Excerpt from Conjunctivitis, Allergic

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The ocular surface may exhibit a wide variety of immunologic responses that may result in conjunctival and corneal inflammation. In the Gell and Coombs classification system for various immunologic hypersensitivity reactions, 5 classes of reactions are recognized.

Type I (immediate) hypersensitivity reactions occur when a sensitized individual comes in contact with a specific antigen. Immunoglobulin E (IgE) has a strong affinity for mast cells, and the cross-linking of 2 adjacent IgE molecules by the antigen triggers mast cell degranulation. This in turn causes the release of various preformed and newly formed mediators of the inflammatory cascade, including histamine, tryptase, chymase, heparin, chondroitin sulfate, prostaglandins, thromboxanes, and leukotrienes. These various inflammatory mediators, together with various chemotactic factors, result in increased vascular permeability and migration of eosinophils and neutrophils. Principal ocular type I hypersensitivity reaction is allergic conjunctivitis, which is discussed in further detail.

Type II hypersensitivity reactions are autoimmune reactions and may be complement mediated. These reactions may be the underlying cause of various ocular conditions such as cicatricial pemphigoid and Mooren ulcer.

Type III hypersensitivity reactions result in antigen-antibody immune complexes, which deposit in tissues and cause inflammation. Classic type III reaction systemically is the Arthus reaction, and ocular type III hypersensitivity reactions include Stevens-Johnson syndrome and marginal infiltrates of the cornea. Corneal immune (Wesley) rings are also an example of type III reactions.

Type IV hypersensitivity reactions, also known as cell-mediated immunity, are mediated by T lymphocytes. While type I reaction is immediate hypersensitivity, this reaction is also known as delayed-type hypersensitivity, since its onset is generally after 48 hours. Type IV hypersensitivity reactions imply immunocompetence on the part of the individual since an intact immune system is required to mount the cell-mediated response. Ocular examples of type IV hypersensitivity include phlyctenular keratoconjunctivitis, corneal allograft rejection, contact dermatitis, and drug allergies. This section focuses primarily on the major type I hypersensitivity reactions involving the conjunctiva, more commonly referred to as allergic conjunctivitis.

Types of allergic conjunctivitis

Allergic conjunctivitis may be divided into 5 major subcategories. Seasonal allergic conjunctivitis (SAC) and perennial allergic conjunctivitis (PAC) are commonly grouped together. Vernal keratoconjunctivitis (VKC), atopic keratoconjunctivitis (AKC), and giant papillary conjunctivitis (GPC) constitute the remaining subtypes of allergic conjunctivitis.

Pathophysiology:

Seasonal and perennial allergic conjunctivitis

Since conjunctiva is a mucosal surface similar to the nasal mucosa, the same allergens that trigger allergic rhinitis may be involved in the pathogenesis of allergic conjunctivitis. Common airborne antigens including pollen, grass, and weeds may provoke the symptoms of acute allergic conjunctivitis such as ocular itching, redness, burning, and tearing. Main distinction between seasonal and perennial allergic conjunctivitis, as implied by the name, is the timing of symptoms.

Individuals with SAC typically have symptoms of acute allergic conjunctivitis for a defined period of time; in spring when the predominant airborne allergen is tree pollen; in summer when the predominant allergen is grass pollen; or in fall when the predominant allergen is weed pollen. Typically, persons with SAC are symptom-free during the winter months in cooler climates because of the decreased airborne transmission of these allerg .....

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