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H. Logan Brooks, Jr, MD; Sergio Caballero, Jr, MS; Charles K. Newell, MD; Robert L. Steinmetz, MD; Debbie Watson, BS, CRA; Mark S. Segal, MD, PhD; Jeffrey K. Harrison, PhD; Edward W. Scott, PhD; Maria B. Grant, MD

Arch Ophthalmol. 2004;122:1801-1807.

Background  Diffuse macular edema (DME) and/or aberrant neovascularization (NV) can cause vision loss in diabetic retinopathy (DR) and may be modulated by growth factors and chemokines. The chemokine stromal-derived factor 1 (SDF-1) is a potent stimulator of vascular endothelial growth factor (VEGF) expression, the main effector of NV, and the key inducer of vascular permeability associated with DME. Circulating endothelial cell precursors migrating in response to SDF-1 participate in NV.

Objective  To investigate the relationship between SDF-1 and (VEGF) in vitreous of patients with varying degrees of DR and DME before and after intraocular injection of triamcinolone acetonide, used to treat refractory DME.

Methods  In this prospective study, 36 patients were included and observed for 6 months. Vitreous VEGF and SDF-1 levels were measured by enzyme-linked immunosorbent assay in samples obtained immediately before and 1 month after injection of triamcinolone.

Results  Both VEGF and SDF-1 were significantly higher (P<.01) in patients with proliferative DR than in patients with nonproliferative DR. Levels of SDF-1 were markedly increased in patients with DME compared with those without DME. Vascular endothelial growth factor correlated with SDF-1 levels and disease severity (r² = 0.88).

Conclusions  Triamcinolone administration resulted in dramatic reductions of VEGF and SDF-1 to nearly undetectable levels, eliminated DME, and caused regression of active NV. Our results support a role for SDF-1 and VEGF in the pathogenesis of the adverse visual consequences of DR and suggest that the elimination of DME with regression and/or initiation of fibrosis of NV after triamcinolone injection may be due to the suppression of VEGF and SDF-1.

Author Affiliations: Southern Vitreoretinal Association, Tallahassee, Fla (Drs Brooks, Newell, and Steinmetz and Ms Watson); and the Departments of Pharmacology and Therapeutics (Mr Caballero and Drs Harrison and Grant), Medicine (Dr Segal), and Molecular Biology (Dr Scott), University of Florida, Gainesville.

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