ABSTRACT
PURPOSE: Three cases of corneal melting caused by a new nonsteroidal anti-inflammatory drug (NSAID), bromfenac sodium, are reported. CASE REPORTS: Case 1: A 58-year-old man with a history of bullous keratopathy caused by Fuchs' corneal dystrophy was treated for episcleritis with topical bromfenac sodium. After 15 days of treatment, melting (80% depth) was observed inferiorly in the paracentral cornea. Case 2: A 71-year-old man underwent uncomplicated pterygium surgery, followed by treatment with topical bromfenac sodium. After 40 days of treatment, a 60%-depth corneal melt occurred in the nasal limbus. Case 3: A 76-year-old woman had a suspected bacterial corneal ulcer that resolved with topical ofloxacin; however, after 5 days of treatment with topical bromfenac sodium, a perforation occurred in the inferonasal cornea. RESULTS: In all three cases, severe corneal melting was characterized by mild hyperemia, very faint infiltration, and mild pain. Conservative treatment, including the use of a bandage soft contact lens and/or antibiotics and lubrication, led to resolution in all cases. CONCLUSIONS: A new NSAID, bromfenac sodium, can lead to severe corneal melting. These findings, together with similar previous reports concerning diclofenac sodium and ketorolac, suggest that careful observation is required when using topical NSAIDs in the treatment of corneal disease.
Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Benzophenones/adverse effects , Bromobenzenes/adverse effects , Cornea/drug effects , Corneal Diseases/chemically induced , Aged , Anti-Inflammatory Agents, Non-Steroidal/administration & dosage , Benzophenones/administration & dosage , Bromobenzenes/administration & dosage , Cornea/pathology , Corneal Diseases/pathology , Female , Humans , Male , Middle Aged , Ophthalmic SolutionsABSTRACT
PURPOSE: A case of sectorial benign flecked retina not associated with an RDH5 gene mutation is reported. METHODS: A 51-year-old woman showed multiple yellow-white flecks in both eyes similar to those of benign flecked retina but in only the upper half of the retina. We carried out clinical, electrophysiological, and molecular genetic examinations of the patient. RESULTS: Visual acuity was 20/20 OD and 20/20 OS. Fluorescein angiography showed diffuse irregular hypofluorescence that did not correspond to the flecked lesions. A Goldmann-Weeker adaptometer test revealed that the visual threshold of the upper retina was approximately 0.6 to 0.8 log units higher than that of the lower retina. No mutations of the RDH5 gene were detected in exons 2-5 or in the flanking intron sequences. CONCLUSIONS: To our knowledge, this is the first report of sectorial benign flecked retina, and the flecks may not be caused by an RDH5 gene mutation.
