Bromfenac-induced neurotrophic keratitis in a corneal graft.

A man in his 30s, with a history of two operated penetrating keratoplasty (PK), primarily for viral keratitis, presented with pain, redness and diminution of vision in his left eye of 4 days duration. Postoperatively, he was prescribed oral antivirals, topical steroid eyedrops, lubricants and antiglaucoma medications. Eight months after transplantation, an epithelial defect with heaped up margins was noted on anterior segment evaluation on a routine follow-up visit. On checking his medications, it was found that the patient was unknowingly using bromfenac drops in place of brimonidine tartrate for the past month. A diagnosis of neurotrophic keratitis was made in the setting of PK performed for viral keratitis, incited by use of topical bromfenac. The patient was prescribed preservative-free lubricants with immediate discontinuation of bromfenac drops. Topical steroid drops were withheld till the epithelial defect healed. Complete healing of the defect was noted after 4 weeks of therapy.

ACE2 Expression Is Upregulated in Inflammatory Corneal Epithelial Cells and Attenuated by Resveratrol.

Purpose: The ocular surface is considered an important route for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) transmission. The expression level of the SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2) is vital for viral infection. However, the regulation of ACE2 expression on the ocular surface is still unknown. We aimed to determine the change in ACE2 expression in inflamed corneal epithelium and explore potential drugs to reduce the expression of ACE2 on the ocular surface. Methods: The expression of the SARS-CoV-2 receptors ACE2 and TMPRSS2 in human corneal epithelial cells (HCECs) was examined by qPCR and Western blotting. The altered expression of ACE2 in inflammatory corneal epithelium was evaluated in TNFα- and IL-1ß-stimulated HCECs and inflamed mouse corneal epithelium, and the effect of resveratrol on ACE2 expression in HCECs was detected by immunofluorescence and Western blot analysis. Results: ACE2 and TMPRSS2 are expressed on the human corneal epithelial cells. ACE2 expression is upregulated in HCECs by stimulation with TNFα and IL-1ß and inflamed mouse corneas, including dry eye and alkali-burned corneas. In addition, resveratrol attenuates the increased expression of ACE2 induced by TNFα in HCECs. Conclusions: This study demonstrates that ACE2 is highly expressed in HCECs and can be upregulated by stimulation with inflammatory cytokines and inflamed mouse corneal epithelium. Resveratrol may be able to reduce the increased expression of ACE2 on the inflammatory ocular surface. Our work suggests that patients with an inflammatory ocular surface may display higher ACE2 expression, which increases the risk of SARS-CoV-2 infection.