2型糖尿病患者角膜神经损伤相关因素分析

Analysis of Related Factors of Corneal Nerve Damage in Patients with Type 2 Diabetes

摘要: 目的：探讨2型糖尿病(Type 2 Diabetes Mellitus, T2DM)患者各项临床及生化指标与糖尿病角膜神经病变的相关性。方法：选择2024年4月至2024年10月我院收治的75例(150眼) T2DM患者为研究对象。利用Pearson相关性分析比较一般资料及生化指标与角膜上皮下神经丛神经纤维长度、密度之间的相关性。构建多重线性回归分析筛选糖尿病角膜神经病变的相关危险因素。按照血尿酸水平三分位间距将所收集的T2DM患者分为3组：A组(SUA < 283 μmol/L, n = 25)、B组(283 ≤ SUA ≤ 366 μmol/L, n = 25)、C组(SUA > 366 μmol/L, n = 25)，进一步分析尿酸水平与角膜神经参数的关系。按照是否存在糖尿病视网膜病变将所收集的T2DM患者分为2组，探讨患者眼底视网膜病变与角膜神经参数的关系。结果：(1) 糖化血红蛋白、糖尿病病程、尿酸、肌酐与角膜神经长度负相关，糖化血红蛋白、肌酐与主干神经密度负相关，糖尿病病程、肌酐、尿酸与分支神经密度负相关(P均<0.05)；(2) 多重线性回归分析显示糖化血红蛋白、糖尿病病程及尿酸与角膜神经长度相关(P均<0.05)。(3) 进一步按照尿酸水平三分位间距分组，C组患者角膜神经纤维长度、分支神经密度均低于A、B两组，差异有统计学意义(P < 0.05)，A、B两组之间各指标无明显差异(P > 0.05)。(4) 按照是否存在糖尿病视网膜病变分组，存在糖尿病视网膜病变的患者角膜神经长度及主干神经密度均低于无糖尿病视网膜病变的患者，差异有统计学意义(P < 0.05)。结论：高尿酸、血糖控制不佳及糖尿病病程延长与糖尿病角膜神经病变密切相关。高尿酸水平的T2DM患者角膜神经损伤更为明显，T2DM患者也应注意尿酸水平的控制。存在糖尿病视网膜病变的患者更容易出现角膜神经病变，行眼底检查时应注意角膜神经的随访观察。

Abstract: Objective: To investigate the correlation between the clinical and biochemical indexes of type 2 diabetes (T2DM) patients and diabetes corneal neuropathy. Method: 75 T2DM patients admitted to our hospital from April 2024 to October 2024 were selected as the study subjects. Using Pearson correlation analysis and multiple linear regression analysis to compare the correlation between general data and biochemical indicators and the length and density of corneal basal plexus nerve fibers under confocal microscopy. The enrolled patients with type 2 diabetes mellitus were stratified into three groups according to serum uric acid (SUA) level tertiles: Group A (SUA < 283 μmol/L, n = 25), Group B (283 ≤ SUA ≤366 μmol/L, n = 25), and Group C (SUA >366 μmol/L, n = 25), to further analyze the impact of uric acid levels on corneal nerve parameters. Additionally, patients were divided into two groups based on the presence or absence of diabetic retinopathy (DR) to investigate the relationship between retinal pathology and corneal nerve parameters. Result: (1) Glycated hemoglobin (HbA1c), diabetes duration, uric acid, and creatinine levels showed negative correlations with corneal nerve fiber length (CNFL) (P < 0.05). HbA1c and creatinine were negatively correlated with corneal nerve fiber density (CNFD), while diabetes duration, creatinine, and uric acid were negatively correlated with corneal nerve branch density (CNBD) (P < 0.05 for all). (2) HbA1c, diabetes duration, and uric acid were independently associated with CNFL (P < 0.05). (3) According to the interquartile range of uric acid levels, the corneal nerve fiber length and branch nerve density of patients in group C were lower than those in groups A and B (P < 0.05), and there were no significant differences in various indicators between groups A and B (P > 0.05). (4) According to whether DR exists, the corneal nerve length and main nerve density of DR patients are lower than those of NDR T2DM patients (P < 0.05). Conclusion: Hyperuricemia, poor glycemic control, and prolonged diabetes duration were significantly associated with diabetic corneal neuropathy. T2DM patients with hyperuricemia exhibited more severe corneal nerve damage, highlighting the importance of uric acid management in this population. Moreover, the presence of diabetic retinopathy was correlated with a higher risk of corneal neuropathic changes, suggesting that corneal nerve evaluation should be incorporated into routine ophthalmic follow-up, particularly during fundus examinations in diabetic patients.