Treatment is aimed at reducing the local inflammation. Ocular mast cells stabilizer drops such asolopatadine are the mainstay of treatment. In addition, treatment of nasal symptoms with nasal anti-inflammatory sprays promotes patency of the nasolacrimal duct. This combination treatment allows the eye to drain excess allergens, therefore diminishing allergic responses in the eye.
Atopic keratokonjungtivitis is observed in approximately 15 to 40% of patients with atopic dermatitis. Whereas allergic conjunctivitis is usually a self-limiting process, atopic keratoconjunctivitis is chronic and can potentially cause loss of vision. Immunological and immunohistochemical studies reveal mast cells, IgE antibody, eosinophils, and other inflammatory cells in similar quantities to those found in allergic conjunctivitis. The finding of lymphocyte involvement explains the chronic nature of the disease as well as the threat to sight. Additional findings include antibodies to ICAM-1 and HLA-DR throughout the ocular epithjelium, suggesting increased antigen presentation. Also, increased level of RANTES, an eosinophil homeostasis chemokine, are observed in immunochemical studies of the epithelium. Fibroblast numbers are increased in the connective tissue with an increased level of collagen compared with normal tissue. This infiltration is likely critical to the sight-threathening nature of the disease.
The major signs and symptoms include itching and a clear or white stringy discharge. A “cobblestone” appearance is typical. It is commonly associated with contact lens use. Foreign bodies and ocular sutures or prosthetics may be causal as well. Treatment typically involves avoidance of the inciting process or use of ocular anti-inflammatory agents such as cromolyn sodium or topical corticosteroid.
Giant papillary conjunctivitis is a chronic inflammatory process that leads to the production of giant mucosal ducts, or papillae, on the conjunctival lining of the upper eyelids. The immunopathologic mechanism is complex and is theorized to be a mechanical trauma culminating in a mast cell-mediated delayed-type hypersensitivity.
Vernal conjunctivitis is a chronic, bilateral conjunctival inflammatory disease found primarily in young males with history of atopy during spring months. Initial symptom onset is before puberty, and symptoms dissipate by the third decade of life. In severe cases, vernal conjunctivitis can lead to corneal scarring and permanent vision loss. Histopathologically, conjunctival infiltration with basophils, eosinophils, plasma cells, lymphocytes, and macrophages characterizes vernal conjunctivitis. With this cellular milieu, it appears that vernal conjunctivitis is a combined immediate and delayed-type hypersensitivity reaction.
Perrennial allergic conjunctivitis, in contrast, is associated with a persistent increase in the number of these allergic cell types throughout the year as well as specific IgE (dust, mold, animal dander) found in the tears of affected individuals.
Inflammatory markers include up-regulation of intercellular adhesion molecules such as ICAM-1. Increased levels of helper T cell 2 subset (TH2) cytokines, including IL-4, are found in the eye tissues during allergy season. Clinically, the conjunctiva is red, with a clear discharge . The eye is almost uniformly pruritic. Seasonal allergic conjunctivitis is commonly associated with rhinitis, but it may be the predominant symptom of allergy.