PURPOSE: To investigate whether angiotensin II (AII) or vascular endothelial growth factor (VEGF) is related to diabetic macular edema (DME) in patients with and without posterior vitreous detachment (PVD). DESIGN: A case-control study. METHODS: Vitreous fluid samples were obtained at vitreoretinal surgery from 28 eyes of 28 DME patients without PVD, 8 eyes of 8 DME patients with PVD, 14 eyes of 14 nondiabetic patients, and 8 eyes of diabetic patients without retinopathy. The VEGF levels in vitreous fluid and plasma were determined by enzyme-linked immunosorbent assay, while AII levels were measured by radioimmunoassay. RESULTS: The vitreous levels of AII and VEGF were significantly higher in DME patients with or without PVD than in nondiabetic patients or diabetic patients without retinopathy (without PVD: P < .0061, P < .0001, P = .0261, and P < .0001; with PVD: P < .0012, P < .0001, P = .0473, and P < .0001, respectively). There was no significant difference in the vitreous levels of AII or VEGF between patients with or without PVD (P = .4948 and P = .6642, respectively). The vitreous level of AII significantly correlated with that of VEGF in DME patients without PVD (P = .576) or with PVD (P = .488). AII and VEGF levels in vitreous fluid were significantly higher than the respective plasma levels. CONCLUSIONS: We found that the vitreous levels of AII and VEGF were elevated in DME patients irrespective of the status of PVD. Angiotensin II and VEGF may be induced in the eyes and be related to the pathogenesis of DME. Copyright 2003 by Elsevier Science Inc.
PURPOSE: To investigate whether angiotensin II (AII) or vascular endothelial growth factor (VEGF) is related to diabetic macular edema (DME) in patients with and without posterior vitreous detachment (PVD). DESIGN: A case-control study. METHODS: Vitreous fluid samples were obtained at vitreoretinal surgery from 28 eyes of 28 DMEpatients without PVD, 8 eyes of 8 DMEpatients with PVD, 14 eyes of 14 nondiabeticpatients, and 8 eyes of diabeticpatients without retinopathy. The VEGF levels in vitreous fluid and plasma were determined by enzyme-linked immunosorbent assay, while AII levels were measured by radioimmunoassay. RESULTS: The vitreous levels of AII and VEGF were significantly higher in DMEpatients with or without PVD than in nondiabeticpatients or diabeticpatients without retinopathy (without PVD: P < .0061, P < .0001, P = .0261, and P < .0001; with PVD: P < .0012, P < .0001, P = .0473, and P < .0001, respectively). There was no significant difference in the vitreous levels of AII or VEGF between patients with or without PVD (P = .4948 and P = .6642, respectively). The vitreous level of AII significantly correlated with that of VEGF in DMEpatients without PVD (P = .576) or with PVD (P = .488). AII and VEGF levels in vitreous fluid were significantly higher than the respective plasma levels. CONCLUSIONS: We found that the vitreous levels of AII and VEGF were elevated in DMEpatients irrespective of the status of PVD. Angiotensin II and VEGF may be induced in the eyes and be related to the pathogenesis of DME. Copyright 2003 by Elsevier Science Inc.
Authors: David J Browning; Michael M Altaweel; Neil M Bressler; Susan B Bressler; Ingrid U Scott Journal: Am J Ophthalmol Date: 2008-09-05 Impact factor: 5.258