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    Managing treatment options for atopic keratoconjunctivitis

    Corticosteroid therapy, calcineurin inhibitors, off-label dermatologic drug may offer relief

    Atopic keratoconjunctivitis (AKC) occurs in 20 to 43% of patients with atopic dermatitis, although flares of ocular surface inflammation may be independent of dermatitis. The corneal complications of AKC can be sight-threatening, and prompt, effective treatment is imperative to reduce the risk of poor vision or blindness, according to Stephen C. Pflugfelder, MD.

    Patients with conjunctival complications from atopic dermatitis often display velvety papillary reaction and thickening of both the inferior and superior palpebral conjunctiva, said Dr. Pflugfelder, professor and James and Margaret Elkins Chair, department of ophthalmology, Baylor College of Medicine, Houston.

    Subepithelial fibrosis may also develop in chronic cases, leading to entropion that can cause corneal microtrauma. Punctal edema or stenosis is another complication and can worsen the clearance of inflammatory mediators from the ocular surface and lead to a vicious cycle.

    Corneal disease manifests in about 70% of patients with AKC; punctate epitheliopathy is the most common pathology and is usually greatest in the superior and inferior peripheral cornea, perhaps due to conjunctival and lid margin changes. Patients may develop a migratory pattern indicating chronic microtrauma.

    “In the most severe cases, that can go on to become a limbal stem cell deficiency,” Dr. Pflugfelder said.

    Neovascularization develops in about 60% of patients, with Horner-Trantas dots sometimes seen at the limbus. The neovascularization may be severe and progressive in some patients, extending into the center of the cornea.

    “Patients with AKC have increased prevalence of herpetic blepharitis and keratitis,” Dr. Pflugfelder said. “When a patient presents with bilateral ocular herpetic eye disease, I almost always look for signs of atopy.”

    Evidence from the past several decades has indicated that T-cells participate in the ocular surface inflammation, he said.

    Cytokines produced primarily by T helper 2 cells—or sometimes by T helper 1 cells, such as interferon gamma—can contribute to goblet cell hyperplasia and mucous secretion, which may be why many of these patients have excessive mucous discharge, he noted.

    “It can lead to conjunctival subepithelial fibrosis and to eosinophil and mast cell recruitment,” he said. “These cells can further release cytokines and inflammatory mediators which can exacerbate the conjunctival and corneal disease.”

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