Allergic Rhinitis: Pathophysiology

7/13/2020 Allergic Rhinitis
Allergic Rhinitis
Jennifer Kendrick, BScPharm, ACPR, PharmD

Date of Revision: August 1, 2018
Peer Review Date: February 28, 2018
Pathophysiology
Allergic rhinitis affects 10–30% of the population, and the prevalence is increasing.[1][2][3] It is estimated
that more than 500 million people worldwide are affected.[3] The prevalence of allergic rhinitis is thought
to be highest in school-age children; 80% of people with allergic rhinitis are diagnosed before 20 years of
age.[1][4] Allergic rhinitis is associated with a genetic predisposition; children have a 30% chance of
developing allergic rhinitis if 1 parent is affected and a 50% chance if both are affected.[5][6]
Allergic rhinitis is characterized by inflammation of the nasal mucosa following inhalation of an allergen.
[1][4][6][7] The allergic reaction is mediated by antigen-antibody responses and takes place in 3 phases.
The 1st phase, sensitization, occurs on 1st contact with the allergen. Immunoglobulin E (IgE) is produced
and binds to receptors on the surface of mast cells and basophils. The 2nd and 3rd phases occur on re-
exposure to an allergen in a sensitized individual. The 2nd phase, immediate reaction, occurs within
minutes of re-exposure and lasts up to 30–90 minutes. In this phase, the allergen binds to allergen-
specific IgE and the mast cells release preformed mediators, histamine and tumor necrosis factor-alpha
(TNF-alpha), and newly generated mediators, leukotrienes LTC4, LTD4, LTE4, prostaglandin D2 and
kinins. The 3rd phase, late reaction, occurs 4–8 hours after exposure. It is characterized by migration of
inflammatory cells, eosinophils, monocytes, macrophages and basophils.
Allergic rhinitis was previously classified as seasonal or perennial; however, this classification was
determined to be inadequate for a number of reasons. For example, outdoor pollens and moulds may be
perennial in some regions and symptoms of perennial allergy may not be present year-round. The
Allergic Rhinitis and its Impact on Asthma (ARIA) guideline proposed the classifications of intermittent
allergic rhinitis (IAR) and persistent allergic rhinitis (PAR) in 2008.[3] IAR is defined as symptoms of
allergic rhinitis occurring <4 days/week or for <4 weeks at a time. PAR is defined as symptoms of allergic
rhinitis occurring ≥4 days/week and for ≥4 weeks at a time. Allergic rhinitis is further classified based on
severity. In mild allergic rhinitis, symptoms are present but not troublesome and there is no impairment in
daily activities, school or work and no sleep disturbance. In moderate/severe allergic rhinitis, 1 or more is
present: troublesome symptoms; impairment in daily activities, school or work; or sleep disturbance.[3][7]
The ARIA classification has been validated in both adults and children.
Rhinitis may also be nonallergic. Drugs associated with rhinitis are listed in Table 1. Conditions
associated with nonallergic rhinitis are listed in Table 2.
[6][8]
Table 1: Drugs Associated with Rhinitis
ACE inhibitors Gabapentin Psychotropics, e.g.,
ASA and other Hydralazine chlorpromazine, risperidone
NSAIDs Oral contraceptives Sympatholytics, e.g., clonidine,
Cocaine doxazosin, methyldopa,
Phosphodiesterase-5 phentolamine, prazosin
Diuretics, e.g., inhibitors, e.g.,
amiloride, sildenafil Topical decongestants
hydrochlorothiazide (prolonged use)
[3][4][6][7]
Table 2: Possible Nonallergic Causes of Acute and Chronic Rhinitis
Drug-induced (see Table 1)
Hormones
https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/allergic_rhinitis_minor 1/28
pregnancy, menstruation, hypothyroidism
Infection
bacterial, fungal, viral, other
Nonallergic rhinitis with eosinophilia syndrome (NARES)
Other
emotions, e.g., stress, sexual arousal
vasomotor rhinitis, e.g., exercise, cold air
anatomic abnormalities, e.g., nasal septal deviation, enlarged adenoids and tonsils,
nasal tumors, choanal atresia[a]
food (e.g., hot, spicy) and alcohol
temperature changes
strong odours
nasal polyps
atrophy
foreign body
[a]
A congenital defect where the posterior nares do not communicate with the nasopharynx.
Goals of Therapy
Prevent symptoms by avoiding exposure to allergen(s)
Alleviate signs and symptoms produced by the allergic response
Minimize adverse effects of treatment
Improve quality of life
Patient Assessment
The sensitization phase of allergic rhinitis is asymptomatic. Symptoms of the 2nd or immediate phase
include sneezing, nasal and palatal pruritus, congestion, and clear rhinorrhea.[9] Symptoms of the
delayed phase are similar but nasal congestion predominates.[4] Patients may also have itchy, red,
watery eyes (allergic conjunctivitis); itchy throat; ear fullness and popping; and a feeling of pressure over
the cheeks and forehead.[4] Facial signs of allergic rhinitis are illustrated in Figure 1. The allergic salute is
a sign more commonly seen in children, where the patient frequently wipes the nose with the palm of the
hand in an upward motion.
Figure 1: Facial Signs of Allergic Rhinitis
Morgan Lines or Dennie sign or folds are extra creases at the lower eyelids due to edema. Allergic shiners describe discoloured
infraorbital areas due to venous stasis resulting from nasal swelling. The transverse nasal crease is a crease seen at the
junction of the bulbous portion of the nose and the nosebridge and is caused by recurrent nose rubbing (allergic salute).
Conjunctival injection refers to conjunctival redness fading toward the edges.
Some patients present primarily with symptoms of sneezing and rhinorrhea, whereas others are mostly
bothered by nasal blockage and have little or no itching or sneezing.[6] Eye symptoms are more
commonly associated with outdoor allergens.[3][7]
Allergic rhinitis can have a significant impact on a patient's quality of life. Patients with allergic rhinitis
report lower overall sense of health than those without the condition. Up to half of patients report that
allergic rhinitis has at least a moderate effect on daily life. Patients may have headache, difficulty
concentrating, low mood, fatigue or sleep disturbance.[6][10] Malaise or fatigue may be presenting
complaints in children.[9] Complications of allergic rhinitis include sinusitis, otitis media, asthma and sleep
apnea. In children, there may be dental overbite and a high-arched palate due to chronic mouth
breathing.[3][6]
An assessment plan for patients suffering from allergic rhinitis is illustrated in Figure 2. During the
assessment, identify duration, frequency and severity of symptoms as well as precipitating factors and
allergens, occupational exposure, and response to current and previous therapy. When recommending
treatment, consider also the effectiveness and adverse effects of the treatment alternatives, patient
preference and cost.[11]
Consider the need for prescription therapy or referral for allergy testing if the patient has already tried
appropriate nonprescription therapy for 2 weeks without an adequate response, or if the allergen
responsible for symptoms cannot be readily identified.[6] Also refer patients for further assessment if they
have signs or symptoms that are unilateral or are not usually associated with allergic rhinitis (e.g., fever,
facial pain, loss of smell or taste, recurrent epistaxis, purulent nasal or ocular secretions, postnasal drip
with or without rhinorrhea) or symptoms suggesting complications such as asthma.[6]
Prevention
Prevention is the 1st step in the management of allergic rhinitis. Although consensus is that improvement
in symptoms should occur with allergen avoidance, little evidence supports individual measures.[3] While
some measures such as washing pets, impermeable covers for bedding, and air filtration have been
shown to reduce the allergen level, a corresponding reduction in allergic symptoms has not been shown.
[9] The benefits of environmental control may take weeks or months to fully manifest. Avoidance
measures for common allergens are presented below.[1][3][6][7]
Pollen
Keep windows and doors closed when at home or in the car.

If using air conditioning, keep the unit on recirculate or the indoor cycle, if the choice is
available.
Do not use window or attic fans.
Monitor weather reports on pollen counts, if available. Decrease outdoor exposure during
periods of high pollen counts. Pollen counts tend to be highest on sunny, windy days.
Do not dry clothing outdoors.
Shower or bathe and wash hair after outdoor activity to remove pollen from hair and skin and
prevent contamination of bedding.
Outdoor Moulds
Remain in a closed environment as much as possible.

If using air conditioning, keep the unit on the indoor cycle, if the choice is available; note,
however, that units can be heavily contaminated with mould.
Use of face masks for activities such as raking leaves or working with compost or dry soil may
have limited value because air seeps around the edges of the mask and the mask does not
protect the eyes.
Indoor Moulds
Use fungicide on sinks, shower stalls, nonrefrigerated vegetable storage areas and garbage
pails. A solution of equal parts household bleach and water effectively kills mould.
Avoid console humidifiers and cool mist vaporizers; if these must be used, keep them
scrupulously clean.
If the home is built over a crawl space, install a plastic vapor barrier over exposed soil and keep
foundation vents open.
If the basement is damp or tends to flood, avoid carpeting or furnishing the basement. Use a
dehumidifier at all times and empty the extracted water from the air frequently; remove any
standing water as soon as possible.
Remove houseplants, which are a common source of mould. Alternatively, keep soil surface dry
and clean of debris to reduce mould.
House Dust Mites
Avoid carpeting the bedroom and main living areas.

Plastic, leather or wood furniture is best.
Some acaricides (e.g., benzyl benzoate, tannic acid) appear to reduce the mite population if
used regularly. However, their clinical effect is not established and they are not routinely
recommended.[3]
If possible, clean while the allergic individual is not at home.
Mite-sensitive persons should avoid vacuuming or making beds. Those who must do their own
cleaning should wear a face mask during cleaning and for 10–15 minutes afterward.
Use a vacuum cleaner with an efficient double filtration system.
Keep indoor humidity between 40% and 45%.
Minimize use of humidifiers as excess humidity promotes mite growth.
Encase all mattresses, box springs and pillows in the allergic individual's bedroom in zippered,
allergen-proof casings.
Consider replacing old mattresses.
Wash bedding in hot (>55°C) water at least every 2 weeks. Cooler water temperatures will not
kill dust mites, nor will detergents.
Avoid stuffed toys that cannot be washed. Alternatively, put stuffed toys or pillows in a hot dryer
or in plastic bags and freeze every 2 weeks to kill dust mites.
Do not store items under the bed.
Use window shades instead of venetian blinds.
Evidence suggests the best strategy is a combination of the above interventions.[12]
Animal Allergens
Permanent removal of pets from the home is the best way to control animal allergens. This
should be followed by thorough cleaning of the house, including washing carpets. “Trial” removal
of pets is not helpful; it can take 20 weeks or longer for cat allergen levels to drop to levels
comparable to homes without cats.
If the family is unable to remove the animal from the home then:
remove carpets and replace with hard flooring
keep the animal away from the allergic individual's bedroom and other living areas where
the allergic individual spends time
a high-efficiency particulate air (HEPA) filter or electrostatic air purifier may be helpful
washing cats weekly and dogs once or twice weekly may help but evidence to support this
approach is lacking
eliminate litter boxes, if possible; otherwise, place them in an area unconnected to the air
supply for the rest of the house
Occupational Allergens
For individuals affected by occupational rhinitis, recommend minimizing or eliminating exposure.

Common causes of occupational rhinitis include animal or vegetable proteins (e.g., mouse, rat,
wheat, grains, latex), enzymes, pharmaceuticals (e.g., antibiotics) and chemicals (e.g., resins).
Nonpharmacologic Therapy
Intranasal saline spray and irrigation has been shown to reduce nasal symptoms and the need for
pharmacologic therapy in children and nonpregnant adults.[13] The effect of intranasal saline irrigation in
pregnant women is less clear.[14] Isotonic saline is preferred to hypertonic saline, as it improves
mucociliary clearance; however, the optimal dose, frequency and delivery have not been established.[13]
Tobacco smoke can aggravate symptoms and should be avoided by all patients with allergic rhinitis.[3]
Other irritants that should be avoided include insect sprays, air pollution, and fresh tar or paint.[3]
Pharmacologic Therapy
When avoidance of allergens is ineffective or impractical, consider pharmacologic options. If it is possible
to predict the onset of symptoms (e.g., intermittent exposure), prophylactic medication should be started
before exposure.
For comparative ingredients of nonprescription products, consult the Compendium of Products for Minor
Ailments—Cough, Cold and Allergy Products.
Table 3 summarizes the pharmacologic activity of different therapies for the treatment of allergic rhinitis.
[7][15]
Table 3: Comparative Symptom Relief of Allergic Rhinitis Therapies
Medication Rhinorrhea Congestion Sneezing Nasal Eye
Itch Symptoms[a]
Oral antihistamines + +/- + + +/-
Decongestants (oral - + - - -
and topical)
Intranasal ++ ++ ++ ++ +/-
corticosteroids
Leukotriene receptor + + +/- +/- +/-

antagonists
Intranasal ++ - - - -
anticholinergics
Intranasal ++ ++ ++ ++ +/-
antihistamines
[a] See Conjunctivitis.
Abbreviations: - = no effect; +/- = modest or variable effect; + = moderately effective; ++ = effective
Medications for treatment of allergic rhinitis are described in Table 5 and Table 6.
Several guidelines for the treatment of allergic rhinitis are available and each provides similar
treatment recommendations.[3][6][7][9][16][17] For mild intermittent allergic rhinitis, second-generation
antihistamines are the drugs of choice, although they produce only a modest improvement in nasal
congestion. First-generation antihistamines are no longer recommended first-line due to their adverse
effect profile.[6] For mild persistent as well as moderate to severe allergic rhinitis, regularly
administered intranasal corticosteroids are recommended as first-line therapy.[18]
Antihistamines
Introduced in the 1940s, antihistamines were the 1st medications used for the treatment of
allergic rhinitis. They act as competitive antagonists for the histamine-1 (H1) receptor found on the
surface of target cells in the nose, lung, conjunctiva and skin.[19] They also act as a reverse
agonist, meaning that they change the three-dimensional configuration of the receptor, decreasing
its affinity for histamine and down-regulating histamine-driven symptoms.[19] Antihistamines
decrease nasal itching, sneezing, rhinorrhea, conjunctival itching and lacrimation but generally do
not relieve nasal congestion. Desloratadine, fexofenadine and cetirizine have modest effects
on nasal congestion.[20] Antihistamines are first-line treatment in mild cases of allergic rhinitis.[3][6]
[9]
Antihistamines are divided into 2 major classes: first- and second-generation. All are similarly
effective; however, adverse effect profiles and pharmacology differ.[19][21][22][23][24][25]
First-generation antihistamines have a rapid onset but relatively short duration of action due to
their short half-life.[26][27] They are poorly selective for the H1 receptor and also exert effects on
cholinergic receptors. The anticholinergic effect manifests as dry mouth and nasal passages,
difficulty voiding urine, constipation and tachycardia. They are also highly lipophilic and therefore
cross the blood-brain barrier and interact with central H1 receptors. This results in CNS effects
such as sedation and psychomotor and cognitive impairment. In children, paradoxical excitation
may occur.[28] Performance impairment has been documented using various measures (e.g.,
reaction time, visual-motor coordination, arithmetical exercises and memory, learning, and driving
tests), although more recent data suggest that the magnitude of these effects has been
overstated.[29][30] CNS depression and impairment can be independent of any subjective
complaints by the patient.[31] First-generation antihistamines also impair learning and academic
performance in children.[31] Workers taking first-generation antihistamines have lower work
performance and are more likely to be involved in workplace accidents. Daytime performance
effects are noted even when the antihistamine is taken only at bedtime.[6][31] The first-generation
antihistamines should be used with caution in patients with narrow-angle glaucoma, stenosing
peptic ulcer, pyloroduodenal obstruction, symptomatic prostatic hypertrophy or bladder-neck
obstruction, cardiovascular disease, and chronic lung disease. First-generation antihistamines can
decrease rhinorrhea, but mucus secretion may be thickened and can be more bothersome for
some patients.[19]
Second-generation antihistamines are more selective for H1 receptors and less lipophilic.
Consequently, they do not have significant anticholinergic adverse effects and do not cross the
blood-brain barrier.[24] Use of cetirizine in standard doses is associated with more sedation
compared with placebo, but less than first-generation antihistamines.[6] Administration of standard
doses of bilastine, desloratadine, loratadine and rupatadine results in an incidence of sedation
equivalent to placebo; however, drowsiness has been reported at higher than recommended
doses, or rarely in susceptible individuals at recommended doses.[6][32][33] Fexofenadine
appears to be nonsedating, even at increased doses. Due to their improved adverse effect profile,
especially with regard to sedation and psychomotor performance, second-generation
antihistamines are the drug of choice compared with first-generation agents for the treatment of
allergic rhinitis.[6][18] Clinical trials comparing various second-generation antihistamines
demonstrate similar reduction of symptoms.[2][23][25][34] They are less effective than intranasal
corticosteroids for most symptoms of allergic rhinitis.[6] Two meta-analyses demonstrated
intranasal corticosteroids were more effective than antihistamines for relieving congestion and
sneezing; for ocular symptoms, no difference was found.[35][36]
The intranasal antihistamine levocabastine is effective for sneezing, nasal pruritus and
rhinorrhea. It has a rapid onset of action (<15 minutes), but must be used 2–4 times daily.[26] The
intranasal antihistamine azelastine (available only in combination with fluticasone in Canada) is
clinically similar to oral second-generation antihistamines for the relief of nasal symptoms.[36]
Antihistamines are more effective when taken before allergen exposure. The best results are
obtained with chronic dosing compared with intermittent dosing; therefore, patients should take
the antihistamine for as long as they are in contact with the allergen.[18] If one antihistamine is not
effective, switching to another antihistamine may be beneficial.[37]
Mast Cell Stabilizers
Sodium cromoglycate (also called cromolyn sodium), an intranasal mast cell stabilizer, modestly
reduces itching, sneezing and rhinorrhea but is not effective for nasal congestion.[3] Treatment
should begin before exposure to the allergen and continue for the entire allergen season.[26] If
treatment begins after allergen exposure, relief may be delayed up to 4 weeks. Sodium
cromoglycate is less effective than corticosteroids for allergic rhinitis and has not been adequately
compared with leukotriene receptor antagonists and antihistamines.[6][36] Sodium cromoglycate is
currently not available in Canada.
Decongestants
Decongestants are occasionally recommended as adjunctive therapy for patients with allergic
rhinitis who experience nasal congestion; however, the risk of systemic adverse effects should be
considered (see Table 5).[6] Decongestants are available in oral and topical formulations. Oral
decongestants generally have a weaker effect on nasal obstruction than the topical formulations.
[26] Oral pseudoephedrine in combination with an oral antihistamine may be more effective
than either medication alone for nasal congestion in allergic rhinitis.[38] Oral phenylephrine is no
more effective than placebo for nasal congestion in allergic rhinitis and should not be
recommended.[39][40] Most available agents do not cause blood pressure elevations in
normotensive persons unless the recommended dose is significantly exceeded.[41] Elevation of
blood pressure may occur at standard doses in hypertensive patients.[42]
Systemic absorption from topical formulations is low, resulting in mainly local adverse effects (see
Table 6). If used for the treatment of congestion with allergic rhinitis, intermittent use is
recommended.[6] Rhinitis medicamentosa (rebound vasodilation) can occur if topical
decongestants are used for more than 3–5 days.[43] In 1 study, 49% of patients reported using an
intranasal decongestant daily for at least 1 year, even though 80% reported having received
education about limiting the duration of use. Intranasal decongestant overuse was less common
in patients who were using intranasal corticosteroid or oral antihistamine.[44] Overuse can lead to
nasal congestion when the topical agent is stopped, and to permanent overgrowth of nasal tissue
with chronic overuse. This condition is more likely to occur with shorter-acting agents
(phenylephrine) than with longer-acting agents (oxymetazoline and xylometazoline). Many
solutions to this problem have been proposed, including slow tapering of the decongestant,
adding or switching to intranasal corticosteroids, or abrupt discontinuation of the topical
decongestant. Abrupt cessation is effective but may be uncomfortable for the patient, as nasal
congestion may persist for several days or weeks.[43]
Corticosteroids
Intranasal corticosteroids are more effective against the nasal symptoms of allergic rhinitis than
oral and intranasal antihistamines, nasal cromoglycate, and leukotriene receptor antagonists.[35]
[36] Intranasal corticosteroids are the drugs of choice for moderate to severe or persistent allergic
rhinitis, and for mild allergic rhinitis that does not respond to antihistamines.[3][6][9][16][17] Some
intranasal corticosteroids (mometasone and fluticasone furoate) have a modest benefit on
allergic conjunctivitis symptoms.[6][12][45][46][47] A meta-analysis suggests that intranasal
corticosteroids as a class are effective for ocular symptoms of allergic rhinitis; however, the
magnitude of effect has not been quantified.[48] Onset of action of intranasal corticosteroids is
within 6–8 hours of 1st dose, although maximum effect may take a few weeks. Short courses of
oral corticosteroids may be required for severe cases of allergic rhinitis that are unresponsive to
other treatment.[6] Patients may prefer intranasal corticosteroids in aerosol form compared with
spray form; therefore, switching to another intranasal corticosteroid formulation may be
recommended if patient tolerability is affecting therapy.[49] Regular use of intranasal steroids is
more effective than intermittent use.[18]
Leukotriene Receptor Antagonists (LTRA)
Montelukast is superior to placebo but less effective than intranasal corticosteroids for nasal
symptoms of allergic rhinitis.[36] A meta-analysis suggests that antihistamines may be more
effective than montelukast for daytime nasal symptoms and eye symptoms, but that montelukast
may be more effective for nighttime symptoms.[50] Montelukast is more effective than oral
antihistamines and comparable to intranasal corticosteroids for reduction of asthma symptoms
and use of rescue asthma medication.[36] As a result, montelukast may be a reasonable option for
allergic rhinitis coexisting with asthma.[6][7][9] Otherwise, montelukast is not recommended as first-
line therapy for allergic rhinitis.[9]
Zafirlukast is no longer available in Canada.
Immunotherapy
According to clinical practice guidelines, allergen immunotherapy should be considered for

patients who continue to have moderate to severe symptoms despite treatment or those who
require systemic corticosteroids.[2][9] Immunotherapy may be indicated when the exposure to
allergens is significant and unavoidable (e.g., grass pollen), and when the symptom complex is
severe enough to warrant the time, expense and small risk of anaphylaxis.[6] Allergen
immunotherapy is the only treatment that can modify the natural history of allergic rhinitis and
potentially induce long-term disease remission after cessation of treatment.[51] It may also prevent
the development of new allergies and reduce the risk of development of asthma in children.
Therefore, allergen immunotherapy may be considered even in milder cases of allergic rhinitis.
Immunotherapy is administered by subcutaneous injection, although sublingual immunotherapy
seems to be somewhat effective as well.[6][52][53][54][55]
Anticholinergics
Intranasal ipratropium is effective for rhinorrhea secondary to allergic rhinitis but not for other
symptoms.[26]
Combination Therapies
Combination therapy is recommended by some guidelines when patients have inadequate response
to monotherapy.[9][16][17] Some combinations have been shown to be more effective than
monotherapy while others have not.
First- and Second-Generation Antihistamines
Some experts suggest a second-generation antihistamine during the day and a first-
generation antihistamine at bedtime to promote sleep. Evidence to support this practice is
lacking and next-day sedation is possible.[2] If sleep is disturbed due to allergies, symptom relief
itself can be expected to improve sleep.
Antihistamine plus Decongestant
Because antihistamines may have only a modest effect on nasal congestion, antihistamines and
decongestants are often combined. Some patients may respond to this combination when
corticosteroids have failed or when either medication alone does not provide adequate relief of
nasal symptoms.[2][36]
Antihistamine plus Corticosteroid
Intranasal corticosteroids are often combined with oral antihistamines to treat severe or
resistant cases of allergic rhinitis.[6] This strategy seems logical because the 2 drugs have
different mechanisms of action. Evidence is insufficient to support the combination of intranasal
corticosteroids and oral antihistamines, as it has not been consistently shown to be superior to
intranasal corticosteroid alone.[2][36] Combination therapy with intranasal corticosteroid and oral
antihistamine is not recommended for initial management of allergic rhinitis.[17] However,
intranasal corticosteroid in combination with intranasal antihistamine (azelastine/fluticasone) is
more effective for the nasal symptoms of allergic rhinitis than either medication alone.[17][36]
Guidelines recommend that the combination of intranasal corticosteroid and intranasal
antihistamine be considered as an alternative to intranasal corticosteroids alone for the initial

management allergic rhinitis if the patient is willing to accept a higher cost and risk of adverse
events.[16][17]
Antihistamine or Intranasal Corticosteroid plus LTRA
An additive effect has been shown when LTRAs and either oral antihistamines or intranasal
corticosteroids are used concomitantly.[36] The efficacy of oral antihistamines in combination with
a LTRA is less than that of intranasal corticosteroids alone.[6] However, antihistamine-LTRA
combination therapy may provide an alternative for patients who are unresponsive or nonadherent
to intranasal corticosteroid therapy.
Special Populations
Children
The guidelines for treatment of allergic rhinitis in children are similar to those for adults; however,
many of the allergic rhinitis studies exclude children <12 years of age.[6] Health-care practitioners
must ensure they select the correct dosage, ensure proper administration and minimize adverse
effects.[3][7][28] Most second-generation antihistamines are now available in pediatric
formulations for children >6 months and are generally preferred over first-generation agents due
to improved adverse effect profiles. Table 5 and Table 6 provide dosage guidelines and age limits
for oral and intranasal agents. Intranasal corticosteroids are also effective and are considered
safe in children >2 years of age, depending on the formulation.[28] Intranasal budesonide and
mometasone have not shown growth suppression with prolonged use at recommended doses.[6]
[56][57] Intranasal beclomethasone, fluticasone furoate and triamcinolone have been shown to
reduce growth velocity by 0.2–0.9 cm per year within the 1st year of treatment.[58][59][60] Longer-
term studies have not been conducted. If intranasal corticosteroids are used, use the lowest
possible dose, monitor growth and use other therapies (e.g., antihistamines) to minimize the dose
of corticosteroid required for symptom control.[6] Decongestants are not recommended for use in
children under 6 years of age.[61][62] In those children, intranasal saline drops or spray may be
used to clear nasal passages before eating or sleeping.
Pregnancy
Intranasal sodium cromoglycate (not available in Canada) and intranasal corticosteroids are both
considered safe during pregnancy although beclomethasone, budesonide and fluticasone
propionate have accumulated more safety data than other intranasal corticosteroids.[6] Neither
first- nor second-generation antihistamines have been associated with teratogenic effects in
pregnancy.[63][64] First-generation antihistamines were previously favoured because of
substantially greater experience; however, safety data for cetirizine and loratadine now indicate
that these are acceptable options.[65] Chlorpheniramine has a good safety record in pregnancy.
Although diphenhydramine has good safety data and is still recommended and frequently used
in pregnancy, there have been isolated reports of cleft palate.[64] Sedation and impaired
performance may limit the use of first-generation antihistamines.
If possible, avoid the use of bilastine and rupatadine in pregnancy as no adequate nor well-
controlled studies have taken place. The effect of intranasal saline irrigation in pregnancy and has
not been established.[14] Oral decongestants should be avoided in the 1st trimester.[64] A topical
decongestant may be used; at usual doses, they do not present a risk to the fetus.
Immunotherapy generally should not be started during pregnancy. Courses of immunotherapy
started prior to conception may be continued if beneficial and not causing systemic reactions;
doses should not be increased during pregnancy.[66]
Breastfeeding
Recommendations for breastfeeding are similar to those during pregnancy. Both first- and
second-generation antihistamines are considered safe while breastfeeding.[67] First-generation
antihistamines may in theory diminish milk production via their anticholinergic effect; however, this
has not been reported in practice. Infant somnolence should be monitored when a first-generation
antihistamine or cetirizine is used. If possible, avoid bilastine and rupatadine in the breastfeeding
mother as no adequate nor well-controlled studies have taken place.
The systemic absorption of topical decongestants is low and transfer into breast milk is
unknown. Consequently, these agents are expected to be reasonably safe during breastfeeding.
The American Academy of Pediatrics considers pseudoephedrine to be compatible with
breastfeeding.[64] Information on the use of other oral decongestants during breastfeeding is
limited.
Information on the use of topical sodium cromoglycate during breastfeeding is not available,
although the manufacturer recommends caution. It is not currently available in Canada.
For more information, see Pregnancy and Breastfeeding: Self-care Therapy for Common
Conditions.
Monitoring of Therapy
Table 4 provides a monitoring plan framework that should be individualized.
Table 4: Monitoring of Therapy for Allergic Rhinitis

Symptoms Monitoring Endpoint of Actions
Therapy
Allergic symptoms Patient: daily Patient able to If nonprescription therapy is

(sneezing, runny Health-care perform daily ineffective after 1 wk,
nose, itchy and practitioner: next activities. optimize allergen avoidance
watery eyes, visit or by telephone Patient able to and medication dose (if
congestion, 1 wk later sleep. applicable). If symptoms not
rhinorrhea) controlled after a further wk
of therapy, consider another
agent. Refer as necessary.
[3]
Drowsiness Patient: daily Patient not drowsy Switch to a less sedating

(antihistamine) Health-care during the day. antihistamine. If using
practitioner: next cetirizine, could give dose at
visit or by telephone bedtime.
when checking for
efficacy
Insomnia Patient: daily No insomnia. Change medication

(oral Health-care schedule so last dose taken
decongestant) practitioner: 1 wk 4–6 h before bedtime or
discontinue medication.
Symptoms Monitoring Endpoint of Actions

Therapy
Elevated blood Patient: daily No elevation in Stop decongestant if blood

pressure in Health-care blood pressure pressure elevated above
hypertensive practitioner: monitor above baseline. baseline.
patients blood pressure of
(oral hypertensive
decongestant) patients twice in the
1st wk
Advice for the Patient

Advise all patients about allergen avoidance. In addition, patients who require drug therapy should
receive counselling regarding proper use of the medication, expected results and management of
adverse effects (see Table 4). Patients should be encouraged to follow up with their health-care provider
should their medication be partially or completely ineffective, if they are experiencing adverse effects or if
they are unable to adhere to therapy.
Algorithms
[3][4][6][7][11]
Figure 2: Assessment and Initial Treatment of Patients with Allergic Rhinitis
Drug Tables
Table 5: Oral Agents for Allergic Rhinitis
Drug/Cost[a] Dosage Adverse Drug Comments
Effects Interactions
Drug Class: Antihistamines, first-generation

chlorpheniramine[b] Adults: 4 mg Q4–6H CNS: sedation, Increased CNS

Chlor-Tripolon, PO; maximum fatigue, depression when
generics 24 mg/day dizziness, combined with
Children: impairment of alcohol,
< $10 0.35 mg/kg/day cognition and sedatives,
divided Q4–6H PO or performance. tranquilizers,
Anticholinergic: barbiturates.
2–5 y: 1 mg Q4–6H Increased
PO; maximum dry mouth and
eyes, anticholinergic
6 mg/day side effects
constipation,
6–11 y: 2 mg Q4–6H urinary when combined
PO; maximum retention. with TCAs,
12 mg/day scopolamine.
Increase
chlorpheniramine
levels resulting in
increased
adverse effects
when combined
with moderate
CYP2D6
inhibitors, e.g.,
amiodarone,
celecoxib.
Avoid
combination with
strong CYP2D6
inhibitors, e.g.,
bupropion,
paroxetine.
diphenhydramine[b] Adults: 25–50 mg CNS: sedation, Increased CNS Available in

Benadryl Q6–8H PO; maximum fatigue, depression when pediatric
Preparations, 300 mg/day dizziness, combined with 1.25 mg/mL
generics Children: impairment of alcohol, liquid
5 mg/kg/day PO given cognition and sedatives, formulation.
< $10 in 3–4 divided doses performance. tranquilizers,
Maximum: Anticholinergic: barbiturates.
dry mouth and Increased
2–5 y: 37.5 mg/day anticholinergic
eyes,
6–11 y: 150 mg/day constipation, side effects
urinary when combined
retention. with TCAs,
scopolamine.
May increase
levels of
CYP2D6
substrates, e.g.,
metoprolol,
venlafaxine.
Drug Class: Antihistamines, second-generation

bilastine Adults and children Minimal to no Grapefruit juice

Blexten ≥12 y: 20 mg Q24H anticholinergic may reduce
PO effects. bilastine’s
< $10 Headache. bioavailability.
cetirizine [b] Adults and children Minimal to no Increased CNS Active

Reactine, generics ≥6 y: 5–10 mg Q24H anticholinergic depression when metabolite of
PO; maximum effects. combined with hydroxyzine.
< $10 20 mg/day Headache. alcohol, Available in
Children: May cause sedatives, pediatric 10 mg
drowsiness in tranquilizers, rapid-dissolve
6–12 months: 2.5 mg barbiturates. tablet and
Q24H PO some individuals
especially at Increased 1 mg/mL syrup.
12–23 months: higher doses. anticholinergic
2.5 mg Q24H PO; side effects
maximum 2.5 mg when combined
Q12H with TCAs,
scopolamine.
2–5 y: 2.5 mg Q24H
PO; maximum
5 mg/day in
1–2 doses
desloratadine [b] Adults and children Minimal to no Pgp inhibitors Active

Aerius, generics ≥12 y: 5 mg Q24H anticholinergic (e.g., metabolite of
PO effects. erythromycin, loratadine.
< $10 Children: Headache. ketoconazole) Available in
may increase pediatric
6–11 months: 1 mg loratadine levels
Q24H PO 0.5 mg/mL liquid
while Pgp formulation.
1–5 y: 1.25 mg Q24H inducers (e.g.,
PO carbamazepine,
dexamethasone)
6–11 y: 2.5 mg Q24H
may decrease
PO
loratadine levels;
clinical effect
probably
minimal.
fexofenadine [b] Adults: 60 mg Q12H Minimal to no Decreased Active

Allegra PO; anticholinergic fexofenadine metabolite of
maximum 180 mg/day effects. level when terfenadine.
< $10 (12-h formulation) or Headache. combined with Only 5% of a
120 mg/day (24-h aluminum- and dose is
formulation) magnesium- metabolized.
Children 2–11 y: containing
30 mg Q12H PO antacids.
Ingestion of fruit
juices such as
apple, grapefruit
or orange may
decrease
bioavailability.

loratadine [b] Adults and children Minimal to no QTc prolongation Available in

Claritin, Claritin >5 y: 10 mg Q24H anticholinergic reported with pediatric
Liquid Capsules, PO effects. concomitant use 1 mg/mL liquid
generics Children 2–5 y: 5 mg Headache. of loratadine and formulation as
Q24H PO amiodarone. well as rapid-
< $10 Caution is dissolve tablets.
advised.
Pgp inhibitors
(e.g.,
erythromycin,
ketoconazole)
may increase
loratadine levels
while Pgp
inducers (e.g.,
carbamazepine,
dexamethasone)
may decrease
loratadine levels;
clinical effect
probably
minimal.
rupatadine Adults and children Minimal to no Increased CNS Available in

Rupall ≥12 y: 10 mg Q24H anticholinergic depression when pediatric
PO effects. combined with 1 mg/mL liquid
< $10 Headache. alcohol, formulation.
Children 2–11 y: oral
solution sedatives,
tranquilizers,
10–25 kg: 2.5 mg barbiturates.
Q24H PO; maximum Grapefruit juice
2.5 mg/day increases
>25 kg: 5 mg Q24H rupatadine
PO; maximum bioavailability
5 mg/day and should be
avoided.
CYP3A4
inhibitors or
inducers may
increase or
decrease
rupatadine
levels,
respectively.
Drug Class: Decongestants

pseudoephedrine Adults and children Mild CNS Beta-blockers: Caution in

[b] ≥12 y: 60 mg Q4–6H stimulation Antihypertensive patients with
Eltor 120, generics PO; maximum (nervousness, effects may be heart disease,
240 mg/day excitability, reduced. high blood
$10–20 Sustained-release: restlessness, Contraindicated pressure,
120 mg Q12H PO; dizziness, with MAOIs and hyperthyroidism,
maximum 240 mg/day weakness, ergot derivatives. diabetes, angle
Children 6–11 y: insomnia). Avoid use with closure
30 mg Q4–6H PO; Peripheral phenothiazines glaucoma and
maximum 120 mg/day vasoconstriction. and selective prostatic
Tachycardia or serotonin enlargement.
palpitation may reuptake Concurrent use
occur. Blood inhibitors. with or use
pressure may be within 2 wk of
increased in MAOIs may
hypertensive cause
subjects. May hypertensive
adversely affect crisis.
blood sugar
control in
diabetics.
Drug Class: Antihistamine, second-generation/decongestant combinations
cetirizine / Adults and children Minimal to no Increased CNS Cetirizine is the

pseudoephedrine ≥12 y: 1 tablet anticholinergic depression when active
[b] (5 mg/120 mg) Q12H effects. combined with metabolite of
PO Headache. alcohol, hydroxyzine.
Reactine Complete
Mild CNS sedatives, Caution in
$10–20 stimulation tranquilizers, patients with
(nervousness, barbiturates. heart disease,
excitability, Increased high blood
restlessness, anticholinergic pressure,
dizziness, side effects hyperthyroidism,
weakness, when combined diabetes, angle
insomnia). with TCAs, closure
Peripheral scopolamine. glaucoma and
vasoconstriction. Beta-blockers: prostatic
Tachycardia or Antihypertensive enlargement.
palpitation may effects may be Concurrent use
occur. Blood reduced. with or use
pressure may be Contraindicated within 2 wk of
increased in with MAOIs and MAOIs may
hypertensive ergot derivatives. cause
subjects. May Avoid use with hypertensive
adversely affect phenothiazines crisis.
blood sugar and selective
control in serotonin
diabetics. reuptake
inhibitors.

desloratadine / Adults and children Minimal to no Pgp inhibitors Desloratadine is

pseudoephedrine ≥12 y: 1 tablet anticholinergic (e.g., the active
[b] (2.5 mg/120 mg) effects. erythromycin, metabolite of
Q12H PO Headache. ketoconazole) loratadine.
Aerius Dual Action
Mild CNS may increase Caution in
12 Hour
stimulation loratadine levels patients with
$10–20 (nervousness, while Pgp heart disease,
excitability, inducers (e.g., high blood
restlessness, carbamazepine, pressure,
dizziness, dexamethasone) hyperthyroidism,
weakness, may decrease diabetes, angle
insomnia). loratadine levels; closure
Peripheral clinical effect glaucoma and
vasoconstriction. probably prostatic
Tachycardia or minimal. enlargement.
palpitation may Beta-blockers: Concurrent use
occur. Blood Antihypertensive with or use
pressure may be effects may be within 2 wk of
increased in reduced. MAOIs may
hypertensive Contraindicated cause
subjects. May with MAOIs and hypertensive
adversely affect ergot derivatives. crisis.
blood sugar Avoid use with
control in phenothiazines
diabetics. and selective
serotonin
reuptake
inhibitors.
fexofenadine / Adults and children Minimal to no Decreased Active

pseudoephedrine ≥12 y: 1 tablet anticholinergic fexofenadine metabolite of
[b] (60 mg/120 mg) effects. level when terfenadine.
Q12H PO Headache. combined with Only 5% of a
Allegra-D
Mild CNS aluminum- and dose is
$10–20 stimulation magnesium- metabolized.
(nervousness, containing Caution in
excitability, antacids. patients with
restlessness, Ingestion of fruit heart disease,
dizziness, juices such as high blood
weakness, apple, grapefruit pressure,
insomnia). or orange may hyperthyroidism,
Peripheral decrease diabetes, angle
vasoconstriction. bioavailability. closure
Tachycardia or Beta-blockers: glaucoma and
palpitation may Antihypertensive prostatic
occur. Blood effects may be enlargement.
pressure may be reduced. Concurrent use
increased in Contraindicated with or use
hypertensive with MAOIs and within 2 wk of
subjects. May ergot derivatives. MAOIs may
adversely affect Avoid use with cause
blood sugar phenothiazines hypertensive
control in and selective crisis.
diabetics. serotonin
reuptake
inhibitors.

loratadine / Adults and children Minimal to no QTc prolongation Caution in

pseudoephedrine ≥12 y: 1 tablet anticholinergic reported with patients with
[b] (5 mg/120 mg) Q12H effects. concomitant use heart disease,
PO Headache. of loratadine and high blood
Claritin Allergy +
or 1 tablet Mild CNS amiodarone. pressure,
Sinus, Claritin
(10 mg/240 mg) stimulation Caution is hyperthyroidism,
Allergy + Sinus
Q24H PO (nervousness, advised. diabetes, angle
Extra Strength
excitability, Pgp inhibitors closure
$10–20 restlessness, (e.g., glaucoma and
dizziness, erythromycin, prostatic
weakness, ketoconazole) enlargement.
insomnia). may increase Concurrent use
Peripheral loratadine levels with or use
vasoconstriction. while Pgp within 2 wk of
Tachycardia or inducers (e.g., MAOIs may
palpitation may carbamazepine, cause
occur. Blood dexamethasone) hypertensive
pressure may be may decrease crisis.
increased in loratadine levels;
hypertensive clinical effect
subjects. May probably
adversely affect minimal.
blood sugar Beta-blockers:
control in Antihypertensive
diabetics. effects may be
reduced.
Contraindicated
with MAOIs and
ergot derivatives.
Avoid use with
phenothiazines
and selective
serotonin
reuptake
inhibitors.
Drug Class: Leukotriene Receptor Antagonists

montelukast Adults and children Headache, Strong CYP2C9 Strong CYP2C9

Singulair, generics ≥15 y: 10 mg QHS abdominal pain, and 3A4 and 3A4
PO flulike inducers (e.g., inducers (e.g.,
$10–20 symptoms. carbamazepine, carbamazepine,
Children:
Aggressive phenobarbital, phenobarbital,
2–5 y: 4 mg QHS PO behaviour or phenytoin, phenytoin,
6–14 y: 5 mg QHS hostility (rare; rifampin) may rifampin) may
PO e.g., temper decrease decrease
tantrums in montelukast montelukast
children). levels whereas, levels whereas,
strong CYP2C9 strong CYP2C9
inhibitors (e.g., inhibitors (e.g.,
sulfadiazine) fluconazole)
may increase may increase
montelukast montelukast
levels; clinical levels; clinical
significance is significance is
uncertain; uncertain;
however, monitor however,
for reduced monitor for
efficacy or reduced efficacy
adverse effects. or adverse
effects.
[a]
Cost of 10-day supply; includes drug cost only.
[b] Available without a prescription.
Dosage adjustment may be required in renal impairment.
Abbreviations: CNS = central nervous system; MAOI = monoamine oxidase inhibitor; Pgp = P-
glycoprotein; TCA = tricyclic antidepressant
Table 6: Intranasal Agents for Allergic Rhinitis

Drug/Cost[a] Dosage Adverse Comments
Effects
Drug Class: Antihistamines
levocabastine Adults (≤65 y) and Nasal Shake well before

Livostin Nasal Spray children (≥12 y): irritation. use.
2 sprays (50 mcg/spray) Initial priming
$20–30 per nostril BID; may required.
increase to 2 sprays
TID–QID Discontinue if no
improvement seen
within 3 days.
Drug Class: Corticosteroids

Effects
beclomethasone Adults and children Burning or Use at regular

generics ≥6 y: 2 sprays stinging, intervals. Slow
(50 mcg/spray) in each nosebleed. onset (7–14 days
$10–20 nostril BID for maximal effect).
May cause
Adults: maximum mild growth Drug may fail to
12 sprays/day suppression reach the site of
with prolonged action if excessive
Children: maximum nasal mucus
8 sprays/day use.[58][59][60]
secretion or
Use lowest effective edema of the nasal
dose for maintenance mucosa is present.
therapy May use a
vasoconstrictor
(intranasal
decongestant)
2–3 days prior to
the suspension.
Aim spray up
towards turbinates
and away from
septum. Liquid
forms may be
more effective than
metered-dose
inhalers.
budesonide Nasal suspension Burning or Use at regular

Rhinocort Aqua, Rhinocort (64 mcg/metered stinging, intervals. Slow
Turbuhaler dose): nosebleed. onset (7–14 days
Adults and children May cause for maximal effect).
$10–30 Drug may fail to
≥6 y: mild growth
suppression reach the site of
Initial dose: 2 sprays in action if excessive
each nostril daily or with prolonged
nasal mucus
1 spray in each nostril use.[58][59][60]
secretion or
BID; may decrease edema of the nasal
maintenance dose to mucosa is present.
1 spray in each nostril May use a
daily vasoconstrictor
Nasal powder (intranasal
(100 mcg/dose): decongestant)
Adults and children 2–3 days prior to
≥6 y: the suspension.
Initial dose: Aim spray up
2 applications in each towards turbinates
nostril in the morning or and away from
1 application in each septum. Liquid
nostril BID; may forms may be
decrease maintenance more effective than
dose to 1 application in metered-dose
each nostril daily inhalers.
Maximum 400 mcg/day For the nasal
suspension, initial
priming needed.
Re-prime if not
used ≥4 days.

Effects
ciclesonide Adults and children Burning or Use at regular

Omnaris, generics ≥12 y: 2 sprays stinging, intervals. Slow
$10–20 nostril daily; maximum for maximal effect).
200 mcg/day Drug may fail to
reach the site of
action if excessive
nasal mucus
secretion or
edema of the nasal
mucosa is present.
May use a
vasoconstrictor
(intranasal
decongestant)
2–3 days prior to
the suspension.
Aim spray up
towards turbinates
and away from
septum. Liquid
forms may be
more effective than
metered-dose
inhalers.
Initial priming
needed.
fluticasone propionate[b] Adults and children Burning or Use at regular

Flonase, generics ≥12 y: 2 sprays stinging, intervals. Slow
$20–30 nostril daily, may May cause for maximal effect).
increase to BID in mild growth Drug may fail to
severe situations; suppression reach the site of
maximum 400 mcg/day with prolonged action if excessive
nasal mucus
Children 4–11 y: use.[58][59][60]
1–2 sprays in each secretion or
nostril daily; maximum edema of the nasal
200 mcg/day mucosa is present.
May use a
vasoconstrictor
(intranasal
decongestant)
2–3 days prior to
the suspension.
Aim spray up
towards turbinates
and away from
septum. Liquid
forms may be
more effective than
metered-dose
inhalers.

Effects
fluticasone furoate Adults and children Burning or Use at regular

Avamys ≥12 y: 2 sprays stinging, intervals. Slow
(27.5 mcg/spray) in nosebleed. onset (7–14 days
$20–30 each nostril once daily; for maximal effect).
maximum 110 mcg/day Drug may fail to
Children 2–11 y: reach the site of
1 spray in each nostril action if excessive
once daily, may nasal mucus
increase to 2 sprays in secretion or
each nostril once daily if edema of the nasal
needed. Decrease to mucosa is present.
1 spray in each nostril May use a
daily for maintenance; vasoconstrictor
maximum 110 mcg/day (intranasal
decongestant)
2–3 days prior to
the suspension.
Aim spray up
towards turbinates
and away from
septum. Liquid
forms may be
more effective than
metered-dose
inhalers.
Initial priming
needed. Re-prime
if not used
≥30 days or if cap
left off for ≥5 days.
mometasone Adults and children Burning or Use at regular

Nasonex, generics ≥12 y: 2 sprays stinging, intervals. Slow
$20–30 nostril daily, may for maximal effect).
decrease to 1 spray in Drug may fail to
each nostril daily for reach the site of
maintenance; may action if excessive
increase to BID in nasal mucus
severe situations secretion or
Children 3–11 y: edema of the nasal
1 spray in each nostril mucosa is present.
daily May use a
vasoconstrictor
(intranasal
decongestant)
2–3 days prior to
the suspension.
Aim spray up
towards turbinates
and away from
septum. Liquid
forms may be
more effective than
metered-dose
inhalers.

Effects
triamcinolone[b] Adults and children Burning or Use at regular

Nasacort AQ, Nasacort ≥12 y: 2 sprays stinging, intervals. Slow
Allergy 24HR (55 mcg/spray) in each nosebleed. onset (7–14 days
nostril once daily, may for maximal effect).
$10–20 decrease to 1 spray in Drug may fail to
each nostril once daily reach the site of
Children 4–11 y: action if excessive
1 spray in each nostril nasal mucus
once daily, may secretion or
increase to 2 sprays in edema of the nasal
each nostril once daily if mucosa is present.
needed. Decrease to May use a
1 spray in each nostril vasoconstrictor
daily for maintenance; (intranasal
maximum 110 mcg/day decongestant)
2–3 days prior to
the suspension.
Aim spray up
towards turbinates
and away from
septum. Liquid
forms may be
more effective than
metered-dose
inhalers.
Drug Class: Decongestants
oxymetazoline[b] Adults and children Burning, Onset of action:

Claritin Allergy ≥6 y: 0.05% solution: stinging, 5–10 min.
Decongestant, Dristan Long 2–3 drops/sprays per sneezing, Long duration,
Lasting Nasal Mist, Drixoral, nostril Q12H dryness of the lasting up to 12 h.
generics nasal mucosa. Do not use longer
Bradycardia, than 3–5 days.
< $10 tachycardia,
hypotension
and
hypertension
have been
reported.
pheniramine/phenylephrine[b] Adults and children Burning, Onset of action:

Dristan Nasal Mist ≥6 y: 0.25% or 0.5% stinging, 5–10 min.
solution: sneezing, Short duration,
< $10 2–3 drops/sprays per dryness of the lasting up to 4 h.
nostril Q4H nasal mucosa. Do not use longer
Bradycardia, than 3–5 days.
tachycardia,
hypotension
and
hypertension
have been
reported.

Effects
xylometazoline[b] Adults and children Burning, Onset of action:

Balminil Nasal ≥6 y: 0.05% or 0.1% stinging, 5–10 min.
Decongestant, Otrivin, solution: 2–3 drops or sneezing, Long duration,
generics 1–2 sprays per nostril dryness of the lasting up to 12 h.
Q8-10H nasal mucosa. Do not use longer
< $10 Bradycardia, than 3–5 days.
tachycardia,
hypotension
and
hypertension
have been
reported.
Drug Class: Antihistamine/Corticosteroid Combinations
azelastine/fluticasone Adults and children Burning or Avoid use with

Dymista ≥12 y: 1 spray stinging, ritonavir due to
(137 mcg/50 mcg) in nosebleed. potential for
$100 each nostril BID systemic
Dysgeusia
may occur if corticosteroid
patient tilts effects.
head back too
far during
administration.
Rarely causes
drowsiness.
[a] Cost of 1 unit (spray pump); includes drug cost only.

[b] Available without a prescription.
Suggested Readings
Bousquet J, Schunemann HJ, Hellings PW et al. MACVIA clinical decision algorithm in adolescents and
adults with allergic rhinitis. J Allergy Clin Immunol 2016;138:367-74.
Dykewicz MS, Wallace DV, Baroody F et al. Treatment of seasonal allergic rhinitis: an evidence-based
focused 2017 guideline update. Ann Allergy Asthma Immunol 2017;119:489-511.
Seidman MD, Gurgel RK, Lin SY et al. Clinical practice guideline: allergic rhinitis. Otolaryngol Head Neck
Surg 2015;152:S1-43.
Wheatley LM, Togias A. Clinical practice. Allergic rhinitis. N Engl J Med 2015;372:456-63.
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Information for the Patient

Allergic Rhinitis
CPhA assumes no responsibility for or liability in connection with the use of this information. For clinical use only and not intended for for use by
patients. Once printed there is no quarantee the information is up-to-date. [Printed on: 07-13-2020 05:02 PM]
RxTx, Compendium of Therapeutics for Minor Ailments © Canadian Pharmacists Association, 2020. All rights reserved

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7/13/2020 Allergic Rhinitis

Jennifer Kendrick, BScPharm, ACPR, PharmD

Figure 1: Facial Signs of Allergic Rhinitis

measures for common allergens are presented below.[1][3][6][7]

Keep windows and doors closed when at home or in the car.

Remain in a closed environment as much as possible.

House Dust Mites

Avoid carpeting the bedroom and main living areas.

For individuals affected by occupational rhinitis, recommend minimizing or eliminating exposure.

Oral antihistamines + +/- + + +/-

Leukotriene receptor + + +/- +/- +/-

[a] See Conjunctivitis.

Abbreviations: - = no effect; +/- = modest or variable effect; + = moderately effective; ++ = effective

Mast Cell Stabilizers

Leukotriene Receptor Antagonists (LTRA)

Zafirlukast is no longer available in Canada.

According to clinical practice guidelines, allergen immunotherapy should be considered for

First- and Second-Generation Antihistamines

Antihistamine plus Decongestant

Antihistamine plus Corticosteroid

antihistamine be considered as an alternative to intranasal corticosteroids alone for the initial

Antihistamine or Intranasal Corticosteroid plus LTRA

Table 4: Monitoring of Therapy for Allergic Rhinitis

Allergic symptoms Patient: daily Patient able to If nonprescription therapy is

Drowsiness Patient: daily Patient not drowsy Switch to a less sedating

Insomnia Patient: daily No insomnia. Change medication

Symptoms Monitoring Endpoint of Actions

Elevated blood Patient: daily No elevation in Stop decongestant if blood

Advice for the Patient

Drug Class: Antihistamines, first-generation

Drug/Cost[a] Dosage Adverse Drug Comments

chlorpheniramine[b] Adults: 4 mg Q4–6H CNS: sedation, Increased CNS

diphenhydramine[b] Adults: 25–50 mg CNS: sedation, Increased CNS Available in

Drug Class: Antihistamines, second-generation

Drug/Cost[a] Dosage Adverse Drug Comments

bilastine Adults and children Minimal to no Grapefruit juice

cetirizine [b] Adults and children Minimal to no Increased CNS Active

desloratadine [b] Adults and children Minimal to no Pgp inhibitors Active

fexofenadine [b] Adults: 60 mg Q12H Minimal to no Decreased Active

Drug/Cost[a] Dosage Adverse Drug Comments

loratadine [b] Adults and children Minimal to no QTc prolongation Available in

rupatadine Adults and children Minimal to no Increased CNS Available in

Drug Class: Decongestants

Drug/Cost[a] Dosage Adverse Drug Comments

pseudoephedrine Adults and children Mild CNS Beta-blockers: Caution in

Drug Class: Antihistamine, second-generation/decongestant combinations

cetirizine / Adults and children Minimal to no Increased CNS Cetirizine is the

Drug/Cost[a] Dosage Adverse Drug Comments

desloratadine / Adults and children Minimal to no Pgp inhibitors Desloratadine is

fexofenadine / Adults and children Minimal to no Decreased Active

Drug/Cost[a] Dosage Adverse Drug Comments

loratadine / Adults and children Minimal to no QTc prolongation Caution in

Drug Class: Leukotriene Receptor Antagonists

Drug/Cost[a] Dosage Adverse Drug Comments

montelukast Adults and children Headache, Strong CYP2C9 Strong CYP2C9

Table 6: Intranasal Agents for Allergic Rhinitis

Drug Class: Antihistamines

levocabastine Adults (≤65 y) and Nasal Shake well before