Late corneal perforation after photorefractive keratectomy associated with topical diclofenac: Involvement of matrix metalloproteinases

To report a case of a 50-year-old man who was initially seen with a corneal perforation in his right eye 2 months after a photorefractive keratectomy (PRK) procedure and to discuss the roles of topical diclofenac and matrix metalloproteinases (MMPs). Case report with tissue analysis. Ocular examination, diagnostic workup, surgical treatment, and histologic, immunofluorescent, zymography, and real time-polymerase chain reaction studies on corneal button. Slit-lamp examination of the right eye revealed a 4-mm diameter area of central corneal thinning with a 2-mm diameter perforation at its center. Predisposing factors included prolonged postoperative topical diclofenac therapy for more than 2 months and a 10-year history of well-controlled diabetes mellitus. An extensive diagnostic workup ruled out a systemic autoimmune disease. A penetrating keratoplasty was performed. Results of immunohistochemical studies of the corneal button showed stromal accumulation of temporary type III and IV collagens, MMP-3, and MMP-9 in the anterior wounded stroma and MMP-9 in the basal corneal epithelial cells of the leading edge. Differential activity and expression of MMP-2 and MMP-9 were found between the central and peripheral corneal buttons. Prolonged use of diclofenac and diabetes mellitus might be responsible for the corneal perforation after PRK in our patient. MMP-9 and MMP-3 might be involved in delayed wound closure and corneal melting.