Fosmark Dag S, Bragadóttir Ragnheidur, Stene-Johansen Ingar, Berg Jens P, Berg Tore J, Lund Terje, Sandvik Leiv, Hanssen Kristian F
Diabetes Research Centre, Aker and Ullevål University Hospitals, Ullevål University Hospital, Oslo, Norway.
Acta Ophthalmol Scand. 2007 Sep;85(6):618-22. doi: 10.1111/j.1600-0420.2007.00913.x. Epub 2007 May 4.
As advanced glycation endproducts (AGEs) and the vitreous body are both considered to be involved in the development of diabetic retinopathy and hydroimidazolone is one of the most prominent AGEs, we compared vitreous and serum hydroimidazolone in diabetes patients with proliferative diabetic retinopathy (PDR) to levels in non-diabetes controls, co-measuring vitreous albumin and vascular endothelial growth factor (VEGF).
In a cross-sectional case-control study design, we used immunoassays to compare vitreous and serum hydroimidazolone and VEGF levels in 23 consecutive type 2 diabetes mellitus patients with a median known diabetes duration of 12 years (range 1-38 years) with those in 32 non-diabetes age-matched controls undergoing vitrectomy.
Vitreous hydroimidazolone was increased in the PDR group (median 1.3 U/ml, range 0.5-3.3 U/ml) compared with controls (median 0.8 U/ml, 0.5-2.5 U/ml) (p = 0.026). Hydroimidazolone levels in serum and vitreous correlated (r = 0.49, p = 0.019). In PDR, vitreous VEGF levels were increased (median 1600 pg/ml, range 20-14 700 pg/ml) compared with controls (median 7 pg/ml, range 2-500 pg/ml) (p < 0.001). Similarly, vitreous albumin concentration was increased in PDR (median 1.6 g/l, range 0.7-3.0 g/l) compared with controls (median 0.3 g/l, range 0.08-1.9 g/l) (p < 0.001). Albumin could not explain the differences in vitreous VEGF levels in a logistic regression analysis. No correlation was found between vitreous levels of VEGF and hydroimidazolone (r = 0.12, p = 0.59).
Increased vitreous hydroimidazolone is associated with diabetic retinopathy, possibly due to a blood-retinal barrier breakdown. Irrespective of origin, it may add to the ocular damage and needs further causal investigation. Increased VEGF in diabetic vitreous is probably of intraocular origin. It is not associated with vitreous hydroimidazolone.
由于晚期糖基化终产物（AGEs）和玻璃体均被认为与糖尿病视网膜病变的发生有关，且氢化咪唑酮是最主要的AGEs之一，我们比较了增殖性糖尿病视网膜病变（PDR）糖尿病患者玻璃体和血清中的氢化咪唑酮水平与非糖尿病对照组的水平，并同时检测了玻璃体白蛋白和血管内皮生长因子（VEGF）。
在一项横断面病例对照研究设计中，我们使用免疫测定法比较了23例连续的2型糖尿病患者（已知糖尿病病程中位数为12年，范围1 - 38年）的玻璃体和血清氢化咪唑酮及VEGF水平，与32例接受玻璃体切除术的年龄匹配的非糖尿病对照组进行比较。
与对照组（中位数0.8 U/ml，范围0.5 - 2.5 U/ml）相比，PDR组的玻璃体氢化咪唑酮升高（中位数1.3 U/ml，范围0.5 - 3.3 U/ml）（p = 0.026）。血清和玻璃体中的氢化咪唑酮水平相关（r = 0.49，p = 0.019）。在PDR中，与对照组（中位数7 pg/ml，范围2 - 500 pg/ml）相比，玻璃体VEGF水平升高（中位数1600 pg/ml，范围20 - 14700 pg/ml）（p < 0.001）。同样，与对照组（中位数0.3 g/l，范围0.08 - 1.9 g/l）相比，PDR中玻璃体白蛋白浓度升高（中位数1.6 g/l，范围0.7 - 3.0 g/l）（p < 0.001）。在逻辑回归分析中，白蛋白无法解释玻璃体VEGF水平的差异。未发现玻璃体VEGF水平与氢化咪唑酮之间存在相关性（r = 0.12，p = 0.59）。
玻璃体氢化咪唑酮升高与糖尿病视网膜病变相关，可能是由于血视网膜屏障破坏。无论其来源如何，它可能会加重眼部损伤，需要进一步进行因果关系研究。糖尿病玻璃体中VEGF升高可能源于眼内。它与玻璃体氢化咪唑酮无关。
