Although allergen avoidance is the most cost-effective means of managing allergic rhinitis, treatment with pharmacologic agents represents the standard approach to seasonal or perennial allergic rhinitis. Oral antihistamines of the H1 class are effective for nasopharyngeal itching, sneezing, and watery rhinorrhea and for such ocular manifestations as itching, tearing, and erythema, but they are not efficacious for the nasal congestion. The older antihistamines are sedating, and they induce psychomotor impairment, including reduced eye-hand coordination and impaired automobile driving skills. Their anticholinergic (muscarinic) effects include visual disturbance, urinary retention, and constipation. Because the newer H1 antihistamines such as fexofenadine, loratadine, desloradine, cetirizine, levocetirizine, olopatadine, bilastine, and azelastine are less lipophilic and more H1 selective, their ability to cross the blood-brain barrier is reduced, and thus their sedating and anticholinergic side effects are minimized. These newer antihistamines do not differ appreciably in efficacy for relief of rhinitis and/or sneezing. Azelastine nasal spray may benefit individuals with nonallergic vasomotor rhinitis, but it has an adverse effect of dysgeusia (taste perversion) in some patients. Because antihistamines have little effect on congestion, α-adrenergic agents such as phenylephrine or oximetazoline are generally used topically to alleviate nasal congestion and obstruction. However, the duration of their efficacy is limited because of rebound rhinitis (i.e., 7- to 14-day use can lead to rhinitis medicamentosa) and such systemic responses as hypertension. Oral α-adrenergic agonist decongestants containing pseudoephedrine are standard for the management of nasal congestion, generally in combination with an antihistamine. While oral antihistamines typically reduce nasal and ocular symptoms by about one third, pseudoephedrine must be added to achieve a similar reduction in nasal congestion. These pseudoephedrine combination products can cause insomnia and are precluded from use in patients with narrow angle glaucoma, urinary retention, severe hypertension, marked coronary artery disease, or a first trimester pregnancy. The CysLT1 blocker montelukast is approved for treatment of both seasonal and perennial rhinitis, and it reduces both nasal and ocular symptoms by about 20%. Cromolyn sodium, a nasal spray, is essentially without side effects and is used prophylactically on a continuous basis during the season. The clinical efficacy of cromolyn sodium used prophylactically is less than that of second-generation oral antihistamines and less than that of intranasal glucocorticoids. Intranasal high-potency glucocorticoids are the most potent drugs available for the relief of established rhinitis, seasonal or perennial, and are effective in relieving nasal congestion. They provide efficacy with substantially reduced side effects as compared with this same class of agent administered orally. Their most frequent side effect is local irritation, with Candida overgrowth being a rare occurrence. The currently available intranasal glucocorticoids-beclomethasone, flunisolide, triamcinolone, budesonide, fluticasone propionate, fluticasone furoate, ciclesonide, and mometasone furoate-are equally effective for nasal symptom relief, including nasal congestion; these agents all achieve up to 70% overall symptom relief with some variation in the time period for onset of benefit. Topical ipratropium is an anticholinergic agent effective in reducing rhinorrhea, including that in patients with perennial symptoms, and it can be additionally efficacious when combined with intranasal glucocorticoids. Local treatment with cromolyn sodium is effective in treating mild allergic conjunctivitis. Topical antihistamines such as olopatadine, azelastine, ketotifen, or epinastine administered to the eye provide rapid relief of itching and redness and are more effective than oral antihistamines.
Immunotherapy, often termed hyposensitization, consists of repeated subcutaneous injections of gradually increasing concentrations of the allergen(s) considered to be specifically responsible for the symptom complex. Controlled studies of ragweed, grass, dust mite, and cat dander allergens administered for treatment of allergic rhinitis have demonstrated at least partial relief of symptoms and signs. The duration of such immunotherapy is 3-5 years, with discontinuation being based on minimal symptoms over two consecutive seasons of exposure to the allergen. Clinical benefit appears related to the administration of a high dose of relevant allergen, advancing from weekly to monthly intervals. Patients should remain at the treatment site for at least 20 minutes after allergen administration so that any anaphylactic consequence can be managed. Local reactions with erythema and induration are not uncommon and may persist for 1-3 days. Immunotherapy is contraindicated in patients with significant cardiovascular disease or unstable asthma and should be conducted with particular caution in any patient requiring β-adrenergic blocking therapy because of the difficulty in managing an anaphylactic complication. The response to immunotherapy is derived from a complex of cellular and humoral effects that likely includes a modulation in T cell cytokine production. Immunotherapy should be reserved for clearly documented seasonal or perennial rhinitis that is clinically related to defined allergen exposure with confirmation by the presence of allergen-specific IgE. Systemic treatment with a monoclonal antibody to IgE (omalizumab) that blocks mast cell and basophil sensitization has efficacy for allergic rhinitis and can be used with immunotherapy to enhance safety and efficacy. However, current approval is only for treatment of patients with persistent allergic asthma not controlled by inhaled glucocorticoid therapy. A sequence for the management of allergic or perennial rhinitis based on an allergen-specific diagnosis and stepwise management as required for symptom control would include the following: (1) identification of the offending allergen(s) by history with confirmation of the presence of allergen-specific IgE by skin test and/or serum assay; (2) avoidance of the offending allergen; and (3) medical management in a stepwise fashion (Fig. 317-4). Mild intermittent symptoms of allergic rhinitis are treated with oral antihistamines, oral CysLT1 receptor antagonists, intranasal antihistamines, or intranasal cromolyn prophylaxis. Moderate to more severe allergic rhinitis is managed with intranasal glucocorticoids plus oral antihistamines, oral CysLT1 receptor antagonists, or antihistamine-decongestant combinations. Persistent allergic rhinitis requiring the daily use of intranasal glucocorticoids with add-on interventions such as oral antihistamines, decongestant combinations, or topical ipratropium merits consideration of allergen-specific immunotherapy. Even a brief course of oral prednisone can be indicated for rapid relief of severe allergic rhinitis symptoms.