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Allergic rhinitis: impact, diagnosis, treatment and
management
pharmaceutical-journal.com/research/review-article/allergic-rhinitis-impact-diagnosis-treatment-andmanagement/20201509.article
Clinical Pharmacist 9 AUG 2016 By Diana S Church , Martin K Church , Glenis K Scadding
Abstract
Allergic rhinitis results from an immunological abnormality in which atopic individuals
produce immunoglobulin E (IgE) to allergens (e.g. pollen, house dust mites, animal
dander and moulds). IgE activates mast cells, which respond by releasing inflammatory
mediators. Histamine stimulates the early symptoms, predominately mucus production,
nasal itching and sneezing. Leukotrienes and cytokines attract and activate eosinophils to
cause allergic inflammation, which is primarily responsible for nasal blockage. When
untreated, these symptoms can potentially impair patients’ ability to sleep and perform
optimally in their daily professional or personal life. Children’s education is also
particularly affected by untreated symptoms. Treatment is primarily with second
generation H1 -antihistamines, which are particularly effective against the early
symptoms, and intranasal corticosteroids, which reduce allergic inflammation and
improve nasal blockage. First generation H1 -antihistamines should be avoided because
they exacerbate the psychogenic effects of allergic rhinitis. This review article aims to
provide pharmacists and other healthcare professionals with an understanding of the
impact of undiagnosed allergic rhinitis and how to diagnose and treat it effectively.
Keywords: allergy, allergens, allergic rhinitis, antihistamine, corticosteroids, histamine,
immunology, inflammation, pollen.
Original submitted: 10 June 2016; Revised submitted: 29 June 2016; Accepted for
publication: 04 July 2016; Published online: 09 August 2016
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Source: CNRI / Science Photo Library
Caused by an allergy to pollen, this inflamed mucosa shows its ciliated (hairy) surface overgrown in patches.
Cilia are common on the epithelium of the respiratory tract, where their beating serves to remove particles of
dust, pollen, and other foreign material. Here, an allergy to pollen has resulted in the cilia lengthening.
Key points:
Allergic rhinitis occurs in atopic individuals who produce IgE to allergens, such as
pollen, house dust mites, animal dander and moulds.
Histamine stimulates the early symptoms, predominately mucus production, nasal
itching and sneezing. This may respond well to non-sedating H1 -antihistamines.
Subsequent allergic inflammation gives rise to nasal blockage. This responds to
nasal steroids.
When untreated, allergic rhinitis can potentially impair patients’ ability to sleep and
perform optimally in their daily professional or personal life. Children’s education is
also particularly affected.
First generation H1 -antihistamines should be avoided because they exacerbate the
psychogenic effects of allergic rhinitis.
Introduction
Allergic rhinitis is a common allergic disease with increasing prevalence; recent estimates
suggest it affects over 30% of individuals, particularly, but not exclusively, teenagers and
young adults[1],[2]. While considered by many as a trivial disease, allergic rhinitis, in addition
to the nasal and ocular symptoms, is crucially linked to impairments in information processing
and changes in attention-related cognitive processes [3]. However, it has been estimated that up
to 90% of allergic rhinitis patients are untreated, insufficiently treated or inappropriately
treated[4]. This has the potential to impair patients’ ability to perform optimally in their daily
professional and personal life.
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Pathological and psychological effects of untreated allergic
rhinitis
Allergic rhinitis generally develops during childhood and it is the most common chronic
allergic disorder seen in children [5]. Studies have shown that these children can experience
significant impairment through multiple physical and psychological aspects. Their symptoms,
particularly a runny nose, mean that children are often embarrassed in school, have decreased
social interaction and are at double the risk of accidental injury[5],[6]. Nasal congestion, in
particular, is associated with sleep disturbance and resultant daytime fatigue[7]. Two studies
have concluded that untreated allergic rhinitis has a marked detrimental effect on children’s
learning and examination performance[8],[9]. This is particularly important considering that a
quarter of UK school-age children suffer with allergic rhinitis[10], most of whom will have
their peak symptoms in spring and summer, which can coincide with important school
examinations. The correlation between allergic rhinitis and negative effects on learning should
be an area of concern for all professionals involved in their care.
The overall quality of life reduction resulting from allergic rhinitis in adults is well established
– it has a detrimental effect on adult cognitive processes (e.g. productivity at work), as well as
other common attention-requiring activities, such as driving[4],[11],[12]. In a study assessing the
effect of nasal allergen provocation of seasonal allergic patients on driving performance, it
was demonstrated that symptomatic and untreated patients had significantly impaired driving
ability, the magnitude of which was comparable to having a blood alcohol level of 0.05%, the
legal limit in many countries[13]. In addition to acute symptoms, sleep disturbances may
exacerbate impairment of psychomotor performance, including driving[14],[15],[16],[17]. Patients
with allergic rhinitis are often affected by physical conditions (e.g. otitis media, eustachian
tube dysfunction, sinusitis[18]) and other allergic conditions (e.g. asthma and eczema[19]).
Therefore, allergic rhinitis is an illness that affects multiple aspects of patient’s life [19], can be
a source of multiple doctor appointments and has complex effects on society as a whole.
Therefore, optimal management of the disease should address both its physical and mental
consequences.
Mechanisms of allergic rhinitis
The roots of allergy are in parasitology, when a nematode parasite attacking the nasal mucosa.
On first presentation, the immune system is stimulated to produce immunoglobulin E (IgE)
that will bind to and prime mast cells and other inflammatory cells. On a subsequent
presentation, nematode antigens interact with the mast cell IgE, causing it to release preformed
histamine to make the local environment hostile (e.g. producing mucus and stimulating
sensory nerves to cause sneezing). Mast cells also produce cytokines to stimulate the influx
inflammatory cells, particularly eosinophils that contain several toxic proteins with which they
kill the nematode and cause local inflammation. Patients with allergies mount the same
response to allergens as nematode antigens[20],[21]. The series of early immune system events
in patients with allergic rhinitis is presented in Figure 1.
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Figure 1: Immune system events in patients with allergic rhinitis
Panel A demonstrates early immune system events, while panel B shows the later inflammatory allergic
response that increases the severity and persistence of the initial symptoms in patients with allergic rhinitis.
See text for an explanation of the events (numbered).
Panel A demonstrates (1) allergens (e.g. pollen, house dust mites, animal dander and moulds)
penetrating the nasal epithelium. (2) Allergen interacts with IgE, shown in red, to activate the
mast cell. (3) Histamine is the primary mediator released in this early phase of the response. It
has three immediate main effects: (4) stimulation of mucosal goblet cells to produce watery
mucus; (5) stimulation of sensory nerves to cause nasal itching and sneezing; and (6)
vasodilation and tissue oedema, which contribute to nasal blockage. These effects are
primarily histamine-mediated so antihistamines are effective in relieving these symptoms.
Panel B shows the later inflammatory allergic response that increases the severity and
persistence of the initial symptoms, resulting in a chronic phase of allergic rhinitis. Mast cell
activation also produces cytokines, responsible for the attraction of more mast cells and the
influx and activation of other inflammatory cells, particularly eosinophils (7)[22]. Eosinophils
contain aggressive proteinaceous mediators (8) that stimulate sensory neurones to
dramatically increase the production and release of neuropeptides (9). These neuropeptides act
on special venous capacitance vessels (10) present in the nasal turbinates, causing dilatation
and reduced emptying. This is the primary cause of nasal blockage.
Mechanisms of ocular symptoms
Patients with allergic rhinitis may also experience ocular symptoms, primarily reddened, itchy
and watery eyes. Classically these symptoms were believed to be caused by the allergen
landing on the conjunctival lining of the eye, with subsequent activation of the conjunctival
mast cells[23]. It is now believed that these symptoms are partly the result of a naso-ocular
reflex in which allergic inflammation in the nose stimulates the trigeminal nerve with
subsequent release of neuropeptides in the tears[24]. These neuropeptides activate conjunctival
mast cells that release histamine but cause little subsequent eosinophil infiltration and allergic
inflammation[23]. During periods of high atmospheric levels, pollen impaction on the
conjunctiva may induce a more severe form of vernal conjunctivitis in which eosinophil
infiltration stimulated allergic inflammation[25]. If a severe form of vernal conjunctivitis is
suspected, the patient should be referred to their GP.
Diagnosis of allergic rhinitis by pharmacists
Historically, diagnosis of allergic rhinitis has been made by primary healthcare practitioners.
However, pharmacists are now being encouraged to make the primary diagnosis of allergic
rhinitis and establish a management and therapy plan[26]. Although it should be emphasised
that complex cases, or cases where there may by an alternative diagnosis, should always be
referred to a GP.
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Allergic rhinitis symptoms, including runny nose, itching, sneezing and nasal blockage, are
similar to those of the common cold and can be present intermittently, giving the false
suggestion of recurrent ‘colds’[27]. This is more common in patients who are allergic to
pollens or outdoor moulds (rather than pets or house dust mites), which are released into the
air and cause symptoms during specific periods of time throughout the year (see ‘Figure 2:
Seasonal considerations’).
Taking a history from the patient
When questioning the patient, pharmacists should listen for indicators that can lead to the
diagnosis of allergic rhinitis, for example:
recurrence at a particular time of year or day, or variability of symptoms, suggesting
worsening on exposure to the relevant allergen;
involvement of the eyes (itching, watering, redness, puffiness); or
predominance of itch as a symptom, which can also involve the pharynx and ears.
Allergic rhinitis is more likely if there is a past or family history of allergic disease, but
can also occur as the first manifestation of allergy in a previously unaffected person.
When taking the patient’s history, it is important to be aware that they might not often offer all
the clues for diagnosis, so pharmacists may have to ask specific questions to find out more
information. For example, a patient with allergy to house dust mites or animals may complain
of sneezing, having a runny nose and blocked nose in the past one or two weeks, but they
might not realise until asked that their nose has been blocked to a less severe degree for a
much longer time. The pharmacist should also enquire about new allergens in the home,
work, or school environment, as well as symptoms of asthma (shortness of breath
accompanied by wheeze, reduced exercise tolerance or nocturnal symptoms), which often
accompany poorly controlled allergic rhinitis.
Seasonal considerations
Patients may be allergic to trees, plants and
fungi that use the wind to disperse their pollen
or spores[28]. Higher amounts of pollens are
released during dry, warmer days when the
chance of their satisfactory dispersion is
maximum (see Figure 2). Visually these plants
are unspectacular in contrast to those with
colourful flowers to attract bees and other
insects to cross-pollinate them. Individuals are
rarely allergic to this latter type[28].
Figure 2: The seasons of major plant
allergens and house dust mite
The lines refer to the times of year at which different
allergens peak. Note that house dust mite levels are
highest in the winter when doors and windows are
closed in centrally heated homes.
While high amounts of pollen and fungal
spores are released during warmer days
compared to colder ones, house dust mite
allergens are present all year round. However,
these tend to be higher indoors during winter
when windows are shut and the humid,
centrally heated atmosphere is optimum for
their reproduction[29].
Further testing
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With a clear patient history, diagnosis can be made without further tests. However, if in doubt,
looking for the likely IgE molecules by skin prick or blood test can be helpful, although this
should be guided by history, rather than performed in a random fashion. Random screening of
multiple possible allergens is inadvisable because positive tests do not always indicate clinical
disease; many individuals with allergen-specific IgE do not develop symptoms[30].
Furthermore, a positive test to an allergen with no pertinence to patient’s history has no
relevance for diagnosis and might result in over-diagnosis and unnecessary stress for the
patient. Testing should always be considered in the context of the possible clinical benefit,
which can be from allergen avoidance, if the patient is able and willing to comply, or allergen
specific immunotherapy.
Treatment
This section assesses the drugs only briefly – further information and the British Society for
Allergy & Clinical Immunology (BSACI) guidelines for the management of allergic and nonallergic rhinitis[31] are included in later sections.
H1 -antihistamines are effective in relieving histamine-induced symptoms, including itch,
runny nose and/or sneezing[31]. They have a lesser effect on nasal blockage but can be
effective as a single medicine in patients with mild to moderate forms of allergic rhinitis[31].
They have a rapid onset of action and can be used as a rescue medicine to help alleviate the
symptoms of the onset of acute allergic rhinitis.
Intranasal corticosteroids are the primary treatment for nasal obstruction [31] and act by
reducing cytokine production thereby reducing eosinophil recruitment. They also reduce
eosinophil activation and mediator release[32].
Leukotriene receptor antagonists (LTRAs) are given as tablets and may be effective in
some patients but not all[33]. They reduce the effects of the leukotriene C 4 (LTC 4) that
activated mast cells and eosinophils secrete in order to enhance the recruitment of more
eosinophils and thereby reduce allergic inflammation [34]. The LTRAs montelukast and
zafirlukast are available on medical prescription only (POM). Leukotriene synthesis inhibitors
(e.g. zileuton), are not available in the UK.
Nasal decongestants (e.g. xylometazoline and oxymetazoline), are asympathetic receptor
stimulants and cause constriction of the arterial vessels delivering blood to the nasal
capacitance vessels, therefore starving them of blood[35]. They may be given locally or orally.
When given as nasal drops, they are briefly effective and rapidly acting but they may only be
used for short periods – usually four to ten days[31]. Regular use induces a decrease in the
number of a-receptors in the blood vessels rendering a reduced effectiveness with time
(tolerance)[35]. If used for longer periods, rhinitis medicamentosa, a condition characterised by
nasal congestion without rhinorrhoea or sneezing, may occur because of a reduction of blood
vessel a-receptors thus paralysing the physiological local vasoconstriction process[7]. Patients
should be counselled regarding this process.
Oral decongestants (e.g. pseudoephedrine) are only weakly effective in reducing nasal
obstruction but have a longer duration of up to six hours (with slow release preparations)[31].
Owing to their sympathomimetic effects, they should not be used by individuals with high
blood pressure or heart problems [36].
Saline douching, although relatively uncommon in UK, is a safe and inexpensive method of
reducing symptoms in children and adults with seasonal rhinitis by washing out sticky mucus
from the nose[31].
The treatment of ocular symptoms of allergic rhinitis is summarised in Box 1.
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Box 1: Treatment of ocular symptoms
1. Intranasal corticosteroids are the most effective treatment for reducing nasal
inflammation and, consequently, are effective in improving conjunctival
symptoms[37].
2. H1-antihistamine eye drops have a similar efficacy profile to oral antihistamines
with the advantage of a significantly faster onset of action[38].
3. Topical chromones, sodium cromoglycate or nedocromil sodium, which are
available as topical eye preparations, are also weakly effective. Although purported
to be mast cell stabilisers, they most likely affect the inhibition of sensory nerve
activation, thereby reducing itching[39].
Selecting the right treatment
Oral antihistamines are the first-line treatment used by most patients, doctors and pharmacists
for all allergic rhinitis.
When selecting the most appropriate antihistamine to manage allergic rhinitis, healthcare
professionals should be aware of the significant detrimental effect of first generation
antihistamines (FGAH) on cognitive processes in all patient groups[40]. Histamine acting on
H 1 -receptors in the brain has a completely different function to that in the periphery. In the
brain, it has an arousal effect and aids concentration and learning[40]. FGAHs (e.g.
chlorpheniramine, diphenhydramine, hydroxyzine and ketotifen) readily penetrate into the
central nervous system (CNS) and bind to the H1 -receptors in the brain, causing drowsiness
and poor attention[40].
Studies in children have demonstrated that FGAHs exacerbate the detrimental effect of
allergic rhinitis on learning ability[8]. Furthermore, in teenagers sitting summer mock GCSE
examinations, untreated allergic rhinitis caused a 40% increased likelihood of students
dropping an examination grade. FGAHs increased this to 70%[9].
In adults the detrimental effects of allergic rhinitis on quality of life and productivity at work
are exacerbated by FGAHs, even at the lowest doses recommended by manufacturers[40]. The
effects of FGAHs on the CNS are similar to and additive with those produced by alcohol or
other CNS-sedatives, and bedtime dosing with FGAHs may have hangover effects the next
day due to their long elimination half-life value[40]. Furthermore, FGAHs may significantly
reduce driving ability to potentially dangerous levels[40],[41], particularly in the elderly and
those who combine the drug with alcohol ingestion. One study suggests that 25% of
individuals older than 65 years of age have some cognitive impairment, often with no overt
sign of dysfunction [42]. Administration of FGAHs to this population increases the risk of
inattention, disorganised speech, altered consciousness and impaired function or
alertness[43],[44]. In addition, because of their anticholinergic activity, FGAHs significantly
increase the risk for development of dementia[45].
7/17
Therefore, the British and European Guidelines for both allergic rhinitis and urticaria specify
that only second generation antihistamines should be used for symptom relief, because they
penetrate less well into the brain than FGAHs and have negligible anticholinergic
effects[31],[46]. In the UK, cetirizine and loratadine are currently the only SGAHs available for
patients to buy over-the-counter (OTC). There are many others (including levocetirizine,
desloratadine, rupatadine, fexofenadine and bilastine) that are available as prescription-only
medicines (POM). Even though SGAHs are stated to be minimally sedating, there are some
patients who suffer sedation and psychomotor retardation, especially if other sedatives or
alcohol are taken concomitantly[40]. Fexofenadine and bilastine are the least sedating SGAHs
currently available because they are actively pumped out of the blood–brain barrier by pglycoprotein (a proton pump)[47]. However, these must be taken on an empty stomach for
adequate absorption.
Intranasal antihistamines are more effective at reducing nasal symptoms than oral
antihistamines, but do not treat extra-nasal symptoms[48]. Azelastine nasal spray is available
OTC.
Although antihistamines demonstrate efficacy, for the control of symptoms like sneezing,
itching and rhinorrhoea or eye streaming, they are considerably less effective than intranasal
corticosteroids that have a much stronger anti-inflammatory effect and are more effective in
treating nasal obstruction[49]. Corticosteroids should be used as the therapeutic of choice for
anything more than mild disease[31].
Intranasal steroids
Intranasal steroids are the most effective treatment for reducing nasal inflammation and
improving conjunctival symptoms[23],[50]. In the UK, beclomethasone dipropionate and
fluticasone propionate are available OTC, while fluticasone furoate and mometasone furoate
are POM.
When bought OTC or even when prescribed by a medical practitioner, nasal steroids are often
wrongly used or not used at all, because of fears of “steroids”. Therefore, it is important to
explain to the patient that the dose of nasal steroids is in microgram quantities and for most of
the common molecules there is minimal systemic bioavailability (i.e. the amount of active
drug reaching the systemic circulation). There is a variation between molecules, with
fluticasone propionate, furoate and mometasone furoate being the least bioavailable from the
nose. It is best to use the spray in the morning, putting it next to the toothbrush to aid memory.
A second dose can be used in the evening if needed, or if the morning one was forgotten.
The method of application for nasal sprays and drops is shown in Figure 3. Spraying the nasal
septum and sniffing the spray straight back into the throat should be avoided.
Figure 3: Method of application for nasal sprays and nasal drops
8/17
Source: Reproduced from the BSACI allergic rhinitis guidelines with permission.
(a) Correct procedure for the application of nasal sprays. (b) Correct procedure for the installation of nasal
drops.
Begin treatment early and take it daily
It is important to inform patients that nasal steroids do not work immediately. Nasal steroids
have been shown to take at least several days to reach full effectiveness and maximal effect
may not be apparent for two weeks[29].
For patients with intermittent symptoms (e.g. those allergic to pollens) it has been
demonstrated that if therapy with topical nasal corticosteroids is begun a week or two before
symptoms are expected, symptoms have delayed onset and reduced severity[51]. Thus, it can
be useful to ask patients with known seasonal allergic rhinitis to make a note of when their
symptoms started in the current year so that in the following year they can start the treatment
earlier.
Similarly, both antihistamines and nasal corticosteroids, particularly the latter, are more
effective if used on a daily basis, rather than being stopped and started[51]. The symptoms for
both persistent and intermittent allergic rhinitis are underlined by an ongoing inflammation
that is usually present at subclinical levels, even in the absence of symptoms[52]. Daily
treatment helps to prevent this low-grade ongoing subclinical allergic inflammation in the
nasal lining increasing to a threshold at which symptoms occur and, thus, reduces the rate and
severity of exacerbations[51]. Therefore, pharmacists should explain to patients that the drug
makes them free of symptoms, rather than curing their disease, so stopping treatment early
will result in the reappearance of symptoms. If they do not get relief from the prescribed
medication, they should seek further advice since other treatment options might be available.
A simple way to keep track of patients’ symptoms is for them to use the MACVIA-ARIA
visual analogue scale, via a mobile phone app[53]. If their total symptom score is over half way
along the line, the treatment needs to be augmented or changed. Switching from one brand of
antihistamine or intranasal corticosteroid to another is not the answer.
BSACI guidelines suggest that in more severe disease nasal corticosteroids and antihistamines
may be used together[31] and the combination of nasal corticosteroid plus nasal antihistamine
(e.g. azelastine plus fluticasone) has been reported to be more effective than either
alone[54],[55]. However, this drug combination is a POM at present.
Management of allergic rhinitis
The BSACI guidelines provide direction to help healthcare professionals direct therapy for
allergic rhinitis[31]. A simple algorithm for the treatment of allergic rhinitis is shown in Figure
4.
9/17
Figure 4: A simple algorithm for the treatment of allergic rhinitis
Source: This figure is adapted from the BSACI allergic rhinitis guidelines.
The progression of treatment goes from left to right as severity increases.
For patients with intermittent allergic rhinitis caused by seasonal allergens, as the season
wanes and pollen levels in the atmosphere reduce, treatment can be gradually reduced, if the
symptoms are completely controlled, and stopped once the season is over.
Patients with persistent allergic rhinitis, such as those allergic to perennial allergens (e.g.
house dust mite, animals or indoor moulds) or those with mixed seasonal and perennial
allergies, need longer term therapy. Once complete control of symptoms has been achieved, a
gradual ‘step down’ can be attempted. The treatment should be continued for at least three to
six months after complete symptom control. If symptoms recur, the treatment should be
restarted, usually for longer periods (e.g. 6–12 months or even for life). There are some
concerns about possible lining atrophy with long-term use of intranasal steroids. However, in
practice, with correct use this does not occur, probably because of rapid movement by
mucocilliary clearance[56]. Spraying the nasal septum repeatedly can result in soreness,
epistaxis (nose bleed) and possibly even perforation, which is why correct technique is
important.
Allergen avoidance
Studies involving concomitant multiple strict allergen control measures showed that it is
possible to achieve a significant reduction in allergen exposure and, consequently, in
symptoms[57],[58]. However, in real life situations, avoiding aeroallergens to an extent where it
would make a difference in patients’ symptoms is difficult to reach. With pollen allergy,
closing windows at night, driving with closed windows or wearing wrap-around glasses
outdoors can prevent symptom exacerbation[31]. Avoiding being outside during thunderstorms
can also help reduce symptoms, because the sudden change from a dry to a wet climate causes
pollen grains to rupture and release their allergenic into smaller particles, which can be easily
inhaled into the lower airways and cause attacks of allergic rhinitis and asthma[59].
Immunotherapy
Allergen-specific immunotherapy is the treatment in which a patient’s immune system is
rendered tolerant to an allergen by giving increasing doses of the allergen in a controlled
fashion[60],[61]. When used correctly, it is the only treatment that can alter disease course[60].
There is also evidence that it can reduce development of further sensitisations and progression
of allergic rhinitis to asthma, although current trials require positive outcomes to determine if
children with allergic rhinitis, who are likely to progress to asthma, will benefit from it[61].
Few seasonal allergic rhinitis patients warrant immunotherapy treatment; it should only be
considered when allergic rhinitis is debilitating and poorly controlled by pharmacotherapy.
Special consideration should be given to badly affected young people who face years of
summertime examinations or adults whose functioning is disturbed (e.g. surgeons who have
severe eye symptoms or sneezing bouts)[61]. Immunotherapy is currently available for allergic
rhinitis caused by pollen, moulds, house dust mite and animal allergens.
There are two main routes by which immunotherapy is administered; subcutaneously and
sublingually. Subcutaneous immunotherapy involves allergen injections at regular time
intervals in a hospital by trained medical staff. With treatment lasting several years, patient
commitment to attending hospital appointments is essential. Sublingual immunotherapy is
considered to be much safer. The initial dose is given under supervision, but can then be
continued on a daily basis at home[62],[63]. However, patients should be warned against poor
compliance, which is a concern with this form of immunotherapy[64].
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Management in specific patient groups
Children with allergic rhinitis
Children metabolise drugs less well than adults because the liver enzymes mature slowly and
only reach maximal levels at around ten years of age[65]. However, renal clearance is well
developed. Consequently, it is preferable that young children are prescribed an antihistamine
that is not metabolised but excreted unchanged in the urine[66]. Of the OTC preparations, this
means cetirizine is preferable, rather than loratadine.
A nasal steroid with low systemic bioavailability should be used at the lowest possible dose to
control symptoms, particularly nasal congestion and obstruction. Compliance and efficacy is
improved if the child is taught how to use the nasal spray [31]. In older children where liver
metabolic enzymes are increasing, it may be preferable to use fluticasone, which is cleared by
first metabolism, rather than beclomethasone that is not and, consequently, may
accumulate[67]. Furthermore, fluticasone is available for children from four years of age, while
beclomethasone is only available for children from six years of age.
Allergic rhinitis in pregnancy
Most medicines cross the placenta, and should only be prescribed when the apparent benefit is
greater than the risk to the foetus[31]. Regular nasal douching may be helpful. Of the
antihistamines, both loratadine and cetirizine are recommended because they appear to have
good safety records because they have been widely used in pregnant women[68]. Similarly,
beclomethasone and fluticasone appear safe. However, decongestants should be avoided[31].
Local application of chromones, which have not demonstrated teratogenic effects in animals,
are probably the safest drug choice for use in the first three months of pregnancy because
systemic absorption is negligible, although they require multiple daily administrations[31].
Conclusion
The treatment of allergic rhinitis involves non-sedating H1 -antihistamines to reduce
rhinorrhoea and nasal itching, and corticosteroids to reduce allergic inflammation and nasal
blockage. They should be used on a daily basis rather than on ad hoc when symptoms are bad.
Pharmacists should advise patients about how to correctly administer their treatment, as well
as reviewing its effectiveness regularly. Patients should be advised of alternative treatment
options where appropriate.
Financial and conflicts of interests dislosure:
Martin Church has been a speaker or consultant for Almirall, FAES Pharma, Menarini,
Moxie, MSD, Novartis, UCB Pharma, Sanofi-Aventis and Uriach. Glenis Scadding has
had research grants from GSK & ALK and has been a speaker or consultant for ALK,
Astra Zeneca, Brittania Pharmaceuticals, Capnia, Church & Dwight, Circassia, GSK,
Groupo Uriach, Meda, Merck, MSD, Ono Pharmaceuticals, Oxford Therapeutics, SanofiAventis, UCB. Diana Church has no relevant affiliations or financial involvement with any
organisation or entity with a financial interest in or financial conflict with the subject
matter or materials discussed in the manuscript apart from those disclosed. No writing
assistance was utilised in the production of this manuscript.
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Citation: Clinical Pharmacist, August 2016, Vol 8, No 8, online | DOI:
10.1211/CP.2016.20201509
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