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Allergic rhinitis is an inflammatory disease of the nasal mucosal membranes that causes sneezing, rhinorrhea, nasal pruritis and congestion. Patients who have seasonal rhinitis (“hay fever”) exhibit symptoms at specific times during the year, while patients who have perennial rhinitis have symptoms all year. Seasonal exacerbations of perennial rhinitis can also occur. Tree, grass and weed pollens are common seasonal allergens. Important perennial allergens include house dust mites, indoor molds, animal dander and occupational allergens.

Lee and Arriola discuss three therapies: (1) allergen avoidance, (2) pharmacologic treatment to prevent and control symptoms and (3) allergen immunotherapy for recalcitrant patients. Allergen avoidance is accomplished through environmental control aimed at reducing exposure to potential allergens. This may require patients to stay indoors as much as possible during times when the offending allergen is at its seasonal peak. Other measures include enclosing mattresses or pillows with allergen-proof casings, and eliminating carpeting. When these measures fail, pharmacologic intervention is appropriate.

Antihistamines are common first-line treatment for patients with allergic rhinitis. By antagonizing histamine at the H1-receptor sites, symptoms caused by histamine release (e.g., sneezing, rhinorrhea, nasal itching and lacrimation) are reduced. Nasal congestion often remains. The first-generation antihistamines, often available as over-the-counter medications, produce a sedating effect. The ethanolamines (e.g., diphenhydramine) and phenothiazines (e.g., promethazine) cause the most severe sedation; the ethylenediamines (e.g., pyrilamine) cause moderate sedation; and the alkylamines (e.g., chlorpheniramine, brompheniramine) cause the least sedation. Bedtime use of these first-generation antihistamines and the daytime use of the newer agents might be the best therapeutic strategy. Other side effects of the first-generation antihistamines include anticholinergic symptoms that include dry mucous membranes, urinary retention or blurred vision. Narrow angle glaucoma or prostatic hypertrophy can also be exacerbated.

The second-generation antihistamines (see accompanying table) have minimal or no anti-cholinergic and sedative side effects, probably because they do not readily cross the blood-brain barrier. The most serious side effect of these medications is the cardiotoxicity associated with astemizole and terfenidine. Both of these medications have recently been removed from the market.

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Nasal decongestants activate alpha-adrenergic receptors in the vascular smooth muscle of the respiratory mucosa, causing vasoconstriction in the turbinates. These agents may also be added to antihistamine therapy. Oral formulations such as pseudoephedrine and phenylpropanolamine are available but may cause insomnia, restlessness, tachycardia, urinary retention and blood pressure elevation. Topical decongestants can improve symptoms but may cause rhinitis medicamentosa (rebound congestion); therefore, they should be taken for only a three- to five-day period.

Intranasal corticosteroids are becoming a popular treatment, especially in patients with moderate or severe perennial allergic rhinitis. Intranasal corticosteroids inhibit allergic inflammation and relieve sneezing, nasal itching, rhinorrhea and congestion. Recent studies have shown intranasal steroids to be more effective than second-generation decongestants in relieving most of the symptoms of allergic rhinitis. All of the nasal steroid products appear to be equivalent. The most common side effect is local irritation and, rarely, mucosal erosion. The spray should be directed upwards and toward the lateral portion of the nose. The long-term systemic effects of corticosteroid therapy appear to be benign, but more studies are needed. In children taking intranasal steroids, growth progress should be monitored to watch for significant growth velocity reduction, and the lowest effective dosage should be prescribed. This drug should be administered daily rather than on an “as-needed” basis. Combination therapy of inhaled corticosteroids and antihistamines can be prescribed for patients who have severe allergic rhinitis.

Inhaled cromolyn sodium relieves some symptoms but does not relieve nasal congestion. Therapy is difficult because of frequent dosing (three to four times daily). In select patients, cromolyn may be a useful preventive therapy against seasonal allergic rhinitis. Intranasal ipratropium bromide reduces hypersecretion but has no effect on sneezing and nasal congestion.

The authors conclude that pharmacotherapy is the major tool in managing patients with allergic rhinitis. Medications can be used singly or in combination on an individualized basis.

editor's note: The American Academy of Allergy, Asthma, and Immunology supports the early use of intranasal steroids in patients with allergic rhinitis, calling these agents the most effective class of medicine. Recalcitrant patients should undergo allergy tests (skin or in vitro) to search for the presence of specific immunoglobulin E. Referral to an allergist might be appropriate when: (1) identification of an allergic trigger is necessary, (2) response to treatment is inadequate, (3) the patient needs further education about allergies, (4) immunotherapy is being initiated, (5) the patient has severe symptoms affecting quality of life, (6) complications such as sinusitis or otitis media occur and (7) systemic steroid therapy is being considered.—r.s.

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