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Allergic Rhinitis
Updated: Dec 26, 2018
Author: Javed Sheikh, MD; Chief Editor: Michael A Kaliner, MD
Overview
Practice Essentials
Rhinitis, which occurs most commonly as allergic rhinitis, is an inflammation of the nasal membranes that is characterized
by sneezing, nasal congestion, nasal itching, and rhinorrhea, in any combination.[1] Although allergic rhinitis itself is not life-
threatening (unless accompanied by severe asthma or anaphylaxis), morbidity from the condition can be significant.
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
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Physical examination
Nasal features of allergic rhinitis can include the following:
Nasal crease: A horizontal crease across the lower half of the bridge of the nose; caused by repeated upward
rubbing of the tip of the nose by the palm of the hand
Thin, watery nasal secretions
Deviation or perforation of the nasal septum: May be associated with chronic rhinitis, although there can be other,
unrelated causes
Manifestations of allergic rhinitis affecting the ears, eyes, and oropharynx include the 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
to vasodilation or nasal congestion
Oropharynx: "Cobblestoning," that is, streaks of lymphoid tissue on the posterior pharynx; tonsillar hypertrophy; and
malocclusion (overbite) and a high-arched palate
See Clinical Presentation for 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 of determining immediate (IgE-mediated)
hypersensitivity to specific allergens
Fluorescence enzyme immunoassay (FEIA): Indirectly measures the quantity of immunoglobulin E (IgE) serving as
an antibody to a particular antigen
Total serum IgE: Neither sensitive nor specific for allergic rhinitis, but the results can 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 other factors
Imaging studies used in the diagnosis and evaluation of allergic rhinitis include the following:
Radiography: Can be helpful for evaluating possible structural abnormalities or to help detect complications or
comorbid conditions, such as sinusitis or adenoid hypertrophy
Computed tomography scanning: Can be very helpful for evaluating acute or chronic sinusitis
Magnetic resonance imaging: Also can be helpful for evaluating sinusitis
See Workup for more detail.
Management
The management of allergic rhinitis consists of the following 3 major treatment strategies:
Environmental control measures and allergen avoidance: These include keeping exposure to allergens such as
pollen, dust mites, and mold to a minimum
Pharmacologic management: Patients are often successfully treated with oral antihistamines, decongestants, or
both; regular use of an intranasal steroid spray may be more appropriate for patients with chronic symptoms
Immunotherapy: This treatment may be considered more strongly with severe disease, poor response to other
management options, and the presence of comorbid conditions or complications; immunotherapy is often combined
with pharmacotherapy and environmental control
See Treatment and Medication for more detail.
Background
Rhinitis is defined as inflammation of the nasal membranes[2] and is characterized by a symptom complex that consists of
any combination of the following: sneezing, nasal congestion, nasal itching, and rhinorrhea.[1] The eyes, ears, sinuses, and
throat can also be involved. Allergic rhinitis is the most common cause of rhinitis. It is an extremely common condition,
affecting approximately 20% of the population.
Although allergic rhinitis is not a life-threatening condition, complications can occur and the condition can significantly impair
quality of life,[3, 4] which leads to a number of indirect costs. The total direct and indirect cost of allergic rhinitis was recently
estimated to be $5.3 billion per year.[5] A 2011 analysis determined that patients with allergic rhinitis averaged 3 additional
office visits, 9 more prescriptions filled, and $1500 in incremental healthcare costs in 1 year than similar patients without
allergic rhinitis.[6]
See All About Allergies: Be Ready for Spring, a Critical Images slideshow, to help identify a variety of allergens and
symptoms.
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 of the
mucous membranes is characterized by a complex interaction of inflammatory mediators but ultimately is triggered by an
immunoglobulin E (IgE)–mediated response to an extrinsic protein.[7]
The tendency to develop allergic, or IgE-mediated, reactions to extrinsic allergens (proteins capable of causing an allergic
reaction) has a genetic component. In susceptible individuals, exposure to certain foreign proteins leads to allergic
sensitization, which is characterized by the production of specific IgE directed against these proteins. This specific IgE coats
the surface of mast cells, which are present in the nasal mucosa. When the specific protein (eg, a specific pollen grain) 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.[7, 8, 9]
The mediators that are immediately released include histamine, tryptase, chymase, kinins, and heparin.[8, 9] The mast cells
quickly synthesize other mediators, including leukotrienes and prostaglandin D2.[10, 11, 12] These mediators, via various
interactions, ultimately lead to the symptoms of rhinorrhea (ie, nasal congestion, sneezing, itching, redness, tearing,
swelling, ear pressure, postnasal drip). Mucous glands are stimulated, leading to increased secretions. Vascular
permeability is increased, leading to plasma exudation. Vasodilation occurs, leading to congestion and pressure. Sensory
nerves are stimulated, leading to sneezing and itching. All of these events can occur in minutes; hence, this reaction is
called the early, or immediate, phase of the reaction.
Over 4-8 hours, these mediators, through a complex interplay of events, lead to the recruitment of other inflammatory cells
to the mucosa, such as neutrophils, eosinophils, lymphocytes, and macrophages.[13] This results in continued inflammation,
termed the late-phase response. The symptoms of the late-phase response are similar to those of the early phase, but less
sneezing and itching and more congestion and mucus production tend to occur.[13] The late phase may persist for hours or
days.
Systemic effects, including fatigue, sleepiness, and malaise, can occur from the inflammatory response. These symptoms
often contribute to impaired quality of life.
Epidemiology
Frequency
United States
The prevalence of allergic rhinitis in the United States ranges from 3% to 19%, and 30 to 60 million people are affected each
year. The development of allergic rhinitis before 20 years of age occurs in 80% of cases.[14] In 2012, 9% of children
younger than 18 years and 7.5% of adults reported allergic rhinitis in the past 12 months.[15]
International
Throughout the world, the prevalence of allergic rhinitis has slightly escalated.[16] Currently, approximately 10 to 30% of
adults and 40% of children are affected.[14] The European Community Resporatory Health survey recorded a prevalence of
10 to 41% in adults with allergic rhinitis.[17] Scandinavian studies have demonstrated a cumulative prevalence rate of 15%
in men and 14% in women.[18] The prevalence of allergic rhinitis may vary within and among countries.[19, 20, 21, 22]
Highest prevalence of severe allergic rhinitis symptoms in children were observed in Africa and Latin America.[23] This may
be due to geographic differences in the types and potency of different allergens and the overall aeroallergen burden.
Mortality/Morbidity
While allergic rhinitis itself is not life-threatening (unless accompanied by severe asthma or anaphylaxis), morbidity from the
condition can be significant. Allergic rhinitis often coexists with other disorders, such as asthma, and may be associated with
asthma exacerbations.[24, 25, 26]
Allergic rhinitis is also associated with otitis media, eustachian tube dysfunction, sinusitis, nasal polyps, allergic
conjunctivitis, and atopic dermatitis.[2, 1, 27] It may also contribute to learning difficulties, sleep disorders, and fatigue.[28,
29, 30]
Numerous complications that can lead to increased morbidity or even mortality can occur secondary to allergic
rhinitis. Possible complications include otitis media, 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 suggests that uncontrolled allergic rhinitis can actually worsen the inflammation
associated with asthma[24, 25, 26] or atopic dermatitis.[27] This could lead to further morbidity 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
school or work days, and traffic accidents. Cost of allergic rhinitis have increased substantially in the United States.
In 1996, the overall cost (direct and indirect) of allergic rhinitis was estimated to be $5.3 billion per year.[5] In 2002,
total costs including indirect costs were estimated at $11.58 billion.[14]
Race
Allergic rhinitis occurs in persons of all races. Prevalence of allergic rhinitis seems to vary among different populations and
cultures, which may be due to genetic differences, geographic factors or environmental differences, or other population-
based factors.
Sex
In childhood, allergic rhinitis is more common in boys than in girls, but in adulthood, the prevalence is approximately equal
between men and women.
Age
Onset of allergic rhinitis is common in childhood, adolescence, and early adult years, with a mean age of onset 8-11 years,
but allergic rhinitis may occur in persons of any age. In 80% of cases, allergic rhinitis develops by age 20 years.[31] The
prevalence of allergic rhinitis has been reported to be as high as 40% in children, subsequently decreasing with age.[32, 33]
In the geriatric population, rhinitis is less commonly allergic in nature.
Presentation
History
Obtaining a detailed history is important in the evaluation of allergic rhinitis. Important elements include an evaluation of the
nature, duration, and time course of symptoms; possible triggers for symptoms; response to medications; comorbid
conditions; family history of allergic diseases; environmental exposures; occupational exposures; and effects on quality of
life. A thorough history may help 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, and malaise.
[1]
Symptoms and chronicity
Determine the age of onset of symptoms and whether symptoms have been present continuously since onset. While the
onset of allergic rhinitis can occur well into adulthood, most patients develop symptoms by age 20 years.[31]
Determine the time pattern of symptoms and whether symptoms occur at a consistent level throughout the year (ie,
perennial rhinitis), only occur in specific seasons (ie, seasonal rhinitis), or a combination of the two. Determine whether the
symptoms are present all day or only at specific times during the day. This information can help suggest the diagnosis and
determine possible triggers.
According to the Allergic Rhinits and its Impact on Asthma (ARIA) study, allergic rhinitis is classified by frequency and
severity of symptoms. A patient has intermittent allergic rhinitis if symptoms occur less than 4 days a week or 4 weeks of the
year. Persistent allergic rhinitis is labeled if symptoms occur more than 4 days per week and more than 4 weeks of the year.
Symptoms are classified as mild when quality of life is not affected. Symptoms are moderate to severe if patients have at
least one of the following: sleep disturbance, impairment of daily activities, sports, or leisure, impairment of school or work,
or troublesome symptoms.[34]
Determine which organ systems are affected and the specific symptoms. Some patients have exclusive involvement of the
nose, while others have involvement of multiple organs. Some patients primarily have sneezing, itching, tearing, and watery
rhinorrhea (the classic hayfever presentation), while others may only complain of congestion. Significant complaints of
congestion, particularly if 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 yard work, specific animals, or dust while cleaning the house.
Irritant triggers such as smoke, pollution, and strong smells can aggravate symptoms in a patient with allergic rhinitis. These
are also common triggers of vasomotor rhinitis. Many patients have both allergic rhinitis and vasomotor rhinitis.
Other patients may describe year-round symptoms that do not appear to be associated with specific triggers. This could be
consistent with nonallergic rhinitis, but perennial allergens, such as dust mite or animal exposure, should also be considered
in this situation. With chronic exposure and chronic symptoms, the patient may not be able to associate symptoms with a
particular trigger.
Response to treatment
Response to treatment with antihistamines supports the diagnosis of allergic rhinitis, although sneezing, itching, and
rhinorrhea associated with nonallergic rhinitis can also improve with antihistamines.[35]
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[24, 25] or atopic dermatitis.[27] Of patients
with allergic rhinitis, 20% also have symptoms of asthma. Uncontrolled allergic rhinitis may cause worsening of asthma[26]
or even atopic dermatitis.[27] Explore this possibility when obtaining the patient history.
Look for conditions that can occur as complications of allergic rhinitis. Sinusitis occurs quite frequently. Other possible
complications include otitis media, sleep disturbance or apnea, dental problems (overbite), and palatal abnormalities.[36]
The treatment plan might be different if one of these complications is present. Nasal polyps occur in association with allergic
rhinitis, although whether allergic rhinitis actually causes polyps remains unclear. Polyps may not respond to medical
treatment and might predispose a patient to sinusitis or sleep disturbance (due to congestion).
Allergic rhinitis is a risk factor for obstructive sleep apnea (OSA) syndrome.[37] Patients who have allergic rhinitis have
increased nighttime awakenings and daytime sleepiness.[38] Nasal airway resistance is increased in those with allergic
rhinitis and it is intesified in the supine position compared to the upright position.[39]
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.
A population-based, case-control study found a strong association between atopic diseases (AD) and attention-
deficit/hyperactivity disorder (ADHD) in children. The results of the study, which included 4692 children with ADHD and
18,768 randomly selected controls, showed that children with ADHD had a higher rate of allergic disease than controls,
particularly allergic rhinitis and allergic conjunctivitis.[40]
Family history
Because allergic rhinitis has a significant genetic component,[41] a positive family history for atopy makes the diagnosis
more likely.
In fact, a greater risk of allergic rhinitis exists if both parents are atopic than if one parent is atopic. However, the cause of
allergic rhinitis appears to be multifactorial, and a person with no family history of allergic rhinitis can develop allergic rhinitis.
Environmental and occupational exposure
A thorough history of environmental exposures helps to identify specific allergic triggers. This should include investigation of
risk factors for exposure to perennial allergens (eg, dust mites, mold, pets).[42, 43] Risk factors for dust mite exposure
include carpeting, heat, humidity, and bedding that does not have dust mite–proof covers. Chronic dampness in the home is
a risk factor for mold exposure. A history of hobbies and recreational activities helps determine risk and a time pattern of
pollen exposure.
Ask about the environment of the workplace or school. This might include exposure to ordinary perennial allergens (eg,
mites, mold, pet dander) or unique occupational allergens (eg, laboratory animals, animal products, grains and organic
materials, wood dust, latex, enzymes).
Effects on quality of life
An accurate assessment of the morbidity of allergic rhinitis cannot be obtained without asking about the effects on the
patient's quality of life. Specific validated questionnaires 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 facial features, eyes, ears, oropharynx, neck, lungs,
and skin is also important. Look for physical findings that may be consistent with a systemic disease that is associated with
rhinitis.
General facial features
"Allergic shiners" are dark circles around the eyes and are related to vasodilation or nasal congestion.[1, 44]
"Nasal crease" is a horizontal crease across the lower half of the bridge of the nose that is caused by repeated upward
rubbing of the tip of the nose by the palm of the hand (ie, the "allergic salute").[1, 44]
Nose
The nasal examination is best accomplished with a nasal speculum or an otoscope with nasal adapter. In the specialist's
office, a rigid or flexible rhinolaryngoscope may be used.
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 vasomotor
rhinitis. While pale, boggy, blue-gray mucosa is typical for allergic rhinitis, mucosal examination findings cannot definitively
distinguish between allergic and nonallergic causes of rhinitis.
Assess the character and quantity of nasal mucus. Thin and watery secretions are frequently associated with allergic
rhinitis, while thick and purulent secretions are usually associated with sinusitis; however, thicker, purulent, colored mucus
can also occur with allergic rhinitis.
Examine the nasal septum to look for any deviation or septal perforation, which may 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 are firm 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 surrounding nasal
mucosa does shrink.
Ears, eyes, and oropharynx
Perform otoscopy to look for tympanic membrane retraction, air-fluid levels, or bubbles. Performing pneumatic otoscopy can
be considered to look for abnormal tympanic membrane mobility. These findings can be associated with allergic rhinitis,
particularly if eustachian tube dysfunction or secondary otitis media is present.
Ocular examination may reveal findings of injection and swelling of the palpebral conjunctivae, with excess tear production.
Dennie-Morgan lines (prominent creases below the inferior eyelid) are associated with allergic rhinitis.[45]
The term "cobblestoning" is used to describe streaks of lymphoid tissue on the posterior pharynx, which is commonly
observed with allergic rhinitis. Tonsillar hypertrophy can also be observed. Malocclusion (overbite) and a high-arched palate
can be observed in patients who breathe from their mouths excessively.[46]
Neck
Look for evidence of lymphadenopathy or thyroid disease.
Lungs
Look for the characteristic findings of asthma.
Skin
Evaluate for possible atopic dermatitis.
Other
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 are seasonal, perennial, or sporadic/episodic.
Some patients are sensitive to multiple allergens and can have perennial allergic rhinitis with seasonal exacerbations. While
food allergy can cause rhinitis, particularly in children, it is rarely a cause of allergic rhinitis in the absence of gastrointestinal
or skin symptoms.
Seasonal allergic rhinitis is commonly caused by allergy to seasonal pollens and outdoor molds.
Pollens (tree, grass, and weed)
Tree pollens, which vary by geographic location, are typically present in high counts 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 grass species are associated with allergic rhinitis,
including Kentucky bluegrass, orchard, redtop, timothy, vernal, meadow fescue, Bermuda, and perennial rye. A number of
these grasses are cross-reactive, meaning that they have similar antigenic structures (ie, proteins recognized by specific IgE
in allergic sensitization). Consequently, a person who is allergic to one species is also likely to be sensitive to a number of
other species. The grass pollens are most prominent from the late spring through the fall but can be present year-round in
warmer climates.
Weed pollens also vary geographically. Many of the weeds, such as short ragweed, which is a common cause of allergic
rhinitis in much of the United States, are most prominent in the late summer and fall. Other weed pollens are present year-
round, particularly in warmer climates. Common weeds associated with allergic rhinitis include short ragweed, western
ragweed, pigweed, sage, mugwort, yellow dock, sheep sorrel, English plantain, lamb's quarters, and Russian thistle.
Outdoor molds
Atmospheric conditions can affect the growth and dispersion of a number of molds; therefore, their airborne prevalence may
vary depending on climate and season.
For example, Alternaria and Cladosporium are particularly prevalent in the dry and windy conditions of the Great Plains
states, where they grow on grasses and grains. Their dispersion often peaks on sunny afternoons. They are virtually absent
when snow is on the ground in winter, and they peak in the summer months and early fall.
Aspergillus and Penicillium can be found both outdoors and indoors (particularly in 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 can also be caused by outdoor allergens that
are present year-round.[47] In warmer climates, grass pollens can be present throughout the year. In some climates,
individuals may be symptomatic due to trees and grasses in the warmer months and molds and weeds in the winter.
House dust mites

In the United States, 2 major house dust mite species are associated with allergic rhinitis. These are Dermatophagoides
farinae and Dermatophagoides pteronyssinus.[42]
These mites feed on organic material in households, particularly the skin that is shed 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 found year-round in many households. On the
other hand, dust mites are rare in arid climates.
Pets
Allergy to indoor pets is a common cause of perennial allergic rhinitis.[42, 43]
Cat and dog allergies are encountered most commonly in allergy practice, although allergy has been reported to occur with
most of the furry animals and birds 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 infested households.[48, 49]
Rodents
Rodent infestation may be associated with allergic sensitization.[50, 51, 52]
Sporadic allergic rhinitis causes
Sporadic allergic rhinitis, intermittent brief episodes of allergic rhinitis, is caused by intermittent exposure to an allergen.
Often, this is due to pets or animals to which a person is not usually exposed. Sporadic allergic rhinitis can also be due to
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 food allergy also usually has some combination of gastrointestinal, skin, and lung
involvement. In this situation, the history findings usually suggest an association with a particular food. Watery rhinorrhea
occurring shortly after eating may be vasomotor (and not allergic) in nature, mediated via the vagus nerve. This often is
called gustatory rhinitis.
Occupational allergic rhinitis
Occupational allergic rhinitis, which is caused by exposure to allergens in the workplace, can be sporadic, seasonal, or
perennial. People who work near animals (eg, veterinarians, laboratory researchers, farm workers) might have episodic
symptoms when exposed to certain animals, daily symptoms while at the workplace, or even continual symptoms (which
can persist in the evenings and weekends with severe sensitivity due to persistent late-phase inflammation). Some workers
who may have seasonal symptoms include farmers, agricultural workers (exposure to pollens, animals, mold spores, and
grains), and other outdoor workers. Other significant occupational allergens that may cause allergic rhinitis include wood
dust, latex (due to inhalation of powder from gloves), acid anhydrides, glues, and psyllium (eg, nursing home workers who
administer it as medication).
DDx
Diagnostic Considerations
Vasomotor rhinitis or nonallergic rhinitis
Gustatory rhinitis (vagally mediated)
Rhinitis medicamentosa (eg, due to topical decongestants, antihypertensives, cocaine abuse)
Hormonal rhinitis (eg, related to pregnancy, hypothyroidism, oral contraceptive use)
Anatomic rhinitis (eg, deviated septum, choanal atresia, adenoid hypertrophy, foreign body, nasal tumor)
NARES
Immotile cilia syndrome (ciliary dyskinesis)
Cerebrospinal fluid leak
Nasal polyps
Granulomatous rhinitis (eg, Wegener granulomatosis, sarcoidosis)
Differential Diagnoses
Acute Sinusitis
Chronic Sinusitis
Workup
Workup
Laboratory Studies
Testing for reaction to specific allergens can be helpful to confirm the diagnosis of allergic rhinitis and to determine specific
allergic triggers. If specific allergic triggers are known, then appropriate avoidance measures can be recommended. It is
essential to know which allergens a patient is sensitive to in order to perform allergen immunotherapy (desensitization
treatment). To an extent, allergy testing provides knowledge of the degree of sensitivity to a particular allergen. The most
commonly used methods of determining allergy to a particular substance are allergy skin testing (testing for immediate
hypersensitivity reactions) and in vitro diagnostic tests, such as the fluorescence enzyme immunoassay (FEIA), for example
ImmunoCAP, which indirectly measures the quantity of specific IgE to a particular antigen.
Allergy skin tests (immediate hypersensitivity testing) are an in vivo method of determining 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 and scratching or
pricking a needle through the epidermis under the drop. Depending on the exact technique used, this testing is referred to
as scratch, prick, or puncture 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 such as histamine (see Pathophysiology). This generally occurs within 15-20 minutes.
The released histamine causes the wheal-and-flare reaction (A central wheal is produced by infiltrating fluid, and
surrounding erythema is produced due to vasodilation, with concomitant itching.). The size of the wheal-and-flare reaction
roughly correlates with the degree of sensitivity to the allergen.
The extract can also be introduced intradermally (ie, injected into the dermis with an intradermal [TB] needle). With this
technique, the extract is allowed to contact the underlying dermal tissues, including skin mast cells. Intradermal testing is
approximately 1000-fold more sensitive than percutaneous testing. This should be performed with care by qualified
specialists. The rate of false-positive results may be high.
In vitro allergy tests, ie, FEIA, allow measurement of the amount of specific IgE to individual allergens in a sample of blood.
The amount of specific IgE produced to a particular allergen approximately correlates with the allergic sensitivity to that
substance. These tests allow determination of specific IgE to a number of different allergens from one blood sample, but the
sensitivity and specificity are not always as good as accurate skin testing (depending on the laboratory and assay used for
the FEIA). As with skin testing, virtually all of the allergens that cause allergic rhinitis (see Causes) can be determined using
the in vitro specific IgE, although testing 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 both skin testing and in vitro specific IgE). When selecting allergens, select from among the
allergens that are present locally and are known to cause clinically significant allergic disease. A clinician who is specifically
trained in allergy testing should select 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 elevated total IgE level than the normal population, this test is neither sensitive nor specific for allergic
rhinitis. As many as 50% of patients with allergic rhinitis have normal levels of total IgE, while 20% of nonaffected individuals
can have elevated total IgE levels. Therefore, this test is generally not used alone to establish the diagnosis of allergic
rhinitis, but the results can be helpful in some cases when combined with other factors.
Total blood eosinophil count

As with the total serum IgE, an elevated eosinophil count supports the diagnosis of 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 allergic rhinitis, they can be helpful for evaluating
possible structural abnormalities or to help detect complications or comorbid conditions, such as sinusitis or adenoid
hypertrophy.
A 3-view sinus series (Caldwell, Waters, and lateral views) can be helpful in evaluating 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 can be helpful for
diagnosing acute sinusitis, but CT scanning of the sinuses is more 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 tissue abnormalities of the nasopharynx, such as adenoid
hypertrophy.
CT
Coronal CT scan images of the sinuses can be very helpful for evaluating acute or chronic sinusitis. In particular, obstruction
of the ostiomeatal complex (a confluence of drainage channels from the sinuses) can be seen quite clearly. CT scanning
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 scan images, largely because the bony structures
are not seen as clearly on MRI images. However, soft tissues are visualized quite well, making MRI images helpful for
diagnosing malignancies of the upper airway.
Other Tests
Nasal cytology
A nasal smear can sometimes be helpful for establishing the diagnosis of allergic rhinitis. A sample of secretions and cells is
scraped from the surface of the nasal mucosa using a special sampling probe. Secretions that are blown from the nose are
not adequate. The presence of eosinophils is consistent with allergic rhinitis but also can be observed with NARES. Results
are neither sensitive nor specific for allergic rhinitis and should not be used exclusively for establishing the diagnosis.
Procedures
Rhinoscopy
While not routinely indicated, upper airway endoscopy (rhinolaryngoscopy) can be performed if a complication or comorbid
condition may be present. It can be helpful for evaluating structural abnormalities (eg, polyps, adenoid hypertrophy, septal
deviation, masses, foreign bodies) and chronic sinusitis (by visualizing the areas of sinus drainage).
Nasal provocation (allergen challenge) testing
This procedure is essentially a research tool and is rarely indicated in the routine evaluation of allergic rhinitis. The possible
allergen is inhaled or otherwise inoculated into the nose. The patient can then be monitored for development of symptoms
or production of secretions, or objective measurements of nasal congestion can be taken. Some consider this test the
criterion standard test for the diagnosis of allergic rhinitis.[53] However, it is not a practical test to perform routinely, and only
an appropriately trained specialist should perform this test.
Treatment
Medical Care
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 the avoidance of known allergens (substances to
which the patient has IgE-mediated hypersensitivity) and avoidance of nonspecific, or irritant, triggers. Consider
environmental control measures, when practical, in all cases of allergic rhinitis.[54] However, global environmental control
without identification of specific triggers is inappropriate.
Pollens and outdoor molds
Because of their widespread presence in the outdoor air, pollens can be difficult to 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 are
present in the spring, grass pollens from the late spring through summer, and weed pollens from late summer through fall,
but exceptions to these seasonal patterns exist (see Causes).
Pollen counts tend to be higher on dry, sunny, windy days. Outdoor exposure can be limited during this time, but this may
not be reliable because pollen counts can also be influenced by a number of other factors. Keeping the windows and doors
of the house and car closed as much as possible during the pollen season (with air conditioning, if necessary, on
recirculating mode) can be helpful. Taking a shower after outdoor exposure can be helpful by removing pollen that is stuck
to the hair and skin.
Despite all of these measures, patients who are allergic to pollens usually continue to be symptomatic during the pollen
season and usually require some other form of management. As with pollens, avoidance of outdoor/seasonal molds may be
difficult.
Indoor allergens
Depending on the allergen, environmental control measures for indoor allergens can be quite helpful. For dust mites,
covering the mattress and pillows with impermeable covers helps reduce exposure.[55] Bed linens should be washed every
2 weeks in hot (at least 130°F) water to kill any mites present.[56, 57] 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 of
chemical agents that kill the mites or denature the protein, but the efficacy of these agents does not appear to be dramatic.
Dust mites thrive when indoor humidity is above 50%, so dehumidification, air conditioning, or both is helpful.[58]
Indoor environmental control measures for mold allergy focus on reduction of excessive humidity and removal of standing
water. The environmental control measures for dust mites can also help reduce mold spores.
For animal allergy, complete avoidance is the best option. For patients who cannot, 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 be of
some benefit.[59] 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 for cases of
cockroach sensitivity.
Occupational allergens
As with indoor allergens, avoidance is the best measure. When this is not possible, a mask or respirator might be needed.
Nonspecific triggers
Exposure to smoke, strong perfumes and scents, fumes, rapid changes in temperature, and outdoor pollution can be
nonspecific triggers in patients with allergic rhinitis. Consider avoidance of these situations or triggers if they seem to
aggravate symptoms.
Pharmacotherapy
See Medication.
Immunotherapy (desensitization)
Injections
A considerable body of clinical research has established the effectiveness of high-dose allergy shots in reducing symptoms
and medication requirements.[60] Success rates have been demonstrated to be as high as 80-90% for certain allergens. It
is a long-term process; noticeable improvement is often not observed for 6-12 months, and, if helpful, therapy should be
continued for 3-5 years. Immunotherapy is not without risk because severe systemic allergic reactions can sometimes occur.
For these reasons, carefully consider the risks and benefits of immunotherapy in each patient and weigh the risks and
benefits of immunotherapy against the risks and benefits of the other management options.
Indications: Immunotherapy may be considered more strongly with severe disease, poor response to other
management options, and the presence of comorbid conditions or complications. Immunotherapy is often combined
with pharmacotherapy and environmental control.
Administration: Administer immunotherapy with allergens to which the patient is known to be sensitive and that are
present in the patient's environment (and cannot be easily avoided). The value of immunotherapy for pollens, dust
mites, and cats is well established.[61, 62, 63, 64, 65] The value of immunotherapy for dogs and mold is less well
established.[60, 61]
Contraindication: A number of potential contraindications to immunotherapy exist and need to be considered.

Immunotherapy should only be performed by individuals who have been appropriately trained, who institute
appropriate precautions, and who are equipped for potential adverse events.
Sublingual
Sublingual immunotherapy (SLIT) is currently increasing in use, particularly in Europe. Differences between SLIT and
subcutaneous immunotherapy (SCIT) need further study, including research on differences in efficacy, durability, and safety.
SLIT can produce significant clinical improvement in elderly patients with allergic rhinitis 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,
as well as allergies to Dermatophagoides pteronyssinus and D farinae.[66]
In 47 patients who underwent 3 years of SLIT, the total nasal symptom score fell by 44%, while in the 48 patients in the
placebo group, the score dropped by just 6%. In addition, the total medication score for the SLIT patients fell by a maximum
of 51%, while only an insignificant score decrease was seen in the placebo group.[66] In addition, the house dust mite
(HDM) SLIT decreases the risk of asthma exacerbation in adults with house dust mite allergy-related asthma.[67]
In April 2014, the 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).[68]
The Oralair SL tablet needs to be initiated 4 months prior to the season for the specific allergen and is approved for patients
5–65 years of age.
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.[69] 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.[70]
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. Ragwitek is approved for adults aged 18 years or older.[71, 72]
A sublingual (SL) house dust mite immunotherapy (Odactra) was approved by the FDA in 2017. It is a standardized allergen
extract indicated as daily SL immunotherapy for allergic rhinitis, with or without conjunctivitis, confirmed by in vitro testing for
IgE antibodies to Dermatophagoides farinae or Dermatophagoides pteronyssinus house dust mites, or skin testing to
licensed house dust mite allergen extracts.
The first dose must be given in a healthcare setting under the supervision of a physician with experience in diagnosis and
treatment of allergic diseases. Patient monitoring for signs or symptoms of a severe systemic or local allergic reaction is
required following administration. Life-threatening allergic reactions are described in a boxed warning within the prescribing
information. The boxed warning also includes the need to prescribe autoinjectable epinephrine for the patient to have while
using HDM immunotherapy.
Approval was based on a double-blind, multicenter trial (n = 1482) in adolescents and adults with HDM allergic rhinitis with
or without conjunctivitis (AR/C). Over a 52-week period, HDM immunotherapy improved rhinoconjunctivitis score and visual
analog scale-assessed AR/C symptoms (P < 0.001).[73]
SLIT immunotherapy may not be appropriate for everyone. Those affected by multiple allergens may not obtain relief of all
of their symptoms by taking immunotherapy for only a single or couple allergens. SLIT is more convenient than weekly
injections in those with with limited, specific allergies that match the SL product. Whether SLIT will be effective for non-
pollen allergens other than dust mites needs additional study. A 2012 meta-analysis of existing studies of SLIT for grass
pollen reported that SCIT is more effective than SLIT in controlling symptoms and in reducing the use of allergy medications
in patients with seasonal allergic rhinoconjunctivitis to grass pollen.[74]
Surgical Care
Surgical care may be indicated for comorbid or complicating conditions, such as chronic sinusitis, severe septal deviation
(causing severe obstruction), nasal polyps, or other anatomical abnormalities.
Turbinoplasty may be effective for persistent allergic rhinitis when refractory to intranasal steroids and antihistamines.[75]
Radiofrequency turbinoplasty has been shown to improve nasal congestion subjectively and objectively through
rhinomanometry more than intranasal steroids even after 12 months from surgery.[76] Intranasal steroids in conjunction with
turbinoplasty shows greater efficacy in controlling allergic rhinitis compared with intranasal steroids alone.[77] However,
radiofrequency reduction of inferior turbinates seems to provide only temporary relief since patients have worsening
symptoms by 5 years post operatively.[78, 79]
Consultations
While the general practitioner can effectively treat most cases of straightforward allergic rhinitis, consider consultation with
an allergist or immunologist for severe disease, poor response to pharmacotherapy, and the presence of comorbid
conditions or complications. Consultation with other specialists also might be needed for comorbid conditions or
complications. Consult with an allergy specialist 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 a consideration.
Guidelines
Guidelines Summary
Joint Task Force on Practice Parameters (JTFPP)
In 2017, the Joint Task Force on Practice Parameters (JTFPP) released updated recommendations for the treatment of
seasonal allergic rhinitis (SAR) in adolescents and adults.[104]
Updated guidelines include the following:
In patients aged 12 years or older, nasal symptoms of SAR should be treated at least initially with an intranasal
corticosteroid (INCS) alone rather than an INCS–oral antihistamine combination.
In patients aged 15 years or older, moderate to severe SAR should be treated with an INCS over a leukotriene
receptor antagonist (LTRA).
Clinicians may recommend combination therapy with an INCS and an intranasal antihistamine (INAH) over either
agent alone.
American Academy of Otolaryngology-Head and Neck Surgery Foundation (AAO-HNS)
In 2015, the American Academy of Otolaryngology-Head and Neck Surgery Foundation (AAO-HNS) released guidelines for
treating patients ages 2 and up who suffer from allergic rhinitis.[80, 81]
Key recommendations include the following:
For patients with a stuffy nose, nasal passage discoloration, and/or red and watery eyes, doctors should forgo sinus
imaging process in favor of specific immunoglobulin E screening. Sinonasal imaging exposes patients to
unnecessary radiation.
Intranasal steroids and oral antihistamines are recommended as first lines of treatment. Oral leukotriene receptor
antagonists are not.
Sublingual or subcutaneous immunotherapy should be offered to patients who do not respond to pharmacologic
therapy.
Medication
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 spray may be more
appropriate for patients with chronic symptoms.[80] Daily use of an antihistamine, decongestant, or both can be considered
either instead of or in addition to nasal steroids. The newer, second-generation (ie, nonsedating) antihistamines are usually
preferable to avoid sedation and other adverse effects associated with the older, first-generation antihistamines. Ocular
antihistamine drops (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
Class Summary
Often referred to as the nonsedating antihistamines. They compete with histamine for histamine receptor type 1 (H1)
receptor sites in the blood vessels, GI tract, and respiratory tract, which, in turn, inhibits physiologic effects that histamine
normally induces at the H1 receptor sites. Some do not appear to produce clinically significant sedation at usual doses,
while others have a low rate of sedation.[82, 83, 84] Other adverse effects (eg, anticholinergic symptoms) are generally not
observed.
All are efficacious in controlling symptoms of allergic rhinitis (ie, sneezing, rhinorrhea, itching) but do not significantly
improve nasal congestion. For this reason, some second-generation antihistamines are available as combination
preparations containing a decongestant. They are often preferred for first-line therapy of allergic rhinitis, especially for
seasonal or episodic symptoms, because of their excellent efficacy and safety profile. They can be used prn or daily.
Topical azelastine and olopatadine are nasal sprays antihistamines that effectively reduce sneezing, itching, and rhinorrhea
but also effectively reduces congestion.[85, 86, 87] Used twice per day, especially when combined with a topical nasal
corticosteroid, azelastine is effective at managing both allergic and nonallergic rhinitis.
The second-generation oral antihistamines currently available in the United States are cetirizine, levocetirizine,
desloratadine, fexofenadine, and loratadine. A limited number of studies comparing these agents suggest no major
differences in efficacy. Only cetirizine causes drowsiness more frequently than placebo.[84] Cetirizine, fexofenadine, and
loratadine are also available in decongestant-containing preparations.
Cetirizine (Zyrtec)
Competes with histamine for H1 receptors in GI tract, blood vessels, and respiratory tract, reducing hypersensitivity
reactions. Once-daily dosing is convenient. Bedtime dosing may be useful if sedation is a problem.
Levocetirizine (Xyzal)
Histamine1-receptor antagonist. Active enantiomer of cetirizine. Peak plasma levels 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.
Fexofenadine (Allegra Allergy, Mucinex Allergy)

Second-generation agent with a rate of sedation not significantly different from that of placebo. Competes with histamine for
H1 receptors in GI tract, blood vessels, and respiratory tract, reducing hypersensitivity reactions. Available in qd and bid
preparations.
Loratadine (Claritin, Loradamed, QlearQuil 24 hr Relief, Triaminic

Allerchews, Alavert)
Selectively inhibits peripheral histamine H1 receptors. Tolerated well, with rate of sedation not significantly different from
placebo.
Pseudoephedrine/loratadine (Alavert Allergy & Sinus, Claritin D-12 Hour

Allergy & Congestion, Claritin-D 24 Hour Allergy & Congestion)
Selectively inhibits peripheral histamine H1 receptors. Tolerated well, with rate of sedation not significantly different from
placebo.
Pseudoephedrine stimulates vasoconstriction by directly activating alpha-adrenergic receptors of the respiratory mucosa.
Induces also bronchial relaxation and increases heart rate and contractility by stimulating beta-adrenergic receptors.
Tolerated well, with rate of sedation not significantly different from that of placebo. Some patients may notice anxiety or
insomnia owing to pseudoephedrine component.
Pseudoephedrine/fexofenadine (Allegra-D 12 Hour, Allegra-D 24 Hour)

Fexofenadine is a nonsedating second-generation medication with fewer adverse effects than first-generation medications.
Competes with histamine for H1 receptors on GI tract, blood vessels, and respiratory tract, reducing hypersensitivity
reactions. Does not sedate.
Desloratadine (Clarinex)
Relieves nasal congestion and systemic effects of seasonal allergy. Long-acting tricyclic histamine antagonist selective for
H1-receptor. Major metabolite of loratadine, which after ingestion is extensively metabolized to active metabolite 3-
hydroxydesloratadine.
Cetirizine/pseudoephedrine (Zyrtec D Allergy & Congestion)

Cetirizine selectively inhibits histamine H1 receptor sites in blood vessels, GI tract, and respiratory tract, which in turn
inhibits physiologic effects that histamine normally induces at H1 receptor sites. Once-daily dosing is convenient. Bedtime
dosing may be useful if sedation is a problem.
Leukotriene receptor antagonists
Class Summary
Alternative to oral antihistamine to treat allergic rhinitis. One of the leukotriene receptor antagonists, montelukast (Singulair),
has been approved in the United States for treatment of seasonal and perennial allergic rhinitis.[88, 89, 90] When used as
single agent, produces modest improvement in allergic rhinitis symptoms.[91]
Montelukast (Singulair)
Selective leukotriene receptor antagonist that inhibits the cysteinyl leukotriene (CysLT 1) receptor. Selectively prevents
action of leukotrienes released by mast cells and eosinophils. When used as a single agent, has been shown to result in a
reduction of seasonal allergic rhinitis symptoms, similar in degree to that of loratadine.
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 a number of adverse effects (eg, drowsiness, anticholinergic effects). They can be used
prn, but adverse effects may limit their usefulness when taken on a daily basis. Some patients tolerate the adverse effects
with prolonged use, but they may experience cognitive impairment, and driving skills may be affected.[92, 93, 94, 95, 96]
Administration at bedtime may help with drowsiness, but sedation and impairment of cognition may continue until the next
day.
The second-generation antihistamines are nonsedating in most patients and are preferred as first-line therapy. Few adverse
effects are reported (cetirizine may cause drowsiness in as many as 10% of patients); therefore, many specialists prefer the
use of second-generation agents for allergic rhinitis. Caution patients taking medications with sedative effects about driving
and operating heavy machinery.[95, 96]
Chlorpheniramine (Chlor-Trimeton, Aller-Chlor, Allergy Relief, Allergy-Time,

Ed-ChlorPed, Pharbechlor)
First-generation agent, available OTC in the United States. Competes with histamine on H1-receptor sites on effector cells
in blood vessels and respiratory tract.
Diphenhydramine (Benadryl, Aler-Dryl, Allergy Relief, Banophen, Diphen,

Genahist, Ormir)
Common first-generation agent available OTC in the United States. Competes with histamine on H1-receptor sites on
effector cells in blood vessels and respiratory tract. For symptomatic relief of symptoms caused by release of histamine in
allergic reactions.
Hydroxyzine (Vistaril)
Effective first-generation agent but frequently produces sedation. Considerable sedation 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 the respiratory mucosa. Pseudoephedrine
produces weak bronchial relaxation (unlike epinephrine or ephedrine) and is not effective for treating asthma. Increases
heart rate and contractility by stimulating beta-adrenergic receptors, and increases blood pressure by stimulating alpha
adrenergic receptors. Used alone or in combination with antihistamines to treat nasal congestion. Anxiety and insomnia may
occur. Expectorants may thin and loosen secretions, although experimental evidence for their efficacy is limited. Numerous
preparations are available containing combinations of various decongestants, expectorants, or antihistamines. Alternatively,
a separate decongestant and antihistamine can be administered to allow for individual dose titration of each drug.
Pseudoephedrine (Sudafed, Genaphed, Psudatabs, SudoGest, Suphedrine,

Zephrex-D)
Stimulates vasoconstriction by directly activating alpha-adrenergic receptors of the respiratory mucosa. Available OTC in the
United States. Helpful for nasal and sinus congestion.
Nasal corticosteroids
Class Summary
The intranasal steroids are divided into three generations based on their bioavailability. First generation corticosteroids, such
as, beclomethasone, are more bioavailable and tend to produce more systemic adverse effects than newer intranasal
corticosteroids. The second- and third-generation categories are less bioavailable and have limited systemic adverse
effects.
Nasal steroid sprays are highly efficacious in treating allergic rhinitis.[97, 98, 99, 100, 101] They control the 4 major
symptoms of rhinitis (ie, sneezing, itching, rhinorrhea, congestion). They are effective as monotherapy, although they do not
significantly affect ocular symptoms. Studies have shown nasal steroids to be more effective than monotherapy with nasal
cromolyn or antihistamines.[98, 99] Greater benefit may occur when nasal steroids are used with other classes of
medication. They are safe to use and not associated with significant systemic adverse effects in adults (this may also be
true for children, but the data are less clear).
In October 2013, the FDA approved once-daily triamcinolone acetonide (Nasacort Allergy 24HR) nasal spray as an over-
the-counter treatment for nasal allergy symptoms in children aged 2 years or older, adolescents, and adults. It is the first
over-the-counter glucocorticoid approved for the treatment of nasal allergy symptoms.Flonase was approved by FDA to be
available over the counter on July 24, 2014, and Rhinocort was recently approved last year March 23, 2015.[102]
Local adverse effects of nasal steroid sprays are limited to minor irritation or nasal bleeding, which resolve with temporary
discontinuation of the medication. Nasal septal perforations are rarely reported and are less common with the newer
corticosteroids and delivery systems. Safety during pregnancy has not been established; however, clinical experience
suggests nasal corticosteroids (particularly beclomethasone, which has most experience in use) are not associated with
adverse fetal effects.
The nasal steroids can be used prn, but seem to be maximally effective when used on a daily basis as maintenance therapy.
They may also be helpful for vasomotor rhinitis or mixed rhinitis (a combination of vasomotor and allergic rhinitis) and can
help to control nasal polyps.
Beclomethasone, intranasal (Beconase AQ, QNASL)

Corticosteroid with potent anti-inflammatory properties. Elicits effects on various cells, including mast cells and eosinophils.
It also elicits effects on inflammatory mediators (eg, histamine, eicosanoids, leukotrienes, cytokines). Available in solution or
suspension forms and delivered as a metered-dose nasal sprays.
Budesonide, intranasal (Rhinocort Aqua, Rhinocort Allergy)

Corticosteroid considered efficacious and safe for allergic rhinitis. May decrease number and activity of inflammatory cells,
resulting in decreased nasal inflammation.
Fluticasone (Flonase Allergy Relief, GoodSense Nasoflow, Ticaspray,

Veramyst)
Intranasal corticosteroid. Indicated for seasonal and perennial allergic rhinitis. Relieves nasal symptoms associated with
allergic rhinitis. Has also demonstrated improvement in allergic eye symptoms. May decrease number and activity of
inflammatory cells, resulting in decreased nasal inflammation.
Ciclesonide (Omnaris, Zetonna)

Newer 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.
Triamcinolone (Nasacort Allergy 24 HR, Nasal Allergy 24 HR)

Intranasal corticosteroid efficacious and safe for allergic rhinitis. May decrease number and activity of inflammatory cells,
resulting in decreased nasal inflammation.
Mometasone, intranasal (Nasonex, Propel Mini)
Nasal spray; may decrease number and activity of inflammatory cells, resulting in decreased nasal inflammation.
Demonstrated no mineralocorticoid, androgenic, antiandrogenic, or estrogenic activity in preclinical trials. Decreases
rhinovirus-induced up-regulation in respiratory epithelial cells and modulate pretranscriptional mechanisms. Reduces
intraepithelial eosinophilia and inflammatory cell infiltration (eg, eosinophils, lymphocytes, monocytes, neutrophils, plasma
cells).
Nasal corticosteroids and antihistamine combinations
Class Summary
These drug combinations may improve compliance. The antihistamine component will inhibit the release of histamine, which
is responsible for causing the allergic response while the corticosteroid component will inhibit inflammatory reactions.
Azelastine/fluticasone intranasal (Dymista)

New formulation of combined intranasal steroids and intranasal antihistamines. More effective than using intranasal steroids
or intranasal azelastine alone. Can be used in adults and children who are at least 6 years old. Patients may experience an
unpleasant taste after use.
Antihistamines, Intranasal
Class Summary
Alternative to oral antihistamines to treat allergic rhinitis.
Azelastine (Astepro)
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 absorption may
occur, resulting in sedation (reported in approximately 11% of patients).
Olopatadine intranasal (Patanase)

For relief of symptoms of seasonal allergic rhinitis. Before initial use, prime product by releasing 5 sprays or until fine mist
appears. When product has not been used for more than 7 days, re-prime by releasing 2 sprays. Avoid spraying into eyes.
Mast Cell Stabilizers
Class Summary
Produce mast cell stabilization and antiallergic effects that inhibit degranulation of mast cells.[103] Have no direct anti-
inflammatory or antihistaminic effects. Effective for prophylaxis. May be used just before exposure to a known allergen (eg,
animal, occupational). Begin treatment 1-2 wk before pollen season and continue daily to prevent seasonal allergic rhinitis.
Effect is modest compared with that of intranasal corticosteroids. Excellent safety profile and are thought to be safe for use
in children and pregnancy.
Cromolyn sodium (Nasalcrom)

Available OTC in the United States. Used daily for seasonal or perennial allergic rhinitis. Significant effect may not be
observed for 4-7 d. For patients with isolated and predictable periods of exposure (eg, animal allergy, occupational allergy),
administer just before exposure. Generally less effective than nasal corticosteroids. 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. No significant effect on other symptoms. Can be
used alone or in conjunction with other medications. In the United States, ipratropium bromide (Atrovent Nasal Spray) is
available in a concentration of 0.03% (officially indicated for treatment of allergic and nonallergic rhinitis) and 0.06%
(officially indicated for the treatment of rhinorrhea associated with common cold). The 0.03% strength is discussed.
Ipratropium (Atrovent Nasal Spray)

Chemically related to atropine. Has anti-secretory properties, and when applied locally, inhibits secretions from serous and
seromucous glands lining the nasal mucosa. Poor absorption by nasal mucosa; therefore, not associated with adverse
systemic effects. Local adverse effects (eg, dryness, epistaxis, irritation) may occur.
Allergy Extracts
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 for patients aged 5-65 years. 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 precise mechanisms of action of allergen immunotherapy is not known. The SL tablet consists of standardized extract
with consistent biological potency. It is indicated for dust mite-induced allergic rhinitis with or without conjunctivitis, confirmed
by in vitro testing for IgE antibodies to Dermatophagoides farinae or Dermatophagoides pteronyssinus house dust mites, or
skin testing to licensed house dust mite allergen extracts, in people aged 18-65 years.
Follow-up
Further Outpatient Care

See the list below:
Immunotherapy (desensitization) is a long-term process; noticeable improvement is often not observed for 6-12
months, and, if helpful, therapy should be continued for 3-5 years.
Deterrence/Prevention
See the list below:
Patients should avoid factors that may cause or exacerbate allergic rhinitis (see Medical Care).
Complications
See the list below:
Possible complications include otitis media, eustachian tube dysfunction, acute sinusitis, and chronic sinusitis.[4]
Patient Education
See the list below:
Educate patients on environmental control measures, which involve both the avoidance of known allergens
(substances to which the patient has IgE-mediated hypersensitivity) and the avoidance of nonspecific, or irritant,
triggers (see Medical Care).
For excellent patient education resources visit eMedicineHealth's Allergies Center. Also, see eMedicineHealth's
patient education articles Hay Fever, Indoor Allergens, and Allergy Shots.
Questions & Answers

Overview
What is allergic rhinitis (hay fever)?
What are the signs and symptoms of allergic rhinitis (hay fever)?
What are the complications of allergic rhinitis (hay fever)?
What are the nasal symptoms of allergic rhinitis (hay fever)?
What are the ear, eye and throat symptoms of allergic rhinitis (hay fever)?
Which lab tests are used in the diagnosis of allergic rhinitis (hay fever)?
How are imaging studies used in the diagnosis and evaluation of allergic rhinitis (hay fever)?
What are the major treatment strategies for allergic rhinitis (hay fever)?
What is allergic rhinitis (hay fever)?
What is the economic burden of allergic rhinitis (hay fever)?
What is the pathophysiology of allergic rhinitis (hay fever)?
What is the role of immunoglobulin E (IgE) in the pathogenesis of allergic rhinitis (hay fever)?
Which mediators are immediately released in the pathogenesis of allergic rhinitis (hay fever)?
What are systemic effects of allergic rhinitis (hay fever)?
What is the prevalence of allergic rhinitis (hay fever) in the US?
What is the global prevalence of allergic rhinitis (hay fever)?
What is the mortality and morbidities of allergic rhinitis (hay fever)?
What are racial predilections of allergic rhinitis (hay fever)?
How does the prevalence of allergic rhinitis (hay fever) vary by sex?
How does the prevalence of allergic rhinitis (hay fever) vary by age?
Presentation
What is the focus of history for suspected allergic rhinitis (hay fever)?
What are symptoms of allergic rhinitis (hay fever)?
At what age is the onset of symptoms for allergic rhinitis (hay fever) most common?
What is the significance of a time pattern to symptoms of allergic rhinitis (hay fever)?
How is allergic rhinitis (hay fever) classified?
What is the significance of congestion in allergic rhinitis (hay fever)?
What are possible trigger factors for allergic rhinitis (hay fever)?
What are irritant triggers associated with allergic rhinitis (hay fever)?
Which perennial allergens may cause chronic allergic rhinitis (hay fever)?
What is indicated by response to treatments for allergic rhinitis (hay fever)?
Which atopic conditions are associated with allergic rhinitis (hay fever)?
What are complications of allergic rhinitis (hay fever)?
Why is the risk for developing obstructive sleep apnea (OSA) increased in patients with allergic rhinitis (hay fever)?
What is the role of concomitant medical conditions in the diagnosis and treatment allergic rhinitis (hay fever)?
Which conditions increase the risk for allergic rhinitis (hay fever) in children?
What is the role of family history in the diagnosis of allergic rhinitis (hay fever)?
Which environmental exposures should be the focus of history in suspected allergic rhinitis (hay fever)?
What is the effect of allergic rhinitis (hay fever) on quality of life?
What is the focus of the physical exam for suspected allergic rhinitis (hay fever)?
What are the facial features characteristic of allergic rhinitis (hay fever)?
How is the nasal exam of allergic rhinitis (hay fever) conducted?
Which nasal exam findings suggest allergic rhinitis (hay fever)?
What should be included in the nasal exam in patients with allergic rhinitis (hay fever)?
What is the role of otoscopy in the workup of suspected allergic rhinitis (hay fever)?
What are ocular exam findings characteristic of allergic rhinitis (hay fever)?
Which physical findings in the throat are characteristic of allergic rhinitis (hay fever)?
What is the focus of the neck exam in suspected allergic rhinitis (hay fever)?
What is the focus in the respiratory exam in suspected allergic rhinitis (hay fever)?
What is the focus of the dermatologic exam in suspected allergic rhinitis (hay fever)?
Which systemic diseases should be considered in the physical exam for suspected allergic rhinitis (hay fever)?
What are the causes of allergic rhinitis (hay fever)?
What is the cause of seasonal allergic rhinitis (hay fever)?
What are common tree pollens that cause allergic rhinitis (hay fever)?
What are common grass pollens that cause allergic rhinitis (hay fever)?
What are some common weed pollens that cause allergic rhinitis (hay fever)?
How do atmospheric conditions affect the dispersion of mold that cause allergic rhinitis (hay fever)?
What is the cause of perennial allergic rhinitis (hay fever)?
Which house dust mite species commonly cause allergic rhinitis (hay fever)?
Which pets are most likely to cause perennial allergic rhinitis (hay fever)?
Which insect is a common cause of perennial allergic rhinitis (hay fever)?
Which pest infestation can cause allergic rhinitis (hay fever)?
What causes sporadic allergic rhinitis (hay fever)?
What is occupational allergic rhinitis (hay fever)?
DDX
Which conditions should be included in the differential diagnoses for allergic rhinitis (hay fever)?
What are the differential diagnoses for Allergic Rhinitis?
Workup
What is the role of allergy testing in the diagnosis of allergic rhinitis (hay fever)?
How are allergy skin tests used to diagnose allergic rhinitis (hay fever)?
How is an allergy skin test performed in the diagnosis of allergic rhinitis (hay fever)?
How are in vitro allergy tests used to diagnose allergic rhinitis (hay fever)?
What is the basis for selecting allergens to test for in the diagnosis of allergic rhinitis (hay fever)?
What is the role of immunoglobulin E (IgE) measurement in the diagnosis of allergic rhinitis (hay fever)?
What is the role of blood eosinophil count in the diagnosis of allergic rhinitis (hay fever)?
What is the role of radiography in the diagnosis of allergic rhinitis (hay fever)?
What is the role of CT scanning in the diagnosis of allergic rhinitis (hay fever)?
What is the role of MRI in the diagnosis of allergic rhinitis (hay fever)?
What is the role of nasal cytology in the diagnosis of allergic rhinitis (hay fever)?
What is the role of upper airway endoscopy (rhinolaryngoscopy) in the diagnosis of allergic rhinitis (hay fever)?
What is the role of nasal provocation (allergen challenge) testing in the diagnosis of allergic rhinitis (hay fever)?
Treatment
What are the treatment options for allergic rhinitis (hay fever)?
How and when is environmental control and allergen avoidance used in the treatment of allergic rhinitis (hay fever)?
What are the environmental control measures for outdoor allergens that cause allergic rhinitis (hay fever)?
What are the environmental control measures for indoor allergens that cause allergic rhinitis (hay fever)?
What are the environmental control measures for indoor mold that cause allergic rhinitis (hay fever)?
What are the indoor environmental control measures for animals that cause allergic rhinitis (hay fever)?
What is the best environmental control measure for occupational allergic rhinitis (hay fever)?
What are possible nonspecific triggers for allergic rhinitis (hay fever)?
What is the role of pharmacotherapies in the treatment of allergic rhinitis (hay fever)?
What is the role of immunotherapy in the treatment of allergic rhinitis (hay fever)?
What is the role of sublingual immunotherapy (SLIT) in the treatment of allergic rhinitis (hay fever)?
Which sublingual (SL) tablet has been approved by the FDA for the treatment of allergic rhinitis (hay fever) caused by grass
pollens?
How should the Oralair SL tablet be administered for the treatment of allergic rhinitis (hay fever)?
What is the role of Grastek in the treatment of allergic rhinitis (hay fever)?
What is the role of Ragwitek in the treatment of allergic rhinitis (hay fever)?
What is the role of Odactra in the treatment of allergic rhinitis (hay fever)?
How is Odactra administered for the treatment of allergic rhinitis (hay fever)?
What is the efficacy of Odactra in the treatment of allergic rhinitis (hay fever)?
What are the limitations of sublingual immunotherapy (SLIT) in the treatment of allergic rhinitis (hay fever)?
When is surgical care for allergic rhinitis (hay fever) indicated?
What is the role of turbinoplasty in the treatment of allergic rhinitis (hay fever)?
When should specialist consultation be considered for the treatment of allergic rhinitis (hay fever)?
Guidelines
What are the Joint Task Force on Practice Parameters (JTFPP) treatment guidelines for seasonal allergic rhinitis (SAR) in
adolescents and adults?
What key recommendations are included in the AAOH-NSF treatment guidelines for allergic rhinitis (hay fever)?
Medications
Which medications are used in the treatment of allergic rhinitis (hay fever)?
Which medications in the drug class Second-generation antihistamines are used in the treatment of Allergic Rhinitis?
Which medications in the drug class Leukotriene receptor antagonists are used in the treatment of Allergic Rhinitis?
Which medications in the drug class First-generation antihistamines are used in the treatment of Allergic Rhinitis?
Which medications in the drug class Decongestants are used in the treatment of Allergic Rhinitis?
Which medications in the drug class Nasal corticosteroids are used in the treatment of Allergic Rhinitis?
Which medications in the drug class Nasal corticosteroids and antihistamine combinations are used in the treatment of
Allergic Rhinitis?
Which medications in the drug class Antihistamines, Intranasal are used in the treatment of Allergic Rhinitis?
Which medications in the drug class Mast Cell Stabilizers are used in the treatment of Allergic Rhinitis?
Which medications in the drug class Intranasal anticholinergic agents are used in the treatment of Allergic Rhinitis?
Which medications in the drug class Allergy Extracts are used in the treatment of Allergic Rhinitis?
Contributor Information and Disclosures
Author
Javed Sheikh, MD Assistant Professor of Medicine, Harvard Medical School; Clinical Director, Division of Allergy and
Inflammation, Clinical Director, Center for Eosinophilic Disorders, Beth Israel Deaconess Medical Center
Javed Sheikh, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology,
American College of Allergy, Asthma and Immunology
Disclosure: Received grant/research funds from Genentech for other.
Coauthor(s)
Tiffany Jean, MD Fellow, Department of Allergy and Immunology, Kaiser Permanente Los Angeles Medical Center
Tiffany Jean, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical
Association
Disclosure: Nothing to disclose.
Specialty Editor Board
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of
Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Stephen C Dreskin, MD, PhD Professor of Medicine, Departments of Internal Medicine, Director of Allergy, Asthma, and
Immunology Practice, University of Colorado Health Sciences Center
Stephen C Dreskin, MD, PhD is a member of the following medical societies: American Academy of Allergy Asthma and
Immunology, American Association for the Advancement of Science, American College of Allergy, Asthma and Immunology,
Clinical Immunology Society, Joint Council of Allergy, Asthma and Immunology, American Association of Immunologists
Disclosure: Received consulting fee from Genentech for consulting; Received grant support from NIH for research;
Received consulting fee from Clinical Immunization and Safety Assessment (CISA) Network (administered by Vanderbilt
University) for consulting; Received consulting fee from o Member, Medical Expert Panel, Division of Vaccine Injury
Compensation (DVIC), Department of Health and Human Services. for med legal reviews; Received consulting fee from o
Member, Medical Expert Panel, Vaccine Review, Pfize.
Chief Editor
Michael A Kaliner, MD Clinical Professor of Medicine, George Washington University School of Medicine; Medical Director,
Institute for Asthma and Allergy
Michael A Kaliner, MD is a member of the following medical societies: American Academy of Allergy Asthma and
Immunology, American Association of Immunologists, American College of Allergy, Asthma and Immunology, American
Society for Clinical Investigation, American Thoracic Society, Association of American Physicians
Additional Contributors
William F Schoenwetter, MD Consultant in Allergic Diseases, Brainerd Medical Center, Brainerd, Minnesota
William F Schoenwetter, MD is a member of the following medical societies: American Academy of Allergy Asthma and
Immunology, American College of Allergy, Asthma and Immunology, American College of Physicians, American Medical
Association, Joint Council of Allergy, Asthma and Immunology, Minnesota Medical Association
Umer Najib, MD Clinical Research Fellow, Department of Medicine, Division of Allergy and Inflammation, Beth Israel
Deaconess Medical Center
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12/2/2019 https://emedicine.medscape.

Signs and Symptoms

Signs and symptoms of allergic rhinitis include the following:

Itching: Nose, eyes, ears, palate

Complications of this allergic rhinitis include the following:

Acute or chronic sinusitis

Sleep disturbance or apnea

Dental problems (overbite): Caused by excessive breathing through the mouth

Eustachian tube dysfunction

Nasal features of allergic rhinitis can include the following:

Thin, watery nasal secretions

Ears: Retraction and abnormal flexibility of the tympanic membrane

See Clinical Presentation for more detail.

Magnetic resonance imaging: Also can be helpful for evaluating sinusitis

See Workup for more detail.

See Treatment and Medication for more detail.

Symptoms and chronicity

Environmental and occupational exposure

Effects on quality of life

Investigate sleep quality and ability to function at work.

General facial features

Ears, eyes, and oropharynx

Look for evidence of lymphadenopathy or thyroid disease.

Look for the characteristic findings of asthma.

Evaluate for possible atopic dermatitis.

Pollens (tree, grass, and weed)

House dust mites

Allergy to indoor pets is a common cause of perennial allergic rhinitis.[42, 43]

Rodent infestation may be associated with allergic sensitization.[50, 51, 52]

Sporadic allergic rhinitis causes

Occupational allergic rhinitis

Gustatory rhinitis (vagally mediated)

Rhinitis medicamentosa (eg, due to topical decongestants, antihypertensives, cocaine abuse)

Hormonal rhinitis (eg, related to pregnancy, hypothyroidism, oral contraceptive use)

Immotile cilia syndrome (ciliary dyskinesis)

Cerebrospinal fluid leak

Granulomatous rhinitis (eg, Wegener granulomatosis, sarcoidosis)

Total serum IgE

Total blood eosinophil count

Nasal provocation (allergen challenge) testing

Pollens and outdoor molds

Contraindication: A number of potential contraindications to immunotherapy exist and need to be considered.

Updated guidelines include the following:

American Academy of Otolaryngology-Head and Neck Surgery Foundation (AAO-HNS)

Key recommendations include the following:

Fexofenadine (Allegra Allergy, Mucinex Allergy)

Loratadine (Claritin, Loradamed, QlearQuil 24 hr Relief, Triaminic

Pseudoephedrine/loratadine (Alavert Allergy & Sinus, Claritin D-12 Hour

Pseudoephedrine/fexofenadine (Allegra-D 12 Hour, Allegra-D 24 Hour)

Cetirizine/pseudoephedrine (Zyrtec D Allergy & Congestion)

Leukotriene receptor antagonists

Chlorpheniramine (Chlor-Trimeton, Aller-Chlor, Allergy Relief, Allergy-Time,

Diphenhydramine (Benadryl, Aler-Dryl, Allergy Relief, Banophen, Diphen,

Pseudoephedrine (Sudafed, Genaphed, Psudatabs, SudoGest, Suphedrine,

Beclomethasone, intranasal (Beconase AQ, QNASL)

Budesonide, intranasal (Rhinocort Aqua, Rhinocort Allergy)

Fluticasone (Flonase Allergy Relief, GoodSense Nasoflow, Ticaspray,

Ciclesonide (Omnaris, Zetonna)

Triamcinolone (Nasacort Allergy 24 HR, Nasal Allergy 24 HR)

Mometasone, intranasal (Nasonex, Propel Mini)

Nasal corticosteroids and antihistamine combinations

Azelastine/fluticasone intranasal (Dymista)

Olopatadine intranasal (Patanase)