Allergic Rhinitis in Otolaryngology and Facial Plastic Surgery

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.

A study by Shahsavan et al found that patients with moderate to severe persistent allergic rhinitis demonstrated significantly greater interleukin 22 (IL-22) and IL-17A production than did healthy controls, suggesting that the development of persistent allergic rhinitis is influenced by these cytokines. Moreover, a correlation was found between IL-22 and IL-17A serum levels, along with the mean number of IL-22– and IL-17A–positive cells in the nasal mucosa, and specific IgE levels, nasal eosinophil count, and total nasal symptom score (TNSS).[3]

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.

A study by Romano et al indicated that sleep problems in adults with perennial allergic rhinitis not only are common, but negatively affect daily functioning in these individuals. In an analysis of 511 adults with perennial allergic rhinitis (either self reported or physician diagnosed), the investigators found that sleep problems were reported by 66.0% of subjects, and that such problems occurred more frequently in persons with both allergic rhinitis and allergic asthma (78.1%) than in those with allergic rhinitis alone (54.7%). Moreover, sleep difficulties significantly impacted daytime functioning in 33.3% of individuals with allergic rhinitis by itself, versus 47.0% of those with a combination of allergic rhinitis and allergic asthma.[4]

A literature review by Rodrigues et al reported an apparent association between allergic rhinitis and an increased risk of depression and anxiety.[5]

Sex

Males and females tend to be affected by allergic rhinitis in fairly equal proportions. A study by Cazzoletti et al found gender-associated age-based differences in the prevalence of self-reported allergic and nonallergic rhinitis, with allergic rhinitis showing an age-based decrease in prevalence that was comparable in males and females (from 26.6% in persons aged 20-44 years to 15.6% in persons aged 65-84 years), and nonallergic rhinitis showing an age-based decrease in prevalence among females (from 12.0% in females aged 20-44 years to 7.5% in females aged 65-84 years) and roughly the same prevalence in younger and older males (10.2% in males aged 20-44 years and 11.1% in males aged 65-84 years).[6]

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.

See the list below:

• Allergy history

  • For the clinician 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.

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.

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 two 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.

In a study of over 58,000 students aged 12-18 years, Lee et al found that the risk of allergic rhinitis, as well as asthma and atopic dermatitis, was increased in association with the use of cigarettes, electronic cigarettes, and heated tobacco products, with the adjusted odds ratios for these multimorbidities being 1.98, 1.83, and 2.48 for the three tobacco sources, respectively.[7]

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.

See the list below:

• 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).

See the list below:

• 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

The three basic approaches to the treatment of allergies are (1) avoidance, (2) pharmacotherapy, and (3) immunotherapy. Treatment should start with avoidance of allergens and with 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.

An international study by Van Bulck et al found the following prevalences of factors behind uncontrolled allergic rhinitis: disease-related factors (64%), treatment-related factors (56%), patient-related factors (54%), and diagnosis-related factors (47%). It was also determined that in 76% of these patients, uncontrolled allergic rhinitis existed for two or more reasons.[8]

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 injections

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.

Sublingual (SL) immunotherapy

A Cochrane Database of Systematic Reviews article concluded that the sublingual (SL) route is a safe and effective method of immunotherapy;[9]  SL immunotherapy is more convenient than weekly injections for individuals with limited, specific allergies that match the SL product. However, SL immunotherapy may not be appropriate for everyone. Those affected by multiple allergens may not obtain relief from all of their symptoms by taking immunotherapy for only a single or several allergens.

In April 2014, the US Food and Drug Administration (FDA) approved an SL tablet consisting of 5 calibrated grass pollen extracts (Oralair). It contains Perennial Ryegrass (Lolium perenne), Kentucky bluegrass (Poa pratensis), Timothy grass (Phleum pratense), Orchard grass (Dactylis glomerata), and Sweet Vernal grass (Anthoxanthum odoratum).[10]

The Oralair SL tablet needs to be initiated 4 months prior to the season for the specific allergen.

A second SL immunotherapy for Timothy grass (Grastek) was also approved in April 2014 for adults and children aged 5 years or older. It should be initiated at least 12 weeks before the start of the grass pollen season.[11] Efficacy and safety in North America was established in a large study (n=1500) of adults and children aged 5-65 years. Results showed a 23% improvement of symptoms in the entire grass pollen season.[12]

A third SL immunotherapy for ragweed (Ragwitek) was also approved in April 2014 for adults aged 18 years or older. Effectiveness studies included about 760 patients. Phase 3 clinical trials showed reduced rhinoconjunctivitis symptoms over the entire season by 27-43% compared with placebo. It is approved for adults aged 18 years or older.[13, 14]

A study by Devillier et al indicated that in patients with allergic rhinitis, administration of prescription SL immunotherapy with grass pollen tablets reduces the need for allergic rhinitis and asthma medications. The investigators found, for example, that asthma therapy was initiated in 1.8% of patients treated with SL immunotherapy, compared with 5.3% of control patients.[15]

An SL immunotherapeutic agent (Odactra) for house dust mites was approved by the FDA in 2017 for adults aged 18 through 65 years. It is a standardized allergen extract indicated as daily SL immunotherapy for allergic rhinitis, with or without conjunctivitis, confirmed using in vitro testing for IgE antibodies to the house dust mite D farinae or D pteronyssinus, or through skin testing using licensed house dust mite allergen extracts.[16]  FDA approval for adolescents was granted in January 2023. 

The first dose must be administered in a healthcare setting and supervised by a doctor experienced in allergic disease diagnosis and treatment. After this initial dose is given, the patient must be monitored for signs or symptoms of a severe systemic or local allergic reaction. Within the prescribing information, a boxed warning describes life-threatening allergic reactions. The boxed warning also specifies that the patient must be prescribed autoinjectable epinephrine to have while using house dust mite immunotherapy.

Approval was based on a double-blind, multicenter trial (n = 1482) in adolescents and adults with house dust mite allergic rhinitis with or without conjunctivitis (AR/C). Over a 52-week period, house dust mite immunotherapy improved the rhinoconjunctivitis score and visual analog scale–assessed AR/C symptoms.[17]

A study by Soh et al indicated that sublingual immunotherapy with extracts from the dust mite Blomia tropicalis is effective in treating allergic rhinitis sensitized to this species. The study, which included 39 children and adults, found patients’ Total Nasal Symptom Scores and Mini Rhinoconjunctivitis Quality of Life Questionnaire scores improved after 3 months of treatment and continued to approve thereafter.[18]

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.

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.

AAO-HNSF

In 2015 the American Academy of Otolaryngology-Head and Neck Surgery Foundation (AAO-HNSF) released clinical practice guidelines for the diagnosis and management of allergic rhinitis. The recommendations are summarized below.[19]

Diagnosis

A clinical diagnosis of allergic rhinitis should be made in patients with a history and physical examination consistent with an allergic cause and one or more of the following symptoms: (Recommendation)

• Nasal congestion
• Runny nose
• Itchy nose
• Sneezing

Findings consistent with an allergic cause include: (Recommendation)

• Clear rhinorrhea
• Nasal congestion
• Pale discoloration of the nasal mucosa
• Red and watery eyes

For patients with a clinical diagnosis of allergic rhinitis who do not respond to empiric treatment, or in situations in which the diagnosis is uncertain or the specific allergen is needed to target therapy, immunoglobulin E (IgE) (skin or blood) testing should be carried out by clinicians who can perform and interpret the testing. (Recommendation)

Sinonasal imaging should not be routinely performed in patients with symptoms consistent with a diagnosis of allergic rhinitis. (Recommendation)

Management

Avoidance of known allergens or environmental controls (eg, removal of pets; the use of air filtration systems, bed covers, and acaricides) may be advised for patients who have identified allergens that correlate with clinical symptoms. (Option)

The presence of any of the following associated conditions should be documented in medical records: (Recommendation)

• Asthma
• Atopic dermatitis
• Sleep-disordered breathing
• Conjunctivitis
• Rhinosinusitis
• Otitis media

Management recommendations also include the following:

• Clinicians should treat allergic rhinitis with intranasal steroids when patients' symptoms impair their quality of life (Strong recommendation)
• Clinicians should recommend second-generation oral antihistamines, which are less likely to cause drowsiness, for patients complaining primarily of sneezing and itching (Strong recommendation)
• For patients with seasonal, perennial, or episodic allergic rhinitis, intranasal antihistamines may be offered (Option)
• Oral leukotriene receptor antagonists (LTRAs) should not be offered as primary therapy (Recommendation against)
• Combination pharmacologic therapy may be offered to patients who do not have an adequate response to monotherapy (Option)
• If patients have an inadequate response to pharmacologic therapy, with or without environmental controls, immunotherapy (sublingual or subcutaneous) should be offered (Recommendation)
• For patients with nasal airway obstruction and enlarged inferior turbinates who have failed medical management, inferior turbinate reduction may be offered (Option)
• For patients who prefer nonpharmacologic therapy, acupuncture may be offered (Option)

As a result of limited knowledge of herbal medicines and concern about the quality of standardization and safety, no recommendation was made on the use of herbal therapy.

JTFPP

In November 2017, the Joint Task Force on Practice Parameters (JTFPP), of the American Academy of Allergy, Asthma, & Immunology; the American College of Allergy, Asthma & Immunology; and the Joint Council of Allergy, Asthma & Immunology, issued an update to its 2008 guidelines for the treatment of seasonal allergic rhinitis. The revised guidelines state that, at least initially, an intranasal corticosteroid should be used alone rather than in combination with an oral antihistamine, to treat nasal symptoms in patients aged 12 years or older.[20]

The revision also states that in patients aged 15 years or older with moderate to severe seasonal allergic rhinitis, an intranasal corticosteroid is preferable over an LTRA for initial treatment.[20]

Thirdly, according to the revised guidelines, clinicians can recommend seasonal allergic rhinitis treatment with a combination of intranasal corticosteroid and intranasal antihistamine as preferable to therapy with either agent alone, although the cost and side-effects risk will be greater.[20]

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.

Class Summary

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

Chlorpheniramine (Chlor-Trimeton, Aller-Chlor, Chlo-Amine)

A representative first-generation antihistamine; competes with histamine for H1 receptor sites on effector cells in blood vessels and in the respiratory tract.

Loratadine (Claritin)

Selectively inhibits peripheral histamine H1 receptors.

Fexofenadine (Allegra)

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.

Azelastine (Astelin)

Topical antihistamine nasal spray; competes with histamine for H1 receptor sites in the blood vessels, GI tract, and respiratory tract.

Desloratadine (Clarinex)

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.

Olopatadine (Patanol)

Topical antihistamine ophthalmic solution.

Class Summary

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.

Mometasone (Nasonex)

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.

Ciclesonide (Omnaris)

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.

Prednisone (Deltasone, Orasone, Sterapred)

Immunosuppressant for treatment of allergic reactions; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity; dosage and tapering schedule vary.

Triamcinolone (Kenalog-40)

Injectable corticosteroid used to treat inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.

Beclomethasone (Beconase AQ, QNASL)

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. QNASL available as intranasal dry powder.

Fluticasone propionate (Flonase)

Topical nasal steroid spray. Has an extremely potent vasoconstrictive and anti-inflammatory activity. Has weak HPA axis inhibitory potency when applied topically.

Class Summary

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.

Cromolyn sodium, intranasal (NasalCrom)

Inhibits degranulation of sensitized mast cells after exposure to specific antigens; available over the counter; may require several days to work.

Class Summary

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

Ipratropium (Atrovent)

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).

Class Summary

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.

Oxymetazoline (Afrin)

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.

Pseudoephedrine (Sudafed)

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.

Class Summary

Immunotherapy with daily sublingual (SL) tablets may be able to replace weekly injections in some individuals, depending on the offending allergens. SL tablets must be initiated 4 months before the allergen season that is being treated.

Grass pollens allergen extract (Oralair)

SL immunotherapy is indicated for grass pollen–induced allergic rhinitis (with or without conjunctivitis) confirmed by positive skin test or in vitro testing for grass pollen–specific immunoglobulin E antibodies for any of the 5 grass species contained in the product. It consists of 5 purified and calibrated pollen extracts: Perennial Ryegrass (Lolium perenne), Kentucky bluegrass (Poa pratensis), Timothy grass (Phleum pratense), Orchard grass (Dactylis glomerata), and Sweet Vernal grass (Anthoxanthum odoratum).

Timothy grass pollen allergen extract (Grastek)

SL immunotherapy is indicated for allergic rhinitis (with or without conjunctivitis) confirmed by positive skin test or in vitro testing for Timothy grass pollen-specific IgE antibodies.

Ragweed allergen extract (Ragwitek)

SL immunotherapy is indicated for allergic rhinitis (with or without conjunctivitis) confirmed by positive skin test or in vitro testing for ragweed (Ambrosia artemisiifolia) grass pollen-specific IgE antibodies.

House dust mite immunotherapy (Odactra)

The SL tablet consists of standardized extract with consistent biological potency (although the precise mechanisms through which allergen immunotherapy works are unknown). It is indicated for dust mite–induced allergic rhinitis with or without conjunctivitis in people aged 12-65 years, with the allergy confirmed using in vitro testing for IgE antibodies to the house dust mite D farinae or D pteronyssinus or through skin testing using licensed house dust mite allergen extracts.

Monitor doses and adverse effects of medication.

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

Candidates for immunotherapy may be transferred to an allergist for care, and therapy is administered at the discretion of the treating physician.

The clinician should be familiar with immunotherapy and its risks. He or she should be able to deal with any allergic emergency.

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

Complications may include bacterial rhinosinusitis and exacerbation of asthma.

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

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).