Objective: To provide evidence for our theory of the cause of fibrin reaction by showing that interleukin 1 (IL-1) and prostaglandin E 2 (PGE 2 ), previously detected by us in the incubation media of human lens epithelial cell culture, are also synthesized in vivo by residual lens epithelial cells during their fibrous metaplasia and cause fibrin reaction breakdown of the blood-aqueous barrier. Topical sodium diclofenac, which is known to inhibit PGE 2 -synthesis, may be effective in its prevention. Study Design, Setting and Patients: A prospective study of the occurrence of fibrin reaction after posterior chamber lens (PCL) implantation, during a postoperative period of 1 month, was performed in 190 patients with senile cataract, selected randomly at Nishi Eye Hospital, Osaka and divided into two surgical groups. One group received diclofenac sodium three times a day postoperatively and the other a placebo for 1 month. Results: One mild fibrin reaction was observed in the diclofenac group (1.8%), whereas there were eight fibrin reactions in the placebo group (8.4%) ( P < 0.05). Conclusions: Topical diclofenac sodium reduced fibrin reaction significantly, supporting the theory that PGE 2 is produced by residual lens epithelial cells in vivo . IL-1 may induce lens epithelial cells to synthesize PGE2 autocrinely and to undergo fibrous metaplasia.