Background: Deficient retinal capillary perfusion results in angioneogenesis of the eye. Its extension depends on the degree of ischemia. Mild stages are restricted to the retina, while marked ischemia results in neovascularization of the iris (rubeosis iridis). The neovascularization may be induced by the release of growth factors into the vitreous. Tumor necrosis factor alpha seems to be an important angiogenetic growth factor.
Patients and methods: The patients were divided up into three groups with different retinal stages of ischemia, as judged by the extension of new vessel formation of the eye: a control group without angioneogenesis, a diabetes group with less severe to moderate angioneogenesis of patients with proliferative diabetic retinopathy and a rubeosis group with massive angiogenesis (rubeosis iridis) resulting from different causes. TNF-alpha was determined by immunological methods.
Results: The TNF-alpha level of vitreous in rubeosis (25.8 pg/ml; n = 6) was 2-fold elevated compared to controls (13.1 pg/ml; n = 10; p < 0.05) and 1.4-fold elevated compared to the diabetes group (18.2 pg/ml; n = 17). The values ranged from unmeasurable values to 41.25 pg/ml. Within the rubeosis group similar changes were observed independently of the causes of ischemia. There was no correlation between TNF-alpha-levels in the diabetes group and serum creatinine.
Conclusions: 1. TNF-alpha is upregulated in ischemia. 2. TNF-alpha seems to be a mediator of angiogenesis in the eye. 3. Changes in diabetes may be secondary to local ischemia rather than being specific for diabetic retinopathy.