Araszkiewicz Aleksandra, Zozulińska-Ziółkiewicz Dorota, Meller Mikołaj, Bernardczyk-Meller Jadwiga, Piłaciński Stanisław, Rogowicz-Frontczak Anita, Naskręt Dariusz, Wierusz-Wysocka Bogna
Department of Internal Medicine and Diabetology, Poznan University of Medical Sciences, Poznań, Poland.
Pol Arch Med Wewn. 2012;122(10):464-70. Epub 2012 Aug 22.
The degeneration of retinal neurons and glial cells has recently been postulated in the pathogenesis of diabetic retinopathy. Optical coherence tomography (OCT) allows to perform qualitative and quantitative measurements of retinal thickness (RT) with identification of individual retinal layers.
We compared RT, retinal nerve fiber layer (RNFL) thickness, and ganglion cell layer (GCL) thickness obtained by OCT in type 1 diabetic patients with and without clinically diagnosed retinopathy.
The study included 77 consecutive patients with type 1 diabetes (39 men, 38 women; median age, 35 years [interquartile range (IQR), 29-42]; median disease duration, 10 years [IQR, 9-14]) and 31 age- and sex-matched controls. We measured RT in the fovea, parafovea, and perifovea, as well as RNFL and GCL thickness. We divided diabetic patients into 2 subgroups, i.e., those with diabetic retinopathy and without retinopathy.
We observed thicker perifoveal retina (P = 0.05), mean RNFL (P = 0.002), inferior RNFL (P <0.0001), and superior and inferior GCL (P = 0.05 and P = 0.04, respectively) in diabetic subjects compared with the control group. We detected retinopathy in 23 diabetic patients (29%). Compared with patients without retinopathy, subjects with retinopathy had thinner parafoveal retina (P = 0.05), mean RNFL (P = 0.002), inferior and nasal RNFL (P = 0.002, P = 0.03), superior (P = 0.05) and inferior GCL (P = 0.006). Significant correlations were found between duration of diabetes and nasal RNFL thickness (r = -0.32, P = 0.004) and parafoveal RT (r = -0.47, P <0.001).
The results might suggest the loss of intraretinal neural tissue in type 1 diabetic patients with retinopathy. Neurodegeneration in diabetic retinopathy is closly associated with disease duration.
近期研究推测视网膜神经元和神经胶质细胞的退化在糖尿病视网膜病变的发病机制中起作用。光学相干断层扫描（OCT）能够对视网膜厚度（RT）进行定性和定量测量，并识别各个视网膜层。
我们比较了1型糖尿病患者有无临床诊断视网膜病变时，通过OCT测量得到的RT、视网膜神经纤维层（RNFL）厚度和神经节细胞层（GCL）厚度。
该研究纳入了77例连续的1型糖尿病患者（39例男性，38例女性；年龄中位数35岁[四分位间距（IQR），29 - 42]；病程中位数10年[IQR，9 - 14]）以及31例年龄和性别匹配的对照组。我们测量了黄斑中心凹、旁黄斑和周边黄斑的RT，以及RNFL和GCL厚度。我们将糖尿病患者分为2个亚组，即患有糖尿病视网膜病变和未患视网膜病变的患者。
与对照组相比，我们观察到糖尿病患者的周边黄斑视网膜更厚（P = 0.05）、平均RNFL更厚（P = 0.002）、下方RNFL更厚（P <0.0001）以及上方和下方GCL更厚（分别为P = 0.05和P = 0.04）。我们在23例糖尿病患者（29%）中检测到视网膜病变。与未患视网膜病变的患者相比，患有视网膜病变的患者旁黄斑视网膜更薄（P = 0.05）、平均RNFL更薄（P = 0.002）、下方和鼻侧RNFL更薄（P = 0.002，P = 0.03）、上方GCL更薄（P = 0.05）以及下方GCL更薄（P = 0.006）。糖尿病病程与鼻侧RNFL厚度（r = -0.32，P = 0.004）和旁黄斑RT（r = -0.47，P <0.001）之间存在显著相关性。
结果可能提示患有视网膜病变的1型糖尿病患者存在视网膜内神经组织的丢失。糖尿病视网膜病变中的神经变性与病程密切相关。
