Systemic allergies affect about 20 percent of the population, and about 20 percent of these systemic allergy patients also have ocular involvement.1
Ocular allergy is a common clinical disorder that includes dry eye syndrome in its differential diagnosis. Because many of the symptoms of dry eye and ocular allergy overlap, the clinical diagnosis becomes more challenging, highlighting the importance of diagnostic testing such as tear film osmolarity. We may even see dry eye syndrome present after years of chronic allergy, a long-lasting result of tear film imbalance and ocular inflammation.
The major type 1 immunologic hypersensitivity reaction involving the conjunctiva is commonly referred to as allergic conjunctivitis. This is a spectrum of disorders including both seasonal allergic conjunctivitis (SAC) and perennial allergic conjunctivitis (PAC).
Seasonal allergic conjunctivitis is the most common form of ocular allergy. It is an acute disorder and is contrasted from perennial (year-round) allergic conjunctivitis by its seasonal onset. Seasonal allergens can include tree pollen, grass pollen, ragweed, or outdoor molds. Perennial allergens can include dust mites, animal dander, cockroaches, and indoor molds.2
A spectrum of more chronic presentations of ocular allergic disorders includes vernal keratoconjunctivitis (VKC), atopic keratoconjunctivitis (AKC), and giant papillary conjunctivitis (GPC).1,3
Related: Differentiating ocular allergy
The acute phase of a Type 1 hypersensitivity response in ocular allergy involves immunoglobulin E (IgE) mediated mast-cell degranulation. There is minimal presence of migratory inflammatory cells.2
A sensitized individual contacts a specific antigen, and then antigen-specific antibodies, such as IgE and IgG, cross-link and trigger mast cell degranulation. This leads to release of pre-formed allergic mediators, such as histamine, from the mast cell.
Other mediators, such as prostaglandins, thromboxanes, and leukotrienes, are formed through activation of the inflammatory cascade. Along with chemotactic factors, these mediators stimulate the early phase of IgE-mediated hypersensitivity.3
Histamine receptor stimulation (H1 is related to itching, and H2 is related to increased vascular permeability) leads to the onset of symptoms. Further activation of the inflammatory cascade and migration of eosinophils and neutrophils result in the later phase ocular allergic response.