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INTRODUCTION
Background
Rhinitis is defined as inflammation of the nasal membranes and is characterized by a symptom
complex that consists of any combination of the following: sneezing, nasal congestion, nasal itching,
and rhinorrhea. 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. While allergic rhinitis is not a life-threatening condition, complications can occur and the
condition can significantly impair quality of life, 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.
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.
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.
The mediators that are immediately released include histamine, tryptase, chymase, kinins, and
heparin. The mast cells quickly synthesize other mediators, including leukotrienes and prostaglandin
D2. 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. 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. 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.
Frequency
United States
Allergic rhinitis affects approximately 40 million people in the United States. Recent US figures
suggest a 20% cumulative prevalence rate.
International
Scandinavian studies have demonstrated a cumulative prevalence rate of 15% in men and 14%
in women. The prevalence of allergic rhinitis may vary within and among countries. 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. It is also associated
with otitis media, eustachian tube dysfunction, sinusitis, nasal polyps, allergic conjunctivitis, and
atopic dermatitis. Allergic rhinitis may also contribute to learning difficulties, sleep disorders, and
fatigue.
A number of 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 or atopic dermatitis. 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
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work and school performance, missed school or work days, and traffic accidents. The overall cost
(direct and indirect) of allergic rhinitis was recently estimated to be $5.3 billion per year.
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. The prevalence of allergic rhinitis has been reported to be as high
as 40% in children, subsequently decreasing with age. In the geriatric population, rhinitis is less
commonly allergic in nature.
CLINICAL
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.
Trigger factors
o 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.
o 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.
o 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
o 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.
o 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
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o Patients with allergic rhinitis may have other atopic conditions such as asthma or
atopic dermatitis. Of patients with allergic rhinitis, 20% also have symptoms of asthma.
Uncontrolled allergic rhinitis may cause worsening of asthma or even atopic dermatitis.
Explore this possibility when obtaining the patient history.
o 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. 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).
o 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
o Because allergic rhinitis has a significant genetic component, a positive family
history for atopy makes the diagnosis more likely.
o 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.
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
o "Allergic shiners" are dark circles around the eyes and are related to vasodilation or
nasal congestion.
o "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").
Nose
o 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.
o 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.
o 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.
o 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.
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o 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.
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.
o 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.
o 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. 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.
o House dust mites
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In the United States, 2 major house dust mite species are associated with
allergic rhinitis. These are Dermatophagoides farinae and Dermatophagoides
pteronyssinus.
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.
o Pets
Allergy to indoor pets is a common cause of perennial allergic rhinitis.
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.
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).
DIFFERENTIALS
Sinusitis, Acute
Sinusitis, Chronic
Other Problems to be Considered
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)
WORKUP
Lab Studies
Allergy testing: 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. The physician needs 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 radioallergosorbent test (RAST), which indirectly measures
the quantity of specific IgE to a particular antigen.
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o 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.
o In vitro allergy tests, ie, RAST, 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
RAST).
As with skin testing, virtually all of the allergens that cause allergic rhinitis
(see Causes) can be determined using the RAST, although testing for some allergens is
less well established compared to others.
o 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 RAST). 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.
o Sinus films: 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.
o Neck films: A lateral view of the neck can be helpful when evaluating for soft tissue
abnormalities of the nasopharynx, such as adenoid hypertrophy.
CT scanning: Coronal CT scan images of the sinuses can be very helpful for evaluating acute
or chronic sinusitis. In particular, obstruction of the osteomeatal 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).
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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.
However, it is not a practical test to perform routinely, and only an appropriately trained
specialist should perform this test.
Histologic Findings
See Other Tests.
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: These 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. However, global environmental control without
identification of specific triggers is inappropriate.
o 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.
o 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. Bed linens should be washed every 2 weeks
in hot (at least 130°F) water to kill any mites present. 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.
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.
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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. 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.
o 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.
MEDICATION
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. 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.
Drug Category: Second-generation antihistamines
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. Other adverse effects (eg, anticholinergic symptoms) are generally not observed.
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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 is a nasal spray antihistamine that effectively reduces sneezing, itching, and
rhinorrhea but also effectively reduces congestion. 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, 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. Cetirizine, fexofenadine, and
loratadine are also available in decongestant-containing preparations.
Drug Name Cetirizine (Zyrtec)
Competes with histamine for H1 receptors in GI tract, blood vessels, and
Description respiratory tract, reducing hypersensitivity reactions. Once-daily dosing is
convenient. Bedtime dosing may be useful if sedation is a problem.
Adult Dose 5-10 mg PO qd
<6 months: Not established
6-12 months: 2.5 mg PO qd
Pediatric Dose 12-24 months: 2.5 mg PO qd/bid
2-5 years: 2.5-5 mg PO qd
>6 years: 5-10 mg PO qd
Contraindications Documented hypersensitivity
Interactions Increases toxicity of CNS depressants; theophylline decreases clearance
Pregnancy B - Usually safe but benefits must outweigh the risks.
Caution in hepatic or renal dysfunction (adjust dose); 10 mg/d may cause
Precautions drowsiness in approximately 10% of patients; caution driving or operating
heavy machinery
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well, with rate of sedation not significantly different from placebo.
Desloratadine is a long-acting tricyclic histamine antagonist selective for H1
receptor. Major metabolite of loratadine, which is extensively metabolized to
active metabolite 3-hydroxydesloratadine after ingestion.
Loratadine: 10 mg PO qd
Adult Dose
Desloratadine: 5 mg PO qd
Loratadine
<2 years: Not established
2-5 years: 5 mg PO qd
Pediatric Dose >5 years: Administer as in adults
Desloratadine
<12 years: Not established
>12 years: Administer as in adults
Contraindications Documented hypersensitivity
Ketoconazole, erythromycin, procarbazine, cimetidine, and alcohol may
increase loratadine levels; limited data exist for desloratadine; erythromycin
Interactions and ketoconazole increase desloratadine and 3-hydroxydesloratadine plasma
concentrations, but no increase observed in clinically relevant adverse effects,
including QTc
Pregnancy B - Usually safe but benefits must outweigh the risks.
Desloratadine is pregnancy category C; initiate therapy at lower dose in liver
Precautions and renal impairment; caution in pregnancy and breastfeeding; may rarely
cause pharyngitis or dry mouth
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Contraindications Documented hypersensitivity
Not indicated to reverse acute asthma attacks; not for use as monotherapy in
Precautions management of exercise-induced bronchospasm; patients with known aspirin
sensitivity should continue avoidance of aspirin or NSAIDS while taking
montelukast
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May suppress histamine activity in subcortical region of CNS.
Adult Dose 10-25 mg PO q6-8h
Pediatric Dose 0.6 mg/kg/dose PO q6h
Contraindications Documented hypersensitivity
Interactions CNS depression may increase with alcohol or other CNS depressants
Pregnancy C - Safety for use during pregnancy has not been established.
May exacerbate porphyria (may not be safe for these patients); ECG
Precautions abnormalities (alterations in T waves) may occur; may cause drowsiness;
adjust dose in hepatic dysfunction
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
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or mixed rhinitis (a combination of vasomotor and allergic rhinitis) and can help to
control nasal polyps.
Beclomethasone (Beconase, Beconase AQ, Vancenase Pockethaler, Vancenase
Drug Name
AQ)
Older topical nasal steroid. Most reliable during pregnancy, as it has been in
use for many years with no significant problems observed. May decrease
Description
number and activity of inflammatory cells, resulting in decreased nasal
inflammation.
1-2 puffs/nostril (42 mcg/puff) qd/bid; titrate to lowest effective dose
Adult Dose Vancenase AQ Double Strength (84 mcg/puff): 1-2 puffs/nostril qd; titrate to
lowest effective dose
<6 years: Not established
Pediatric Dose
>6 years: Administer as in adults
Contraindications Documented hypersensitivity
Interactions None reported
Pregnancy C - Safety for use during pregnancy has not been established.
Monitor for growth suppression in children; caution in pregnancy and
Precautions
breastfeeding
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Adult Dose 2 puffs/nostril (137 mcg/puff) bid
Interactions Potentiates CNS depression with alcohol and other CNS depressants; caution
with concurrent oral antihistamines; cimetidine increases serum levels
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Avoid contact with eyes; may cause sedation; caution in pregnancy and
breastfeeding
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
Description 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.
Adult Dose 1 puff/nostril (5.3 mg/puff) q4-6h
Precautions Not for use in severe renal or hepatic impairment; symptoms may recur when
withdrawing drug
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Interactions Drugs with anticholinergic properties (eg, dronabinol) may increase toxicity
FOLLOW-UP
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 be continued for 3-5 years.
Deterrence/Prevention
Patients should avoid factors that may cause or exacerbate allergic rhinitis
Complications
Possible complications include otitis media, eustachian tube dysfunction, acute sinusitis, and
chronic sinusitis.
Patient Education
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).
MISCELLANEOUS
Medical/Legal Pitfalls
While no major medicolegal pitfalls are associated with allergic rhinitis, 2 issues deserve
mention.
o While patients with allergic rhinitis may experience sedation and fatigue secondary
to the disease process itself, sedation may occur due to medications. Most commonly,
sedation is related to antihistamines, particularly the first-generation agents. In many states,
driving while taking a first-generation, or sedating, antihistamine is illegal. Caution any
patient who is taking a medication that has potential sedative effects about driving and
operating heavy machinery.
o A potential area of medicolegal concern is the failure to diagnose a comorbid
condition or complication. Allergic rhinitis can occur in conjunction with other atopic diseases,
such as asthma. Because asthma can be severe and even fatal, failure to diagnose
concomitant asthma can lead to serious adverse events. Failure to diagnose potentially
serious medical conditions that should be considered in the differential diagnosis of allergic
rhinitis (eg, intranasal malignancy) might lead to serious consequences. Also, complications
of allergic rhinitis (eg, sinusitis) can be serious and must be recognized when present.
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