TOPICAL AND SUBCUTANEOUS ALPHA-INTERFERON FAILS TO SUPPRESS CORNEAL NEOVASCULARIZATION

Corneal neovascularization is a potentially blinding complication of a variety of corneal disorders. alpha-Interferon has been shown to inhi bit endothelial cell migration and proliferation. It has been used suc cessfully in the treatment of pediatric pulmonary hemangioma and hairy cell leukemia. This study was undertaken to evaluate the effect of to pical and subcutaneous (s.c.) alpha-interferon on corneal neovasculari zation. Corneal neovascularization was induced in 40 male New Zealand white rabbits by placing silk sutures (7.0) bilaterally in each rabbit eye at the 3 and 9 o'clock positions of the cornea, 3 mm from the lim bus. Animals were randomized into two main treatment groups for topica l (group 1) and s.c. (group 2) administration of interferon. Group 1 ( n = 24) was then randomized into four subgroups and treated daily with topical doses of (a) rabbit specific alpha-interferon; (b) alpha-inte rferon plus 1% prednisolone acetate; (c) 1% prednisolone acetate; and (d) buffered phosphate control. Group 2 (n = 16) was randomized into t wo subgroups that received s.c, injections every other day of (a) alph a-interferon and (b) phosphate buffer. Rate of corneal neovascularizat ion was documented photographically, with the endpoint being the arriv al of vessels at the suture for each group. The results of this study indicated that at the concentration and dosing regimens we used, neith er topical nor s.c. alpha-interferon inhibits the rate of corneal vasc ular growth significantly when compared with our phosphate buffered so lution control group (p = 0.88 and p = 0.84, respectively). Prednisolo ne acetate appeared to be the most effective in inhibiting corneal neo vascularization (p = 0.003). Additionally, no additive effect was evid ent when alpha-interferon was used in conjunction with prednisolone ac etate (p = 0.031).