Agents For Allergy
BY WILLIAM TOWNSEND, OD
Vonda, a 40-year-old female with a long history of immune-related problems, presented for evaluation. She suffered from atopic dermatitis. We had intermittently treated her atopic keratoconjunctivitis when seasonal
exacerbations occurred. During the latest episode, she suffered from very itchy eyes and eyelids as well as blurry vision. Acuities were OD 20/20, OS 20/30. Biomicroscopy revealed mild superficial punctate corneal changes (more prevalent OS) and conjunctival injection. Eversion of the lids showed giant papillae with apical scarring in both eyes. The lids were erythematous and scaly.
The Allergic Response
It is important to understand the phases of allergic eye disease. When an allergen attaches to IgE antibodies on the surface of a mast cell, calcium influx into the cell initiates changes in the cell membrane that cause the cell to degranulate. Within minutes, pre-formed mediators such as histamine are released and cause vascular and tissue changes. Alcon's Emadine (emadastine) and CIBA Vision's Livostin (levocabastine) are effective topical antihistamines that, to some extent, block the ocular effects of this early phase of allergic response.
The late phase has two "sub-phases." When the mast cell degranulates, arachidonic acid is released from cell membranes and converted to leukotrienes and prostaglandins. Prostaglandins cause increased sensitivity to pain and increased vascular permeability. Leukotrienes attract leukocytes to the area. Allergan's Acular (ketorolac tromethamine) and CIBA's Voltaren (diclofenac sodium) inhibit prostaglandin synthesis. There are no topical leukotriene antagonists currently available.
The late phase also attracts eosinophils and neutrophils to the area. Eosinophils activate mast cells and release substances that prolong or worsen the allergic response. Their importance in the development of vernal and atopic keratoconjunctivitis is only now being understood. Eosinophil major basic protein is thought to cause corneal changes in atopic keratoconjunctivitis and other ocular allergic conditions.
CIBA's Zatidor (ketotifen) and Alcon's Patanol (olopatadine HCl) have both direct antihistamine and mast cell stabilizing properties for treating moderate to serious allergy-related eye disease. They effectively diminish or block the early and late phases of keratoconjunctivitis.
A Newer Alternative
We initially treated Vonda with a combination mast cell stabilizer/antihistamine. When symptoms and signs showed little improvement, we prescribed Santen's Alamast (pemirolast potassium). Within a week, the itching, conjunctival signs and corneal changes significantly diminished.
Alamast has mast cell stabilizing and indirect antihistaminic activity that blocks mast cell degranulation. It also inhibits chemotaxis of eosinophils and blocks the release of mediators from eosinophils. By blocking chemotaxis of eosinophils and preventing release of mediators from these leukocytes, Alamast may reduce signs and symptoms associated with these conditions.
Alamast may not be the best choice for an acute condition because the drug takes days to weeks to achieve maximum effect. It will be valuable for chronic conditions such as seasonal allergic conjunctivitis and perennial allergic conjunctivitis. Alamast's greatest value may be in treating allergic eye conditions in which eosinophils play a major role.
The recommended dosage of Alamast is qid, although some studies have shown bid dosing effective. In our area, Alamast costs $53.00 per 10 ml bottle. It is not recommended for children under three years of age.
Dr. Townsend is in private practice in Canyon, Texas, and is a consultant at the Amarillo VA Medical Center. E-mail him at
Contact Lens Spectrum, Issue: April 2001