Allergic rhinitis (inflammation of nasal mucosa; hay fever, chronic allergic rhinitis, pollinosis) is the most common form of respiratory allergy presumed to be mediated by an immediate (type I hypersensitivity) immunologic reaction. It affects about 8% to 10% of the U.S. population (20% to 30% of adolescents). The symptoms are similar to viral rhinitis but are usually more persistent and demonstrate seasonal variation (Tierney, McPhee Papadakis, 2001). It often occurs with other conditions, such as allergic conjunctivitis, sinusitis, and asthma. Allergic rhinitis is associated with impaired work and school performance and de-creased quality of life (Ratner, Ehrlich, Fineman et al., 2002). When untreated, many complications may result, such as allergic asthma, chronic nasal obstruction, chronic otitis media with hear-ing loss, anosmia (absence of the sense of smell), and, in children, orofacial dental deformities. Early diagnosis and adequate treat-ment are essential to reduce complications and relieve symptoms.
Because allergic rhinitis is induced by airborne pollens or molds, it is characterized by the following seasonal occurrences:
· Early spring—tree pollen (oak, elm, poplar)
· Early summer—rose pollen (rose fever), grass pollen (Timothy, red-top)
· Early fall—weed pollen (ragweed)
Each year, attacks begin and end at about the same time. Air-borne mold spores require warm, damp weather. Although there is no rigid seasonal pattern, these spores appear in early spring, are rampant during the summer, and taper off and disappear by the first frost.
Sensitization begins by ingestion or inhalation of an antigen. On re-exposure, the nasal mucosa reacts by the slowing of ciliary ac-tion, edema formation, and leukocyte (primarily eosinophil) in-filtration. Histamine is the major mediator of allergic reactions in the nasal mucosa. Tissue edema results from vasodilation and increased capillary permeability.
Typical signs and symptoms of allergic rhinitis include nasal con-gestion; clear, watery nasal discharge; intermittent sneezing; and nasal itching. Itching of the throat and soft palate is common. Drainage of nasal mucus into the pharynx initiates multiple at-tempts to clear the throat and results in a dry cough or hoarseness. Headache, pain over the paranasal sinuses, and epistaxis can ac-company allergic rhinitis. The symptoms of this chronic condition depend on environmental exposure and intrinsic host responsive-ness. Allergic rhinitis may affect quality of life by also producing fatigue, loss of sleep, and poor concentration (Ratner et al., 2002).
Diagnosis of seasonal allergic rhinitis is based on history, physi-cal examination, and diagnostic test results. Diagnostic tests in-clude nasal smears, peripheral blood counts, total serum IgE, epicutaneous and intradermal testing, RAST, food elimination and challenge, and nasal provocation tests. Results indicative of allergy as the cause of rhinitis include increased IgE and eosinophil levels and positive reactions on allergen testing. False-positive and false-negative responses to these tests, particularly skin testing and provocation tests, may occur.
The goal of therapy is to provide relief from symptoms. Therapy may include one or all of the following interventions: avoidance therapy, pharmacotherapy, and immunotherapy (Kay, 2001b). Verbal instructions must be reinforced by written information. Knowledge of general concepts regarding assessment and therapy in allergic diseases is important so that patients can learn to manage certain conditions as well as prevent severe reactions and illnesses.
In avoidance therapy, every attempt is made to remove the aller-gens that act as precipitating factors. Simple measures and envi-ronmental controls are often effective in decreasing symptoms. Examples include use of air conditioners, air cleaners, humidifiers and dehumidifiers, and smoke-free environments. In many cases, it is impossible to avoid exposure to all environmental allergens, so pharmacologic therapy or immunotherapy is needed.
Antihistamines, now classified as H1-receptorantagonists (or H1-blockers), are used in managing mild allergic disorders. (H2-receptor antagonists are used to treat gastric and duodenal ulcers.) H1-blockers bind selectively to H1 receptors, preventing the actions of histamines at these sites. They do not prevent the release of histamine from mast cells or basophils. The H1-antagonists have no effect on H2-receptors, but they do have the ability to bind to nonhistaminic receptors. The ability of cer-tain antihistamines to bind to and block muscarinic receptors un-derlies several of the prominent anticholinergic side effects of these medications.
Oral antihistamines, which are readily absorbed, are most ef-fective when given at the first occurrence of symptoms because they prevent the development of new symptoms by blocking the actions of histamine at the H1-receptors. The effectiveness of these medications is limited to certain patients with hay fever, va-somotor rhinitis, urticaria (hives), and mild asthma. They are rarely effective in other conditions or in any severe conditions.Antihistamines are the major class of medications prescribed for the symptomatic relief of allergic rhinitis. The major side ef-fect is sedation, although histamine H1 antagonists are less sedat-ing than earlier antihistamines (Kay, 2001b). Additional side effects include nervousness, tremors, dizziness, dry mouth, palpi-tations, anorexia, nausea, and vomiting. Antihistamines are con-traindicated during the third trimester of pregnancy; for nursing mothers and newborns; in children and elderly people; and in pa-tients whose conditions can be aggravated by muscarinic blockade (ie, asthma, urinary retention, open-angle glaucoma, hyperten-sion, and prostatic hyperplasia).
Newer antihistamines are called second-generation or non-sedating H1-receptor antagonists. Unlike first-generation H1-receptor antagonists, they do not cross the blood–brain barrier and do not bind to cholinergic, serotonin, or alpha-adrenergic re-ceptors. They bind to peripheral rather than central nervous sys-tem H1-receptors, causing less sedation. Examples of these medications are loratadine (Claritin), cetirizine (Zyrtec), and fex-ofenadine (Allegra). These are summarized in Table 53-2.tion to the oral route. The topical route (drops and sprays) causes fewer side effects than oral administration; however, the use of drops and sprays should be limited to a few days to avoid rebound congestion. Adrenergic nasal decongestants are used for the relief of nasal congestion when applied topically to the nasal mucosa. They activate the alpha-adrenergic receptor sites on the smooth muscle of the nasal mucosal blood vessels, reducing local blood flow, fluid exudation, and mucosal edema. Topical ophthalmic drops are used for symptomatic relief of eye irritations due to al-lergies. Potential side effects include hypertension, dysrhythmias, palpitations, central nervous system stimulation, irritability, tremor, and tachyphylaxis (acceleration of hemodynamic status). Examples of adrenergic decongestants and their routes of admin-istration are found in Table 53-3.
Intranasal cromolyn sodium (Nasalcrom)is a spray that acts by stabilizing the mast cell membrane, thus re-ducing the release of histamine and other mediators of the aller-gic response. In addition, it inhibits macrophages, eosinophils, monocytes, and platelets involved in the immune response (Ratner et al., 2002). Cromolyn interrupts the physiologic response to nasal antigens and is used prophylactically before exposure to
Adrenergic agents, vasoconstrictors of mu-cosal vessels, are used topically (nasal and ophthalmic) in addition to the oral route. The topical route (drops and sprays) causes fewer side effects than oral administration; however, the use of drops and sprays should be limited to a few days to avoid rebound congestion. Adrenergic nasal decongestants are used for the relief of nasal congestion when applied topically to the nasal mucosa. They activate the alpha-adrenergic receptor sites on the smooth muscle of the nasal mucosal blood vessels, reducing local blood flow, fluid exudation, and mucosal edema. Topical ophthalmic drops are used for symptomatic relief of eye irritations due to al-lergies. Potential side effects include hypertension, dysrhythmias, palpitations, central nervous system stimulation, irritability, tremor, and tachyphylaxis (acceleration of hemodynamic status). Examples of adrenergic decongestants and their routes of admin-istration are found in Table 53-3.
Intranasal cromolyn sodium (Nasalcrom)is a spray that acts by stabilizing the mast cell membrane, thus re-ducing the release of histamine and other mediators of the aller-gic response. In addition, it inhibits macrophages, eosinophils, monocytes, and platelets involved in the immune response (Ratner et al., 2002). Cromolyn interrupts the physiologic response to nasal antigens and is used prophylactically before exposure to allergens to prevent the onset of symptoms and to treat symptoms once they occur.
It is also used therapeutically in chronic allergic rhinitis. This spray is as effective as antihistamines but less effec-tive than intranasal corticosteroids in the treatment of seasonal allergic rhinitis. Patients must be informed that the beneficial ef-fects of the medication may take a week or so to occur. The med-ication is of no benefit in the treatment of nonallergic rhinitis. Adverse effects (ie, sneezing, local stinging, and burning sensa-tions) are usually mild.
Intranasal corticosteroids are indicated in moresevere cases of allergic and perennial rhinitis that cannot be con-trolled by more conventional medications such as decongestants, antihistamines, and intranasal cromolyn. These medications include beclomethasone (Beconase, Vancenase), budesonide (Rhinocort), dexamethasone (Decadron Phosphate Turbinaire), flunisolide (Nasalide), fluticasone (Cutivate, Flonase), and tri-amcinolone (Nasacort).
Because of their anti-inflammatory actions, these medications are equally effective in preventing or suppressing the major symp-toms of allergic rhinitis. Corticosteroids are administered by metered-spray devices. If the nasal passages are blocked, a topical decongestant can be used to clear the passages before the adminis-tration of the intranasal corticosteroid. Patients must be aware that full benefit may not be achieved for several days to 2 weeks. Ad-verse effects of intranasal corticosteroids are mild and include dry-ing of the nasal mucosa and burning and itching sensations caused by the vehicle used to administer the medication. Systemic effects are more likely with dexamethasone. Recommended use of this medication is limited to 30 days. Beclomethasone, budesonide, flu-nisolide, fluticasone, and triamcinolone are deactivated rapidly after absorption, so they do not achieve significant blood levels. Corticosteroids suppress host defenses, so they must be used with caution in patients with tuberculosis or untreated bacterial infec-tions of the lungs. Patients on corticosteroids are at risk for infec-tion and for suppression of typical manifestations of inflammation because host defenses are compromised. Inhaled corticosteroids do not affect the immune system to the same degree as systemic cor-ticosteroids (ie, oral corticosteroids). As corticosteroids are inhaled into the upper respiratory tract, tuberculosis or untreated bacte-rial infections of the lungs may become apparent and progress. Whenever possible, patients with tuberculosis and other bacterial infections of the lungs should avoid inhaled corticosteroids.
Oral and parenteral corticosteroids are used when conven-tional therapy has failed and symptoms are severe and of short du-ration. They can control symptoms of allergic reactions such as hay fever, medication-induced allergies, and allergic reactions toinsect stings. Because the response to corticosteroids is delayed, they have little or no value in acute therapy for severe reactions such as anaphylaxis. Patients who receive corticosteroids must be cautioned not to stop taking the medication suddenly or without specific instructions from the physician. The patient is also in-structed about side effects, which include fluid retention, weight gain, hypertension, gastric irritation, glucose intolerance, and adrenal suppression.
Allergen desensitization (allergen immunotherapy, hyposensitiza-tion) is primarily used to treat IgE-mediated diseases by injections of allergen extracts. This type of therapy provides an adjunct to symptomatic pharmacologic therapy and can be used when aller-gen avoidance is not possible (Parslow et al., 2001). Specific im-munotherapy has been used in the treatment of allergic disorders for about 100 years. It consists of administering increasing con-centrations of extracts of specific allergens over a long period (Kay, 2001b). Goals of immunotherapy include reducing the level of circulating IgE, increasing the level of blocking antibody IgG, and reducing mediator cell sensitivity. Immunotherapy has been most effective for ragweed pollen; however, treatment for grass, tree pollen, cat, and house dust mite allergens has also been effective.
Correlation of a positive skin test with a positive allergy his-tory is an indication for immunotherapy if the allergen cannot be avoided. The value has been fairly well established in instances of allergic rhinitis and bronchial asthma that are clearly due to sen-sitivity to one of the common pollens, molds, and household dust. Although helpful in most patients, immunotherapy does not cure the condition. Before immunotherapy is initiated, the patient must understand what to expect and the importance of continuing therapy for several years. When skin tests are per-formed, the results are correlated with clinical manifestations; treatment is based on the patient’s needs rather than on skin tests.
The most common method of treatment is the serial injection of one or more antigens that are selected in each particular case on the basis of skin tests. This method provides a simple and ef-ficient technique for identifying IgE antibodies to specific anti-gens. Specific treatment consists of injecting extracts of the pollens or mold spores that cause symptoms in a particular pa-tient. Injections begin with very small amounts and are gradually increased, usually at weekly intervals, until a maximum tolerated dose is attained. Maintenance booster injections are given at 2- to 4-week intervals, frequently for a period of several years, before maximum benefit is achieved There are three methods of injection therapy: coseasonal, pre-seasonal, and perennial. When treatment is given on a coseasonal basis, therapy is initiated during the season in which the patient experiences symptoms. This method has been proved ineffective and is used infrequently. Also, there is an increased risk of sys-temic reactions. Preseasonal therapy injections are given 2 to 3 months before symptoms are expected, allowing time for hypo-sensitization to occur. This treatment is discontinued after the season begins. Perennial therapy is administered all year round, usually on a monthly basis, and is the preferred method because it has more effective, longer-lasting results.
Any patient who receives specific immunotherapy is at risk for general, and potentially fatal, anaphylaxis. This occurs most fre-quently at the induction or “up-dosing” phase. Attempts have been made to minimize the risk of systemic reactions by pre-treating allergen extracts with agents such as formaldehyde. This approach decreases the binding of the allergen by IgE, but it also results in decreased immunogenicity (Kay, 2001b).
Because of the risk for anaphylaxis, injections should not be given by a lay person or by the patient. The patient remains in the office or clinic for at least 30 minutes after the injection and is ob-served for possible systemic symptoms. If a large, local swelling de-velops at the injection site, the next dose should not be increased, because this may be a warning sign of a possible systemic reaction.
Therapeutic failure is evident when a patient does not experi-ence a decrease of symptoms within 12 to 24 months, fails to de-velop increased tolerance to known allergens, and cannot decrease the use of medications to reduce symptoms. Potential causes of treatment failure include misdiagnosis of allergies, inadequate doses of allergen, newly developed allergies, and inadequate en-vironmental controls.