photopic ERG of cone cells in the group of no capillary vessel zone enlargein macula lutea with DR, and aggravated with the development of diabetic maculopathy (P<0.05).;and the amplitude of OPS decrease, latency of OPS delayed,and aggravated withthe development of diabetic maculopathy (P <0.05).Conclusion:(1) The structure and functional changes may appeared in rods and conescells in the group of normal ocular fundus in FFA with diabetes, and aggravated with thedevelopment of diabetic maculopathy.(2) Blood-retinal barrier of retina was damaged, andmay accompanied choroid-retinal barrier damaged in diabetic maculopathy.更多还原