Vascular adhesion molecules in vitreous from eyes with proliferative diabetic retinopathy.

Purpose: To investigate whether proliferative vitreoretinopathy (PDR) is associated with a selective increase in vitreous levels of soluble vascular cell adhesion molecules that mediate leukocyte extravasation and interaction with endothelium during processes of inflammation and neovascularization.

Methods: Vitreous from 55 patients undergoing vitrectomy for treatment of PDR complicated by vitreous hemorrhage and/or traction retinal detachment was assayed for the presence of the soluble vascular cell adhesion molecules sICAM-1, sVCAM-1, and sE-selectin using a standard enzyme-linked immunosorbent assays (ELISA). Vitreous from 12 cadaveric eyes matching age and sex of the patients were used as control samples.

Results: Vitreous levels of sICAM-1, sVCAM-1, and sE-selectin were significantly higher in eyes with PDR than in control cadaveric vitreous, and levels of all three molecules did not relate to the type or duration of diabetes mellitus. However, eyes with either traction retinal detachment alone or both traction retinal detachment and vitreous hemorrhage exhibited significantly higher levels of sICAM-1 and sE-selectin than eyes with vitreous hemorrhage alone. Vitreous levels of sVCAM-1 were similar in eyes with either vitreous hemorrhage or traction retinal detachment alone.

Conclusions: The present observations suggest that molecular inflammatory mechanisms may contribute to processes of neovascularization and fibrosis observed in PDR, possibly not as the causative event, but as a result of endothelial, Müller, and retinal pigment epithelial cell activation. The results also indicate that retinal detachment amplifies the existing inflammation within the diabetic retina. Identification of any abnormalities in the production and control of specific adhesion molecules could have important implications in the design of new therapeutic regimens to treat and prevent this sight-threatening complication of diabetes mellitus.