Allergic rhinitis occurs when an allergen such as dust mites, insect waste, animal dander, molds, pollens, and other pollutants (e.g., cigarette smoke) penetrate the nasal mucosa, enters the underlying tissue, and interacts with IgE antibodies on the surfaces of previously sensitized mast cells and basophiles.4-6 The allergen cross-links IgE/Fc receptor-complexes and causes the release histamine, which binds to histaminergic receptors in the nasal mucosa and surrounding tissues.
Histamine-induced venule dilation engorges the local microvasculature with blood and the contraction of vascular endothelial cells allows the escape of plasma proteins and fluid from capillary venules. The accompanying itchy palate, sneezing, coughing, and runny nose; and allergic conjunctivitis result from the combined action of histamine and the release of other chemical mediators of inflammation (e.g., kinins, prostaglandins, and leukotrienes).
Patients should be informed about their condition and advised to avoid known allergens. Intranasal corticosteroids are the most common treatment for persistent symptoms.2,3,5,6 Patients with more severe disease that does not respond to intranasal corticosteroids may be taking an antihistamine, and a cysteinyl leukotriene (CysLT)-receptor antagonist.2,3,5,6 Other therapies may include decongestants such as pseudoephedrine; and intranasal cromolyn, an agent that inhibits mast cell degranulation.5,6
Allergic rhinitis is a systemic illness and may be associated with fatigue and malaise.5,6 Symptoms may be mild, i.e., do not interfere with the patient’s quality of life; or severe, i.e., they may affect participation in sports, sleep, and school or work performance; and in susceptible patients exacerbate asthma. Severe allergic rhinitis may interfere with the clinical process. Patients with an uncertain diagnosis or severe symptoms require a medical referral.