Pathophysiology

The development of allergic rhinitis is the result of interplay of genetic factors with environmental factors. This complex interaction begins in utero and continues throughout life. One study demonstrated that the offspring of mothers who experienced allergic rhinitis in early pregnancy had a higher risk of developing allergic rhinitis than the offspring of mothers who had no symptoms during pregnancy . The environment contributes to the development of this disease as has been shown by many groups. In one study, children who are raised in rural areas have a significantly lower prevalence of allergic sensitization and symptoms than their urban counterparts as demonstrated via skin prick testing .

The highly effective filtration of aeroallergens by the nose could contribute to the prevalence of allergic rhinitis. The filtration system reaches near complete efficacy for particles larger than 10 μm in diameter, thereby removing nearly all of them from inhaled air. The efficiency of filtration drops as the particle size decreases, approaching zero for particles between 1 and 2 μm in diameter. Most aeroallergens are 10 to 100 μm in size, allowing for easy removal from inhaled air and deposition on the nasal mucosa . Simple deposition on the nasal mucosa, however, is insufficient to cause allergic rhinitis.

The characteristic inflammation of allergic rhinitis initiated by the deposition of filtered aeroallergens begins with the processing of the allergen and is followed by a complex inflammatory cascade composed of early and late phases. The allergen interacts with a specific allergen-presenting cell that results in the presentation of the processed allergen to a helper T cell. Allergen-presenting cells are abundant in the nose. The activated T cells then induce B cells to differentiate and produce immunoglobulin E (IgE). This allergen-specific IgE enters the circulation and initiates the early phase of allergic inflammation. During the early phase, mast cells and basophils degranulate, releasing histamine, leukotrienes, cytokines, and chemokines . These inflammatory mediators cause microvascular leak, resulting in mucosal edema, mucous secretion, and vasodilation. Symptoms of the early phase of allergic inflammation include rhinorrhea, sneezing, lacrimation, pruritis, and bronchospasm. The time frame of this response is short—starting within 5 minutes and lasting 30 minutes to 1 hour . The late phase, which follows, begins between 2 and 6 hours after the initial response and is associated with the synthesis of new mediators and the infiltration of a variety of inflammatory cells, including eosinophils, neutrophils, basophils, macrophages, and lymphocytes. Nasal congestion is the predominant feature of the late phase . Repetitive allergen exposure will result in progressively increased inflammatory mediator release and worse clinical symptoms.

Burden of illness

Allergic rhinitis results in a significant burden of illness including associated headaches, fatigue, poor concentration, loss of sleep, fatigue, adverse effects of medical therapies, and the potential development of other conditions . All of these findings can have a significant impact on work/school performance and quality of life . Adverse effects from therapies vary in severity from anaphylaxis resulting from immunotherapy to more mild symptoms such as somnolence, dizziness, dry mouth, and headaches that result from antihistamine use. Finally, in addition to these direct outcomes, allergic rhinitis can result in the development of asthma, sinusitis, or otitis media .

Burden of illness

Allergic rhinitis results in a significant burden of illness including associated headaches, fatigue, poor concentration, loss of sleep, fatigue, adverse effects of medical therapies, and the potential development of other conditions . All of these findings can have a significant impact on work/school performance and quality of life . Adverse effects from therapies vary in severity from anaphylaxis resulting from immunotherapy to more mild symptoms such as somnolence, dizziness, dry mouth, and headaches that result from antihistamine use. Finally, in addition to these direct outcomes, allergic rhinitis can result in the development of asthma, sinusitis, or otitis media .

The unified airway

There is extensive evidence linking the upper and lower airways, described together as the unified airway . Epidemiologic studies have demonstrated a strong link between allergic rhinitis and asthma through their incidence together, and the two disease processes are now beginning to be considered as results of the same underlying inflammatory process. In these studies, asthma has been demonstrated in up to 40% of adults with rhinitis . The prevalence of rhinitis in adults with asthma is variably reported as occurring in up to 80% of patients . Children without the diagnosis of asthma that have allergic rhinitis demonstrate increased bronchial hyperresponsiveness to methacholine bronchial challenges when compared with healthy nonatopic controls . Adults with asthma as well as allergic rhinitis were found to have higher rates of hospitalization and increased medication expenses than those who did not carry both diagnoses . Finally, treatment of rhinitis has been shown to improve control of asthma in patients that carry both diagnoses .

In addition to asthma, there is evidence of a link between allergic rhinitis and rhinosinusitis. This evidence points to an increased prevalence of allergic sensitization, increased incidence of skin test positivity in response to aeroallergens, and increased levels of IgE in patients with sinusitis . There is also strong evidence that treatment of allergic rhinitis reduces the severity of sinusitis, results in improved outcomes following sinus surgery, and could result in improved outcomes from medical management of chronic rhinosinusitis . Allergic rhinitis is also proposed to lead to the development of rhinosinusitis as a result of mechanical obstruction and mucous stasis .

Allergic rhinitis can also contribute to the development of otitis media and otitis media with effusion through immunologic and mechanical methods. Allergic inflammation incited by aeroallergens deposited in the nasopharynx results in inflammation around the Eustachian tube and mechanically impairs the clearance of secretions . Resulting edema can hinder mucocilliary function. The incidence of allergic rhinitis among children with chronic otitis media with effusion has been reported to be between 40% and 50% as determined by positive skin testing and the increased expression of IgE to specific allergens .

Allergic rhinitis represents only a component of the spectrum of inflammatory diseases involving the unified airway. The link between allergic rhinitis, asthma, sinusitis, and otitis media with effusion has strong support. It is important to identify and appropriately treat allergic rhinitis in patients to minimize the potential development of complications, enhance the treatment of associated conditions, and improve overall quality of life.