Download Allergic Rhinitis: A Review of Current Data

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CEU
NATIONAL CONTINUING EDUCATION PROGRAM
Allergic Rhinitis:
A Review of Current Data
STATEMENT OF OBJECTIVES
Upon successful completion of this lesson,
the pharmacist should be able to:
1. Describe the pathophysiology of allergic
rhinitis
2. Recognize the common signs and
symptoms of allergic rhinitis
3. Outline the link between allergic rhinitis
and asthma
4. Review current drugs of choice for allergic
rhinitis as well as second-line therapy
5. Counsel patients with allergic rhinitis about
the mechanism(s) of action, the correct
way to administer medication(s), and
possible adverse effects
6. Highlight unique issues affecting subpopulations of allergic rhinitis sufferers including
pregnant women, children, and elderly
individuals.
INSTRUCTIONS
1. After carefully reading this lesson, study
each question and select the one
answer you believe to be correct. Circle
the appropriate letter on the attached
reply card.
2. Indicate if you are already registered as
an annual CE Club Member or if you
would like to become a member.
3. Complete the card and mail, or fax to
(416) 764-3937.
4. Your reply card will be marked and you
will be advised of your results in a letter
from Pharmacy Post.
5. To pass this lesson, a grade of 70%
(14 out of 20) is required. If you pass,
your CEU(s) will be recorded with the
relevant provincial authority(ies). (Note:
Some provinces require individual
pharmacists to notify them.)
Lori Bonertz, BSc Pharm
INTRODUCTION
Allergic rhinitis (AR) is a prevalent, chronic
condition, and patients with this condition
often self-medicate. For these reasons, and
because a pharmacist may be the first healthcare professional that a patient consults, pharmacists must have a thorough understanding
of the pathophysiology and treatment of this
disease.
PREVALENCE
The prevalence of AR is increasing in developed countries.1-3 Based on a study of almost
500,000 children aged 13 to 14 in over 155
centres in 56 countries, Canada has one of the
highest rates of AR in the world, approaching
30%.1,2 Prevalence is highest in adolescence
and young adulthood.4 On average, onset is
prior to adolescence,3 and incidence decreases
with age.4 The costs associated with AR are
high, accounting for at least $1.8 billion annually in the U.S. in direct costs (physician visits
and medication expenses).5 The indirect costs
associated with absence from work and school
and impaired performance are high as AR is
common in individuals in the work force and
in children.6,7
PATHOPHYSIOLOGY
AR is an immunologic response initiated by
exposure to inhalant allergens and mediated
by immunoglobulin (Ig)E.3,7,8 Once the allergen is introduced to the body, it is engulfed by
antigen-presenting cells (macrophages, den-
dritic cells, Langerhans cells, B-lymphocytes)
and broken down within their phagolysosomes.7 The resulting allergen peptides associate with the molecules of the major histocompatibility complex and move to the surface of
the cell where they are recognized by T-helper
(TH) cells. The TH cells, particularly the
TH2, release cytokines including interleukin4 (IL-4), which results in isotype switching of
B-lymphocytes to produce specific IgE. These
IgE molecules attach to numerous cells,
notably mast cells in the nasal mucosa and circulating basophils.2,5 The individual is now
sensitized to the allergen.7 When there is further exposure to allergen, it is recognized by
the IgE receptors on mast cells or basophils
and cross-linkage of adjacent IgE occurs, leading to the immediate release of mediators such
as histamine and leukotrienes, prostaglandins,
tryptase and others. The actions of these
mediators on nerves, mucous glands, and
blood vessels produce the early-phase response
characteristic of AR: sneezing, itching, rhinorrhea, and nasal congestion. In addition to this
early-phase response that occurs within minutes of allergen exposure and fades within one
hour, up to one-half of AR sufferers experience symptoms, particularly nasal congestion,
three to 12 hours later without additional
allergen exposure.3,7,8 This late response is
caused by an infiltration of inflammatory cells
(e.g. eosinophils, basophils, TH2 cells) which
sets up chronic inflammation of the nasal tissues and exacerbates the reaction of the nasal
Supported by an unrestricted educational grant from:
mucosa to further allergen exposure (priming)
and to non-allergic/irritant stimuli, such as
smoke, strong odours and air pollutants.3,7,8
AR can have a substantial negative impact
on quality of life.7 and is associated with other
medical conditions.3,7 Chronic nasal obstruction in children can have serious consequences, such as excessive mouth breathing,
which may cause facial abnormalities. 3 A
number of individuals with AR may also have
asthma (21 to 58%). AR is common in those
with asthma (28 to 92%),3,7 and there is evidence that individuals with AR are more likely to develop asthma.3 Theoretically, adequate
treatment of AR should decrease the chance
of progression to asthma, but this has not yet
been proven.5 However, studies have shown
that treating AR improves asthma symptom
control and decreases health-care visits for
asthma.3,7,9 AR is also associated with sinusitis
and otitis media. Therefore, adequate treatment of AR may reduce the frequency of
these conditions in atopic individuals.3,7
DIAGNOSIS
Family history of atopy (hereditary tendency
to be sensitive to certain allergens) is the most
important risk factor for AR.8 Diagnosis is
based mainly on clinical history, confirmed by
skin tests or radioallergosorbent tests to detect
the presence of allergen-specific IgE in
serum.2 Apart from sneezing, itching, rhinorrhea, and nasal congestion, patients may
describe symptoms such as weakness, malaise,
irritability, and decreased appetite.3 Signs
include the “allergic shiner”, a darkening of
the lower eyelid caused by suborbital edema;
the Dennie-Morgan line with linear folds or
lines in the lower eyelid of children secondary
to edema occurring in this area; the “allergic
salute”, the upward rubbing of the nose with
the palm of the hand; and the resulting “allergic crease”, a transverse skin line below the
bridge of the nose caused by constant
rubbing.3
Traditionally AR has been classified as
either seasonal (hay fever) or perennial,3 with
perennial AR defined as nasal symptoms for
more than two hours a day for more than nine
months of the year.7 The majority of patients
exhibit seasonal AR,3 but medical costs, associated co-morbid diseases and use of concomitant medications are higher in those with
perennial AR.10
Notably there is much variation between
patients in the pattern of symptoms and there
has been a move to change the terminology
to intermittent versus persistent AR. 11
Intermittent AR is defined as symptoms present for less than four days a week or for less
than four weeks with “persistent AR” defined
as symptoms present for more than four days
per week and for more than four weeks.
PREVENTIVE MEASURES
A meta-analysis of six prospective studies concluded that exclusive breastfeeding during the
infant’s first three months of life helps prevent
AR regardless of whether there is a family history of atopy or not.12 Reducing exposure to
perennial allergens such as animal dander,
mould, and house-dust mites in the home
environment may reduce a child’s likelihood
of developing AR. Once an individual is diagnosed with AR, reducing contact with known
allergens is certainly important. Mould is less
likely in homes where the humidity is kept
low and condensation is avoided.13,14 Some
measures to reduce dust mites include weekly
vacuuming and washing bedding in hot water
(>130°F), removing stuffed animals from the
bed, and covering mattresses and pillows with
impermeable covers.14 For those with seasonal
AR, minimizing time spent outdoors on
windy days or on days when the pollen count
is high, and showering after spending time
outdoors may be helpful.15 These individuals
should not wear clothing or use bedding that
has been dried outside.
TREATMENT
The Allergic Rhinitis and Its Impact on
Asthma
(ARIA)—World
Health
Organization (WHO) initiative classifies AR
symptoms as mild and moderate-severe.11
The guidelines are summarized in Table 1.
Patients who do not experience improvement
after two to four weeks should be assessed for
medication compliance, heavy persistent allergen exposure, and accuracy of diagnosis.11 The
Patient Self-Care textbook provides a useful
flow chart for assessment and initial treatment
of patients with AR.15
Prevention of bronchial hyper-reactivity
in patients with asthma and AR has been
demonstrated subsequent to treatment with
intranasal corticosteroids, intranasal cromolyn
sodium, oral antihistamines (cetirizine, lorata-
CE FACULTY
This Month:
Allergic Rhinitis: A Review of Current Data
Author:
Lori Bonertz is a community pharmacist at
Fort St. John Pharmacy & Wellness Centre,
Fort St. John, BC. She has worked as a hospital and community pharmacist in Australia and
as a medical writer for Adis International Ltd.
in England.
Reviewers:
All lessons are reviewed by three pharmacists for accuracy, completeness and relevance to current pharmacy practice.
CE Scientific Editor:
Rose Pavlakovic, BScPhm, CGP
Toronto, Ont.
This lesson has been approved
for 1 CE unit by the Canadian
Council on Continuing Education
in Pharmacy. File # 092-0204.
Approved for 1 CEU by l’Ordre
des pharmaciens du Québec.
This CE lesson is published by Rogers Media Healthcare/Santé, One Mount Pleasant Rd., Toronto, Ont., M4Y 2Y5. Tel.: (416) 764-3916
Fax: (416) 764-3931. No part of this CE lesson may be reproduced, in whole or in part, without the written permission of the publisher.
2 Pharmacy Post/CE
May 2004
Table 1. Treatment guidelines from the Allergic Rhinitis in Asthma-World Health Organization initiative11
Severity and classification
of allergic rhinitis
Treatment option
Mild* intermittent
Oral or intranasal antihistamines
Intranasal decongestants (< 10 days consecutively and not more than twice
a month)
Oral decongestants
Moderate-severe** intermittent
Mild persistent
Oral or intranasal antihistamines
Oral antihistamines and decongestants
Intranasal corticosteroids
Sodium cromoglycate
Moderate-severe persistent
Intranasal corticosteroids
* no sleep disturbance or impairment of daily activities, school, or work
** impairment of daily activities, school/work
dine) and pseudoephedrine.16-19
Oral Antihistamines
Oral antihistamines remain a first-line treatment for AR.3 They block the H1 receptor,
inhibiting numerous pathways that contribute
to inflammatory cell recruitment and accumulation. They effectively ameliorate the classic
symptoms of sneezing, itching, rhinorrhea,
and conjunctivitis.3 Generally, nasal congestion does not respond well to antihistamine
treatment.
The newer second- (e.g. cetirizine, fexofenadine, loratadine) and third-generation
(desloratadine) antihistamines have not been
shown to be more effective than first-generation antihistamines (e.g. chlorpheniramine,
clemastine),4 with the possible exception of
desloratadine for nasal congestion.20 However,
because of their greater specificity for the H1
receptor, they have fewer anticholinergic
effects, and therefore less potential for drugdisease interactions (e.g. aggravation of glaucoma). This group does not cross the bloodbrain barrier so drowsiness is less of an issue3
and there is less potential for additive interactions with other medications that cause sedation3. The pharmacist must be sensitive to the
fact that AR can have an immense impact on
a patient’s health-related quality of life
(HRQL). Several trials have demonstrated
quality-of-life benefits of some second-generation oral antihistamines when used to treat
AR in adults. Two randomised, double-blind
placebo-controlled studies in adults with seaMay 2004
sonal AR have demonstrated significant
improvements in HRQL with cetirizine
10 mg once daily versus placebo. 21,22
Fexofenadine (120 mg or 180 mg) was also
shown to be significantly better than both
placebo and loratadine (10 mg) in randomised, double-blind, placebo-controlled
trials over two weeks.23,24 It should be noted
that the absorption of fexofenadine is
decreased by co-administration with aluminum or magnesium and dosage must be
modified in renal impairment.25 Although two
second-generation antihistamines (terfenadine, astemizole) were removed from the
Canadian market because of the propensity to
cause prolongation of the QTc interval, currently marketed second-generation antihistamines do not appear to have this risk. 3
Antihistamine therapy should be initiated
prior to the allergen season for seasonal/intermittent AR so histamine blockade is in place
before exposure to allergen and symptoms
have developed and taken regularly during
that time. Dosage information and adverse
effect profiles of the antihistamines available
in Canada (except for desloratadine) are summarized in the textbook, Patient Self-Care.15
Topical Antihistamines
Levocabastine is a potent and selective antihistamine26,27 and currently the only ophthalmic or nasal spray antihistamine formulation available in Canada. Levocabastine nasal
spray or ophthalmic drops would not generally
be used first-line except for mild persistent
AR with symptoms limited to either the eye
or nose.27 The tolerability of intranasal levocabastine is similar to that of sodium cromoglycate. The most common adverse effects
associated with intranasal levocabastine
include headache (4%), nasal irritation (3%),
somnolence (3%), and fatigue (2%).26 The
only adverse effects that were noted more
commonly with levocabastine ophthalmic
drops compared to placebo were eye irritation
(16.4% vs 15.8%) and tiredness (2% vs
1.4%).26
Oral Decongestants
Pseudoephedrine is available as a single entity
product, in combination with an antihistamine, and/or a pain reliever. It is suitable addon therapy to antihistamines as it helps alleviate nasal congestion for which antihistamines
are generally not effective. Phenylepherine is
available in combination products. These
drugs are sympathomimetic amines, and
should be used with caution in people with
high blood pressure, cardiac or thyroid disease, diabetes, glaucoma, or prostatic hypertrophy.28 Dosage information and common
adverse effects are listed in Patient Self-Care.15
Patients taking non-selective monoamine oxidase inhibitors should avoid taking oral
decongestants because of the potential for
increased pressor effect that can result in
severe hypertension, hyperpyrexia, seizures,
arrhythmias and death.29
Topical Decongestants
Topical decongestants (xylometzoline,
oxymetazoline, naphazoline and phenylephrine are available in Canada), can provide
short-term relief of nasal congestion but
should not be used for more than five to 10
consecutive days to avoid developing rhinitis
medicamentosa, characterized by rebound
congestion, nasal hyper-reactivity, tolerance
and histologic changes of the nasal mucosa.30
If a patient has developed rhinitis medicamentosa, treatment with nasal corticosteroids
has been shown to be effective. Individuals
who have experienced rhinitis medicamentosa
in the past should be particularly careful when
using topical decongestants again as rebound
Pharmacy Post/CE 3
congestion can occur more quickly.30
Intranasal Corticosteroids
Intranasal corticosteroids are the most effective medications for treating AR and are recommended first-line treatment for moderatesevere AR and/or persistent symptoms. 11
They inhibit the release of mediators from
basophils and the influx of eosinophils and
other inflammatory cells and are effective for
all the symptoms of allergic inflammation.3
There are currently six intranasal corticosteroids marketed in Canada: budesonide, fluticasone, flusinolide, beclomethasone,
mometasone and triamcinolone.31-36 No therapeutic advantage has been shown for one
product over another when administered at
equivalent dosages in adults, although patients
may prefer one formulation over another27 or
a once-daily versus twice-daily dosing schedule.3 Cost may also be a factor in patient
choice.3 Interestingly, combination of intranasal corticosteroid with oral antihistamine
has not been shown to be more effective than
intranasal corticosteroid therapy alone.27
In counselling, it should be emphasized to
patients that this is not a relieving medication.
While some patients may experience symptom relief within 12 hours,35 the maximal
effect may not be achieved until after several
days to weeks of regular use because these
agents prevent the release and recruitment
rather than block the effect of inflammatory
mediators. 27 The American Academy of
Otolaryngology - Head and Neck Surgery
Foundation published a review of the techniques of intranasal steroid use.37 Because no
convincing evidence emerged regarding
whether any particular technique provided
maximal efficacy or safety, the panel recommended a seven-step standard technique.1
Hold head in an upright neutral position.2
Clear nose of any thick or excessive mucus.3
Insert spray nozzle into the nostril.4 Direct the
spray away from the septum and toward the
outer portion of the eye or the top of the ear
on that side. (If possible, use the right hand to
spray the left nostril and left hand to spray the
right nostril, to direct the spray away from the
septum.)5 Activate the device as recommend4 Pharmacy Post/CE
ed by the manufacturer and with the number
of sprays recommended by the doctor. 6
Gently breathe in or sniff during the
spraying.7 Breathe out through the nose.
Intranasal corticosteroids are well tolerated. Local adverse effects include sneezing
and irritation of the nose and throat. 27
Crusting, transient dryness and minor epistaxis are also possible. The greatest concern
with intranasal corticosteroid use is the possible effect on the hypothalamic-pituitary
adrenal axis and growth in children. Overall,
the published clinical and pharmacokinetic
literature indicates that “intranasal corticosteroids are unlikely to cause any significant
suppression of the HPA axis when administered short-term (<1 year) at the recommended therapeutic dosage.”27 Reassuringly,
adding intranasal corticosteroids to inhaled
corticosteroid treatment does not appear to
increase suppression of the HPA axis. In
prospective studies with standard doses of
mometasone and fluticasone propionate, no
inhibitory effect on growth in children was
shown.27
Sodium Cromoglycate
Sodium cromoglycate stabilizes mast cells
and prevents degranulation and release of
histamine and other mediators.38,39 It has no
effect on basophils nor any effect against
histamine that has already been released so
is most effective if administered prior to the
development of symptoms. It can be administered intranasally or intraocularly for AR.
It has poor systemic absorption, therefore
the adverse-effect profile is mainly comprised of local reactions such as nasal stinging or burning, sneezing and local irritation
for the intranasal preparation and transient
stinging and burning for the ophthalmic
preparation.39 The ophthalmic preparation
primarily targets ocular symptoms,39 whereas
the intranasal preparation has some impact
on sneezing, rhinorrhea, nasal obstruction
and nasal itch. One of the drawbacks of
sodium cromoglycate is that it needs to be
administered four times a day. Contact lenses should not be worn when using the ophthalmic preparation.39
Ipratropium Bromide
Administered intranasally, this anticholinergic
agent can be effective for reducing watery rhinorrhea in AR40 because histamine- and
antigen-induced submucosal secretion is
cholinergically mediated. Ipratropium has
minimal systemic absorption. Associated
adverse effects include mild and transient
epistaxis, local irritation and nasal dryness.
Leukotriene Antagonists
Leukotriene antagonists (i.e. montelukast,
zafirlukast) would appear to be logical choices
for the treatment of AR because leukotrienes
are implicated in causing congestion and rhinorrhea.20 However, a review of current literature by Nathan41 concluded that these agents
are “sometimes more effective than placebo;
no more effective than nonsedating antihistamines; and less effective than intranasal
corticosteroids in the treatment of allergic
rhinitis.” Moreover, the combination of a
leukotriene antagonist and an antihistamine
has not been shown to be better than monotherapy with either agent. 41 Leukotriene
antagonists have a low incidence of adverse
effects, with headache being the most common, but with a similar incidence as that
reported with placebo.42
Anti-IgE Antibody
Because IgE initiates the inflammatory
processes underlying AR, it is a prime target
for drug therapy.20 Omalizumab is a recombinant, humanized murine anti-IgE antibody
that binds to circulating IgE.43 It is administered subcutaneously once every three to four
weeks for four months and has demonstrated
efficacy and good tolerability in seasonal and
perennial AR, with rates of adverse events
similar to placebo injection.20,43 It is currently
undergoing phase II clinical trials for AR in
Canada.44
Immunotherapy
The three clinical indications for immunotherapy are: IgE-mediated rhinoconjunctivitis, allergic asthma and severe anaphylactic
reactions to bee stings.3 Immunotherapy can
also be considered when allergen avoidance
May 2004
and pharmacologic treatment is unsuccessful.
Immunotherapy involves the administration
of gradually increasing quantities of an extract
of a specific allergen in order to desensitize the
allergic individual over a period of years.
Immunotherapy down-regulates the allergic
phenotype and may reduce the progression of
rhinitis to asthma.3 Injection therapy has several drawbacks, notably the potential for local
and systemic reactions including anaphylaxis.
Results with sublingual immunotherapy have
been encouraging. A Cochrane review of sublingual immunotherapy for AR concluded
that it is a safe treatment that significantly
reduces symptoms and need for pharmacotherapy compared to placebo.45
Alternative Therapy
It is helpful to have reliable sources of information to consult in order to answer questions
from patients or other healthcare professionals
about the putative efficacy of an alternative
therapy. The Natural Medicines Database46 is
extensive, well-organized, referenced, and
user-friendly.
Butterbur (Petasites hybridus) is one herbal
preparation that is being touted for AR.47
Importantly, butterbur should not be used by
women who are pregnant or breastfeeding,
and it is not recommended in children.47
SPECIAL POPULATIONS
AR in Pregnancy
Approximately one-third of women with AR
will experience increased symptoms during
pregnancy.48 The possibility of vasomotor
rhinitis, related to increased estrogen and
progesterone levels can make the diagnosis
more complicated. 48 Allergen avoidance
should be attempted. If possible, drug treatment should be reserved until after the first
trimester when major organ formation in the
fetus is complete. Nasal saline spray and elevating the head of the bed may be helpful.
There are differing opinions regarding the
safety of intranasal decongestants. Demoly et
al. recommend avoiding intranasal decongestants even after the first trimester because data
is lacking.49 In contrast, Blaiss states that nonprescription nasal sprays such as oxymetazoMay 2004
line can be recommended for occasional use.48
Oral decongestants, except for pseudoephedrine, have demonstrated teratogenicity in animals and should be avoided in pregnancy.48,49
Because oral pseudoephedrine taken during
the first trimester has been associated with a
rare condition, infant gastroschisis, it should
not be used during the first trimester. 48
Intranasal sodium cromoglycate can be used
as first-line treatment for AR in pregnancy. It
has minimal systemic absorption and has not
been associated with a risk of congenital malformations. Because they have been in use
longer, first-generation antihistamines rated
Federal Drug Administration category B are
recommended over second-generation antihistamines. However, cetirizine or loratadine,
both of which are currently rated category B,
can be used for those who do not tolerate or
do not respond to the recommended firstgeneration agents.49,50 Intranasal corticosteroids are an option. Corticosteroids are teratogenic in animals and systemic corticosteroids are known to increase risk of abnormalities in humans.49 However, inhaled corticosteroids (rated category C except budesonide which is category B) are used by pregnant women with asthma and have not been
implicated in causing abnormalities. Intranasal
fluticasone propionate has been shown to be
effective for treating vasomotor rhinitis over
an eight-week period; no adverse effects were
noted in the offspring.49 Intranasal ipratropium has poor systemic absorption and may be
used for symptoms of rhinorrhea.49 Although
there is consensus that specific immunotherapy should not be initiated during pregnancy,
women may continue with a regimen that was
begun prior to pregnancy.48,49 Herbal medicines should not be taken due to insufficient
efficacy and safety data.
Although the data are limited for some
drugs, none of the medications used to treat
AR would appear to be incompatible with
breastfeeding. In light of the likely protective
effect of breastfeeding for preventing AR, it
may be particularly important for women with
AR to breastfeed. Because of the low systemic
bioavailability of corticosteroids administered
intranasally, little if any drug is excreted into
breast milk.35 Although pseudoephedrine is
excreted in breast milk, the American
Academy of Pediatrics considers oral pseudoephedrine to be compatible with breastfeeding.51 Similarly oral antihistamines are
excreted in breast milk but are considered to
be compatible with breastfeeding; 50 nonsedating agents would be preferable to sedating agents to minimize any possible adverse
effects in the infant.
AR in Children
Children do not generally exhibit seasonal
allergies until after the age of two or three
because it takes at least two seasons of exposure to induce sensitivity.3 Allergen control
measures should be strongly encouraged
(see Preventive Measures). Newer generation
antihistamines, loratadine and cetirizine, are
available in liquid form and are appropriate
first-line treatment. Intranasal sodium cromoglycate has a very benign adverse effect
profile in children, but compliance may be an
issue because of the frequent dosage schedule.
Some intranasal corticosteroids are approved
for use in children as young as three years and
have good efficacy. As discussed above, the
risk of systemic effects is low.
AR in the Elderly (>65 Years)
Because elderly patients are at increased risk of
drug-drug and drug-disease interactions, second-generation antihistamines are preferred
over first-generation antihistamines. Kidney
function decreases with age, therefore the
dosage of agents that are eliminated renally,
such as fexofenadine,25 may need to be adjusted. Intranasal ipratropium can be useful for
rhinorrhea in elderly individuals and has a low
risk of interactions with other drugs. 40
However, individuals with or predisposed to
glaucoma (the prevalence of which increases
with age), must take care that the spray does
not come into contact with the eyes as there
are isolated reports of aerosolized ipratropium
causing ocular complications.40
ROLE OF THE PHARMACIST
Patients often feel frustrated until the optimal
regimen for symptom control is found.
Pharmacy Post/CE 5
Ensuring that the patient understands the
purpose of each medication, correct administration, and possible adverse effects will
contribute to achieving this goal. Preventive
measures should be encouraged. There are,
several useful websites to which patients can
be directed (http://www.aaaai.org/patients/
resources/fastfacts/rhinitis.stm and http://
www.lung.ca/asthma/allergies/).
Pharmacists are also an information
resource for patients and health-care professionals regarding alternative therapy and treatment options mentioned in the media.
SUMMARY
AR is a common, chronic condition affecting
both children and adults. Antihistamines continue to be the foundation of pharmacotherapy; intranasal corticosteroids are also first-line
treatment. Decongestants are often useful
add-on therapy. Leukotriene antagonists are
another treatment option and anti-IgE antibody treatment is undergoing clinical investigation. Immunotherapy is useful in individuals who have a single allergy for which pharmacologic treatment has not been effective.
Pharmacists have a role to play in educating
patients about the disease, ensuring correct
use of non-prescription and prescription pharmacotherapy, and providing information on
alternative therapy and new treatment
options.
REFERENCES
1. The International Study of Asthma and Allergies in
Childhood (ISAAC) Steering Committee. Worldwide
variation in prevalence of symptoms of asthma, allergic
rhinoconjunctivitis, and atopic eczema: ISAAC. Lancet
1998;351(9111):1225-32.
2. Habbick BF, Pizzichini MMM, Taylor B, et al.
Prevalence of asthma, rhinitis and eczema among children in 2 Canadian cities: The International Study of
Asthma and Allergies in Childhood. CMAJ 1999;
160:1824-8.
3. Berger WE. Overview of allergic rhinitis. Ann Allergy
Asthma Immunol 2003;90 (Suppl 3):7-12.
4. Bellanti JA, Wallerstedt DB. Allergic rhinitis update:
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5. Management of Allergic and Non-Allergic rhinitis.
Summary, Evidence Report/Technology Assessment:
Number 54. AHRQ Publication No. 02-E023, May
2002. Agency for Healthcare Research and Quality,
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rhinsum.htm (accessed November 7, 2003).
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and Quality, Rockville, MD. http://www.ahrq.gov/clinic/
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childhood? A meta-analysis of prospective studies. Acta
Paediatr 2002;91:275-9.
13. BC Health Files. Indoor air quality: Moulds and
other biological contaminants. Ministry of Health
Planning, Health File #65b, April 1998, http://www.
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Williams & Wilkins, 1998.
QUESTIONS
1. A local mothers’ group has invited you
to do a presentation. You select allergic
rhinitis (AR) as your topic because this
condition is common in children and young
adults.
What has been identified as a risk factor for
a child developing AR?
a) Parental history of smoking
b) Parental history of AR/atopy
c) <32 weeks gestation at birth
d) >3 siblings
2. These are all valid reasons for early
diagnosis and appropriate treatment of AR
in children EXCEPT
a) improving quality of life.
b) decreasing the incidence of the common
cold.
c) decreasing the chance of developing facial
abnormalities.
d) decreasing the likelihood of developing
asthma.
3. The late-phase response in AR:
a) occurs in up to 50% of those with the
condition
b) is manifested primarily by a recurrence of
sneezing
c) is noted one hour after the early-phase
response
d) does not occur in immunoglobulin(Ig)
A-deficient individuals.
May 2004
4. A.N., a 20-year-old landscaper, consults
you for help regarding his allergies, which
typically flare up in Spring. In the past he
has used topical decongestants and experienced what sounds like rhinitis medicamentosa. He takes no other medication,
smokes one package of cigarettes daily,
and has no other medical conditions.
Which statement is TRUE?
a) If untreated, his seasonal (intermittent) AR
may progress to perennial (persistent) AR.
b) His allergic symptoms will likely become
more severe as he gets older.
c) He will likely have a higher tolerance to
developing rhinitis medicamentosa from topical decongestants having experienced it
before.
d) He should wear goggles or sunglasses
while working and shower at the end of each
day to lessen allergen exposure.
e) All of the above.
5. A.N. begins taking loratadine 10 mg
daily and returns for a smoking cessation
appointment. Issues to consider include:
a) any form of nicotine replacement therapy
reduces the blood levels of loratadine.
b) his allergic symptoms may worsen as his
sense of smell improves after quitting smoking
c) some individuals who do very physical
work find that the nicotine patch does not
adhere well.
d) nicotine replacement therapy is contraindicated for use in anyone with a concomitant medical condition.
6. A. N. read a newspaper article about a
new treatment – omalizumab – for AR that
only needs to be given every three to four
weeks. What is the mechanism of action of
this agent?
a) Blunting the effects of cytokines.
b) Increasing the ratio of T helper cell (TH)1
to TH2.
c) Inhibition of phosphodiesterase.
d) Acting as an antibody against IgE and
binding to it in the circulation.
7. B.G. is a 35-year-old who has been experiencing very itchy eyes and some sneezing
for the past two months. Upon questioning
her you learn that three months ago she
brought her mother’s cat to live with them
because her mother is currently too ill to
care for it. B.G. takes no medication, has no
other medical conditions, and does not
smoke. Other information that would be
most relevant to learn before making any
recommendations would be:
a) whether the cat is short- or long-haired.
b) B.G.’s diet
c) whether or not B.G. wears contacts
d) all of the above
e) a and c
Pharmacy Post/CE 7
QUESTIONS
8. B.G. begins taking fexofenadine 120 mg
daily and restricts the cat to a non-carpeted
room far from her bedroom and has some
improvement in symptoms. However, she
subsequently experiences 2 episodes of
coughing and chest tightness. Her peak
flow measured in the pharmacy is 70% of
expected so you refer her to her doctor.
The most likely scenario is:
a) She is not actually allergic to cats.
b) The symptoms suggestive of asthma are
unrelated to the allergy.
c) The allergy has led to the development of
asthma.
d) B.G. is experiencing anxiety because of
her mother’s illness.
9. J.W., a 36-year-old woman, asks to
speak with you about her hay fever, which
she experiences every year at this time.
Upon questioning, she does have the typical symptoms of sneezing, itchy eyes and
nasal congestion, which make sleeping difficult. She has used cetirizine in the past
with good effect but is concerned about
using medication because she is 14 weeks
pregnant. Which statement is TRUE?
a) Experts agree that intranasal decongestants are safe to use during pregnancy.
b) Saline nose drops may provide some
relief.
c) Cetirizine must be avoided in pregnancy.
d) Symptoms of AR always improve during
pregnancy.
e) All of the above
10. J.W. has read about the herbal preparation butterbur on the Internet and she
wants to know more. You respond by:
a) asking what information she has read.
b) asking whether her AR symptoms have
worsened.
c) stating that you do not recommend butterbur in pregnancy
d) a and c
e) all of the above
11. Following a prenatal check-up, J.W.
presents a prescription for intranasal fluticasone. Which statement regarding
intranasal fluticasone is TRUE?
a) It will provide immediate relief.
b) It has been used in a trial of vasomotor
rhinitis of pregnancy and showed no adverse
effects on the baby.
c) It is rated category B in pregnancy.
8 Pharmacy Post/CE
d) The patient should breathe out through
the mouth after administering a dose.
12. J.W. is wondering whether she can
take any medication for AR when she is
breastfeeding. You respond that:
a) All the medications used to treat AR
appear to be compatible with breastfeeding.
b) A sedating antihistamine may be preferred
because of its shorter duration of action
compared to a non-sedating antihistamine.
c) Atopic women should not breastfeed
because IgE is transferred to breastmilk,
inducing allergy in the infant.
d) Antihistamines decrease milk production.
13. C.M., an 80-year-old with rheumatoid
arthritis and hypertension controlled with
medication, presents a prescription for
ipratropium nasal spray for her runny nose.
An issue of particular concern would be:
a) the potential for adverse effects to outweigh possible benefits of this treatment in
this patient.
b) the potential for drug interactions with her
current medications.
c) whether the patient is able to manipulate
the delivery device given her conditions.
d) the potential for drug-disease interactions.
14. A mother presents a prescription for
intranasal sodium cromoglycate for her fiveyear-old daughter, N.M. How would you
counsel the mother on this medication?
a) It can cause drowsiness, so observe her
performance at kindergarten.
b) It commonly causes nose bleeds.
c) It commonly causes nasal stinging.
d) It commonly causes dry mouth; sugarless
gum or ice chips may offset this adverse
effect.
15. After two weeks, N.M. still has troubling
symptoms. Possible reasons for this include
all of the following EXCEPT
a) poor compliance with the frequent dosing
schedule.
b) sodium cromoglycate is ineffective in this
age group.
c) initiation of the drug after the pollen season has begun.
d) excessive pollen exposure.
16. N.M.’s physician prescribes intranasal
mometasone. Her mother is reluctant to fill
the prescription because she has heard
that steroids stunt growth. What is your
response?
a) Intranasal mometasone is less effective
than some other intranasal corticosteroids.
b) Intranasal mometasone should be avoided
in case her child requires inhaled corticosteroid treatment for asthma in the future.
c) Immunotherapy would be a simpler
option.
d) At dosages recommended by the manufacturer, intranasal mometasone has not
been shown to affect children’s growth.
17. D.V. is a 32-year-old lawyer with asthma and persistent AR. He is allergic to
ASA. He is currently receiving inhaled fluticasone 500 mcg twice daily and intranasal
budesonide one spray into each nostril
twice daily. He mentions that he still experiences nasal congestion and presents a
prescription for montelukast 10 mg daily
from an ear, nose and throat specialist.
Which of the following is TRUE of montelukast?
a) It is rational therapy in someone with concomitant asthma, AR and ASA allergy.
b) It is prescribed at a lower dosage for AR
than for asthma.
c) It has a well-defined role as second-line
therapy in persistent AR.
d) All of the above
18. You counsel D.V. that montelukast:
a) should be taken on an empty stomach.
b) commonly causes sedation.
c) is unlikely to interact with his current
medications.
d) none of the above
19. Levocabastine ophthalmic drops are
most appropriate to treat AR when used
a) in children.
b) with predominantly ocular symptoms.
c) in elderly patients.
d) where severe nasal congestion precludes
intranasal administration.
20. Which combination has proven benefits
over monotherapy with either agent alone?
a) Nonsedating antihistamine + intranasal
corticosteroid
b) Nonsedating antihistamine + oral decongestant
c) Oral decongestant + topical decongestant
d) Antihistamine + leukotriene antagonist
May 2004
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