Emed Rhinitis Allergy

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    Practice Essentials

    Rhinitis, which occurs most commonly as allergic rhinitis, is an inflammation ofthe nasal membranes that is characterized by sneezing, nasal congestion, nasalitching, and rhinorrhea, in any combination.[2] While allergic rhinitis itself is not life-threatening (unless accompanied by severe asthma or anaphylaxis), morbidityfrom the condition can be significant.

    Essential update: Allergic rhinitis associated with increased risk ofADHD

    A population-based, case-control study found a strong association betweenatopic diseases (AD) and attention-deficit/hyperactivity disorder (ADHD) inchildren. The study involved 4692 children with ADHD and 18,768 randomlyselected controls. Results showed that children with ADHD had a higher rate of

    AD than controls, particularly allergic rhinitis and allergic conjunctivitis. In addition,children with atopic dermatitis and asthma were also at higher risk of ADHD.[7]

    Signs and symptoms

    History

    Signs and symptoms of allergic rhinitis include the following:

    Sneezing Itching: Nose, eyes, ears, palate Rhinorrhea Postnasal drip Congestion Anosmia Headache Earache Tearing Red eyes Eye swelling Fatigue Drowsiness Malaise

    Complications of this allergic rhinitis include the following:

    Acute or chronic sinusitis Otitis media Sleep disturbance or apnea Dental problems (overbite): Caused by excessive breathing through the mouth Palatal abnormalities Eustachian tube dysfunction

    Physical examination

    Nasal features of allergic rhinitis can include the following:

    Nasal crease: A horizontal crease across the lower half of the bridge of thenose; caused by repeated upward rubbing of the tip of the nose by the palm ofthe hand

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    Thin, watery nasal secretions Deviation or perforation of the nasal septum: May be associated with chronic

    rhinitis, although there can be other, unrelated causesManifestations of allergic rhinitis affecting the ears, eyes, and oropharynx includethe following:

    Ears: Retraction and abnormal flexibility of the tympanic membrane Eyes: Injection and swelling of the palpebral conjunctivae, with excess tear

    production; Dennie-Morgan lines (prominent creases below the inferior eyelid);and dark circles around the eyes (allergic shiners), which are related tovasodilation or nasal congestion

    Oropharynx: "Cobblestoning," that is, streaks of lymphoid tissue on theposterior pharynx; tonsillar hypertrophy; and malocclusion (overbite) and ahigh-arched palate

    SeeClinical Presentationfor more detail.

    Diagnosis

    Laboratory tests used in the diagnosis of allergic rhinitis include the following:

    Allergy skin tests (immediate hypersensitivity testing): An in vivo method ofdetermining immediate (IgE-mediated) hypersensitivity to specific allergens

    Radioallergosorbent test (RAST): Indirectly measures the quantity ofimmunoglobulin E (IgE) serving as an antibody to a particular antigen

    Total serum IgE: Neither sensitive nor specific for allergic rhinitis, but the resultscan be helpful in some cases when combined with other factors

    Total blood eosinophil count: Neither sensitive nor specific for the diagnosis, but,

    as with total serum IgE, can sometimes be helpful when combined with otherfactors

    Imaging studies used in the diagnosis and evaluation of allergic rhinitis includethe following:

    Radiography: Can be helpful for evaluating possible structural abnormalities orto help detect complications or comorbid conditions, such as sinusitis oradenoid hypertrophy

    Computed tomography scanning: Can be very helpful for evaluating acute orchronic sinusitis

    Magnetic resonance imaging: Also can be helpful for evaluating sinusitisSeeWorkupfor more detail.

    Management

    The management of allergic rhinitis consists of the following 3 major treatmentstrategies:

    Environmental control measures and allergen avoidance: These includekeeping exposure to allergens such as pollen, dust mites, and mold to aminimum

    Pharmacologic management: Patients are often successfully treated with oralantihistamines, decongestants, or both; regular use of an intranasal steroidspray may be more appropriate for patients with chronic symptoms

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    Immunotherapy: This treatment may be considered more strongly with severedisease, poor response to other management options, and the presence of

    comorbid conditions or complications; immunotherapy is often combined withpharmacotherapy and environmental controlSeeTreatmentandMedicationfor more detail.

    Background

    Rhinitis is defined as inflammation of the nasal membranes[1] and is characterizedby a symptom complex that consists of any combination of the following:sneezing, nasal congestion, nasal itching, and rhinorrhea.[2] The eyes, ears,sinuses, and throat can also be involved. Allergic rhinitis is the most commoncause of rhinitis. It is an extremely common condition, affecting approximately 20%of the population.

    Although allergic rhinitis is not a life-threatening condition, complications canoccur and the condition can significantly impair quality of life,[3, 4] which leads to anumber of indirect costs. The total direct and indirect cost of allergic rhinitis wasrecently estimated to be $5.3 billion per year.[5]A 2011 analysis determined thatpatients with allergic rhinitis averaged 3 additional office visits, 9 moreprescriptions filled, and $1500 in incremental healthcare costs in 1 year thansimilar patients without allergic rhinitis.[6]

    Pathophysiology

    Allergic rhinitis involves inflammation of the mucous membranes of the nose,eyes, eustachian tubes, middle ear, sinuses, and pharynx. The nose invariably is

    involved, and the other organs are affected in certain individuals. Inflammation ofthe mucous membranes is characterized by a complex interaction ofinflammatory mediators but ultimately is triggered by an immunoglobulin E (IgE)mediated response to an extrinsic protein.[8]

    The tendency to develop allergic, or IgE-mediated, reactions to extrinsic allergens(proteins capable of causing an allergic reaction) has a genetic component. Insusceptible individuals, exposure to certain foreign proteins leads to allergicsensitization, which is characterized by the production of specific IgE directedagainst these proteins. This specific IgE coats the surface of mast cells, whichare present in the nasal mucosa. When the specific protein (eg, a specific pollengrain) is inhaled into the nose, it can bind to the IgE on the mast cells, leading to

    immediate and delayed release of a number of mediators.[8, 9, 10]

    The mediators that are immediately released include histamine, tryptase,chymase, kinins, and heparin.[9, 10] The mast cells quickly synthesize othermediators, including leukotrienes and prostaglandin D2.[11, 12, 13] These mediators,via various interactions, ultimately lead to the symptoms of rhinorrhea (ie, nasalcongestion, sneezing, itching, redness, tearing, swelling, ear pressure, postnasaldrip). Mucous glands are stimulated, leading to increased secretions. Vascularpermeability is increased, leading to plasma exudation. Vasodilation occurs,leading to congestion and pressure. Sensory nerves are stimulated, leading tosneezing and itching. All of these events can occur in minutes; hence, thisreaction is called the early, or immediate, phase of the reaction.

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    Over 4-8 hours, these mediators, through a complex interplay of events, lead tothe recruitment of other inflammatory cells to the mucosa, such as neutrophils,

    eosinophils, lymphocytes, and macrophages.[14]

    This results in continuedinflammation, termed the late-phase response. The symptoms of the late-phaseresponse are similar to those of the early phase, but less sneezing and itchingand more congestion and mucus production tend to occur.[14] The late phase maypersist for hours or days.

    Systemic effects, including fatigue, sleepiness, and malaise, can occur from theinflammatory response. These symptoms often contribute to impaired quality oflife.

    Epidemiology

    Frequency

    United StatesAllergic rhinitis affects approximately 40 million people in the UnitedStates.[15]Recent US figures suggest a 20% cumulative prevalence rate.[16, 17]

    InternationalScandinavian studies have demonstrated a cumulative prevalence rate of 15% inmen and 14% in women.[18] The prevalence of allergic rhinitis may vary within andamong countries.[19, 20, 21, 22] This may be due to geographic differences in the typesand potency of different allergens and the overall aeroallergen burden.

    Mortality/Morbidity

    While allergic rhinitis itself is not life-threatening (unless accompanied by severeasthma or anaphylaxis), morbidity from the condition can be significant. Allergicrhinitis often coexists with other disorders, such asasthma, and may beassociated with asthma exacerbations.[23, 24, 25]

    Allergic rhinitis is also associated withotitis media,eustachian tubedysfunction,sinusitis,nasal polyps,allergic conjunctivitis, andatopic dermatitis.[1, 2,26] It may also contribute to learning difficulties, sleep disorders, and fatigue.[27, 28, 29]

    Numerous complications that can lead to increased morbidity or even mortalitycan occur secondary to allergic rhinitis. Possible complications include otitismedia, eustachian tube dysfunction, acute sinusitis, and chronic sinusitis.

    Allergic rhinitis can be associated with a number of comorbid conditions,including asthma, atopic dermatitis, and nasal polyps. Evidence now suggeststhat uncontrolled allergic rhinitis can actually worsen the inflammationassociated with asthma[23, 24, 25] or atopic dermatitis.[26] This could lead to furthermorbidity and even mortality.

    Allergic rhinitis can frequently lead to significant impairment of quality of life.Symptoms such as fatigue, drowsiness (due to the disease or to medications),and malaise can lead to impaired work and school performance, missed schoolor work days, and traffic accidents. The overall cost (direct and indirect) ofallergic rhinitis was recently estimated to be $5.3 billion per year.[5]

    Race

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    Allergic rhinitis occurs in persons of all races. Prevalence of allergic rhinitisseems to vary among different populations and cultures, which may be due to

    genetic differences, geographic factors or environmental differences, or otherpopulation-based factors.

    Sex

    In childhood, allergic rhinitis is more common in boys than in girls, but inadulthood, the prevalence is approximately equal between men and women.

    Age

    Onset of allergic rhinitis is common in childhood, adolescence, and early adultyears, with a mean age of onset 8-11 years, but allergic rhinitis may occur inpersons of any age. In 80% of cases, allergic rhinitis develops by age 20

    years.[30]

    The prevalence of allergic rhinitis has been reported to be as high as 40%in children, subsequently decreasing with age.[16, 17] In the geriatric population,rhinitis is less commonly allergic in nature.

    History

    Obtaining a detailed history is important in the evaluation of allergic rhinitis.Important elements include an evaluation of the nature, duration, and time courseof symptoms; possible triggers for symptoms; response to medications; comorbidconditions; family history of allergic diseases; environmental exposures;occupational exposures; and effects on quality of life. A thorough history mayhelp identify specific triggers, suggesting an allergic etiology for the rhinitis.

    Symptoms that can be associated with allergic rhinitis include sneezing, itching(of nose, eyes, ears, palate), rhinorrhea, postnasal drip, congestion, anosmia,headache, earache, tearing, red eyes, eye swelling, fatigue, drowsiness, andmalaise.[2]

    Symptoms and chronicity

    Determine the age of onset of symptoms and whether symptoms have beenpresent continuously since onset. While the onset of allergic rhinitis can occurwell into adulthood, most patients develop symptoms by age 20 years.[30]

    Determine the time pattern of symptoms and whether symptoms occur at a

    consistent level throughout the year (ie, perennial rhinitis), only occur in specificseasons (ie, seasonal rhinitis), or a combination of the two. During periods ofexacerbation, determine whether symptoms occur on a daily basis or only on anepisodic basis. Determine whether the symptoms are present all day or only atspecific times during the day. This information can help suggest the diagnosisand determine possible triggers.

    Determine which organ systems are affected and the specific symptoms. Somepatients have exclusive involvement of the nose, while others have involvementof multiple organs. Some patients primarily have sneezing, itching, tearing, andwatery rhinorrhea (the classic hayfever presentation), while others may onlycomplain of congestion. Significant complaints of congestion, particularly if

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    unilateral, might suggest the possibility of structural obstruction, such as a polyp,foreign body, or deviated septum.

    Trigger factors

    Determine whether symptoms are related temporally to specific trigger factors.This might include exposure to pollens outdoors, mold spores while doing yardwork, specific animals, or dust while cleaning the house.

    Irritant triggers such as smoke, pollution, and strong smells can aggravatesymptoms in a patient with allergic rhinitis. These are also common triggers ofvasomotor rhinitis. Many patients have both allergic rhinitis and vasomotor rhinitis.

    Other patients may describe year-round symptoms that do not appear to beassociated with specific triggers. This could be consistent with nonallergic rhinitis,

    but perennial allergens, such as dust mite or animal exposure, should also beconsidered in this situation. With chronic exposure and chronic symptoms, thepatient may not be able to associate symptoms with a particular trigger.

    Response to treatment

    Response to treatment with antihistamines supports the diagnosis of allergicrhinitis, although sneezing, itching, and rhinorrhea associated with nonallergicrhinitis can also improve with antihistamines.[31]

    Response to intranasal corticosteroids supports the diagnosis of allergic rhinitis,although some cases of nonallergic rhinitis (particularly the nonallergic rhinitis

    with eosinophils syndrome [NARES]) also improve with nasal steroids.Comorbid conditions

    Patients with allergic rhinitis may have other atopic conditions such as asthma[23,24] or atopic dermatitis.[26] Of patients with allergic rhinitis, 20% also havesymptoms of asthma. Uncontrolled allergic rhinitis may cause worsening ofasthma[25] or even atopic dermatitis.[26] Explore this possibility when obtaining thepatient history.

    Look for conditions that can occur as complications of allergic rhinitis. Sinusitisoccurs quite frequently. Other possible complications include otitis media, sleepdisturbance or apnea, dental problems (overbite), and palatal

    abnormalities.[32] The treatment plan might be different if one of thesecomplications is present. Nasal polyps occur in association with allergic rhinitis,although whether allergic rhinitis actually causes polyps remains unclear. Polypsmay not respond to medical treatment and might predispose a patient to sinusitisor sleep disturbance (due to congestion).

    Investigate past medical history, including other current medical conditions.Diseases such as hypothyroidism or sarcoidosis can cause nonallergic rhinitis.Concomitant medical conditions might influence the choice of medication.

    Family history

    Because allergic rhinitis has a significant genetic component,

    [33]

    a positive familyhistory for atopy makes the diagnosis more likely.

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    In fact, a greater risk of allergic rhinitis exists if both parents are atopic than if oneparent is atopic. However, the cause of allergic rhinitis appears to be

    multifactorial, and a person with no family history of allergic rhinitis can developallergic rhinitis.

    Environmental and occupational exposure

    A thorough history of environmental exposures helps to identify specific allergictriggers. This should include investigation of risk factors for exposure to perennialallergens (eg, dust mites, mold, pets).[34, 35] Risk factors for dust mite exposureinclude carpeting, heat, humidity, and bedding that does not have dust miteproofcovers. Chronic dampness in the home is a risk factor for mold exposure. Ahistory of hobbies and recreational activities helps determine risk and a timepattern of pollen exposure.

    Ask about the environment of the workplace or school. This might includeexposure to ordinary perennial allergens (eg, mites, mold, pet dander) or uniqueoccupational allergens (eg, laboratory animals, animal products, grains andorganic materials, wood dust, latex, enzymes).

    Effects on quality of life

    An accurate assessment of the morbidity of allergic rhinitis cannot be obtainedwithout asking about the effects on the patient's quality of life. Specific validatedquestionnaires are available to help determine effects on quality of life.[3, 4]

    Determine the presence of symptoms such as fatigue, malaise, drowsiness

    (which may or may not be related to medication), and headache.

    Investigate sleep quality and ability to function at work.

    Physical

    The physical examination should focus on the nose, but examination of facialfeatures, eyes, ears, oropharynx, neck, lungs, and skin is also important. Look forphysical findings that may be consistent with a systemic disease that isassociated with rhinitis.

    General facial features

    "Allergic shiners" are dark circles around the eyes and are related to vasodilationor nasal congestion.[2, 36]

    "Nasal crease" is a horizontal crease across the lower half of the bridge of thenose that is caused by repeated upward rubbing of the tip of the nose by thepalm of the hand (ie, the "allergic salute").[2, 36]

    Nose

    The nasal examination is best accomplished with a nasal speculum or anotoscope with nasal adapter. In the specialist's office, a rigid or flexiblerhinolaryngoscope may be used.

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    The mucosa of the nasal turbinates may be swollen (boggy) and have a pale,bluish-gray color. Some patients may have predominant erythema of the mucosa,

    which can also be observed with rhinitis medicamentosa, infection, or vasomotorrhinitis. While pale, boggy, blue-gray mucosa is typical for allergic rhinitis,mucosal examination findings cannot definitively distinguish between allergic andnonallergic causes of rhinitis.

    Assess the character and quantity of nasal mucus. Thin and watery secretionsare frequently associated with allergic rhinitis, while thick and purulent secretionsare usually associated with sinusitis; however, thicker, purulent, colored mucuscan also occur with allergic rhinitis.

    Examine the nasal septum to look for any deviation or septal perforation, whichmay be present due to chronic rhinitis, granulomatous disease, cocaine abuse,

    prior surgery, topical decongestant abuse, or, rarely, topical steroid overuse.Examine the nasal cavity for other masses such as polyps or tumors. Polyps arefirm gray masses that are often attached by a stalk, which may not be visible.After spraying a topical decongestant, polyps do not shrink, while the surroundingnasal mucosa does shrink.

    Ears, eyes, and oropharynx

    Perform otoscopy to look for tympanic membrane retraction, air-fluid levels, orbubbles. Performing pneumatic otoscopy can be considered to look for abnormaltympanic membrane mobility. These findings can be associated with allergicrhinitis, particularly if eustachian tube dysfunction or secondary otitis media is

    present.

    Ocular examination may reveal findings of injection and swelling of the palpebralconjunctivae, with excess tear production. Dennie-Morgan lines (prominentcreases below the inferior eyelid) are associated with allergic rhinitis.[37]

    The term "cobblestoning" is used to describe streaks of lymphoid tissue on theposterior pharynx, which is commonly observed with allergic rhinitis. Tonsillarhypertrophy can also be observed. Malocclusion (overbite) and a high-archedpalate can be observed in patients who breathe from their mouths excessively.[38]

    Neck

    Look for evidence of lymphadenopathy or thyroid disease.

    Lungs

    Look for the characteristic findings of asthma.

    Skin

    Evaluate for possible atopic dermatitis.

    Other

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    Look for any evidence of systemic diseases that may cause rhinitis (eg,sarcoidosis, hypothyroidism, immunodeficiency, ciliary dyskinesia syndrome,

    other connective tissue diseases).

    Causes

    The causes of allergic rhinitis may differ depending on whether the symptoms areseasonal, perennial, or sporadic/episodic. Some patients are sensitive to multipleallergens and can have perennial allergic rhinitis with seasonal exacerbations.While food allergy can cause rhinitis, particularly in children, it is rarely a cause ofallergic rhinitis in the absence of gastrointestinal or skin symptoms.

    Seasonal allergic rhinitis is commonly caused by allergy to seasonal pollens andoutdoor molds.

    Pollens (tree, grass, and weed)

    Tree pollens, which vary by geographic location, are typically present in highcounts during the spring, although some species produce their pollens in the fall.Common tree families associated with allergic rhinitis include birch, oak, maple,cedar, olive, and elm.

    Grass pollens also vary by geographic location. Most of the common grassspecies are associated with allergic rhinitis, including Kentucky bluegrass,orchard, redtop, timothy, vernal, meadow fescue, Bermuda, and perennial rye. Anumber of these grasses are cross-reactive, meaning that they have similarantigenic structures (ie, proteins recognized by specific IgE in allergic

    sensitization). Consequently, a person who is allergic to one species is also likelyto be sensitive to a number of other species. The grass pollens are mostprominent from the late spring through the fall but can be present year-round inwarmer climates.

    Weed pollens also vary geographically. Many of the weeds, such as shortragweed, which is a common cause of allergic rhinitis in much of the UnitedStates, are most prominent in the late summer and fall. Other weed pollens arepresent year-round, particularly in warmer climates. Common weeds associatedwith allergic rhinitis include short ragweed, western ragweed, pigweed, sage,mugwort, yellow dock, sheep sorrel, English plantain, lamb's quarters, andRussian thistle.

    Outdoor molds

    Atmospheric conditions can affect the growth and dispersion of a number ofmolds; therefore, their airborne prevalence may vary depending on climate andseason.

    For example,Alternaria and Cladosporium are particularly prevalent in the dryand windy conditions of the Great Plains states, where they grow on grasses andgrains. Their dispersion often peaks on sunny afternoons. They are virtuallyabsent when snow is on the ground in winter, and they peak in the summermonths and early fall.

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    Aspergillus and Penicillium can be found both outdoors and indoors (particularlyin humid households), with variable growth depending on the season or climate.

    Their spores can also be dispersed in dry conditions.

    Perennial allergic rhinitis is typically caused by allergens within the home but canalso be caused by outdoor allergens that are present year-round.[39] In warmerclimates, grass pollens can be present throughout the year. In some climates,individuals may be symptomatic due to trees and grasses in the warmer monthsand molds and weeds in the winter.

    House dust mites

    In the United States, 2 major house dust mite species are associated with allergicrhinitis. These are Dermatophagoides farinae and Dermatophagoidespteronyssinus.[34]

    These mites feed on organic material in households, particularly the skin that isshed from humans and pets. They can be found in carpets, upholstered furniture,pillows, mattresses, comforters, and stuffed toys.

    While they thrive in warmer temperatures and high humidity, they can be foundyear-round in many households. On the other hand, dust mites are rare in aridclimates.

    Pets

    Allergy to indoor pets is a common cause of perennial allergic rhinitis.[34, 35]

    Cat and dog allergies are encountered most commonly in allergy practice,although allergy has been reported to occur with most of the furry animals andbirds that are kept as indoor pets.

    Cockroaches

    While cockroach allergy is most frequently considered a cause of asthma,particularly in the inner city, it can also cause perennial allergic rhinitis in infestedhouseholds.[40, 41]

    Rodents

    Rodent infestation may be associated with allergic sensitization.[42, 43, 44]

    Sporadic allergic rhinitis causes

    Sporadic allergic rhinitis, intermittent brief episodes of allergic rhinitis, is causedby intermittent exposure to an allergen. Often, this is due to pets or animals towhich a person is not usually exposed. Sporadic allergic rhinitis can also be dueto pollens, molds, or indoor allergens to which a person is not usually exposed.While allergy to specific foods can cause rhinitis, an individual affected by foodallergy also usually has some combination of gastrointestinal, skin, and lunginvolvement. In this situation, the history findings usually suggest an associationwith a particular food. Watery rhinorrhea occurring shortly after eating may bevasomotor (and not allergic) in nature, mediated via the vagus nerve. This often

    is called gustatory rhinitis.

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    Occupational allergic rhinitis

    Occupational allergic rhinitis, which is caused by exposure to allergens in theworkplace, can be sporadic, seasonal, or perennial. People who work nearanimals (eg, veterinarians, laboratory researchers, farm workers) might haveepisodic symptoms when exposed to certain animals, daily symptoms while atthe workplace, or even continual symptoms (which can persist in the eveningsand weekends with severe sensitivity due to persistent late-phase inflammation).Some workers who may have seasonal symptoms include farmers, agriculturalworkers (exposure to pollens, animals, mold spores, and grains), and otheroutdoor workers. Other significant occupational allergens that may cause allergicrhinitis include wood dust, latex (due to inhalation of powder from gloves), acidanhydrides, glues, and psyllium (eg, nursing home workers who administer it asmedication).

    Differential Diagnoses Sinusitis, Acute Sinusitis, Chronic

    Laboratory Studies

    Testing for reaction to specific allergens can be helpful to confirm the diagnosis ofallergic rhinitis and to determine specific allergic triggers. If specific allergictriggers are known, then appropriate avoidance measures can be recommended.It is essential to know which allergens a patient is sensitive to in order to performallergen immunotherapy (desensitization treatment). To an extent, allergy testingprovides knowledge of the degree of sensitivity to a particular allergen. The most

    commonly used methods of determining allergy to a particular substance areallergy skin testing (testing for immediate hypersensitivity reactions) and in vitrodiagnostic tests, such as the radioallergosorbent test (RAST), which indirectlymeasures the quantity of specific IgE to a particular antigen.

    Allergy skin tests (immediate hypersensitivity testing) are an in vivo method ofdetermining immediate (IgE-mediated) hypersensitivity to specific allergens.Sensitivity to virtually all of the allergens that cause allergic rhinitis (see Causes)can be determined with skin testing.

    By introducing an extract of a suspected allergen percutaneously, an immediate(early-phase) wheal-and-flare reaction can be produced. Percutaneous

    introduction can be accomplished by placing a drop of extract on the skin andscratching or pricking a needle through the epidermis under the drop. Dependingon the exact technique used, this testing is referred to as scratch, prick, orpuncture testing.

    The antigen in the extract binds to IgE on skin mast cells, leading to the early-phase (immediate-type) reaction, which results in the release of mediators suchas histamine (see Pathophysiology). This generally occurs within 15-20 minutes.The released histamine causes the wheal-and-flare reaction (A central wheal isproduced by infiltrating fluid, and surrounding erythema is produced due tovasodilation, with concomitant itching.). The size of the wheal-and-flare reactionroughly correlates with the degree of sensitivity to the allergen.

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    The extract can also be introduced intradermally (ie, injected into the dermis withan intradermal [TB] needle). With this technique, the extract is allowed to contact

    the underlying dermal tissues, including skin mast cells. Intradermal testing isapproximately 1000-fold more sensitive than percutaneous testing. This shouldbe performed with care by qualified specialists. The rate of false-positive resultsmay be high.

    In vitro allergy tests, ie, RAST, allow measurement of the amount of specific IgEto individual allergens in a sample of blood. The amount of specific IgE producedto a particular allergen approximately correlates with the allergic sensitivity to thatsubstance. These tests allow determination of specific IgE to a number ofdifferent allergens from one blood sample, but the sensitivity and specificity arenot always as good as accurate skin testing (depending on the laboratory andassay used for the RAST). As with skin testing, virtually all of the allergens that

    cause allergic rhinitis (see Causes) can be determined using the RAST, althoughtesting for some allergens is less well established compared to others.

    Testing every patient for sensitivity to every allergen known is not practical.Therefore, select a limited number of allergens for testing (this applies to bothskin testing and RAST). When selecting allergens, select from among theallergens that are present locally and are known to cause clinically significantallergic disease. A clinician who is specifically trained in allergy testing shouldselect allergens for testing.

    Total serum IgE

    This is a measurement of the total level of IgE in the blood (regardless of

    specificity). While patients with allergic rhinitis are more likely to have an elevatedtotal IgE level than the normal population, this test is neither sensitive nor specificfor allergic rhinitis. As many as 50% of patients with allergic rhinitis have normallevels of total IgE, while 20% of nonaffected individuals can have elevated totalIgE levels. Therefore, this test is generally not used alone to establish thediagnosis of allergic rhinitis, but the results can be helpful in some cases whencombined with other factors.

    Total blood eosinophil count

    As with the total serum IgE, an elevated eosinophil count supports the diagnosisof allergic rhinitis, but it is neither sensitive nor specific for the diagnosis. The

    results can sometimes be helpful when combined with other factors.

    Imaging Studies

    Radiography

    While radiographic studies are not needed to establish the diagnosis of allergicrhinitis, they can be helpful for evaluating possible structural abnormalities or tohelp detect complications or comorbid conditions, such as sinusitis or adenoidhypertrophy.

    A 3-view sinus series (Caldwell, Waters, and lateral views) can be helpful inevaluating for sinusitis of the maxillary, frontal, and sphenoid sinuses. The

    ethmoid sinuses are difficult to visualize clearly on x-ray films. Plain x-ray films

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    can be helpful for diagnosing acute sinusitis, but CT scanning of the sinuses ismore sensitive and specific. For chronic sinusitis, plain x-ray films are often

    inconclusive, and CT scan is much preferred.

    A lateral view of the neck can be helpful when evaluating for soft tissueabnormalities of the nasopharynx, such as adenoid hypertrophy.

    CT scanning

    Coronal CT scan images of the sinuses can be very helpful for evaluating acuteor chronic sinusitis. In particular, obstruction of the ostiomeatal complex (aconfluence of drainage channels from the sinuses) can be seen quite clearly. CTscanning may also help delineate polyps, turbinate swelling, septal abnormalities(eg, deviation), and bony abnormalities (eg, concha bullosa).

    MRI

    For evaluating sinusitis, MRI images are generally less helpful than CT scanimages, largely because the bony structures are not seen as clearly on MRIimages. However, soft tissues are visualized quite well, making MRI imageshelpful for diagnosing malignancies of the upper airway.

    Other Tests

    Nasal cytology: A nasal smear can sometimes be helpful for establishing thediagnosis of allergic rhinitis. A sample of secretions and cells is scraped from thesurface of the nasal mucosa using a special sampling probe. Secretions that areblown from the nose are not adequate. The presence of eosinophils is consistentwith allergic rhinitis but also can be observed with NARES. Results are neithersensitive nor specific for allergic rhinitis and should not be used exclusively forestablishing the diagnosis.

    Procedures

    Rhinoscopy: While not routinely indicated, upper airway endoscopy(rhinolaryngoscopy) can be performed if a complication or comorbid conditionmay be present. It can be helpful for evaluating structural abnormalities (eg,polyps, adenoid hypertrophy, septal deviation, masses, foreign bodies) andchronic sinusitis (by visualizing the areas of sinus drainage).

    Nasal provocation (allergen challenge) testing: This procedure is essentially aresearch tool and is rarely indicated in the routine evaluation of allergic rhinitis.

    The possible allergen is inhaled or otherwise inoculated into the nose. Thepatient can then be monitored for development of symptoms or production ofsecretions, or objective measurements of nasal congestion can be taken. Someconsider this test the criterion standard test for the diagnosis of allergicrhinitis.[45] However, it is not a practical test to perform routinely, and only anappropriately trained specialist should perform this test.

    Histologic Findings

    See Other Tests.

    Medical Care

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    The management of allergic rhinitis consists of 3 major categories of treatment,(1) environmental control measures and allergen avoidance, (2) pharmacological

    management, and (3) immunotherapy.

    Environmental control measures and allergen avoidance involve both theavoidance of known allergens (substances to which the patient has IgE-mediatedhypersensitivity) and avoidance of nonspecific, or irritant, triggers. Considerenvironmental control measures, when practical, in all cases of allergicrhinitis.[46]However, global environmental control without identification of specifictriggers is inappropriate.

    Pollens and outdoor molds

    Because of their widespread presence in the outdoor air, pollens can be difficultto avoid. Reduction of outdoor exposure during the season in which a particular

    type of pollen is present can be somewhat helpful. In general, tree pollens arepresent in the spring, grass pollens from the late spring through summer, andweed pollens from late summer through fall, but exceptions to these seasonalpatterns exist (see Causes).

    Pollen counts tend to be higher on dry, sunny, windy days. Outdoor exposure canbe limited during this time, but this may not be reliable because pollen counts canalso be influenced by a number of other factors. Keeping the windows and doorsof the house and car closed as much as possible during the pollen season (withair conditioning, if necessary, on recirculating mode) can be helpful. Taking ashower after outdoor exposure can be helpful by removing pollen that is stuck tothe hair and skin.

    Despite all of these measures, patients who are allergic to pollens usuallycontinue to be symptomatic during the pollen season and usually require someother form of management. As with pollens, avoidance of outdoor/seasonalmolds may be difficult.

    Indoor allergens

    Depending on the allergen, environmental control measures for indoor allergenscan be quite helpful. For dust mites, covering the mattress and pillows withimpermeable covers helps reduce exposure.[47] Bed linens should be washedevery 2 weeks in hot (at least 130F) water to kill any mites present.[48, 49]Thorough

    and efficient vacuum cleaning of carpets and rugs can help, but, ultimately,carpeting should be removed. The carpet can be treated with one of a number ofchemical agents that kill the mites or denature the protein, but the efficacy ofthese agents does not appear to be dramatic. Dust mites thrive when indoorhumidity is above 50%, so dehumidification, air conditioning, or both is helpful.[50]

    Indoor environmental control measures for mold allergy focus on reduction ofexcessive humidity and removal of standing water. The environmental controlmeasures for dust mites can also help reduce mold spores.

    For animal allergy, complete avoidance is the best option. For patients whocannot, or who do not want to, completely avoid an animal or pet, confinement of

    the animal to a noncarpeted room and keeping it entirely out of the bedroom can

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    be of some benefit.[51] Cat allergen levels in the home can be reduced with high-efficiency particulate air (HEPA) filters and by bathing the cat every week

    (although this may be impractical). Cockroach extermination may be helpful forcases of cockroach sensitivity.

    Occupational allergens

    As with indoor allergens, avoidance is the best measure. When this is notpossible, a mask or respirator might be needed.

    Nonspecific triggers

    Exposure to smoke, strong perfumes and scents, fumes, rapid changes intemperature, and outdoor pollution can be nonspecific triggers in patients withallergic rhinitis. Consider avoidance of these situations or triggers if they seem to

    aggravate symptoms.

    Pharmacotherapy

    See Medication.

    Immunotherapy (desensitization)

    A considerable body of clinical research has established the effectiveness ofhigh-dose allergy shots in reducing symptoms and medicationrequirements.[52]Success rates have been demonstrated to be as high as 80-90%for certain allergens. It is a long-term process; noticeable improvement is oftennot observed for 6-12 months, and, if helpful, therapy should be continued for 3-5

    years. Immunotherapy is not without risk because severe systemic allergicreactions can sometimes occur. For these reasons, carefully consider the risksand benefits of immunotherapy in each patient and weigh the risks and benefitsof immunotherapy against the risks and benefits of the other managementoptions.

    Sublingual immunotherapy (SLIT) is currently increasing in use, particularly inEurope. It is not yet approved in the United States but clinical trials are underway,with plans for application for FDA approval. Differences between SLIT andsubcutaneous immunotherapy (SCIT) need further study, including research ondifferences in efficacy, durability, and safety.

    SLIT can produce significant clinical improvement in elderly patients with allergicrhinitis caused by house dust mites (HDMs), according to a study by Bozek et al.The report looked at a group of patients aged 60-75 years with allergic rhinitis, aswell as allergies to Dermatophagoides pteronyssinus and D farinae.[53]

    In 47 patients who underwent 3 years of SLIT, the total nasal symptom score fellby 44%, while in the 48 patients in the placebo group, the score dropped by just6%. In addition, the total medication score for the SLIT patients fell by amaximum of 51%, while only an insignificant score decrease was seen in theplacebo group.[53]

    Whether SLIT will be effective for non-pollen allergens as well as pollens also

    needs additional study. A 2012 meta-analysis of existing studies of SLIT for grass

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    pollen reported that SCIT is more effective than SLIT in controlling symptoms andin reducing the use of allergy medications in patients with seasonal allergic

    rhinoconjuntivitis to grass pollen.[54]

    Indications: Immunotherapy may be considered more strongly with severedisease, poor response to other management options, and the presence ofcomorbid conditions or complications. Immunotherapy is often combined withpharmacotherapy and environmental control.

    Administration: Administer immunotherapy with allergens to which the patient isknown to be sensitive and that are present in the patient's environment (andcannot be easily avoided). The value of immunotherapy for pollens, dust mites,and cats is well established.[55, 56, 57, 58, 59] The value of immunotherapy for dogsand mold is less well established.[52, 55]

    Contraindication: A number of potential contraindications to immunotherapy

    exist and need to be considered. Immunotherapy should only be performed byindividuals who have been appropriately trained, who institute appropriateprecautions, and who are equipped for potential adverse events.

    Surgical Care

    Surgical care is not indicated for allergic rhinitis but may be indicated forcomorbid or complicating conditions, such as chronic sinusitis, severe septaldeviation (causing severe obstruction), nasal polyps, or other anatomicalabnormalities. The value of turbinectomy is not established.

    Consultations

    While the general practitioner can effectively treat most cases of straightforward

    allergic rhinitis, consider consultation with an allergist or immunologist for severedisease, poor response to pharmacotherapy, and the presence of comorbidconditions or complications. Consultation with other specialists also might beneeded for comorbid conditions or complications. Consult with an allergyspecialist when identification or clarification of specific allergic triggers is needed,when detailed counseling regarding environmental control measures is needed,when quality of life is significantly impaired, or when immunotherapy may be aconsideration.

    Medication Summary

    Most cases of allergic rhinitis respond to pharmacotherapy. Patients with

    intermittent symptoms are often treated adequately with oral antihistamines,decongestants, or both as needed. Regular use of an intranasal steroid spraymay be more appropriate for patients with chronic symptoms. Daily use of anantihistamine, decongestant, or both can be considered either instead of or inaddition to nasal steroids. The newer, second-generation (ie, nonsedating)antihistamines are usually preferable to avoid sedation and other adverse effectsassociated with the older, first-generation antihistamines. Ocular antihistaminedrops (for eye symptoms), intranasal antihistamine sprays, intranasal cromolyn,intranasal anticholinergic sprays, and short courses of oral corticosteroids(reserved for severe, acute episodes only) may also provide relief.

    Second-generation antihistamines

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    Class Summary

    Often referred to as the nonsedating antihistamines. They compete withhistamine for histamine receptor type 1 (H1) receptor sites in the blood vessels,GI tract, and respiratory tract, which, in turn, inhibits physiologic effects thathistamine normally induces at the H1 receptor sites. Some do not appear toproduce clinically significant sedation at usual doses, while others have a low rateof sedation.[60, 61, 62] Other adverse effects (eg, anticholinergic symptoms) aregenerally not observed.

    All are efficacious in controlling symptoms of allergic rhinitis (ie, sneezing,rhinorrhea, itching) but do not significantly improve nasal congestion. For thisreason, some second-generation antihistamines are available as combinationpreparations containing a decongestant. They are often preferred for first-linetherapy of allergic rhinitis, especially for seasonal or episodic symptoms, becauseof their excellent efficacy and safety profile. They can be used prn or daily.

    Topical azelastine and olopatadine are nasal sprays antihistamines thateffectively reduce sneezing, itching, and rhinorrhea but also effectively reducescongestion.[63, 64, 65] Used twice per day, especially when combined with a topicalnasal corticosteroid, azelastine is effective at managing both allergic andnonallergic rhinitis.

    The second-generation oral antihistamines currently available in the UnitedStates are cetirizine, levocetirizine, desloratadine, fexofenadine, and loratadine. Alimited number of studies comparing these agents suggest no major differencesin efficacy. Only cetirizine causes drowsiness more frequently than

    placebo.[62]Cetirizine, fexofenadine, and loratadine are also available indecongestant-containing preparations.

    View full drug information

    Cetirizine (Zyrtec)

    Competes with histamine for H1 receptors in GI tract, blood vessels, andrespiratory tract, reducing hypersensitivity reactions. Once-daily dosing isconvenient. Bedtime dosing may be useful if sedation is a problem.

    View full drug information

    Levocetirizine (Xyzal)

    Histamine1-receptor antagonist. Active enantiomer of cetirizine. Peak plasmalevels reached within 1 h and half-life is about 8 h. Available as a 5-mg breakable(scored) tab. Indicated for seasonal and perennial allergic rhinitis.

    View full drug information

    Fexofenadine (Allegra)

    Second-generation agent with a rate of sedation not significantly different fromthat of placebo. Competes with histamine for H1 receptors in GI tract, bloodvessels, and respiratory tract, reducing hypersensitivity reactions. Available in qdand bid preparations.

    View full drug information

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    Loratadine (Claritin)

    Selectively inhibits peripheral histamine H1 receptors. Tolerated well, with rate ofsedation not significantly different from placebo.

    Loratadine/pseudoephedrine (Claritin-D 24 Hour, Claritin-D 12 Hour)

    Selectively inhibits peripheral histamine H1 receptors. Tolerated well, with rate ofsedation not significantly different from placebo.

    Pseudoephedrine stimulates vasoconstriction by directly activating alpha-adrenergic receptors of the respiratory mucosa. Induces also bronchial relaxationand increases heart rate and contractility by stimulating beta-adrenergicreceptors.

    Tolerated well, with rate of sedation not significantly different from that of placebo.Some patients may notice anxiety or insomnia owing to pseudoephedrinecomponent.

    Fexofenadine/pseudoephedrine (Allegra-D)

    Fexofenadine is a nonsedating second-generation medication with fewer adverseeffects than first-generation medications. Competes with histamine for H1receptors on GI tract, blood vessels, and respiratory tract, reducinghypersensitivity reactions. Does not sedate.

    Pseudoephedrine stimulates vasoconstriction by directly activating alpha-adrenergic receptors of the respiratory mucosa. Induces also bronchial relaxationand increases heart rate and contractility by stimulating beta-adrenergicreceptors.

    View full drug information

    Desloratadine (Clarinex)

    Relieves nasal congestion and systemic effects of seasonal allergy. Long-actingtricyclic histamine antagonist selective for H1-receptor. Major metabolite ofloratadine, which after ingestion is extensively metabolized to active metabolite 3-hydroxydesloratadine.

    Cetirizine and pseudoephedrine (Zyrtec-D)

    Cetirizine selectively inhibits histamine H1 receptor sites in blood vessels, GI tract,and respiratory tract, which in turn inhibits physiologic effects that histaminenormally induces at H1 receptor sites. Once-daily dosing is convenient. Bedtimedosing may be useful if sedation is a problem.

    Pseudoephedrine stimulates vasoconstriction by directly activating alpha-adrenergic receptors of the respiratory mucosa. Induces also bronchial relaxationand increases heart rate and contractility by stimulating beta-adrenergicreceptors.

    Leukotriene receptor antagonists

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    Class Summary

    Alternative to oral antihistamine to treat allergic rhinitis. One of the leukotrienereceptor antagonists, montelukast (Singulair), has been approved in the UnitedStates for treatment of seasonal and perennial allergic rhinitis.[66, 67, 68] When usedas single agent, produces modest improvement in allergic rhinitis symptoms.[69]

    View full drug information

    Montelukast (Singulair)

    Selective leukotriene receptor antagonist that inhibits the cysteinyl leukotriene(CysLT 1) receptor. Selectively prevents action of leukotrienes released by mastcells and eosinophils. When used as a single agent, has been shown to result ina reduction of seasonal allergic rhinitis symptoms, similar in degree to that ofloratadine.

    First-generation antihistamines

    Class Summary

    The older, first-generation H1 antagonists (eg, diphenhydramine, hydroxyzine)are effective in reducing most symptoms of allergic rhinitis, but they produce anumber of adverse effects (eg, drowsiness, anticholinergic effects). They can beused prn, but adverse effects may limit their usefulness when taken on a dailybasis. Some patients tolerate the adverse effects with prolonged use, but theymay experience cognitive impairment, and driving skills may be affected.[70, 71, 72, 73,74]Administration at bedtime may help with drowsiness, but sedation andimpairment of cognition may continue until the next day.

    The second-generation antihistamines are nonsedating in most patients and arepreferred as first-line therapy. Few adverse effects are reported (cetirizine maycause drowsiness in as many as 10% of patients); therefore, many specialistsprefer the use of second-generation agents for allergic rhinitis. Caution patientstaking medications with sedative effects about driving and operating heavymachinery.[73, 74]

    View full drug information

    Chlorpheniramine (Chlor-Trimeton)

    First-generation agent, available OTC in the United States. One of the safest

    antihistamines to use during pregnancy. Competes with histamine on H1-receptorsites on effector cells in blood vessels and respiratory tract.

    View full drug information

    Diphenhydramine (Benadryl, Benylin)

    Common first-generation agent available OTC in the United States. Competeswith histamine on H1-receptor sites on effector cells in blood vessels andrespiratory tract. For symptomatic relief of symptoms caused by release ofhistamine in allergic reactions.

    View full drug information

    Hydroxyzine (Atarax, Vistaril, Vistazine)

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    Effective first-generation agent but frequently produces sedation. Considerablesedation may occur with higher doses. Antagonizes H1 receptors in periphery.

    May suppress histamine activity in subcortical region of CNS.

    Decongestants

    Class Summary

    Stimulate vasoconstriction by directly activating alpha-adrenergic receptors of therespiratory mucosa. Pseudoephedrine produces weak bronchial relaxation (unlikeepinephrine or ephedrine) and is not effective for treating asthma. Increasesheart rate and contractility by stimulating beta-adrenergic receptors. Used aloneor in combination with antihistamines to treat nasal congestion. Anxiety andinsomnia may occur. Expectorants may thin and loosen secretions, althoughexperimental evidence for their efficacy is limited. Numerous preparations are

    available containing combinations of various decongestants, expectorants, orantihistamines. Alternatively, a separate decongestant and antihistamine can beadministered to allow for individual dose titration of each drug.

    View full drug information

    Pseudoephedrine (Sudafed)

    Stimulates vasoconstriction by directly activating alpha-adrenergic receptors ofthe respiratory mucosa. Available OTC in the United States. Helpful for nasal andsinus congestion.

    Nasal corticosteroids

    Class Summary

    Nasal steroid sprays are highly efficacious in treating allergic rhinitis.[75, 76, 77, 78,79] They control the 4 major symptoms of rhinitis (ie, sneezing, itching, rhinorrhea,congestion). They are effective as monotherapy, although they do notsignificantly affect ocular symptoms. Studies have shown nasal steroids to bemore effective than monotherapy with nasal cromolyn or antihistamines.[76,77] Greater benefit may occur when nasal steroids are used with other classes ofmedication. They are safe to use and not associated with significant systemicadverse effects in adults (this may also be true for children, but the data are lessclear).

    Local adverse effects are limited to minor irritation or nasal bleeding, whichresolve with temporary discontinuation of the medication. Nasal septalperforations are rarely reported and are less common with the newercorticosteroids and delivery systems. Safety during pregnancy has not beenestablished; however, clinical experience suggests nasal corticosteroids(particularly beclomethasone, which has most experience in use) are notassociated with adverse fetal effects.

    The nasal steroids can be used prn, but seem to be maximally effective whenused on a daily basis as maintenance therapy. They may also be helpful forvasomotor rhinitis or mixed rhinitis (a combination of vasomotor and allergicrhinitis) and can help to control nasal polyps.

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    View full drug information

    Mometasone (Nasonex)

    Nasal spray; may decrease number and activity of inflammatory cells, resulting indecreased nasal inflammation.[80] Demonstrated no mineralocorticoid, androgenic,antiandrogenic, or estrogenic activity in preclinical trials. Decreases rhinovirus-induced up-regulation in respiratory epithelial cells and modulatepretranscriptional mechanisms. Reduces intraepithelial eosinophilia andinflammatory cell infiltration (eg, eosinophils, lymphocytes, monocytes,neutrophils, plasma cells).

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    Beclomethasone (Beconase AQ, QNASL)

    Intranasal steroid. Most reliable during pregnancy, as it has been in use for many

    years with no significant problems observed. May decrease number and activityof inflammatory cells, resulting in decreased nasal inflammation. QNASLavailable as intranasal dry powder.

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    Budesonide inhaled (Rhinocort Aqua)

    Newer topical steroid considered efficacious and safe for allergic rhinitis. Maydecrease number and activity of inflammatory cells, resulting in decreased nasalinflammation.

    View full drug information

    Fluticasone (Flonase)Newer topical steroid considered efficacious and safe for allergic rhinitis. Maydecrease number and activity of inflammatory cells, resulting in decreased nasalinflammation.

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    Ciclesonide (Omnaris)

    Corticosteroid nasal spray indicated for allergic rhinitis. Prodrug that isenzymatically hydrolyzed to pharmacologic active metabolite C21-desisobutyryl-ciclesonide following intranasal application. Corticosteroids have a wide range ofeffects 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 50mcg.

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    Fluticasone furoate (Veramyst)

    Intranasal corticosteroid. Indicated for seasonal and perennial allergic rhinitis.Relieves nasal symptoms associated with allergic rhinitis. Has also demonstratedimprovement in allergic eye symptoms. Contains 27.5 mcg/spray.

    View full drug information

    Triamcinolone (Nasacort AQ)

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    Injectable corticosteroid used to treat inflammatory dermatosis responsive tosteroids; decreases inflammation by suppressing migration of polymorphonuclear

    leukocytes and reversing capillary permeability.

    Intranasal antihistamines

    Class Summary

    Alternative to oral antihistamines to treat allergic rhinitis.

    View full drug information

    Azelastine (Astelin)

    Use prn or on a regular basis. Use alone or in combination with other medications.Unlike oral antihistamines, has some effect on nasal congestion. Helpful for

    vasomotor rhinitis. Some patients experience a bitter taste. Systemic absorptionmay occur, resulting in sedation (reported in approximately 11% of patients).

    View full drug information

    Olopatadine intranasal (Patanase)

    For relief of symptoms of seasonal allergic rhinitis. Before initial use, primeproduct by releasing 5 sprays or until fine mist appears. When product has notbeen used for more than 7 days, re-prime by releasing 2 sprays. Avoid sprayinginto eyes.

    Intranasal cromolyns

    Class SummaryProduce mast cell stabilization and antiallergic effects that inhibit degranulation ofmast cells.[81] Have no direct anti-inflammatory or antihistaminic effects. Effectivefor prophylaxis. May be used just before exposure to a known allergen (eg,animal, occupational). Begin treatment 1-2 wk before pollen season and continuedaily to prevent seasonal allergic rhinitis. Effect is modest compared with that ofintranasal corticosteroids. Excellent safety profile and are thought to be safe foruse in children and pregnancy.

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    Cromolyn sodium (Nasalcrom)

    Available OTC in the United States. Used daily for seasonal or perennial allergicrhinitis. Significant effect may not be observed for 4-7 d. For patients with isolatedand predictable periods of exposure (eg, animal allergy, occupational allergy),administer just before exposure. Generally less effective than nasalcorticosteroids. Protective effect lasts 4-8 h, frequent dosing is necessary.

    Intranasal anticholinergic agents

    Class Summary

    Used for reducing rhinorrhea in patients with allergic or vasomotor rhinitis. Nosignificant effect on other symptoms. Can be used alone or in conjunction withother medications. In the United States, ipratropium bromide (Atrovent NasalSpray) is available in a concentration of 0.03% (officially indicated for treatment of

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    allergic and nonallergic rhinitis) and 0.06% (officially indicated for the treatment ofrhinorrhea associated with common cold). The 0.03% strength is discussed.

    View full drug information

    Ipratropium (Atrovent Nasal Spray 0.03%)

    Chemically related to atropine. Has anti-secretory properties, and when appliedlocally, inhibits secretions from serous and seromucous glands lining the nasalmucosa. Poor absorption by nasal mucosa; therefore, not associated withadverse systemic effects. Local adverse effects (eg, dryness, epistaxis, irritation)may occur.

    Further Outpatient Care

    Immunotherapy (desensitization) is a long-term process; noticeable improvement

    is often not observed for 6-12 months, and, if helpful, therapy should becontinued for 3-5 years.

    Deterrence/Prevention

    Patients should avoid factors that may cause or exacerbate allergic rhinitis (seeMedical Care).

    Complications

    Possible complications include otitis media, eustachian tube dysfunction, acutesinusitis, and chronic sinusitis.[4]

    Patient Education

    Educate patients on environmental control measures, which involve both the

    avoidance of known allergens (substances to which the patient has IgE-mediatedhypersensitivity) and the avoidance of nonspecific, or irritant, triggers (seeMedical Care).

    For excellent patient education resources visit eMedicineHealth'sAllergiesCenter. Also, see eMedicineHealth's patient education articlesHay Fever,IndoorAllergens, andAllergy Shots.

    http://reference.medscape.com/drug/atrovent-atrovent-hfa-ipratropium-343416http://reference.medscape.com/drug/atrovent-atrovent-hfa-ipratropium-343416http://reference.medscape.com/drug/atrovent-atrovent-hfa-ipratropium-343416http://reference.medscape.com/drug/atrovent-atrovent-hfa-ipratropium-343416http://www.emedicinehealth.com/Collections/CO1661.asphttp://www.emedicinehealth.com/Collections/CO1661.asphttp://www.emedicinehealth.com/Collections/CO1661.asphttp://www.emedicinehealth.com/Collections/CO1661.asphttp://www.emedicinehealth.com/articles/8589-1.asphttp://www.emedicinehealth.com/articles/8589-1.asphttp://www.emedicinehealth.com/articles/8589-1.asphttp://www.emedicinehealth.com/articles/8633-1.asphttp://www.emedicinehealth.com/articles/8633-1.asphttp://www.emedicinehealth.com/articles/8633-1.asphttp://www.emedicinehealth.com/articles/8633-1.asphttp://www.emedicinehealth.com/articles/8423-1.asphttp://www.emedicinehealth.com/articles/8423-1.asphttp://www.emedicinehealth.com/articles/8423-1.asphttp://www.emedicinehealth.com/articles/8423-1.asphttp://www.emedicinehealth.com/articles/8633-1.asphttp://www.emedicinehealth.com/articles/8633-1.asphttp://www.emedicinehealth.com/articles/8589-1.asphttp://www.emedicinehealth.com/Collections/CO1661.asphttp://www.emedicinehealth.com/Collections/CO1661.asphttp://reference.medscape.com/drug/atrovent-atrovent-hfa-ipratropium-343416http://reference.medscape.com/drug/atrovent-atrovent-hfa-ipratropium-343416