Allergic rhinitis involves inflammation of nasal mucous membranes in sensitized individuals when inhaled allergenic particles contact mucous membranes and elicit a response mediated by immunoglobulin E (IgE). There are two types: seasonal and persistent (formerly called “perennial”) allergic rhinitis.
Seasonal (hay fever) allergic rhinitis occurs in response to specific allergens (pollen from trees, grasses, and weeds) present at predictable times of the year (spring and/ or fall) and typically causes more acute symptoms. Persistent allergic rhinitis occurs year-round in response to nonseasonal allergens (eg, dust mites, animal dander, and molds) and usually causes more subtle, chronic symptoms.
Many patients have a combination of both types, with symptoms year-round and seasonal exacerbations. Symptoms include clear rhinorrhea, sneezing, nasal congestion, postnasal drip, allergic conjunctivitis, and pruritic eyes, ears, or nose.
In children, physical examination may reveal dark circles under the eyes (allergic shiners), a transverse nasal crease caused by repeated rubbing of the nose, adenoidal breathing, edematous nasal turbinates coated with clear secretions, tearing, and periorbital swelling.
Patients may complain of loss of smell or taste, with sinusitis or polyps the underlying cause in many cases. Postnasal drip with cough or hoarseness can be bothersome. Untreated rhinitis symptoms may lead to insomnia, malaise, fatigue, and poor work or school performance.
Airborne allergens enter the nose during inhalation and are processed by lymphocytes, which produce antigen-specific IgE, sensitizing genetically predisposed hosts to those agents. On nasal reexposure, IgE bound to mast cells interacts with airborne allergens, triggering release of inflammatory mediators.
An immediate reaction occurs within seconds to minutes, resulting in rapid release of preformed and newly generated mediators from the arachidonic acid cascade. Mediators of immediate hypersensitivity include histamine, leukotrienes, prostaglandin, tryptase, and kinins. These mediators cause vasodilation, increased vascular permeability, and production of nasal secretions. Histamine produces rhinorrhea, itching, sneezing, and nasal obstruction.
A late-phase reaction may occur 4 to 8 hours after initial allergen exposure due to cytokine release from mast cells and thymus-derived helper lymphocytes. This inflammatory response causes persistent chronic symptoms, including nasal congestion.
The symptoms of “hay fever” are similar to those of viral rhinitis but are usually persistent and may show seasonal variation. Nasal symptoms are often accompanied by eye irritation, pruritus, conjunctival erythema, and excessive tearing. Many patients have a strong family history of atopy or allergy.
The clinician should be careful to distinguish allergic rhinitis from vasomotor (nonallergic) rhinitis. Vasomotor rhinitis is caused by increased sensitivity of the vidian nerve and is a common cause of clear rhinorrhea in elderly persons. Often patients will report that they have troubling rhinorrhea in response to numerous nasal stimuli, including warm or cold air, odors or scents, light, or particulate matter.
On physical examination, the mucosa of the turbinates is usually pale or violaceous because of venous engorgement. This is in contrast to the erythema of viral rhinitis. Nasal polyps, which are yellowish boggy masses of hypertrophic mucosa, are associated with long-standing allergic rhinitis.
Intranasal corticosteroid sprays are the mainstay of treatment of allergic rhinitis. They are more effective—and frequently less expensive—than nonsedating antihistamines, though patients should be reminded that there may be a delay in onset of relief of 2 or more weeks.
Corticosteroid sprays may also shrink hypertrophic nasal mucosa and nasal polyps, thereby providing an improved nasal airway and ostiomeatal complex drainage. Because of this effect, intranasal corticosteroids are critical in treating allergy in patients prone to recurrent acute bacterial rhinosinusitis or chronic rhinosinusitis.
Available preparations include beclomethasone (42 mcg/spray twice daily per nostril), flunisolide (25 mcg/spray twice daily per nostril), mometasone furoate (200 mcg once daily per nostril), budesonide (100 mcg twice daily per nostril), and fluticasone propionate (200 mcg once daily per nostril). All are considered equally effective. Probably the most critical factors are compliance with regular use and proper introduction into the nasal cavity. In order to deliver medication to the region of the middle meatus, proper application involves holding the bottle straight up with the head tilted forward and pointing the bottle toward the ipsilateral ear when spraying.
Side effects are limited, the most annoying being epistaxis (perhaps related to incorrect delivery of the drug toward the nasal septum).
Antihistamines offer temporary, but immediate, control of many of the most troubling symptoms of allergic rhinitis. Effective antihistamines include nonsedating loratadine (10 mg orally once daily), desloratadine (5 mg once daily), and fexofenadine (60 mg twice daily or 120 mg once daily), and minimally sedating cetirizine (10 mg orally once daily).
Brompheniramine or chlorpheniramine (4 mg orally every 6–8 hours, or 8–12 mg orally every 8–12 hours as a sustained-release tablet) and clemastine (1.34–2.68 mg orally twice daily) may be less expensive but are usually associated with some drowsiness.
The H1 -receptor antagonist nasal spray azelastine (1–2 sprays per nostril daily) is also effective, but many patients object to its bitter taste.
Other side effects of oral antihistamines besides sedation include xerostomia and antihistamine tolerance (with eventual return of allergy symptoms despite initial benefit after several months of use). In such patients, typically those with perennial allergy, alternating effective antihistamines periodically can control symptoms over the long term.
Measures Antileukotriene medications, such as montelukast (10 mg/day orally), alone or with cetirizine (10 mg/day orally) or loratadine (10 mg/day orally), may improve nasal rhinorrhea, sneezing, and congestion. Cromolyn sodium and sodium nedocromil are also useful adjunct agents for allergic rhinitis. They work by stabilizing mast cells and preventing proinflammatory mediator release.
Topical agents, they have very few side effects. The most useful form of cromolyn is probably the ophthalmologic preparation. Intranasal cromolyn is cleared rapidly and must be administered four times daily for continued symptom relief, and it is not nearly as effective as inhaled corticosteroid.
Intranasal anticholinergic agents, such as ipratropium bromide 0.03% or 0.06% sprays (42–84 mcg per nostril three times daily), may be helpful adjuncts when rhinorrhea is a major symptom. They are not as effective for treating allergic rhinitis but are more useful for treating vasomotor rhinitis.
Avoiding or reducing exposure to airborne allergens is the most effective means of alleviating symptoms of allergic rhinitis. Depending on the allergen, this can be extremely difficult. Maintaining an allergen-free environment by covering pillows and mattresses with plastic covers, substituting synthetic materials (foam mattress, acrylics) for animal products (wool, horsehair), and removing dust-collecting household fixtures (carpets, drapes, bedspreads, wicker) is worth the attempt to help more troubled patients.
Air purifiers and dust filters may also aid in maintaining an allergen-free environment. Nasal saline irrigations are a useful adjunct in the treatment of allergic rhinitis to mechanically flush the allergens from the nasal cavity. There is no clear benefit to hypertonic saline over commercially available normal saline preparations (eg, Ayr or Ocean Spray).
When symptoms are extremely bothersome, a search for offending allergens may prove helpful. This can either be done by serum radioallergosorbent test (RAST) testing or skin testing by an allergist.
In some cases, allergic rhinitis symptoms are inadequately relieved by medication and avoidance measures. Often, such patients have a strong family history of atopy and may also have lower respiratory manifestations, such as allergic asthma.
Referral to an allergist may be appropriate for consideration of immunotherapy. This treatment course is quite involved, with proper identification of offending allergens, progressively increasing doses of allergen(s), and eventual maintenance dose administration over a period of 3–5 years.
Immunotherapy has been proven to reduce circulating IgE levels in patients with allergic rhinitis and reduce the need for allergy medications. Both subcutaneous and sublingual immunotherapy have been shown to be effective in the long-term treatment of refractory allergic rhinitis.
Treatments are initiated at a suitable medical facility with monitoring following treatment because of the risk of anaphylaxis during dose escalation; later, sublingual immunotherapy may be administered at home. Local reactions from subcutaneous injections are common and usually self-limited.