Updated: Jun 1, 2009
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.
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.
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.
Males and females tend to be affected by allergic rhinitis in fairly equal proportions.
Patients with allergies frequently have a characteristic physical appearance.
For practical purposes, allergens can be divided into seasonal and perennial groups.
Allergic Fungal Sinusitis
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.
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.2
A pulmonologist may be consulted.
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.
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.
These medications are H1 receptor antagonists and relieve sneezing, itching, and rhinorrhea.
A representative first-generation antihistamine; competes with histamine for H1 receptor sites on effector cells in blood vessels and in the respiratory tract.
4 mg PO q6h
<6 years: Not established
6-12 years: 4 mg PO q12h
>12 years: Administer as in adults
CNS toxicity increases with coadministration of other CNS depressants, tricyclic antidepressants, MAOIs, and phenothiazines
Documented hypersensitivity; asthma attacks; narrow-angle glaucoma; symptomatic prostate hypertrophy; bladder neck obstruction; stenotic peptic ulcer
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May cause significant confusion; not for use in premature or full-term neonates
Selectively inhibits peripheral histamine H1 receptors.
10 mg PO qd
<6 years: Not established
>6 years: Administer as in adults
Ketoconazole, erythromycin, procarbazine, and alcohol may increase levels
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Initiate therapy with lower doses in liver impairment
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.
60 mg PO q12h or 180 mg PO qd
<6 years: not established
6-12 years: 30 mg PO q12h
>12 years: Administer as in adults
Toxicity increases with coadministration of erythromycin and ketoconazole
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
No data about use while breastfeeding
Topical antihistamine nasal spray; competes with histamine for H1 receptor sites in the blood vessels, GI tract, and respiratory tract.
2 sprays in each nostril q12h
<5 years: Not established
5-11 years: 1 spray in each nostril q12h
>12 years: Administer as in adults
Increases CNS toxicity of depressants
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Adverse effects include local irritation and unpleasant taste; caution in hepatic or renal dysfunction; doses >10 mg/d may cause drowsiness
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.
5 mg PO qd
<12 years: Not established
>12 years: Administer as in adults
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
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Decrease dose in hepatic impairment; rarely causes pharyngitis or dry mouth
Topical antihistamine ophthalmic solution.
1-2 gtt OU bid
<3 years: Not established
3-12 years: 1 gtt OU bid
>12 years: Administer as in adults
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Do not use with contact lenses; not for injection; caution in hepatic or renal dysfunction, doses >10 mg/d may cause drowsiness
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.
Nasal spray; demonstrated no mineralocorticoid, androgenic, antiandrogenic, or estrogenic activity in preclinical trials. Decreases rhinovirus-induced up-regulation in respiratory epithelial cells and modulate pretranscriptional mechanisms.
2 sprays (50 mcg/spray)each nostril qd
<2 years: Not established
2-11 years: 1 spray (50 mcg/spray) each nostril qd
>12 years: Administer as in adults
None reported
Documented hypersensitivity, nasal septal perforation, nasal surgery, nasal trauma
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Use with caution inpatients with active or quiescent tuberculosis of the respiratory tract;untreated fungal, bacterial, systemic viral infections; or ocular herpes
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.
2 sprays (50 mcg/spray) in each nostril qd (ie, 200 mcg/d)
<12 years: Not established
>12 years: Administer as in adults
Data limited; oral ketoconazole increases desciclesonide AUC by approximately 3.5-fold at steady state
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
Immunosuppressant for treatment of allergic reactions; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity; dosage and tapering schedule vary.
40-60 mg PO qd; taper over 7-10 d
Not established
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
Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
Injectable corticosteroid used to treat inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.
0.5 cc into each inferior turbinate q6-8wk
Not established
Coadministration with barbiturates, phenytoin, and rifampin decreases effects
Documented hypersensitivity; fungal, viral, and bacterial skin infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
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.
2 sprays in each nostril bid
<6 years: Not established
6-12 years: 1 spray in each nostril bid
>12 years: Administer as in adults
Coadministration with ketoconazole may increase plasma levels (does not appear to be clinically significant)
Documented hypersensitivity; bronchospasm; status asthmaticus; other types of acute episodes of asthma
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Weight gain, increased bruising, cushingoid features, acneiform lesions, mental disturbances, and cataracts may occur (taper medication slowly if these occur)
Topical nasal steroid spray. Has an extremely potent vasoconstrictive and anti-inflammatory activity. Has weak HPA axis inhibitory potency when applied topically.
2 sprays in each nostril qd
<4 years: Not established
4-12 years: 1 spray in each nostril qd
>12 years: Administer as in adults
None reported
Documented hypersensitivity; viral, fungal, and bacterial skin infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
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.
Inhibits degranulation of sensitized mast cells after exposure to specific antigens; available over the counter; may require several days to work.
1 spray in each nostril tid/qid
<6 years: Not established
>6 years: Administer as in adults
None reported
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Do not use in severe renal or hepatic impairment; symptoms may reoccur when withdrawing drug
These drugs relieve rhinorrhea but have no effect on other symptoms of allergy.
Chemically related to atropine; has antisecretory properties; when applied locally, inhibits secretions from serous and seromucous glands lining the nasal mucosa; available in 0.03% and 0.06% strengths; also effective in relieving rhinorrhea from other causes (eg, cold air, gustation).
2 sprays in each nostril bid/qid
<6 years: Not established
6-12 years: 1-2 sprays each nostril bid
>12 years: Administer as in adults
Drugs with anticholinergic properties, such as dronabinol, may increase toxicity; albuterol may increase effects
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Not indicated for acute episodes of bronchospasm; caution in narrow-angle glaucoma, prostatic hypertrophy, bladder neck obstruction
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.
A representative topical decongestant applied directly to mucous membranes, where it stimulates alpha-adrenergic receptors and causes vasoconstriction. Decongestion occurs without drastic changes in BP, vascular redistribution, and cardiac stimulation.
2-3 sprays in each nostril q12h
<6 years: Not established
6-12 years: 1-2 sprays in each nostril q12h
>12 years: Administer as in adults
Hypotensive action of guanethidine may be reversed; concurrent administration with methyldopa may increase vasopressor response; concurrent use of MAOIs and ephedrine may cause hypertensive crisis; pressor sensitivity to mixed-acting agents (eg, ephedrine) may be increased; guanethidine potentiates epinephrine effects and inhibits ephedrine effects; phenothiazines may reverse action; TCAs potentiate vasopressor response and may cause dysrhythmias
Documented hypersensitivity; MAOI therapy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Prolonged use can lead to rebound rhinitis; caution in hyperthyroidism, coronary artery and ischemic heart disease, diabetes mellitus, increased intraocular pressure, prostatic hypertrophy; because of increased vasoconstriction, patients with hypertension may have change in BP; do not use topical decongestants for longer than 3-5 d
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.
30 mg PO q4-6h
<2 years: Not established
2-6 years: 15 mg PO q6h
>6 years: Administer as in adults
Propranolol, MAOIs, and sympathomimetic agents may increase toxicity; methyldopa and reserpine may reduce effects
Documented hypersensitivity; severe anemia; postural hypertension or hypotension; closed-angle glaucoma; head trauma; cerebral hemorrhage
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in cardiovascular disease, diabetes mellitus, prostatic hypertrophy, increased intraocular pressure
Monitor doses and adverse effects of medication.
Regimen depends on the patient's symptoms and other coexisting medical problems.
See Avoidance of allergens and environmental controls for methods of deterrence and prevention.
Most patients with allergic rhinitis can expect an improved quality of life with appropriate environmental control measures; pharmacotherapy; and, when necessary, immunotherapy.
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allergic rhinitis, sinus allergies, rhinosinusitis, allergy, seasonal allergy, allergen, nasal catarrh, hay fever, autumnal catarrh, rhinitis nervosa, otitis media
Quoc A Nguyen, MD, Associate Clinical Professor, Director, Sinus and Allergy Center, Department of Otolaryngology-Head & Neck Surgery, University of California, Irvine Medical Center
Quoc A Nguyen, MD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngic Allergy, American Academy of Otolaryngology-Head and Neck Surgery, American Laryngological Rhinological and Otological Society, American Rhinologic Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.
Lanny Garth Close, MD, Chair, Professor, Department of Otolaryngology-Head and Neck Surgery, Columbia University College of Physicians and Surgeons
Lanny Garth Close, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American College of Physicians, American Laryngological Association, American Society for Head and Neck Surgery, and New York Academy of Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Stephen G Batuello, MD, Consulting Staff, Colorado ENT Specialists
Stephen G Batuello, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Physician Executives, American Medical Association, and Colorado Medical Society
Disclosure: Nothing to disclose.
Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders
Christopher L Slack, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Medical Association
Disclosure: Nothing to disclose.
Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine
Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Head and Neck Society
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