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Laboratory Tests Although examination of the ocular discharge in allergic conjunctivitis typically reveals large numbers of eosinophils, this test is almost never performed. Instead, allergic conjunctivitis is generally diagnosed clinically. As with any allergy, skin testing may be performed to identify

the offending allergen or allergens, however, it is rarely undertaken.


ALLERGEN AVOIDANCE The most effective but least practical treatment is to prevent exposure to the allergen. Since this is not usually possible, patients should be instructed to frequently use cold compresses,

artificial tears and ointments to soothe and lubricate the eyes and wash away the allergens. Artificial tear substitutes provide a barrier function and help to improve the first-line defence at the level of the conjunctival mucosa. These products help to dilute various allergens and inflammatory mediators that may be present on the ocular surface, and they help flush the

ocular surface of these agents

MEDICAL TREATMENT The main strategy of medical treatment is to combine different therapeutic pharmacological agents, that are active on different mediators involved in allergy pathogenesis. These phar- macological agents may include:

Topical Vasoconstrictors Vasoconstrictors are available either alone or in conjunction with antihistamines to provide short-term relief of vascular injection and redness. Common vasoconstrictors include napha- zoline, phenylephrine, oxymetazoline, and tetrahydrozoline.


Generally, the common problem with vasoconstrictors is that they may cause rebound con- junctival injection, inflammation and dryness. These pharmacological agents are ineffective against severe ocular allergies and against other more severe forms of allergic conjunctivitis, such as atopic and vernal disease. [6]

Antihistamines Systemic and/or topical antihistamines may be given to relieve acute symptoms due to inter- action of histamine at ocular H1 and H2 receptors.

Two kinds of systemic H1 receptor antagonist are available: a The first generation drugs, such as chlorpheniramine and hydroxyzine. These easily pass the blood-brain barrier and cause sedation, they also may have anticholinergic activity leading to elevation of IOP and problems with accommodation. b The second generation drugs, such as astemizole, cetirizine, loratadine, terfenadine are non-sedating.



While systemic antihistamines often relieve ocular allergic symptoms, patients may experience

systemic side effects such as drowsiness and dry mouth.

Topical antihistamines competitively and reversibly block histamine receptors and relieve itching and redness but only for a short time. These medications do not affect other proin- flammatory mediators, such as prostaglandins and leukotrienes, which remain uninhibited.

Topical levocabastine is a second generation anti-H1 agent with a rapid onset of action and good local tolerance and does not affect accommodation or IOP. Newer topical anti-histami- nes, such as emedastine difumarate 0.5 % have been seen to be very effective in relieving the signs and symptoms of allergic conjunctivitis. [7]

Mast cells stabilisers Mast cell stabilisers have a mechanism of action that is unclear. They may aid in the phospho- rylation of a 78,000-d protein that terminates secretion of mast cell granules; they may incre-

ase calcium influx into the cell preventing membrane changes; and/or they may reduce mem- brane fluidity prior to mast cell degranulation. The end result is a decrease in degranulation of mast cells, which prevents release of histamine and other chemotactic factors that are pre- sent in the preformed and newly formed state. Mast cell stabilisers do not relieve existing symptoms and are to be used on a prophylactic basis to prevent mast cell degranulation with subsequent exposure to the allergen. Therefore, they need to be used long term in conjunc- tion with various other classes of medication. Common mast cell stabilisers include cromolin sodium and lodoxamide.

Dual action drugs If the goal of the therapy is to be both treatment and prevention, an agent which has both antihistamine and mast cell stabilising activities should be considered. There are several pro- ducts on the market claiming to show this dual effect or even multiple effects. Among these agents only olopatadine hydrochloride 0.1 % targets tryptase/chymase mast cells, the predominant mast cells in human conjunctival tissue and is the only antihistamine and mast-cell stabiliser approved to treat all the signs and symptoms of allergic conjunctivitis. Studies demonstrate that this formulation effectively controls the signs and symptoms associ- ated with allergic conjunctivitis for at least 16 to 24 hours post-instillation.

Non-steroidal anti-inflammatory drugs (NSAIDs) These act on the cyclooxygenase metabolic pathway and inhibit production of prostaglandins and thromboxanes. They have no role in blocking mediators formed by the lipoxygenase path- way, such as leukotrienes. Common NSAIDs that are approved for allergic indications include ketorolac tromethamine and diclofenac sodium. They are useful in reducing itching and conjunctival injection but not very helpful in ridding the eye of excess immune cells. [8]

Corticosteroids Corticosteroids remain one of the most potent pharmacologic agents used in the treatment of allergic conjunctivitis. They act at the first step of the arachidonic acid pathway by inhibiting phospholipase, which is responsible for converting membrane phospholipid into arachidonic acid. By preventing the formation of arachidonic acid, corticosteroids effectively block both

cyclooxygenase and lipoxygenase pathways, in contrast to NSAIDs, which act only on the cyclooxygenase pathway. Corticosteroids do have limitations, including ocular side effects such



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