Abstract. Background/Aim: Acute allergic rhinoconjuctivitis is the most common form of ocular allergies. The pathogenetic mechanisms are based on an immunoglobulin E (IgEAcute allergic rhinoconjuctivitis is the most common form of ocular allergies, affecting at least 15-20% of the population. It is divided into seasonal (hay fever), which is released by pollen in the spring and summer, and perennial, which appears throughout the year and is induced by dust mites, animal dander and mold allergens (1, 2). The pathogenetic mechanisms of acute allergic conjunctivitis are based on an immunoglobulin E (IgE)-mediated hypersensitivity reaction, where IgE binds initially to highaffinity receptors on mast cells and basophils and then to the aforementioned allergens. The subsequent activation of mast cells results in the release of inflammatory mediators, including histamine, tryptase, prostaglandins, chemokines and leukotrienes (1). Monocytes, eosinophils and platelets also afford low-affinity IgE receptors (2). Subjects experience acute episodes of redness, tearing, ocular and nasal itching, sneezing, congestion and rhinorrhoea. Slit lamp examination usually reveals bilateral eyelid edema along with conjunctival swelling, chemosis and papillary reaction (1, 2).
403