Management of Allergic Rhinitis: Introduction
Allergic rhinitis refers to inflammation of the nasal membrane caused by exposure to inhaled antigens. The sixth most prevalent condition in the United States, it affects 20% or 40 million Americans (10%-30% of adults and up to 40% of children) each year. Patients 18 to 44 years of age are most commonly affected, as the prevalence of allergic rhinitis increases throughout childhood and peaks in the late second and third decades of life. The estimated annual direct costs are 4.5 billion dollars and the indirect costs related to absenteeism and productivity loss from work and school are 3.8 million dollars. If severe allergic rhinitis is not properly treated, it can lead to asthma, rhinosinusitis and otitis media.
Allergic rhinitis is an immunologic response characterized by symptoms of sneezing, rhinorrhea, nasal congestion, post-nasal drip due to posterior drainage of mucus hypersecretion, and pruritic eyes. A combination of strategies involving environmental modification and pharmacologic management should be used to provide symptomatic relief. The guidelines developed by the Joint Task Force on Practice Parameters in Allergy, Asthma and Immunology have been challenged by recently published clinical trials suggesting a change in the stepwise approach to pharmacologic treatment. With less than 15% of symptomatic patients seeking treatment from a physician, pharmacists are in a key position to identify patients with allergic rhinitis, address environmental factors, target pharmacologic therapy to patient-specific symptoms and prevent complications from allergic rhinitis.
Allergic rhinitis can be divided into seasonal and perennial forms, based on the time of symptom onset and duration. In seasonal allergic rhinitis, the nasal and ocular symptoms, such as tearing and conjunctivitis, occur during well-defined seasons. Perennial allergic rhinitis refers to allergy symptoms that persist most of the year because of allergy to antigens present year-round. Other conditions that mimic signs and symptoms of allergic rhinitis include benign and malignant tumors, nasal septal deviation, nasal polyps and pregnancy.
Pathophysiology
The induction and elicitation of the allergic response can be divided into an immediate- and a late-phase reaction. The immediate reaction occurs within minutes as allergens enter the body through inhalation and interact with T-cell and B-cell lymphocytes to produce IgE antibodies. These antibodies will then attach to mast cells and basophils. Upon re-exposure to the same allergen, the mast cell- and basophil-bound IgE cross-link, leading to degranulation of mast cells and release of preformed mediators (histamine, leukotrienes, prostaglandin and bradykinin). The clinical responses to these inflammatory mediators are rhinorrhea, sneezing, itching and vascular engorgement resulting in nasal congestion.Four to 24 hours later, a late-phase inflammatory reaction follows via migration and activation of inflammatory cells, including eosinophils, neutrophils, macrophages, basophils and monocytes in the nasal mucosa. The patient experiences renewed allergic symptoms (worsening nasal secretions and congestion) without additional allergen exposure.
Allergens
Seasonal: Pollens and outdoor mold spores most frequently cause seasonal allergic rhinitis; the most troublesome allergen in North America is ragweed pollen. Tree pollen occurs predominately in April to May, grass pollen in May to June, and ragweed pollen in August to October. Outdoor mold spores occur in soil, water and rotting matter, and are released into the air when lawns are disturbed by mowing of grass and by raking of leaves. The spores are ubiquitous, stay airborne over long periods, and are most prominent from July through November.
Perennial: Perennial allergic rhinitis is caused by indoor allergens, such as house dust mites, animal dander, cockroaches and indoor mold spores. Dust mites thrive in humidity >50% and damp conditions within the home encourage the growth of indoor molds, particularly Cladosporium and Penicillium.
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