Systemic levels contribute significantly to increased intraocular IGF-I, IGF-II and IGF-BP3 [correction of IFG-BP3] in proliferative diabetic retinopathy.
Systemic levels contribute significantly to increased intraocular IGF-I, IGF-II and IGF-BP3 [correction of IFG-BP3] in proliferative diabetic retinopathy.
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在增殖性糖尿病视网膜病变中，全身水平对眼内 IGF-I、IGF-II 和 IGF-BP3 [IFG-BP3 的校正] 增加有显着贡献。
DOI：
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发表时间：
2000
期刊：
影响因子：
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通讯作者：
Andreas F. H. Pfeiffer
中科院分区：
文献类型：
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作者：
Jochen Spranger;J. Bühnen;V. Jansen;M. Krieg;R. Meyer;W. Blum;H. Schatz;Andreas F. H. Pfeiffer
增殖性糖尿病视网膜病变 (PDR) 中已证实眼内血管生成生长因子（例如胰岛素样生长因子 I (IGF-I)）水平升高。目前尚不清楚血视网膜屏障渗漏增加或局部合成是否主要决定人类眼内 IGF 水平，这对于 PDR 中生长抑素类似物的可能治疗选择特别令人感兴趣。这是第一项平行研究血清和玻璃体 IGF-I/II、IGF-BP3 和肝源性通透性标记物白蛋白的水平，以确定体内循环源性眼内 IGF 的量。将无视网膜增殖的对照组与患有 PDR 的患者进行比较。通过免疫学方法测定IGF-I/II、IGF-BP3和白蛋白的水平。与对照组 (115.7 +/- 36.2 mg/dl; n = 10) 相比，PDR 患者玻璃体白蛋白水平升高 2.2 倍 (254.1 +/- 37.2 mg/dl; n = 27; p = 0.0027)，而糖尿病患者的血清水平略有下降 (5049 +/- 196 mg/dl vs. 4330 +/- 196 mg/dl) 186 毫克/分升；p = 0.0283)。这与 PDR 患者玻璃体中 IGF-I/11 和 IGF-BP3 的增加相当（IGF-I：2.3 +/- 1.1 ng/ml p = 0.005。IGF-II：37.9 +/- 4.9 ng/ml；p = 0.0003。IGF-BP3：97.9 +/- 26.9 ng/ml；p = 0.0001；n = 34）与对照相比（IGF-I：0.7 +/- 0.1 ng/ml。IGF-II：21.3 +/- 4.2 ng/ml。IGF-BP3：31.3 +/- 4.9 ng/ml：n = 19）。 IGF-I、II 和 IGF-BP3 的血清水平在各组之间没有显着差异。眼内白蛋白和 IGF-I 水平计算为各自血清水平的百分比，显着相关（r = 0.42；p = 0.012）。这项研究表明，PDR 中 IGF-I、II 和 IGF-BP3 的流入量与肝脏来源的血清蛋白白蛋白的流入量平行，表明血视网膜屏障的渗漏和 IGF 的血清水平主要决定玻璃体内的 IGF 水平，而不是局部合成。因此，通过新型高效生长抑素类似物抑制全身 IGF 水平为预防 PDR 提供了一种有前景的方法。
Increased intraocular levels of angiogenic growth factors such as insulin-like growth factor I (IGF-I) have been demonstrated in proliferative diabetic retinopathy (PDR). It is unclear whether increased leakage of the blood retina barrier or local synthesis primarily determine intraocular levels of IGFs in man, which is of special interest regarding possible therapeutic options with somatostatin analogues in PDR. This is the first study investigating parallelly serum and vitreous levels of IGF-I/II, IGF-BP3 and the liver-derived permeability marker albumin to determine in vivo the amount of circulation-derived intraocular IGFs. A control group without retinal proliferation and patients with PDR were compared. Levels of IGF-I/II, IGF-BP3 and albumin were determined by immunological methods. Vitreous levels of albumin were 2.2-fold elevated in patients with PDR (254.1 +/- 37.2mg/dl; n = 27; p = 0.0027) compared to controls (115.7 +/- 36.2mg/dl; n =10), whereas serum levels were slightly decreased in diabetes patients (5049 +/- 196 mg/dl vs. 4330 +/- 186 mg/dl; p = 0.0283). This was comparable to an increase of IGF-I/11 and IGF-BP3 in vitreous from PDR patients (IGF-I: 2.3 +/- 1.1 ng/ml p = 0.005. IGF-II: 37.9 +/- 4.9 ng/ml; p = 0.0003. IGF-BP3: 97.9 +/- 26.9 ng/ml; p = 0.0001; n = 34) compared to controls (IGF-I: 0.7 +/- 0.1 ng/ml. IGF-II: 21.3 +/- 4.2 ng/ml. IGF-BP3: 31.3 +/- 4.9 ng/ml: n = 19). Serum levels did not differ significantly among the groups regarding IGF-I, II and IGF-BP3. Intraocular albumin and IGF-I levels calculated as percentage of the respective serum levels correlated significantly (r = 0.42; p = 0.012). This study demonstrates that influx of IGF-I, II and IGF-BP3 in PDR quantitatively parallels influx of the liver derived serum protein albumin suggesting that leakage of the blood retina barrier and serum levels of IGF primarily determine intravitreal IGF levels rather than local synthesis. Suppression of systemic IGF levels by new, highly effective somatostatin-analogues therefore provides a promising approach to prevent PDR.