Epidemiology
Allergic rhinitis affects as many as 8% to 10% of children in the United States. Many of these children suffer significant morbidity, leading to millions of lost school days annually. Morbidity is amplified when these children concurrently suffer from complications of allergic rhinitis, such as recurrent otitis media or chronic sinus disease.
Typically, children who have allergic rhinitis have a family history of atopic disorders. Upper airway allergy may become manifest at any age, but the appearance of symptoms is most common during childhood or young adulthood. Clinical signs of rhinitis may be perennial, seasonal, or episodic, and the primary focus of complaints may relate to secondary problems, including ear, sinus, or lung disease.
Pathophysiology
In the allergic patient, disease is mediated by the production of antigenspecific IgE by the patient's B lymphocytes. Current research suggests that the primary defect may be the excessive production of interleukin 4 (IL-4) or a deficient level of gamma interferon (γ-INF) when a T-cell is presented with an antigen. This constellation of immunomodulators directs the B-cell to produce IgE rather than the IgG response of the non-allergic patient.
Clinical disease occurs when an allergen reacts with antigen-specific IgE on the patient's nasal mast cells. When these factors combine, the mast cell is activated to release a variety of preformed and newly produced mediators, including histamine, leukotrienes, and prostaglandins (Fig 1).
Expression of Interferon‐γ, Interleukin‐4 and Interleukin‐5 mRNA in the Nasal Mucosal Membrane of Rats with Allergic Rhinitis
