Abstract

Dear Editor, Staphylococcus-associated marginal keratitis is an immunemediated corneal disorder secondary to blepharoconjunctivitis. Marginal infiltrates (also referred to as catarrhal infiltrates) usually occur where the eyelid margins intersect with the corneal surface. Marginal infiltrates in staphylococcal blepharitis are typically gray–white, wellcircumscribed, and located approximately 1 mm inside the limbus, with a characteristic clear zone of cornea between the infiltrate and the limbus. Superficial blood vessels cross the clear interval into the area of infiltration, and pannus may develop in chronic disease. Therapy includes reduction of toxin-producing microorganisms by eyelid hygiene, application of topical antibiotics and corticosteroids [1]. We are unaware of previous reports about the treatment of staphylococcus-associated marginal keratitis with topical cyclosporine. A 19-year-old boy presented with redness, discomfort, photophobia, and decreased vision in his left eye. He previously had blepharitis history for 3 years and keratitis history for 8 months. He was prescribed various topical antibiotics, nonsteroids, and corticosteroids, including fluoromethalone, dexamethasone by other clinics, but his complaints have not recovered. His best-corrected visual acuity was 20/200, and intraocular pressure was 15 mmHg with air-puff tonometry in the left eye. Slit-lamp biomicroscopic examination revealed matted anterior eyelid crusting, papillary reaction of the tarsal conjunctiva, severe conjunctival hyperemia, and especially inferior corneal neovascularization involved the pupillary axis (Fig. 1a). Fundoscopic examination was normal. We diagnosed marginal keratitis associated with staphylococcal blepharoconjunctivitis. The diagnosis of staphylococcal blepharoconjunctivitis was confirmed by growth of staphylococcus aureus in eyelid and conjunctival cultures. Daily eyelid hygiene was advised and topical cyclosporine 0.05% ophthalmic suspension was started 2 times daily because of unresponsiveness to corticosteroid treatment. His complaints began to decrease after 2 weeks, and completely improved after 6 weeks of treatment. Conjunctival hyperemia, and corneal neovascularization completely regressed (Fig. 1b), and his best-corrected visual acuity increased to 20/40 after 6 weeks of treatment. After 6 months of cyclosporine treatment, neither recurrence of neovascularization nor complaints of the patient were observed. Cyclosporine has been used successfully as a systemic immunomodulator for more than 2 decades, but an ophthalmic formulation, topical cyclosporine 0.05% ophthalmic emulsion, was approved by the US Food and Drug Administration to treat dry eye disease in 2003. Treatment with topical cyclosporine has been shown to reduce cell surface markers of activated T lymphocytes, expression of a proinflammatory cytokine, and apoptotic cells, and to increase goblet cell densities in conjunctival epithelium. Many chronic ocular surface disorders share features with dry eye disease, and their responses to immunomodulation therapy with cyclosporine have been evaluated. Because of this, in a number of previous studies, cyclosporine 0.05% ophthalmic emulsion has shown efficacy for management of vernal and atopic keratoconjunctivitis, ocular rosacea, posterior blepharitis, contact lens intolerance, greft-versusElectronic supplementary material The online version of this article (doi:10.1007/s00417-009-1290-4) contains supplementary material, which is available to authorized users.

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