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Allergic Rhinitis

Allergic rhinitis is characterized by symptoms of nasal obstruction, rhinorrhea, sneezing, and nasal itching. Components of inhaled dust, such as mites, molds, or animal dander, can cause IgE-mediated response in atopic individuals, activating mast cells to release potent chemical mediators and then attracting inflammatory cells to induce symptoms of allergic rhinitis.

Although allergic rhinitis (AR) is a benign disease, it is now recognized as causing a significant impairment in the quality of life (QOL) of affected individuals and is associated with other diseases of the upper and lower respiratory tracts such as asthma, sinusitis, and otitis media with effusion (OME). Poor control of AR symptoms can lead to subsequent poor therapeutic control of these comorbid conditions. Consequently, early diagnosis and treatment ofAR should be a priority, not only to control AR but also to manage any associated comorbid disease. Understanding the underlying pathophysiology of AR and its comorbid diseases can improve the selection of treatments for the management of these conditions.

ALLERGIC RHINITIS: PATHOPHYSIOLOGY

AR is an immunologic response modulated by immunoglobulin E (IgE), and it can be classified as seasonal, perennial, or episodic. Seasonal AR is defined as Symptoms that occur during exposure to seasonal allergens such as ragweed, grasses, outdoor molds, and tree pollens. Perennial AR, defined as nasal symptoms for more than 2 hours per day for more than 9 months of the year, occurs when allergies develop to house dust mites, indoor molds, animal dander, and cockroaches or when a person develops sensitivities to multiple seasonal allergens such as those that occur in warmer parts of the country where the pollen season may last all year. Episodic AR refers to symptoms from exposure to allergens that are not normally present in the environment, such as an individual allergic to cats becoming symptomatic on entering the home of cat-owning relatives. Once allergic symptoms are present, irritants such as strong odors or perfumes, tobacco smoke, paint, newspaper ink, soap powders, and air pollutants may exacerbate them. This represents nonspecific hyperresponsiveness. AR shares several features with asthma, the most important being that both are chronic inflammatory diseases.

COMORBID DISEASES

AR shares many features with other inflammatory diseases of the upper and lower airways. Among the inflammatory cells, eosinophils are the most constantly elevated in these diseases compared with a normal state. Eosinophils are also elevated in sinus tissues obtained from children with chronic rhinosinusitis at the time of endoscopic sinus surgery and in middle ear biopsy samples of patients with OME. In asthma, eosinophils are elevated in sputum, and sputum eosinophilia correlates with asthma severity. Eosinophils thus can be considered the common thread of cellular inflammation in both the upper and lower airways, forming a common therapeutic target of underlying inflammation in AR, asthma, rhinosinusitis, or OME.

Allergic Rhinitis and Asthma

Allergic rhinitis and asthma are both inflammatory diseases of the upper and lower airways, respectively, and are often comorbid conditions. Asthma has been diagnosed in 21% to 58% of patients with AR, and of patients with asthma, 28% to 92% have also been diagnosed with AR. When AR and asthma coexist, AR may exacerbate asthma, and, conversely, treating nasal symptoms in these patients has had positive effects on their asthma status. Treating AR in patients with atopic asthma has shown that reducing mouth breathing and restoring normal nasal physiologic conditions reduced asthma symptoms and exacerbations.

Allergic Rhinitis and Rhinosinusitis

Allergic rhinitis and rhinosinusitis are both inflammatory diseases of the upper airway . Allergy is a known contributing factor to both acute and chronic rhinosinusitis.Several possible mechanisms have been proposed to explain the interaction between AR and rhinosinusitis: First, AR creates edema of the nasal passages, blocking proper drainage of the sinus cavities and subsequently leading to stasis of secretions and bacterial infection.

Second, the penetration of allergen into the sinus cavities creates allergic inflammation within the sinus mucosa. Third, AR causes priming and upregulation of adhesion molecules of circulating leukocytes, making them more likely to migrate to sites of ongoing inflammation such as the ones caused by bacterial or viral rhinosinusitis. Fourth, subjects with an allergic diathesis may have a different inflammatory response to a bacterial infection compared with nonallergic subjects.

Allergic Rhinitis and Oitiis Media

Otitis media is primarily a disease of children younger than 15 years.Treating AR may help improve existing OME or the risk of its development in predisposed children. Adding antiallergy treatment might enhance resolution of OME only in allergic children. Rhinitis may be related to otitis media etiology through either of 2 ways: Eustachian tube dysfunction caused by allergic reaction of nasal mucosa or an impaired mucociliary function.Tympanometry is an objective test that assesses transmission and pressure system integrity at middle ear, it also measures auditory canal volume and Eustachian tube function by introducing air under pressure.

ALLERGIC RHINITIS: A REVIEW OF THE TREATMENT OPTIONS

Treatment can include avoidance of allergen, pharmacotherapy, and/or allergen immunotherapy. The treatment plan must also consider co-morbid conditions.

Avoidance of Allergens

Guidelines for the treatment of allergic rhinitis recommend allergen avoidance.Although reducing one’s exposure to dust, pets, high pollen count, and other triggers will certainly reduce allergen exposure, doing so is impractical for many patients.

Pharmacotherapy for Allergic Rhinitis

Antihistamines are the cornerstone of treatment for allergic rhinitis.improvement in quality of life, work productivity, and daily activities leading to symptomatic relief of nasal itching, sneezing, rhinorrhea, and nasal congestion, nonresponders to one may respond favorably to another.

The introduction of topical steroid therapy in the early 1970s has beencharacterized as the most important progress in the treatment of allergic rhinitis since the arrival of antihistamines in late 1940s. Intranasal corticosteroid preparations can relieve symptoms of rhinitis by decreasing capillary permeability and mucous secretions in addition to reducing the numbers of inflammatory cells and chemical mediators in nasal secretions. Locally applied steroids are able to significantly inhibit the allergen-induced type I reaction and to reduce IgE binding to target cells. They also inhibit the influx and activation of inflammatory cells in the nasal mucosa.

Topical steroids are readily absorbed from the airway mucosa and have a high glucocorticoid activity. Their plasma half-life is short and thus theoretically do not exert significant systemic activity. Intranasal corticosteroids are generally safe, and can be used on a regular basis without mucosal atrophy. Transient, local effects are the most commonly reported adverse events, including nasal bleeding, burning, stinging, and irritation as well as altered taste and smell.Although many fear “corticosteroid-like” adverse effects, patients using intranasal corticosteroids are at very low risk of systemic effects (eg, hypothalamic-pituitary-adrenal axis suppression, growth suppression in children). Increased intraocular pressure and nasal septum perforation are rare.

Immunotherapy

Allergen immunotherapy (also known as allergy shots) is an appropriate approach to treatment for patients whose rhinitis is allergic in etiology (IgE mediated) and due to allergens for which a potent extract is available; symptoms are sufficiently severe to justify the time, expense, and risk of immunotherapy; and exposure to allergens is unavoidable. The patient’s age, co-morbidities, duration and progression of illness, and prior experience with pharmacotherapy should also be considered. A patient’s decision to initiate immunotherapy is accompanied by a commitment to frequent office visits, which are required for administration of injections. In addition, the low but serious risk of anaphylaxis is also a concern.

With proper management and patient education, allergic rhinitis can be controlled, and affected people can lead normal and productive lives. Treatment for allergic rhinitis should focus on: rapid onset and convenience; safety and cost effectiveness; immune tolerance; improving patient adherence; and recognizing and treating co-morbidities.

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