Background: This study of 86 patients with 12 months of follow-up was designed to determine whether topical corticosteroids or plasmin inhibitors have an effect on the outcome of photorefractive keratectomy.
Methods: Patients were allocated randomly to either steroid (0.1% fluorometholone for 6 months), plasmin-inhibitor (aprotinin 40 IU/ml for 3 weeks), or control (no treatment) groups and underwent either -3.00- or -6.00-diopter (D) corrections.
Results: With -3.00-D corrections, the mean refractive change was significantly greater at 3 and 6 months (P < 0.05) in the steroid group compared with the control group. When steroids were discontinued, the difference became insignificant within 3 months. Similarly, with -6.00-D procedures the mean refractive change was greater at 6 weeks and 3 and 6 months (P < 0.01), but the refractive change again became insignificant 3 months after stopping steroid treatment. Four patients treated with steroids had a hyperopic shift greater than +2.00 D of that intended at 12 months. Similar overcorrections were not noted in the other treatment groups. There were no differences in refractive outcome between the aprotinin and control groups at any stage. With -6.00-D procedures, objective measurements of haze were significantly greater in the aprotinin group compared with the control group at 9 and 12 months (P < 0.05). With this exception, there were no differences in haze, forward or backward scatter of light, best-corrected visual acuity, or halo measurements between the groups.
Conclusions: Corticosteroids can maintain a hyperopic shift during their administration, but this effect is reversed on cessation of treatment. Objective tests have shown that steroids have no effect on corneal haze or visual performance after PRK. There is no justification for routinely submitting all patients to long-term steroid regimens and their associated side effects. Treatment with aprotinin produced no beneficial effect on refractive outcome, and haze was greater in the -6.00-D procedures. The concept of modulating the plasminogen activator/plasmin system to regulate wound healing after PRK is discussed.