Ocular symptoms of allergies for many are as severe as rhinitis symptoms said Stephen C. Pflugfelder, MD. Ocular manifestations of seasonal allergies include seasonal allergic conjunctivitis (SAC), perennial allergic conjunctivitis (PAC), vernal keratoconjunctivitis (VKC), and atopic keratoconjunctivitis (AKC), said Dr. Pflugfelder. The ideal therapy should include multiple steps in the allergy cascade, perhaps by neutralizing both the H1 and H2 receptors, stabilizing the mast cells, and having anti-inflammatory properties.
Ocular manifestations of seasonal allergies include seasonal allergic conjunctivitis (SAC), perennial allergic conjunctivitis (PAC), vernal keratoconjunctivitis (VKC), and atopic keratoconjunctivitis (AKC), said Dr. Pflugfelder, professor and holder of the James and Margaret Elkins Chair, Department of Ophthalmology, The Cullen Eye Institute, Baylor College of Medicine, Houston.
One recently published study showed that SAC can have a dramatic impact on patients' daily activities: more than 70% of patients said that it limits their ability to go outdoors or read, and about 50% reported that it affects their ability to drive, concentrate on daily tasks, sleep, or apply make-up.
"There is always something blooming," he said.
AKC is a much more serious but, fortunately, less common form of ocular allergy that can affect a subset of patients with atopic dermatitis and can cause potentially blinding keratopathy.
"Interestingly, Staphylococcus aureus may drive this immune response," Dr. Pflugfelder said. "Some of those patients have heavy colonization on the conjunctival and eyelid margins. At times, treating them with a short course of an oral cephalosporin can have quite a beneficial effect both on their eyes and their skin."
VKC affects mostly young men living in warmer climates. Clinical features include ropy discharge and severe giant papillae along with keratopathy. It can cause shield corneal ulcers and Trantas-Horner dots, he said.
Mechanisms of allergy
"We know a lot more about the mechanisms of allergy now than we did even a decade ago," Dr. Pflugfelder said. "In addition to mast cells, there are other cells involved, including a certain subset of T cells called Th2 lymphocytes. Cytokine produced by activated T cells promotes IgE production by B cells. IgE binds to mast cells, causing sensitization."
Airborne or topical allergens bind to IgE on mast cells, he said, and that process results in degranulation. An immediate reaction of histamine occurs, and the late-phase reaction features histamine and other inflammatory mediators. Each allergic syndrome has its own complement of inflammatory cells and mediators.
"SAC and PAC are usually histamine-mediated diseases with a slight influx of eosinophils and basophils, but usually with self-limited resolution as the allergy goes away," he said. "With VKC and AKC, there is a greater influx of T lymphocytes, resulting in chronic inflammation and much more tissue destruction."
Those facts have implications for therapy, Dr. Pflugfelder explained.
"The ideal therapy should include multiple steps in the allergy cascade, perhaps by neutralizing both the H1 and H2 receptors, stabilizing the mast cells, and having anti-inflammatory properties," he said.
"Systemic therapies such as oral antihistamines are generally reserved for systemic or nasal symptoms," he continued. "They may have only minimal effect on ocular symptoms and often have anticholinergic side effects that can cause ocular dryness."