Atopic keratoconjunctivitis

Abstract
Atopic keratoconjunctivitis (AKC) is a potentially blinding disease characterized by a bilateral chronic keratoconjunctivitis associated with atopic dermatitis. The disease usually manifests as severe itching and burning, excessive tearing, foreign body sensation, and mucoid discharge. The clinical characteristics of AKC show a broad spectrum including lid dermatitis, chronic blepharitis, cicatrizing conjunctivitis with fornix foreshortening and symblepharon formation, punctate epithelial keratitis, persistent epithelial defects, corneal scarring and neovascularization, lipid keratopathy, conjunctivalization of peripheral cornea, and peripheral ulcerative keratitis. The underlying pathophysiologic mechanism in AKC involves a combination of type-I IgE-mediated, and type-IV delayed hypersensitivity reactions. The immunoregulatory defect responsible for the overproduction of allergen-specific IgE antibody, the key component responsible for antigen binding, and subsequent mast cell degranulation, is probably multifactorial. The histopathologic characteristics of the conjunctiva in AKC include a mast cell and eosinophil invasion of the epithelium, epithelial pseudotubule formation, and prominent mast cell and mononuclear cell infiltration of the substantia propria. A number of ocular conditions have been reported to be associated with AKC, including keratoconus, herpes simplex keratitis, and cataracts. Successful long-term control of this potentially blinding disease requires a multidisciplinary approach involving systemic and environmental aspects. Scrupulous long-term environmental control of allergens is the single most important aspect in the management of patients with AKC. Systemic anti-histamine therapy, and long-term topical mast cell stabilizing therapy are also mandatory. Topical steroids should be reserved for exacerbations of the disease.

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