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    Immune mechanisms in allergic eye disease

    Understanding the role of different mechanisms will help increase treatment options


    Types of ocular allergy

    True ocular allergy involves both IgE- and non-IgE-mediated mechanisms. Seasonal and perennial allergic conjunctivitis are primarily IgE-mediated and can be treated using topical and oral antihistamines and topical mast cell stabilisers, whereas non-IgE-mediated disorders such as contact blepharoconjunctivitis require anti-allergic drugs and topical corticosteroids to treat.

    Atopic and vernal keratoconjunctivitis (VKC) have a mixture of IgE-mediated and non-IgE-mediated components and require intense and prolonged anti-allergic drugs, frequently in combination with corticosteroids or topical immunomodulators such as cyclosporine.5

    The diagnosis of ocular allergy is relatively simple, being based mostly on clinical history, signs and symptoms, and being confirmed by the results of allergy tests. In general, asking the right questions to patients should reveal not only signs and symptoms but also their frequency, duration and severity.6

    VKC is a severe ocular disease that occurs predominantly in children living in warm climates. It is frequently complicated by corneal involvement that manifests in a variety of forms including Tranta’s dots; superficial punctuate keratitis; shield ulcer; corneal plaque; corneal neovascularisation; lipid infiltration; bacterial or fungal keratitis; keratoconus; pseudogerontoxon; and corneal opacification.

    Even though it is relatively easily diagnosed because of its distinct clinical history and ocular manifestations, VKC requires particular attention and is not easy to manage.

    Warm climates and sun exposure probably explain the characteristic north-south gradient prevalence of this form of ocular allergy. VKC is associated with other allergic manifestations in approximately half of patients and often arises in response to exposure to specific allergenic triggers: these observations suggest it does indeed have an allergic component.

    Tear levels of IgE and mast cell mediators are high, which supports this conclusion. However, this does not explain the length of the disease, its typical regression after puberty or the fact that it most often manifests in response to non-allergenic triggers such as sunlight, heat and wind. Antigen-specific Th2 cells have not been demonstrated infiltrating the conjunctiva, and several non-IgE-mediated mechanisms are believed to also be involved.

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