Peripheral Corneal Infiltrates Following Oral Diclofenac Administration

Diclofenac sodium is a nonsteroidal anti-inflammatory drug that has been used systemically and topically for the control of many forms of inflammation. Diclofenac and other topical nonsteroidal anti-inflammatory drugs have been used topically for the control of discomfort and pain following photorefractive keratectomy.^1,2 The drug has been shown to decrease corneal sensitivity following topical use.³ Peripheral corneal infiltrates have been observed following topical application of diclofenac and soft contact bandage lens following photorefractive keratectomy.^1,4

To my knowledge, peripheral corneal infiltrates following the use of oral diclofenac have not been previously reported. Here I report a case of peripheral corneal infiltrates following oral use of diclofenac.

A 37-year-old male physician had a history of pain, redness, irritation, and photophobia in the left eye of 2 days' duration. His medical history revealed a history of backache, for which he received diclofenac sodium, 50 mg orally twice daily for a period of 1 week. The patient denied a history of systemic illness and had no previous episodes of blepharitis or conjunctivitis. He also denied using contact lenses for the past year.

On examination, the patient was found to have a visual acuity of 20/20 OD and 20/20 OS with correction. Biomicroscopy of the right eye revealed normal conjunctiva and peripheral 360° corneal micropannus. Biomicroscopy of the left eye revealed normal eyelids with no eyelid disease and no blepharitis. There was mild conjunctival hyperemia. A 360° corneal micropannus was noted, and 2 peripheral corneal infiltrates measuring 1.0 mm in diameter each were noted at the 2-o'clock and 6-o'clock positions. The corneal epithelium was intact and no staining with fluorescein was noted. The infiltrates were subepithelial with a 1.0-mm lucid interval between the corneal infiltrates and the limbus. Cultures of the eyelids and corneal infiltrates on blood agar, chocolate agar, and thioglycolate medium were negative for organisms. Giemsa-stained corneal scraping revealed polymorphonuclear cells. The patient was treated with topical 0.1% fluorometholone eyedrops to the left eye 3 times daily and was asked to discontinue use of the oral diclofenac. During the next 5 days the peripheral corneal infiltrates resolved. One month later, the patient developed backache and resumed oral administration of diclofenac sodium, 100 mg daily. Two days after the initiation of systemic treatment with diclofenac, he developed peripheral corneal infiltrates, one in the right eye and one in the left eye. He was advised to discontinue the use of oral diclofenac and was prescribed 0.1% fluorometholone eyedrops 3 times daily. Once again, the peripheral corneal infiltrates subsided completely within 7 days. Three months later, the patient resumed diclofenac administration and after 3 days developed 2 peripheral corneal infiltrates in the left eye. This time, the patient was asked to discontinue the use of diclofenac and no topical treatment was given. The infiltrates subsided within 7 days after the discontinuation of the use of oral diclofenac.

Peripheral corneal infiltrates have been reported with the topical use of diclofenac. Sher et al¹ noted peripheral corneal infiltrates in 3 patients following administration of topical diclofenac. The peripheral corneal infiltrates of my patient occurred at 3 different occasions following 3 different courses of diclofenac. The appearance of these peripheral corneal infiltrates is probably secondary to the use of oral diclofenac. The mechanism may be similar to that seen with topical diclofenac. The presence of preexisting contact lens–induced peripheral corneal vascularization may have predisposed to peripheral corneal infiltrations. Although the exact mechanism is not well understood, it could be due to inhibition of cyclooxygenase 1 and 2 with a subsequent shunt to the lipooxygenase pathway leading to the synthesis of leukotrienes such as LTB4—a chemotactic factor that may attract polymorphonuclear cells to the corneal periphery.

This study was supported in part by The Eye Foundation for Research in Ophthalmology, The Eye Center, Riyadh, Saudi Arabia.

The author has no proprietary interest in any of the materials or products used in this study.

Corresponding author: Khalid F. Tabbara, MD, The Eye Center, PO Box 55307, Riyadh 11534, Saudi Arabia (e-mail: k.tabbara@nesma.net.sa).