Allergic rhinitis is a widespread condition, affecting 20 to 40 million persons in the United States each year, including up to 40% of children.1 The direct costs of treatment and indirect costs related to worker absences and loss of productivity are significant. In 1995, the total economic impact of allergic rhinitis was estimated at $2.7 billion, not including the costs of associated problems, such as rhinosinusitis and asthma.1 Among children, rhinitis is a significant cause of lost school days.1
In part 1 of this article, I will discuss the use of antihistamines, decongestants, anticholinergics, and cromolyn in the management of allergic rhinitis. In part 2, to be published in a coming issue of The Journal of Respiratory Diseases, I will review the use of intranasal corticosteroids, leukotriene modifiers, and combination therapy; I also will discuss the role of allergen immunotherapy.
PATHOPHYSIOLOGYAllergic rhinitis is an inflammatory disease of the nasal mucosa; symptoms include sneezing, itching, rhinorrhea, and nasal congestion. Active symptoms and the underlying inflammation are the result of a process that begins when mast cells in the nasal mucosa of sensitized persons bind allergens through IgE expressed on the cell surface. Binding causes mast cell degranulation and the release of a host of preformed and newly formed mediators, including histamine and cysteinyl leukotrienes, which are important targets for drug intervention (Figure).
The events immediately following allergen binding to IgE cause the early-phase allergic response and provoke symptoms within minutes of allergen exposure. Increased vascular permeability of nasal vessels, along with glandular stimulation and vessel dilation, results in watery rhinorrhea, mucinous secretion, and nasal airways occlusion; nerve stimulation leads to nasal itching and sneezing.
A late-phase response develops hours later. In this phase, the mediators that were generated dur- ing the early response induce a variety of migratory cells--including eosinophils, basophils, and neutrophils--to infiltrate the nasal mucosa.2 Activation of these cells elicits and sustains an inflammatory response that causes the tissue damage and persistent nasal blockage characteristic of chronic allergic reaction.
Allergic rhinitis is characterized as seasonal or perennial according to whether symptoms appear in a predictable cyclic pattern or throughout the year. Seasonal allergic rhinitis is the result of IgE-mediated responses to seasonal aeroallergens, typically pollens and molds. In perennial allergic rhinitis, the response is to aeroallergens that persist in the environment year-round, such as house dust mites, molds, and animal dander. Nasal obstruction may be the dominant symptom of chronic rhinitis, which is attributable to the ongoing inflammatory response associated with perennial allergy.1
EVALUATIONAllergic rhinitis can sometimes be confused with nonallergic, non-IgE-mediated forms of rhinitis, which include infectious rhinitis, vasomotor rhinitis, occupational rhinitis, and nonallergic rhinitis with eosinophilia syndrome.1 The evaluation of rhinitis begins with a careful history, followed by a physical examination that includes examination of the nasal passageways and secretions and determination of whether nasal polyps are present.
An important step in making an unequivocal diagnosis of allergic rhinitis is testing for specific IgE. This is usually accomplished by skin testing to allergens, although in vitro tests for specific subclasses of IgE can also be performed. Identification of a specific allergen(s) is an invaluable guide to appro- priate avoidance measures and to immunotherapy.1
