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Most people develop allergies in childhood. A second subset of individuals develop allergies as adults between the ages of 18 and 35.
Causes of allergic conjunctivitis
- Environmental: air pollution, pollens, climate, geographical locale
- Genetic: 4-fold increase in a child's chance of developing allergy if 1 parent is atopic; 10-fold if both parents are atopic
- Medications and cosmetics
- Devices (contact lenses, sutures)
Allergic cascade: The hypersensitivity can be divided into 3 phases
- Sensitization
- Early--starts within minutes of exposure to the allergen
- Late--starts about 2 hours after allergan exposure
Sensitized individuals are exposed to allergen proteins which dissolve in tears. Macrophages engulf the allergen and degrade it into fragments. These fragments are then displayed on the macrophages which activate helper T cells. Helper T cells bind to the fragments, causing plasma B cells in the blood and lymphatic tissue to mature. Plasma B cells make antigen specific IgE antibodies which adhere to the fragments. These antibodies will then in turn attach to mast cells. The next time the patient is exposed to the allergen, the allergan will bind to the antibodies and cause degranulation of the mast cell.
What escapes from the mast cells?
- Histamine: H1 and H2 receptors are present in the conjunctiva. Itching is caused by histamine (H1) binding to the nerve cells and increased vascular permeability (from endothelial cell contraction). Hyperemia in ocular allergy is caused by histamine (H2) binding on blood vessels causing vasodilation and redness.
- Preformed molecules: neutral protease (tryptase), eosinophil chemotactic factor (ECF-A), heparin, chymase, tumor necrosis factor, other factors
- Newly synthesized molecules: prostaglandins (cause inflammation, vasodilation, and smooth muscle contraction), leukotrienes (increase mucus production, stimulate neutrophil chemotaxis, enhance capillary permeability, cause vasodilation), cytokines (stimulate B cells to synthesize IgE, control migration of inflammatory cells)
- Chemotactic factors: molecules that attract inflammatory cells to the site of exposure and contribute to late phase reaction
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Late phase is responsible for corneal damage such as keratitis, limbal infiltrates, and ulcers. It is associated with more serious conditions such as vernal and atopic keratoconjunctivitis. Eosinophils and other inflammatory cells are not present in large numbers on conjunctival scrapings in seasonal or perennial conjunctivitis. |
Mast cell degranulation is involved in the wound healing process by activating proteases, heparin, growth factors, and fibroblasts which either help regenerate new tissue or remove unhealthy tissue. There may be a role for mast cell stabilizers to help regulate the wound healing process and complications after LASIK;
decreasing itch may help prevent patients from rubbing eyes postoperatively.
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