Hernández C, Burgos R, Cantón A, García-Arumí J, Segura R M, Simó R
Endocrinology Division, Hospital General Vall d'Hebron, Barcelona, Spain.
Diabetes Care. 2001 Mar;24(3):516-21. doi: 10.2337/diacare.24.3.516.
To evaluate the intravitreous concentration of vascular cell adhesion molecule (VCAM)-1 in diabetic patients with proliferative diabetic retinopathy (PDR) and the relationship of VCAM-1 with vascular endothelial growth factor (VEGF).
Serum and vitreous fluid samples were obtained simultaneously at the onset of vitrectomy from 20 diabetic patients with PDR and 20 nondiabetic control subjects with nonproliferative ocular disease. Both groups were matched by serum levels of VCGM-1 and VEGF. VCAM-1 and VEGF were determined by enzyme-linked immunosorbent assay. Statistics were determined using the Mann-Whitney U test and Spearman's rank correlation test.
The intravitreous concentration of VCAM-1 was signifcantly elevated in diabetic patients with PDR compared with control subjects (26 ng/ml [19-118] vs. 22 ng/ml [20-47], P < 0.05). A direct correlation between VCAM-1 and total vitreous proteins was detected in diabetic patients (r = 0.64, P = 0.003), but not in control subjects. After adjusting for total intravitreous proteins, VCAM-1 was significantly lower in diabetic patients with PDR than in control subjects (8.2 ng/ml [4-31.4] vs. 43.1 ng/ml [9.7-100], P < 0.001). Intravitreous VEGF concentrations were higher in patients with PDR than in control subjects in absolute terms (1.34 ng/ml [0.16-6.22] vs. 0.009 ng/ml [0.009-0.044], P < 0.0001) and after correcting for total vitreal proteins (0.33 ng/ml [0.01-2.3] vs. 0.013 ng/ml [0.003-0.035], P = 0.0001). Finally, the vitreous ratio of VCAM-1 to proteins correlated with the vitreous ratio of VEGF to proteins in both diabetic patients (r = 0.74, P = 0.001) and control subjects (r = 0.84, P = 0.005).
The low proportion of VCAM-1 in relation to total vitreal proteins observed in diabetic patients with PDR suggests that VCAM-1 is quenched by diabetic retina. In addition, the direct correlation detected between VCAM-1 and VEGF suggests that cellular adhesion and neovascularization may be linked processes.
评估增殖性糖尿病视网膜病变（PDR）糖尿病患者玻璃体内血管细胞黏附分子（VCAM）-1的浓度，以及VCAM-1与血管内皮生长因子（VEGF）的关系。
在玻璃体切割术开始时，同时采集20例PDR糖尿病患者和20例非增殖性眼病的非糖尿病对照者的血清和玻璃体液样本。两组在血清VCGM-1和VEGF水平上进行匹配。采用酶联免疫吸附测定法测定VCAM-1和VEGF。使用Mann-Whitney U检验和Spearman等级相关检验进行统计学分析。
与对照者相比，PDR糖尿病患者玻璃体内VCAM-1浓度显著升高（26 ng/ml [19 - 118] vs. 22 ng/ml [20 - 47]，P < 0.05）。在糖尿病患者中检测到VCAM-1与玻璃体内总蛋白之间存在直接相关性（r = 0.64，P = 0.003），而在对照者中未检测到。在调整玻璃体内总蛋白后，PDR糖尿病患者的VCAM-1显著低于对照者（8.2 ng/ml [4 - 31.4] vs. 43.1 ng/ml [9.7 - 100]，P < 0.001）。PDR患者玻璃体内VEGF浓度绝对值高于对照者（1.34 ng/ml [0.16 - 6.22] vs. 0.009 ng/ml [0.009 - 0.044]，P < 0.0001），在校正玻璃体内总蛋白后也是如此（0.33 ng/ml [0.01 - 2.3] vs. 0.013 ng/ml [0.003 - 0.035]，P = 0.0001）。最后，糖尿病患者和对照者中VCAM-1与蛋白的玻璃体比率均与VEGF与蛋白的玻璃体比率相关（糖尿病患者：r = 0.74，P = 0.001；对照者：r = 0.84，P = 0.005）。
PDR糖尿病患者中观察到的VCAM-1相对于玻璃体内总蛋白的低比例表明，VCAM-1被糖尿病视网膜淬灭。此外，检测到的VCAM-1与VEGF之间的直接相关性表明，细胞黏附与新生血管形成可能是相关过程。
