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首页> 外文期刊>Cornea >Diabetes and corneal cell densities in humans by in vivo confocal microscopy.
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Diabetes and corneal cell densities in humans by in vivo confocal microscopy.

机译:通过体内共聚焦显微镜观察人的糖尿病和角膜细胞密度。

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摘要

PURPOSE: Diabetes is accompanied by an increased autofluorescence of the cornea, probably because of accumulation of advanced glycation end products (AGEs). The pathogenic mechanism is still unknown. This study aimed to quantify differences in corneal cell densities between diabetic patients and healthy controls. METHODS: The left cornea of 15 patients with non-insulin-dependent diabetes mellitus (NIDDM) with level of retinopathy 20 according to the Early Treatment of Diabetic Retinopathy Study (ETDRS) and of 15 healthy controls were examined by noninvasive in vivo confocal microscopy in an observational prospective study. The cell densities in 6 corneal layers were determined along the optical axis of the cornea by using stereologic methods. RESULTS: The average cell density per unit area in the superficial and basal epithelium and the endothelial layer was 725 +/- 171, 5950 +/- 653, and 2690 +/- 302 cells/mm in controls and 815 +/- 260, 5060 +/- 301, and 2660 +/- 364 cells/mm in diabetic patients. The cell density per unit volume in the anterior, mid-, and posterior stroma was 26,300 +/- 4090, 19,390 +/- 3120, and 25,700 +/- 3260 cells/mm in controls and 27,560 +/- 3880, 21,930 +/- 2110, and 25,790 +/- 3090 cells/mm in patients with diabetes. In both groups, the density in the midstroma was significantly lower than in both the anterior stroma and the posterior stroma (P < 0.02). The cell density in the basal layer of diabetic patients was significantly lower than in healthy controls (-15.0%, P < 0.0004). In the other layers, no significant differences between both groups (P > 0.07) were observed. CONCLUSIONS: The lower basal cell density found in patients with diabetes may result from a combination of different mechanisms including decreased innervation at the subbasal nerve plexus, basement membrane alterations, and higher turnover rate in basal epithelial cells. The lower cell density in the midstroma of diabetic patients and healthy controls may be attributed in part to differences in oxygen concentration in the stromal layers (depths). Changes in cellular density did not seem to be responsible for the increased autofluorescence in diabetes.
机译:目的:糖尿病伴有角膜自发荧光增加,可能是由于晚期糖基化终末产物(AGEs)的积累。其致病机理尚不清楚。这项研究旨在量化糖尿病患者和健康对照者之间角膜细胞密度的差异。方法:通过无创体内共聚焦显微镜检查了15例糖尿病视网膜病变早期治疗研究(ETDRS)的15例非胰岛素依赖型糖尿病(NIDDM)视网膜病水平为20的左角膜和15例健康对照者的左眼角膜。观察性前瞻性研究。使用立体学方法沿着角膜的光轴确定6个角膜层中的细胞密度。结果:浅层和基底上皮以及内皮层的单位面积平均细胞密度分别为725 +/- 171、5950 +/- 653和2690 +/- 302细胞/ mm,而对照组为815 +/- 260,糖尿病患者的5060 +/- 301和2660 +/- 364细胞/ mm。对照中前,中,后基质的单位体积细胞密度分别为26,300 +/- 4090、19,390 +/- 3120和25,700 +/- 3260个细胞/ mm,以及27,560 +/- 3880、21,930 + / -糖尿病患者的2110和25,790 +/- 3090个细胞/毫米。在两组中,中间基质的密度均显着低于前基质和后基质(P <0.02)。糖尿病患者基底层的细胞密度显着低于健康对照组(-15.0%,P <0.0004)。在其他层中,两组之间均未观察到显着差异(P> 0.07)。结论:糖尿病患者的基底细胞密度较低可能是由多种机制共同导致的,这些机制包括基底神经丛神经支配减少,基底膜改变以及基底上皮细胞更新率较高。糖尿病患者和健康对照者中层中较低的细胞密度可能部分归因于基质层中的氧浓度差异(深度)。细胞密度的变化似乎并不与糖尿病中自体荧光增加有关。

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