AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
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INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Allergic rhinitis is a common health problem for which many patients do not seek appropriate medical care. Although not a life-threatening condition in most cases, it has a substantial impact on public health and the economy.

According to findings in a recent study, the total estimated cost of allergic rhinitis in 1994 was between 1.2 and 1.5 billion dollars.¹ The illness resulted in more than 6 million missed work days, 2 million missed school days, and 28 million reduced-activity days. These figures are certainly higher today because of the higher cost of new medications and the increasing prevalence of the condition.

Pathophysiology

Because the nose is the most common port of entry for allergens, in patients with allergies, signs and symptoms of allergic rhinitis, not surprisingly, are the most common complaints.

Four types of hypersensitivity responses exist, as initially classified by Gell and Coombs and later modified by Shearer and Huston. Individuals with allergic rhinitis are thought to have type I reactions.

After initial exposure to an antigen, antigen-processing cells (macrophages) present the processed peptides to T helper cells. Upon subsequent exposure to the same antigen, these cells are stimulated to differentiate into either more T helper cells or B cells. The B cells may further differentiate into plasma cells and produce immunoglobulin E (IgE) specific to that antigen. Allergen-specific IgE molecules then bind to the surface of mast cells, sensitizing them.

Further exposures result in the bridging of 2 adjacent IgE molecules, leading to the release of preformed mediators from mast cell granules. These mediators (ie, histamine, leukotrienes, kinins) cause early-phase symptoms such as sneezing, rhinorrhea, and congestion. Late-phase reactions begin 2-4 hours later and are caused by newly arrived inflammatory cells. Mediators released by these cells prolong the earlier reactions and lead to chronic inflammation.

Frequency

United States

Approximately 39 million Americans are reported to have allergic rhinitis. From various studies, 17-25% of the population in the United States are estimated to have the condition.

Mortality/Morbidity

• Allergic rhinitis is frequently associated with otitis media, rhinosinusitis, and asthma, either as a precipitating and/or aggravating factor or a symptomatic comorbid condition.
• Allergic rhinitis can significantly decrease the quality of life and impair social and work functions, either directly or indirectly, because of the adverse effects of medications taken to relieve the symptoms.

Sex

• Males and females tend to be affected by allergic rhinitis in fairly equal proportions.

Age

• Allergic rhinitis appears mainly to affect individuals younger than 45 years.
• The condition may begin to appear in patients as young as 2 years and usually reaches a peak in those aged 21-30 years.
• It then tends to remain stable or slowly decrease until patients are aged 60 years, when again the prevalence may increase slightly.

CLINICAL

Section 3 of 11  

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• Clinical
• Differentials
• Workup
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• Medication
• Follow-up
• Miscellaneous
• Multimedia
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History

• Allergy history
• • For the physician who treats patients with allergic rhinitis, nothing is more crucial than the allergy history. It is important not only in identifying an allergy but also in guiding the treatment plan.
  • Although history taking begins at the initial encounter, it should not be completed at a single sitting, and it should be continued during subsequent visits, as needed.
  • Details about the presenting symptoms (eg, onset, fluctuation, severity) should be obtained. In addition, the interviewer should note any recent changes in the patient's life (eg, at home, in the workplace, in leisure activities, in diet).
• Family history
• • Children of individuals with allergies have been shown to have a higher incidence of allergies than that of other children.
  • If both parents have allergies, their child has a 50% chance of having the same problem.
• Past medical history
• • In children, a history of recurrent otitis media, upper respiratory tract infection, asthma, chronic rashes, and formula intolerance are suggestive of allergies.
  • Other pertinent medical problems (eg, asthma, aspirin hypersensitivity) and the use of medications (eg, beta-blockers, tranquilizers) that could interfere with the treatment for allergies should be evaluated.
  • Inquire about the results of previous allergy tests and treatment.

Physical

Patients with allergies frequently have a characteristic physical appearance.

• Face
• • Patients with allergic rhinitis frequently grimace and twitch their face, in general, and nose, in particular, because of itchy mucus membranes.
  • Chronic mouth breathing secondary to nasal congestion can result in the typical adenoid facies.
• Eyes
• • Patients may have injected conjunctiva; increased lacrimation; and long, silky eyelashes.
  • Dennie-Morgan lines (creases in the lower eyelid skin) and allergic shiners (dark discoloration below the lower eyelids) caused by venous stasis may be present.
• Ears
• • Ears are frequently unremarkable.
  • Eczematoid otitis externa and middle ear effusion may be present.
• Nose
• • A transverse nasal crease may be present because of the patient's repeated lifting of the nasal tip to relieve itching and open the nasal airway.
  • The turbinates are frequently hypertrophic and covered with a boggy pale or bluish mucosa.
  • Nasal secretions can range from clear and profuse to stringy and mucoid.
  • The presence of polyps does not necessarily indicate that the affected individual has allergic rhinitis.
• Mouth
• • A high arched palate, narrow premaxilla, and receding chin may be present secondary to long-term mouth breathing.
  • The posterior oropharynx may be granular because of irritation from persistent postnasal discharge.

Causes

For practical purposes, allergens can be divided into seasonal and perennial groups.

• Seasonal allergens are primarily pollens. In general, trees bloom in the spring; grasses, in the summer; and weeds, in the fall. Information about regional allergens can be obtained from manufacturers of allergy-treatment supplies, local botanic gardens, universities, and newspapers.
• Perennial allergens of importance are molds, house dust, and animal danders. Although these allergens are present throughout the year, they tend to be more problematic during the winter, when people spend most of their time indoors.
• • Molds can be either indoor or outdoor allergens. Perennial symptoms that worsen in cool, humid weather suggest mold sensitivity. The major manufacturers of allergy-treatment supplies have lists of predominant molds in each region. Significant reservoirs of molds include indoor plants, refrigerator drip pans, areas under sinks, and compost piles.
  • House dust is a mixture of approximately 28 allergenic components. The actual major allergen appears to be a collection of degrading lysine residues.
    • For practical reasons, the component of house dust that most closely resembles the overall extract consists of dust mites (although they are much less immunologically potent than the overall extract).
    • The 2 major dust mites in the United States are Dermatophagoides pteronyssinus and Dermatophagoides farina. These mites thrive in warm (65-80°F), humid (>70% relative humidity) environments. They are abundant in mattresses, pillows, upholstered furniture, and carpets.
    • Another significant ingredient of house dust is decomposing cockroach body parts, which can be a problem even in buildings that appear to be free of the live insect.
  • A person does not need to own a pet to be exposed to dander, such as cat dander, which can cling to clothing and be brought into classrooms and homes. Dog dander, however, tends to be primarily a problem for its owner. The dander of other pets such as rabbits and hamsters is also highly allergenic.

DIFFERENTIALS

Section 4 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

WORKUP

Section 5 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• The diagnosis of allergic rhinitis is based on the history, and tests are used only to confirm atopy.
• Nasal cytologic studies may be needed.
• • Nasal secretions are stained with hematoxylin and eosin.
  • In general, the presence of eosinophils and goblet cells is suggestive of allergy, whereas the presence of neutrophils and bacteria is characteristic of infection.
• An elevated eosinophil count can occur in patients with asthma, nonallergic rhinitis with eosinophilia syndrome (NARES), and parasitic infection. Therefore, this finding is not specific to allergic rhinitis.
• Skin tests may be performed.
• • Skin testing is generally considered to be the standard of allergy workup. The classic wheal-and-flare responses result from the interaction between the antigen and sensitized mast cells in the skin.
  • In general, the acute phase starts within 2-4 minutes and reaches a maximum in 10-20 minutes. It may be followed by a late phase 4-6 hours later.

    A number of factors affect the responses; these include the following:

    • Volume and potency of the antigen
    • Reactivity of the skin
    • Age and race of the patient
    • Area of body tested
    • Distance between the injections and time of day of testing
    • Medications (eg, antihistamines and tricyclic antidepressants)
  • Because of these variables, positive and negative controls must be used to ensure the validity of the results.
  • In addition, patients receiving beta-blocker therapy are at risk for severe reactions, and the drugs should be switched to another class of medication before testing is initiated.
  • Currently, 3 types of skin tests are in use.
    • Prick testing is rapid and safe, and scores are graded from 0-4 according to both wheal and flare responses. However, low-grade sensitivities can be missed. Therefore, the test is often used as a screening tool, which is followed by intradermal testing if necessary.
    • Single-dilution intradermal testing involves injecting 0.01-0.05 mL of antigen into the epidermis. The resulting wheal and flare are measured after 10-20 minutes and graded as in prick testing. This test can be used to detect most low-degree atopies if a 1:500 concentration is used. However, as with prick testing, it does not permit accurate quantitation of the sensitivity to the antigen involved.
    • Progressive-dilution intradermal testing (skin endpoint titration) involves a series of 5-fold dilutions, starting with a concentration that is sufficiently dilute to be nonreactive. Progressively stronger concentrations are injected until a wheal forms. The endpoint is confirmed when the wheal with the next stronger dilution is 2 mm larger than the previous wheal. This endpoint indicates the relative sensitivity of the patient to the allergen and designates the starting point for immunotherapy. This method allows both qualitative and quantitative assessment of sensitivity to the antigen in question.
• The IgE count may be determined.
• • In contrast to total IgE, which has a poor clinical correlation, antigen-specific IgE antibodies are important in the diagnosis of inhalant allergy.
  • Compared with skin testing, in vitro testing is more specific, and it is not affected by skin reactivity or medications. It also has no risk of systemic reaction and is better tolerated, because it is less traumatic. However, in vitro testing is less sensitive than skin testing, especially in regard to molds. Also, the results are not available immediately and must be verified with skin testing before immunotherapy can be started.
  • The original method for obtaining an IgE count, the radioallergosorbent test (RAST), has evolved from a radioimmunoassay to a test that involves enzymatic or fluorometric processes (eg, enzyme-linked immunosorbent assay [ELISA]).
    • Fadal and Nalebuff have modified the test to increase its sensitivity and to improve the correlation of its findings to those obtained with the skin endpoint titration method.
    • Scores do not necessarily correlate with the severity of the clinical symptoms. Although they can be used to establish the starting dose for immunotherapy, a vial test still is required before immunotherapy can be initiated.

Imaging Studies

• No radiologic studies are necessary in the evaluation of patients with allergies because the diagnosis is made on the basis of the history and confirmed with relevant physical findings and test results.
• Imaging findings, if available for other reasons, are usually nonspecific and may be the same as those in other types of rhinosinusitis (eg, mucosal thickening, turbinate hypertrophy).

Other Tests

• Many other alternative tests for allergies are available, but they have not been fully validated yet.
• These include the following:
• • Basophilic histamine-release test
  • Cytotoxic test
  • Leukocyte antibody test for related antigens

TREATMENT

Section 6 of 11  

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Medical Care

The 3 basic approaches for the treatment of allergies are (1) avoidance, (2) pharmacotherapy, and (3) immunotherapy. Treatment should start with avoidance of allergens and environmental controls. In almost all cases, however, some pharmacotherapy is needed because the patient is either unwilling or unable to avoid allergens and to control the occasional exacerbations of symptoms. For patients with a severe allergy that is not responsive to environmental controls and pharmacotherapy or for those who do not wish to use medication for a lifetime, immunotherapy may be offered.

• Avoidance of allergens and environmental controls
• • Patients who have seasonal allergies should avoid outdoor activities when allergens are in the air. The patient's house and workplace should be kept as clean as possible.
  • House dust mites thrive in warm, humid conditions, and the antigen is found in their feces. Control measures include removing reservoirs (eg, stuffed animals, carpets, heavy drapes), covering bedding with dust-mite–proof covers, and washing potential reservoirs in hot water. Frequent vacuuming with a high-efficiency particulate-arresting (HEPA) vacuum and use of acaricides (eg, benzyl benzoate) and products that denature dust mite antigen (eg, tannic acid) are encouraged. In addition, lowering the relative humidity to less than 50% and lowering the temperature to less than 70°F are helpful in controlling the dust mite population.
  • If removing pets is not feasible, they should be kept at least out of the bedroom. Also, frequent vacuuming with an HEPA vacuum and washing the animals are helpful in decreasing the allergen load.
  • Molds are present throughout the year in damp areas, both indoors and outdoors. Attention should be paid to reservoirs such as refrigerator drip pans, areas around air conditioner condensers and under sinks, indoor plants, and decaying vegetation in the yard. The use of a dehumidifier and an HEPA air-filtration system is also encouraged.
• Immunotherapy
  • Immunotherapy is indicated for patients whose symptoms are not well controlled with avoidance measures and pharmacotherapy. It is also appropriate for those with symptoms lasting more than 1 season and documented allergen-specific IgE antibodies.
  • Immunotherapy should be considered only in individuals who can comply with weekly injections for approximately 3 years.
  • Immunotherapy should be avoided in those receiving beta-blockers and those who have poorly controlled asthma, autoimmune disorders, or immunodeficiency disorders.
  • During pregnancy, injections should not be initiated, and doses should not be increased.
  • Although the exact mechanisms of immunotherapy are not known, they are associated with decreased allergen-specific IgE levels and increased allergen-specific immunoglobulin G (IgG) levels. These IgG molecules are thought to be blocking antibodies that are important in impeding the allergic reaction.
  • Immunotherapy involves regular injections (every 5-7 d) of increasing amounts of each reacting allergen until the symptoms are relieved or the maximum tolerated dose is reached, at which time a maintenance dose is given every 2-4 weeks. This dose is maintained until symptoms are controlled for 2-3 seasons and then tapered.
  • Although systemic reactions are rare when immunotherapy is properly administered, only qualified personnel should give injections, and resuscitative equipment should be available.

Surgical Care

Although allergic rhinitis is a medical condition, adjunctive surgery may be offered to alleviate obstructive symptoms in appropriate individuals. Examples are nasal polypectomy in the patients who have severe polyposis and various inferior turbinate reduction maneuvers in patients who have nasal obstruction caused by turbinate hypertrophy that persists despite maximal medical therapy.

Consultations

A pulmonologist may be consulted.

Diet

Food allergies can cause nasal symptoms similar to those caused by inhalant allergies. Therefore, a workup for possible food allergies should be considered if the patient has a history of food reactions, if findings of the inhalant allergy evaluation are negative, and if appropriate treatments fail to yield improvement.

Activity

• In general, patients with allergies should avoid working and playing in areas that are known to exacerbate symptoms.
• Outdoor activities should be restricted when the inciting allergens are in season.
• Individuals who are sensitive to pollen should stay indoors in the morning, and patients who are allergic to molds should remain indoors in the early evening, because the allergens are more prevalent in the air at these times.

MEDICATION

Section 7 of 11  

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At one time or another, most patients with allergies require pharmacologic intervention.

Many classes of medications are available; the use of each must be tailored to the individual patient's symptoms.

Drug Category: Antihistamines

These medications are H1 receptor antagonists and relieve sneezing, itching, and rhinorrhea.

Drug Name	Loratadine (Claritin)
Description	Selectively inhibits peripheral histamine H1 receptors.
Adult Dose	10 mg PO qd
Pediatric Dose	<6 years: Not established >6 years: Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	Ketoconazole, erythromycin, procarbazine, and alcohol may increase levels
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	Initiate therapy with lower doses in liver impairment

Drug Name	Fexofenadine (Allegra)
Description	A representative third-generation antihistamine; competes with histamine for H1 receptors in the GI tract, blood vessels, and respiratory tract, reducing hypersensitivity reactions; does not cause sedation.
Adult Dose	60 mg PO q12h or 180 mg PO qd
Pediatric Dose	<6 years: not established 6-12 years: 30 mg PO q12h >12 years: Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	Toxicity increases with coadministration of erythromycin and ketoconazole
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	No data about use while breastfeeding

Drug Name	Azelastine (Astelin)
Description	Topical antihistamine nasal spray; competes with histamine for H1 receptor sites in the blood vessels, GI tract, and respiratory tract.
Adult Dose	2 sprays in each nostril q12h
Pediatric Dose	<5 years: Not established 5-11 years: 1 spray in each nostril q12h >12 years: Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	Increases CNS toxicity of depressants
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Adverse effects include local irritation and unpleasant taste; caution in hepatic or renal dysfunction; doses >10 mg/d may cause drowsiness

Drug Name	Desloratadine (Clarinex)
Description	Long-acting tricyclic histamine antagonist selective for H1 receptor. Relieves nasal congestion and systemic effects of seasonal allergy. Is a major metabolite of loratadine, which, after ingestion, is metabolized extensively to active metabolite 3-hydroxydesloratadine.
Adult Dose	5 mg PO qd
Pediatric Dose	<12 years: Not established >12 years: Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	Limited data exist; erythromycin and ketoconazole increase desloratadine and 3-hydroxydesloratadine plasma concentrations, but no increase in clinically relevant adverse effects, including QTc, was observed
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Decrease dose in hepatic impairment; rarely causes pharyngitis or dry mouth

Drug Name	Olopatadine (Patanol)
Description	Topical antihistamine ophthalmic solution.
Adult Dose	1-2 gtt OU bid
Pediatric Dose	<3 years: Not established 3-12 years: 1 gtt OU bid >12 years: Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	None reported
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Do not use with contact lenses; not for injection; caution in hepatic or renal dysfunction, doses >10 mg/d may cause drowsiness

Drug Category: Corticosteroids

These agents have a potent anti-inflammatory action. Oral preparations affect late-phase reactions. Intranasal preparations reduce both acute and late-phase reactions after several days of use. These medications relieve rhinorrhea, sneezing, itching, and congestion. Many physicians currently consider intranasal steroid use to be the first-line therapy for allergic rhinitis.

Drug Name	Ciclesonide (Omnaris)
Description	Corticosteroid nasal spray indicated for allergic rhinitis. Prodrug that is enzymatically hydrolyzed to pharmacologic active metabolite C21-desisobutyryl-ciclesonide following intranasal application. Corticosteroids have a wide range of effects on multiple cell types (eg, mast cells, eosinophils, neutrophils, macrophages, lymphocytes) and mediators (eg, histamines, eicosanoids, leukotrienes, cytokines) involved in allergic inflammation. Each spray delivers 50 mcg.
Adult Dose	2 sprays (50 mcg/spray) in each nostril qd (ie, 200 mcg/d)
Pediatric Dose	<12 years: Not established >12 years: Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	Data limited; oral ketoconazole increases desciclesonide AUC by approximately 3.5-fold at steady state
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Caution when replacing systemic corticosteroids because of risk of adrenal insufficiency; may decrease growth velocity in pediatric patients; caution with active or quiescent tuberculosis infection or with untreated fungal, viral, or bacterial infections; rare instances of wheezing, nasal septum perforation, cataracts, glaucoma, and increased intraocular pressure reported

Drug Name	Prednisone (Deltasone, Orasone, Sterapred)
Description	Immunosuppressant for treatment of allergic reactions; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity; dosage and tapering schedule vary.
Adult Dose	40-60 mg PO qd; taper over 7-10 d
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease
Interactions	Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression; infections may occur with glucocorticoid use; adverse effects include adrenal suppression, hyperglycemia, hypokalemia, edema, tachycardia, hypertension, GI irritation, anxiety, insomnia, osteoporosis, cataracts

Drug Name	Triamcinolone (Kenalog-40)
Description	Injectable corticosteroid used to treat inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.
Adult Dose	0.5 cc into each inferior turbinate q6-8wk
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; fungal, viral, and bacterial skin infections
Interactions	Coadministration with barbiturates, phenytoin, and rifampin decreases effects
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Multiple complications (eg, severe infections, hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression) may occur; abrupt discontinuation of glucocorticoids may cause adrenal crisis

Drug Name	Beclomethasone (Beconase AQ, Vancenase AQ)
Description	Topical nasal steroid spray that inhibits bronchoconstriction mechanisms and produces direct smooth muscle relaxation; may decrease number and activity of inflammatory cells, decreasing airway hyper-responsiveness.
Adult Dose	2 sprays in each nostril bid
Pediatric Dose	<6 years: Not established 6-12 years: 1 spray in each nostril bid >12 years: Administer as in adults
Contraindications	Documented hypersensitivity; bronchospasm; status asthmaticus; other types of acute episodes of asthma
Interactions	Coadministration with ketoconazole may increase plasma levels (does not appear to be clinically significant)
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Weight gain, increased bruising, cushingoid features, acneiform lesions, mental disturbances, and cataracts may occur (taper medication slowly if these occur)

Drug Name	Fluticasone propionate (Flonase)
Description	Topical nasal steroid spray. Has an extremely potent vasoconstrictive and anti-inflammatory activity. Has weak HPA axis inhibitory potency when applied topically.
Adult Dose	2 sprays in each nostril qd
Pediatric Dose	<4 years: Not established 4-12 years: 1 spray in each nostril qd >12 years: Administer as in adults
Contraindications	Documented hypersensitivity; viral, fungal, and bacterial skin infections
Interactions	None reported
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Prolonged use, application over large surface areas, application of potent steroids, and occlusive dressings may increase systemic absorption of corticosteroids and cause Cushing syndrome, reversible HPA-axis suppression, hyperglycemia, and glycosuria

Drug Category: Mast cell stabilizer

Mast cell stabilizers inhibit mast cell degranulation and influence granulocyte chemotaxis. They are most effective when used prophylactically, and they have an excellent safety profile.

Drug Category: Anticholinergic

These drugs relieve rhinorrhea but have no effect on other symptoms of allergy.

Drug Category: Decongestants

Decongestants are available in oral and topical preparations. These drugs act on alpha-adrenergic receptors in the nasal mucosa, causing vasoconstriction that concomitantly reduces turbinate edema and rhinorrhea.

Drug Name	Pseudoephedrine (Sudafed)
Description	A representative oral decongestant; stimulates vasoconstriction by directly activating alpha-adrenergic receptors in the respiratory mucosa; also induces bronchial relaxation and increases the heart rate and contractility by stimulating beta-adrenergic receptors.
Adult Dose	30 mg PO q4-6h
Pediatric Dose	<2 years: Not established 2-6 years: 15 mg PO q6h >6 years: Administer as in adults
Contraindications	Documented hypersensitivity; severe anemia; postural hypertension or hypotension; closed-angle glaucoma; head trauma; cerebral hemorrhage
Interactions	Propranolol, MAOIs, and sympathomimetic agents may increase toxicity; methyldopa and reserpine may reduce effects
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Caution in cardiovascular disease, diabetes mellitus, prostatic hypertrophy, increased intraocular pressure

FOLLOW-UP

Section 8 of 11  

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• Follow-up
• Miscellaneous
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Further Outpatient Care

• Monitor doses and adverse effects of medication.

In/Out Patient Meds

• Regimen depends on the patient's symptoms and other coexisting medical problems.

Transfer

• Candidates for immunotherapy may be transferred to another physician for care, and therapy is administered at the discretion of the treating physician.
• The physician should be familiar with immunotherapy and its risks. He or she should be able to deal with any allergic emergency.

Deterrence/Prevention

• See Avoidance of allergens and environmental controls for methods of deterrence and prevention.

Complications

• Bacterial rhinosinusitis
• Exacerbation of asthma

Prognosis

• Most patients with allergic rhinitis can expect an improved quality of life with appropriate environmental control measures; pharmacotherapy; and, when necessary, immunotherapy.

Patient Education

• The clinic should have literature about allergies, and the office staff should continually educate patients and reinforce their understanding of avoidance and environmental control techniques.
• Patients undergoing immunotherapy should be instructed to report any reactions from the previous injection and any changes in their health status during each visit (eg, change in medication, new onset of upper respiratory tract infection, worsening of asthma).

MISCELLANEOUS

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Medical/Legal Pitfalls

• Only qualified personnel should administer immunotherapy.
• A protocol to treat anaphylaxis must be in place, and drills must be conducted at regular intervals.
• Patients must stay in the office for 15-20 minutes after each injection. They should report any reaction or change in their medical status before the next injection is administered, because doses may need to be adjusted.

MULTIMEDIA

Section 10 of 11  

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• Medication
• Follow-up
• Miscellaneous
• Multimedia
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Media file 1:  Boggy inferior turbinate in an allergic patient.
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Media type:  Image

REFERENCES

Section 11 of 11

• Authors and Editors
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1. Malone DC, Lawson KA, Smith DH, et al. A cost of illness study of allergic rhinitis in the United States. J Allergy Clin Immunol. Jan 1997;99(1 Pt 1):22-7. [Medline].
2. Alho OP, Karttunen R, Karttunen TJ. Nasal mucosa in natural colds: effects of allergic rhinitis and susceptibility to recurrent sinusitis. Clin Exp Immunol. Aug 2004;137(2):366-72. [Medline].
3. Berger WE. Treatment update: allergic rhinitis. Allergy Asthma Proc. Jul-Aug 2001;22(4):191-8. [Medline].
4. Crystal-Peters J, Crown WH, Goetzel RZ, Schutt DC. The cost of productivity losses associated with allergic rhinitis. Am J Manag Care. Mar 2000;6(3):373-8. [Medline].
5. Davis WE, Holt GR, Johnson JT, et al. Policy statements. In: The Bulletin -American Academy of Otolaryngology-Head & Neck Surgery. Mosby-Year Book;1998:9.
6. deShazo RD. Allergic Rhinitis. Cecil Textbook of Medicine, 21st edition. 2000;1445-1450.
7. King HC, Mabry RL, Mabry CS. Allergy in ENT Practice: A Basic Guide. New York, NY:. Thieme Medical Publishers;1998:1-403.
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Article Last Updated: Nov 16, 2007