Allergic rhinitis

The right clinical information, right where it's needed

Last updated: Jun 13, 2018

 Table of Contents
Summary 3

Basics 4
Definition 4
Epidemiology 4
Aetiology 4
Pathophysiology 5
Classification 5

Prevention 7
Primary prevention 7
Secondary prevention 7

Diagnosis 8
Case history 8
Step-by-step diagnostic approach 8
Risk factors 9
History & examination factors 12
Diagnostic tests 13
Differential diagnosis 15
Diagnostic criteria 16

Treatment 17
Step-by-step treatment approach 17
Treatment details overview 21
Treatment options 23
Emerging 48

Follow up 49
Recommendations 49
Complications 49
Prognosis 50

Guidelines 52
Diagnostic guidelines 52
Treatment guidelines 52

Evidence scores 54

References 55

Disclaimer 62
 Summary

◊ Presumptive diagnosis of allergic rhinitis may be made in the presence of nasal congestion,
sneezing, and itchy nose/palate/eyes with a pattern of allergic triggers.

◊ Definitive diagnosis would require specific IgE reactivity during skin-prick or in vitro testing, but a trial
of therapy may be ordered on the basis of a presumptive clinical diagnosis.

◊ Treatment consists of allergen avoidance where possible and pharmacotherapy (antihistamines,

corticosteroids, cromoglicate, decongestants, leukotriene receptor antagonists). Immunotherapy may
be an option in patients with persistent symptoms.

◊ Intranasal corticosteroids remain the single most effective class of medications for treating allergic
rhinitis.

◊ Reducing exposure to environmental allergens (e.g., dander, dust mites, and tobacco smoke) is an
important measure for patients sensitive to these items, and can often be recommended empirically
based on the patient's history.
 Allergic rhinitis Basics

Definition
Allergic rhinitis (AR) is a common, yet under-appreciated inflammatory condition of the nasal mucosa,
characterised by nasal pruritus, sneezing, rhinorrhoea, and nasal congestion, the last of which is often
BASICS

deemed the most bothersome symptom. Frequently, there is associated palate, throat, ear, and eye itching
as well as eye redness, puffiness, and watery discharge. AR is mediated by an IgE-associated response to
ubiquitous indoor and/or outdoor environmental allergens.

Epidemiology
Allergic rhinitis (AR) is a common disease that affects up to 30% of adults and up to 40% of children in
industrialised countries worldwide.[2] In the US, prevalence of physician-diagnosed AR has been reported to
be 14% in adults and 7% in children.[3] In Europe, prevalence of AR was reported as 13%.[4]

AR affects people of all ages, but approximately 80% of individuals diagnosed with AR develop symptoms
before the age of 20 years.[5] Older children have a higher prevalence of AR than younger ones, with a peak
occurring at ages 13 to 14 years.[6] During early childhood, boys are more likely than girls to be affected
by AR;[7] beginning in puberty, girls have a higher rate of new AR symptoms, and by age >20 years the
prevalence of AR is equal among men and women.[7]

The prevalence of AR varies significantly between countries, as demonstrated by the landmark International
Study of Asthma and Allergies in Childhood (ISAAC) study, which reviewed self-reported symptoms of
allergic rhinoconjunctivitis, asthma, and atopic dermatitis among 463,801 children aged 13 to 14 years
from 56 countries.[8] The initial phase of the study (carried out between 1992 and 1998) found the highest
prevalence of AR in the UK, Australia, New Zealand, and Ireland, followed by North, Central, and South
America; the lowest prevalence was found in Eastern European countries, Indonesia, Greece, China, Taiwan,
Uzbekistan, India, and Ethiopia. There was an overall increase in prevalence of AR across most countries,
particularly among young children, when the ISAAC study was repeated between 2002 and 2003.[9]

Aetiology
Allergic rhinitis (AR) is not easily explained by the presence of any one genetic or environmental variable.
It is likely that multiple genes, in combination with one another and specific environmental variables, are
responsible for causing the clinical manifestation of AR.[10] [11] Atopic disorders have been linked to loci
on chromosomes 2, 5, 6, 7, 11, 13, 16, and 20, suggesting family history represents a major risk factor for
the development of AR. The risk of developing atopic disease in the absence of parental family history was
reported to be 13%.[12] The risk increased to 29% if one parent or sibling is atopic, 47% if both parents are
atopic, and 72% if both parents have the same atopic manifestation.[12] The prevalence of AR continues
to increase in the Western world.[13] While no single variable can account for this increase, the 'hygiene
hypothesis' has been frequently cited as a possible explanation. Supporters of this hypothesis propose that
inadequate exposure to animals and other microorganism-rich environments in early life may favour an
allergic phenotype.[14]

Changes to the intestinal microbiome have also been implicated in the development of allergy (the 'microflora
hypothesis').[15] [16] [17] [18] [19] According to this hypothesis, the intestinal microbiome of Westerners may
be altered by certain lifestyle factors (e.g., antibiotic use and dietary factors) which may predispose to the
development of allergy.[15]

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Allergic rhinitis Basics

Pathophysiology
In susceptible individuals, exposure to a variety of environmental aero-allergens leads to allergic
sensitisation, which is characterised by the production of specific IgE directed against these proteins. This

BASICS
process begins with the binding of the allergen by antigen-presenting cells, such as dendritic cells, in the
nasal mucosa that process the captured allergen and present it to T cells. Ultimately, this may lead to the
production of allergen-specific IgE, which binds to high-affinity IgE receptors present on the surface of mast
cells in the nasal mucosa.

Once mast cells are sensitised to specific allergens, re-exposure to the allergen in quantities sufficient to
cause cross-linking between allergen and adjacent IgE molecules will lead to degranulation of the mast cell
and initiation of various pro-inflammatory events, such as synthesis of interleukins and inflammatory cell
infiltration. The effects of mast cell activation may be separated into two separate processes termed the early
phase and the late-phase response.

The early phase begins within minutes of allergen exposure and is primarily due to mast cell release of
pre-formed mediators, including histamine, tryptase, chymase, kinins, and heparin. Other substances that
are rapidly synthesised include cysteinyl leukotrienes (CysLTs) and interleukins, among others. Clinically,
this process results in mucous gland stimulation leading to rhinorrhoea, sensory nerve stimulation (which
leads to sneezing and itching), and vasodilation (which results in mucosal and sinusoidal swelling and nasal
obstruction).

Over 4 to 8 hours, the events of the early phase result in the recruitment and migration of other inflammatory
cells to the nasal mucosa, including eosinophils, lymphocytes, and macrophages. These cells become
activated and release their mediators into the milieu, perpetuating the inflammatory process. Symptoms of
the late-phase response are characterised less by sneezing and itching than the early phase and more by
congestion and mucus production.

Classification
Traditional classification of AR: seasonal or perennial
AR has traditionally been classified as being seasonal or perennial, depending on whether an individual was
sensitised to cyclic pollens or year-round allergens such as dust mites, pets, cockroaches, and moulds. This
classification scheme has been shown to be artificial and often inconsistent, because, depending on the
locale, allergic sensitisation to multiple seasonal allergens can result in year-round disease, and, conversely,
allergic sensitisation to 'perennial' allergens such as animal dander can result in symptoms during only a
limited period of time. Nevertheless, this classification system continues to be used in clinical research and
guidelines.

ARIA (allergic rhinitis and its impact on asthma) classification[1]

The ARIA classification of AR is based on severity, duration of symptoms, and impact of social life, school,
and work.

Intermittent: symptoms are present

• <4 days a week or for <4 consecutive weeks.

Persistent: symptoms are present

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 Allergic rhinitis Basics

• >4 days a week and for >4 consecutive weeks.

Mild: none of the following items are present

• Sleep disturbance
BASICS

• Impairment of daily activities, leisure, and/or sport

• Impairment of school or work
• Troublesome symptoms.
Moderate/severe: one or more of the following items are present

• Sleep disturbance
• Impairment of daily activities, leisure, and/or sport
• Impairment of school or work
• Troublesome symptoms.

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Allergic rhinitis Prevention

Primary prevention
For primary prevention of AR, smoking cessation in smoking mothers, exclusive breastfeeding during the first
3 months of life, and exposure to solid foods only after the sixth month of life may be advocated.

A meta-analysis of randomised controlled trials on probiotics taken by pregnant or nursing mothers for the
primary prevention of atopic disorders in infants did not show a protective effect of probiotics for allergic
conditions other than eczema.[39] However, despite the limited evidence for probiotics in preventing atopic
disorders, guidelines from the World Allergy Organization (WAO) recommend the use of probiotics in
pregnant women at high risk for having an allergic child, in women who are breastfeeding infants at high risk
of developing allergy, and in infants at high risk of developing allergy.[18] WAO guidelines also recommend
using prebiotics in not-exclusively breastfed infants, but not in exclusively breastfed infants.[19]

A Cochrane review has found no evidence that polyunsaturated fatty acid (PUFA) supplementation in infancy
has an effect on infant or childhood allergy or other atopic conditions.[40]

Secondary prevention

PREVENTION
Avoidance of allergens known or suspected to trigger AR symptoms may minimise (or fully alleviate)
symptoms and reduce medication use. However, this may not be the case for all AR patients.

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 Allergic rhinitis Diagnosis

Case history
Case history #1
A 22-year-old student presents with a 5-year history of worsening nasal congestion, sneezing, and
nasal itching. Symptoms are year-round but worse during the spring season. On further questioning it
is revealed that he has significant eye itching, redness, and tearing as well as palate and throat itching
during the spring season. He remembers that his mother told him at some point that he used to have
eczema in infancy.

Step-by-step diagnostic approach

Allergic rhinitis (AR) is mediated by an IgE-associated response to indoor and outdoor environmental
allergens. However, none of these individual findings are very sensitive or specific, so their presence does
not distinguish between allergic and non-allergic nasal disease. Similarly, the absence of pertinent findings
does not rule out allergic disease, so determination of specific IgE reactivity using skin-prick testing or in vitro
specific IgE determination represents the only confirmed means of diagnosing AR.

Signs and symptoms

Nasal signs and symptoms:

• Pruritus
• Sneezing
• Rhinorrhoea
• Nasal congestion, often the most bothersome.
Associated signs and symptoms:

• Associated palate, throat, ear, and eye itching

DIAGNOSIS

• Eye redness, puffiness, and watery discharge.

Constitutional signs and symptoms:

• Fatigue
• Irritability.
The diagnosis of AR may be made presumptively based on the types of signs and symptoms and the
history of allergen triggers. Patients should also be asked about the presence of chest symptoms, food
allergies, and atopic dermatitis (eczema).

Unilateral rhinorrhoea should prompt evaluation for cerebrospinal fluid leak. Unilateral disease, with the
exception of unilateral nasal congestion due to a deviated septum, should warrant referral to an ENT
physician.

Physical examination
Physical examination of the nose is necessary. Findings may include swelling of the turbinates and nasal
mucosa, the presence of clear nasal mucus and/or a pale mucosa, and nasal crease (a transverse crease
resulting from repetitive nose rubbing and manipulation).

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Allergic rhinitis Diagnosis
Physical examination of the face may identify allergic shiners (bluish discoloration in the infraorbital
region), conjunctival injection, ocular mucoid discharge, and, rarely, Dennie-Morgan lines (creases
present under the lower eyelids).

Trial of therapy
A trial of symptom-driven pharmacotherapy with intranasal corticosteroids, or oral or intranasal
antihistamine, may be a pragmatic and reasonable first step. A trial of intranasal corticosteroids should be
considered a preferred first choice in moderate or severe AR, especially if nasal obstruction is an issue.
A sufficient response to the chosen medication should be assessed after 4 weeks of therapy. Because
symptoms from AR are often very subjective, the patient's perceived improvement in symptoms and
quality of life is paramount in determining whether there has been an adequate response or whether
further investigation is required. Validated quality of life questionnaires specific for AR can be used to
assess therapy response (e.g., Rhinoconjunctivitis Quality of Life Questionnaire [RQLQ] and Rhinitis
Control Assessment Test [RCAT]).[41] [42] [43]

Allergy testing
Determination of specific IgE reactivity using skin-prick testing[44] or in vitro specific IgE determination is
advisable if there is an inadequate response to trial of therapy.

• In vitro IgE determination or skin testing usually suffice; although, on some occasions both tests are
used for optimal management.
• The choice of test often depends on availability. In vitro IgE determination tends to be more
readily available but is more expensive, and has traditionally been felt to provide less sensitivity
and specificity than skin testing. However, it may be preferable in patients with severe eczema
affecting the testing area, in patients with significant dermatographism, or for those unwilling or
unable to stop their antihistamines or medications with antihistaminic properties (e.g., tricyclic
antidepressants).
• Most medical laboratories offer a variety of allergen panels that should incorporate the most
important perennial allergens such as animal danders and dust mites as well as geographically

DIAGNOSIS
important local pollens such as grasses, weeds, and trees.
• Some of the panels including foods need only be ordered if there has been possible association
with food triggers or history of food allergy.
• Results may not only confirm the presence of allergic disease but also help in directing
environmental control interventions and determining whether a patient may be suitable for
immunotherapy.

Risk factors
Strong
family history of atopy
• The best established risk factor is a family history of atopic disease, especially AR.[11] Various
modalities, such as genetic linkage analysis, have been employed to collectively identify a multitude of
genetic loci associated with a higher incidence of AR.[10]

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 Allergic rhinitis Diagnosis
age <20 years
• Approximately 80% of individuals diagnosed as having AR develop symptoms before the age of 20
years.[12] Onset after age 20 years raises suspicion of non-allergic rhinitis rather than AR.

positive allergen skin-prick tests

• Even though sensitisation to a specific allergen does not always equate with clinical disease, allergen
reactivity remains one of the strongest risk factors for the presence of upper (as well as lower) allergic
respiratory disease. The degree of association was explored in the second National Health and
Nutrition Examination Survey (NHANES II).[20] The survey sampled 4295 white people in the US
between 1976 and 1980 and found that AR was associated with a positive skin test to ragweed (odds
ratio [OR] 2.3, 95% CI 1.5 to 3.3), rye-grass (OR 2.8, 95% CI 1.8 to 4.3), house dust (OR 2.5, 95% CI
1.6 to 3.9), and Alternaria (OR 2.3, 95% CI 1.5 to 3.4).

inadequate exposure to animals and other micro-organism-rich

environments in early life
• Children of families with exposure to a farming lifestyle (farming animals, unpasteurised milk) in
rural areas of Germany, Austria, and Switzerland were less likely to develop allergic sensitisation,
hay fever, and asthma than children of non-farmers living in the same localities.[21] Continual long-
term exposure to stables until age 5 years was associated with the lowest frequencies of allergic
sensitisation and disease.[21]

Western lifestyle
• The landmark International Study of Asthma and Allergies in Childhood (ISAAC) study delineated
the worldwide variation in prevalence of allergic rhinoconjunctivitis and other allergic disorders by
reviewing self-reported symptoms from 463,801 children aged 13 to 14 years in 56 countries.[8] The
initial phase of the study (carried out between 1992 and 1998) found the highest prevalence of AR
in the UK, Australia, New Zealand, and Ireland, followed by North, Central, and South America. The
lowest prevalence was found in Eastern European countries, Indonesia, Greece, China, Taiwan,
Uzbekistan, India, and Ethiopia. There was an overall increase in prevalence of AR across most
DIAGNOSIS

countries, particularly among young children, when the ISAAC study was repeated between 2002 and
2003.[9]

Weak
ethnicity
• In the US, atopic sensitisation (including asthma) appear to be more prevalent among certain ethnic
groups, such as African Americans and Puerto Ricans.[22] [23]
• In the UK, the prevalence of AR in men was found to be 79% higher among West Indians and 92%
higher among Asians than among white British people. However, this difference may rapidly vanish in
children of immigrants, who appear to have a prevalence of AR more closely resembling that of the
native population.
• In one UK study, significantly more West Indian women consulted primary care physicians for AR
compared with the white British population.[24]

higher socio-economic status

• Children of parents with higher education or social class occupations appear to have a higher
incidence of AR, as documented in the US, UK, and Guinea-Bissau.[25]

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Allergic rhinitis Diagnosis
environmental pollution
• Environmental pollution is a multi-faceted variable whose contribution to AR has not been fully
elucidated. Pollution can be divided into outdoor and indoor pollution. Outdoor pollution includes
particulate matter, including diesel exhaust, ozone, NO2, and airborne toxins, among others. Indoor
pollutants include smoke and particles set free by wood and coal burning equipment as well as
tobacco smoke, among others. While certain physiological effects stemming from pollution are well
understood (e.g., diesel exhaust particles seem to augment allergic inflammation), it remains unclear
how strongly these variables influence the prevalence and severity of upper airway allergic disease.
• Although controversial, there is evidence to suggest that environmental pollution and climatic change
may be associated with increased expression of allergenic proteins in several pollen grains in a variety
of plants.[26] However, the association with allergic respiratory disease is unclear.

exposure to indoor allergens such as animal dander and dust mites

• Although controversial, it has been suggested that exposure to sufficient quantities of certain allergens
(e.g., dog) early in life may be protective against development of allergic sensitisation and allergic
disease. In contrast, exposure to perennial allergens such as dust mites and cockroaches is usually
associated with an increased risk of allergic sensitisation and atopic disease.[27] [28]

birth during a pollen season

• Several studies have suggested that perinatal exposure to specific allergens may lead to a higher
incidence of AR. The overall effects of birth during a pollen season are probably modest at most.[29]

lack of older siblings

• Several studies have found an inverse relationship between sibship size and AR.[30] [31] Firstborns
also seem to be at a higher risk of developing AR. The exact mechanism has not been fully elucidated;
however, an increase in reported early respiratory illnesses is unlikely to be the full explanation.

heavy maternal smoking (20 or more cigaret tes/day during the first year of
life)

DIAGNOSIS
• In the prospective Tucson children's respiratory study, early introduction of solid foods, heavy maternal
smoking in the first year of life (20 or more cigarettes/day), and higher IgE were all associated with the
development of AR in the first few years of life.[25]

higher serum IgE levels (>100 IU/mL before age 6 years)

• In the prospective Tucson children's respiratory study, early introduction of solid foods, heavy maternal
smoking in the first year of life (20 or more cigarettes/day), and higher IgE were all associated with the
development of AR in the first few years of life.[25]

early introduction of foods or formula

• In the prospective Tucson children's respiratory study, early introduction of solid foods, heavy maternal
smoking in the first year of life (20 or more cigarettes/day), and higher IgE were all associated with the
development of AR in the first few years of life.[25]

breast feeding
• The effect of breastfeeding on risk of allergic diseases, such as asthma, AR, and eczema, is
controversial. While exclusive breastfeeding during the first 4 to 6 months has been advocated for the
prevention of atopic disorders,[32] the evidence appears to be inconclusive.[33] [34] [35] Furthermore,

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 Allergic rhinitis Diagnosis
several studies have found this practice to actually increase the likelihood of developing atopic
disease.[36] [37] One possible explanation centres on the IgE levels of the breastfeeding mother. In
one study, children who were exclusively breastfed for at least 4 months by mothers with high serum
IgE levels had higher serum IgE (and atopy) levels compared with non-breastfed children or children
breastfed for less than 4 months.[38] Conversely, children who were breastfed by mothers with low
serum IgE levels (regardless of duration) had lower serum IgE levels compared with non-breastfed
children.

presence of other atopic conditions (eczema, food allergies, wheezing/

asthma)
• Eczema and food allergies usually present before allergic rhinitis, while wheezing/asthma may develop
at any time in relation to the onset of rhinitis.

History & examination factors

Key diagnostic factors
presence of risk factors (common)
• Risk factors include: family history of atopy; age <20 years; Western lifestyle; inadequate exposure to
animals and other micro-organism-rich environments in early life.

sneezing (common)
• More likely in AR than non-allergic rhinitis.

nasal pruritus (common)

• More likely in AR than non-allergic rhinitis.

Other diagnostic factors

palate, throat, ear, and eye itching (common)
DIAGNOSIS

• is a diagnostic factor

eye redness, puffiness, and watery discharge (common)

• is a diagnostic factor

fatigue and irritability (common)

• is a diagnostic factor

nasal congestion (common)

• is a diagnostic factor

rhinorrhoea (common)
• Unilateral rhinorrhoea should prompt evaluation for cerebral spinal fluid leak. Unilateral disease, with
the exception of unilateral nasal congestion due to a deviated septum, should warrant referral to an
ENT physician.

allergic shiners (common)

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Allergic rhinitis Diagnosis
• Bluish discoloration in the infra-orbital region.

conjunctival injection (common)

• is a diagnostic factor

ocular mucoid discharge (common)

• is a diagnostic factor

nasal crease (common)

• A transverse crease on the exterior of the nose resulting from repetitive nose rubbing and
manipulation.

mucosal pallor (common)

• is a diagnostic factor

swelling of the nasal mucosa and turbinates (common)

• is a diagnostic factor

abundant clear nasal secretions (common)

• is a diagnostic factor

Dennie-Morgan lines (creases present under the lower eyelids) (uncommon)

• is a diagnostic factor

Diagnostic tests
1st test to order

Test Result

DIAGNOSIS
therapeutic trial of antihistamine or intranasal corticosteroid clinical improvement
• Oral or intranasal antihistamine can be used. In moderate or severe
AR, a trial of an intranasal corticosteroid should be considered a
preferred first choice, especially if nasal obstruction is an issue. Re-
assessed after a 4-week trial.
• Amelioration of symptoms and improvement in quality-of-life
parameters such as sleep quantity and quality, activities of daily
living, and ability to pursue hobbies, sports, and social activities
without limitation should guide the clinician in determining whether
a specific treatment regimen represents a failure. Validated quality
of life questionnaires specific for AR can be used to assess therapy
response (e.g., Rhinoconjunctivitis Quality of Life Questionnaire
[RQLQ] and Rhinitis Control Assessment Test [RCAT]).[41] [42] [43]

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 Allergic rhinitis Diagnosis

Other tests to consider

Test Result
allergen skin-prick testing wheal and flare reaction
after specific allergen is
• Provides superior sensitivity and specificity compared with in vitro
introduced into the skin is
specific IgE determination testing, as long as the test is performed
3 mm larger than negative
by a properly trained individual. However, it is not suitable for
(saline) control
patients with severe eczema affecting the testing area, those with
significant dermatographism, or those unwilling or unable to stop their
antihistamines or medications with antihistaminic properties (e.g.,
tricyclic antidepressants).
• Also offers rapid results and lower costs, especially if the number of
individual skin tests performed is limited.
• Panel should include perennial allergens (e.g., dust mite, animal
dander, cockroach if inner city) and locally prominent pollens (e.g.,
grasses, ragweed, birch, etc.) depending on location.
• Interpretation of results can be challenging. Individuals with very
high IgE levels may have multiple positives that may or may not be
clinically relevant.
• Size of individual wheal and flare levels do not necessarily correlate
with clinical reactivity to that particular allergen.
in vitro specific IgE determination specific allergen response
• Sandwich-type assay that utilises the patient's serum to bind to
specific allergens present on a solid phase/chip.
• Tends to be more expensive than skin-prick testing, and results are
not immediately available. However, can be ordered by physicians not
trained in skin testing and employed in patients with severe eczema,
significant dermatographism, or those unwilling or unable to stop their
antihistamines (because antihistamine use may cause false-negative
results in skin-prick tests).
• Interpretation can be challenging.
• IgE levels do not necessarily correlate with clinical reactivity to that
particular allergen.
• RAST results - and, to a lesser degree, skin tests - can be difficult to
DIAGNOSIS

interpret in individuals with very high IgE levels, as they often have
multiple positives that may or may not be clinically relevant.

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Allergic rhinitis Diagnosis

Differential diagnosis

Condition Differentiating signs / Differentiating tests

symptoms
Non-allergic rhinitis • Sporadic or persistent • Other than the absence of
perennial symptoms not positive allergy tests, no
resulting from IgE-mediated single, specific differentiating
immunopathological events. feature exists.
• Pain/pressure, and a post-
nasal drip sensation are
common.
• Presence of nasal itching
and sneezing less likely.
• Non-allergic triggers such
as strong odours, perfumes,
cigarette smoke, and
weather-related changes
may be present.
• Not common in children.
Onset of symptoms after age
20 years more likely.[45]

Acute sinusitis • Acute (<2 weeks), sub-acute • Diagnosis is usually clinical.

(2-6 weeks).
• Acute disease often due to
an infectious cause.
• May present with cough,
discoloured nasal mucus,
and facial pressure/pain.[46]

Chronic sinusitis • Symptoms >12 weeks. • Sinus CT scans are

Usually diagnosed with the abnormal, by definition, in
aid of radiological studies. people with chronic sinusitis.
One of the more common

DIAGNOSIS
clinical characteristics of
chronic sinusitis is the
presence of hyposmia or
anosmia.
• More commonly
characterised by chronic
inflammation than a bacterial
infection, especially in
adults.[46]
• Frequently characterised
as chronic sinusitis with
nasal polyposis, and chronic
sinusitis without nasal
polyposis.

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 Allergic rhinitis Diagnosis

Condition Differentiating signs / Differentiating tests

symptoms
Viral rhinosinusitis • Acute (<2 weeks) episode of • Diagnosis is usually clinical.
rhinitis presenting with nasal
congestion, rhinorrhoea,
sneezing, and varying
degrees of nasal pruritus.
May present with a sore
throat, myalgias, headaches,
discoloured mucus, and
fever. More common during
the autumn to spring
months.

Diagnostic criteria
ARIA (allergic rhinitis and its impact on asthma) guidelines
Intermittent: symptoms are present

• <4 days a week

• Or for <4 consecutive weeks.

Persistent: symptoms are present

• >4 days a week

• And for >4 consecutive weeks.

Mild: none of the following items are present

• Sleep disturbance
DIAGNOSIS

• Impairment of daily activities, leisure, and/or sport

• Impairment of school or work
• Troublesome symptoms.
Moderate/severe: one or more of the following items are present

• Sleep disturbance
• Impairment of daily activities, leisure, and/or sport
• Impairment of school or work
• Troublesome symptoms.

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Allergic rhinitis Treatment

Step-by-step treatment approach

The goal of symptom amelioration or cessation may require institution of allergy avoidance measures,
pharmacotherapy, immunotherapy, or a combination thereof. The clinician should ask about nasal, palate,
and eye symptoms, so that pharmacotherapy can be selected to target all of the affected areas. It is
sometimes easy to ignore common non-nasal symptoms that frequently accompany allergic rhinitis (AR) and
contribute to an impaired quality of life.

• Allergen avoidance is one of the guiding principles of treatment. While environmental control measures
can sometimes lead to complete symptom control (e.g., by removing a pet), they can at other times
prove impractical, ineffective, or difficult to implement.
• After an initial pharmacological treatment regimen has been initiated, follow-up should take place in a
reasonable amount of time and therapy stepped up or stepped down as deemed necessary.
• While the treatments available are usually considered to be safe and relatively free from adverse
effects, sedation associated with the use of first-generation antihistamines probably represents the
most commonly encountered problem.
• Intranasal corticosteroids remain the single most effective class of medications for treating AR.
However, for many patients, especially those with mild symptoms, it is recommended that other
therapies (e.g., antihistamines and leukotriene receptor antagonists) be attempted prior to starting
intranasal corticosteroids.[47]

Allergen avoidance and control

Pollen (grasses, trees, weeds):

• Keeping windows of homes and cars closed and employing an air conditioner in the recycling/
indoor mode.
• Minimising time spent outdoors during times of high pollen count.
• Utilising HEPA (high-efficiency particulate air) filters may prove helpful.[48]
• Using nasal filters.[49]
Dust mites:

• Encasing mattresses, pillows, and quilts/duvets in impermeable covers. A study showed that only
'tightly woven' or impermeable plastic covers provided protection against dust mite penetration.[50]
• Washing all bedding weekly in a hot cycle (55°C to 60°C [131°F to 140°F]) to reduce dust-mite
allergen levels and live dust mites.
• Employing HEPA filters can reduce allergen loads and may lead to symptom improvement in those
with allergic sensitisation to dust mites.
• Applying acaricides such as disodium octaborate tetrahydrate can lower the number of live dust
mites in carpets; however, it remains unknown whether this results in symptom amelioration.
• Dehumidification, with target reduction of relative humidity below 50%, should suppress dust mite
growth. However, a randomised controlled trial in the UK showed that dehumidifiers did not have a
major effect on house dust mite counts or allergen levels.1[C]Evidence
TREATMENT

• A systematic review of house dust mite avoidance measures (including use of acaricides and
extensive bedroom-based environmental control measures) found that these may help reduce
rhinitis symptoms, although evidence from high-quality studies was lacking.[52]
Pet dander:

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 Allergic rhinitis Treatment

• Individuals allergic to cats and dogs have few effective ways to reduce their exposure to pet
allergens short of ridding themselves of the animals. It is important to counsel patients that pet
allergen levels only slowly decline over several months when a pet is removed from the home;
therefore, rapid improvement is not expected. Ultimately though, the affected individual willing to
take that drastic step is frequently rewarded with significant symptom amelioration. While some
people may react differently to individual dogs, 'hypoallergenic' dogs are a myth that has been
debunked.[53]
• Washing of cats has not been shown to be an effective approach to reducing allergen exposure.
Although weekly washings can reduce allergens, clinical studies have shown neither a persistent
reduction of airborne allergens nor a clear reduction in rhinitis symptoms.[54] [55]
• HEPA filters do not appear to lead to significant symptom improvement in cat-sensitised individuals,
as noted in one placebo-controlled study.[56]
Cockroach infestation:

• Cockroach infestation is associated with AR and asthma, especially in the inner city.[28]
• Control measures are based on eliminating suitable environments and restricting access by
sealing, caulking, and controlling the food supply as well as using chemical control and [Link]
cockroach extermination by professionals may reduce allergen levels by 80% to 90%, no studies
have evaluated the clinical significance of this reduction.[57]
• Re-infestation from adjacent apartments is a frequent problem, and thus extermination efforts will
probably need to be repeated and extended beyond the affected space.
Moulds:

• Moulds are ubiquitous both indoors and outdoors.

• Mould-allergic individuals should carefully inspect their home for mould damage, with special
attention to more humid areas of the dwelling.
• Localised mould growth may be removed with a dilute bleach solution.
• More extensive mould damage may require more aggressive measures such as replacing the
affected surface/material.
• Controlled clinical studies have not been undertaken to show that these measures effectively
reduce the symptoms of rhinitis.

Intermit tent mild symptoms

Direct comparison of antihistamines (oral or intranasal) and leukotriene receptor antagonists is difficult,
as good head-to-head comparison studies are lacking, and meta-analyses have been problematic due to
differing outcome measures in different studies. These agents have shown superiority to placebo in well-
controlled, prospective studies. First-line treatment should be with an oral or intranasal antihistamine. If
one agent is ineffective, changing to a different one is appropriate. Leukotriene receptor antagonists can
be used as an alternative to antihistamines, especially in those who also have mild persistent asthma.[58]
Combining different agents or using treatment options usally reserved for more severe disease may be
considered if symptoms are not controlled by single agent therapy.
TREATMENT

Oral or intranasal antihistamines:

• Effective for rhinorrhoea, sneezing, and itching.

• Oral antihistamines only have a modest effect on congestion.[47]

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Allergic rhinitis Treatment
• Second-generation oral antihistamines are preferred to first-generation agents because they cause
less or no sedation. Cetirizine has been found to be particularly effective in AR, but may cause
some mild sedation.[59]
• Intranasal antihistamines (e.g., azelastine, olopatadine) are particularly effective for rhinorrhoea
and congestion, but they do not improve symptoms at non-nasal sites. They have a fast onset of
action after initial dosing (usually 15-30 minutes, and no later than 3 hours) and are effective over a
12-hour period, but they may cause sedation.
• There is a risk of paradoxical hyperactivity with use of sedating antihistamines, particularly in
children.
Leukotriene receptor antagonist:

• Althought effective for congestion, they are less effective than antihistamines for rhinorrhoea,
sneezing, and itching.
• They may be associated with adverse neuropsychiatrical events (mood changes, aggression, and
depression, among others).

Persistent mild or intermit tent moderate or severe symptoms

First-line treatments:

• Oral antihistamine
• Intranasal antihistamine
• Intranasal sodium cromoglicate
• Leukotriene receptor antagonist (used as an alternative to antihistamines and cromolyn, particularly
in those with mild persistent asthma).
Second-line treatment:

• An intranasal corticosteroid may be used if first-line agents fail to achieve symptom control.
Intranasal corticosteroids are superior (or at least equivalent) to first-line agents, even when first-
line agents are combined. They may also provide additional benefit in reducing AR-associated
ocular symptoms.[60] [61] No significant increase in complications, such as local atrophy,
hypothalamic pituitary adrenal (HPA) axis suppression, and bone fractures among older people
have been found with intranasal corticosteroids.[62] One notable exception may be intranasal
dexamethasone, which has significantly higher systemic bioavailability than other intranasal
corticosteroids and has also been linked to Cushing syndrome.[63] The delayed onset of action
with intranasal corticosteroids means they should be used for at least 2 weeks on a daily basis
before any conclusions can be drawn on their clinical effects. Therefore, while being the single
most effective group of pharmacologic agents for AR, they may not always lend themselves to
treatment of intermittent symptoms.
Third-line treatment:

• Immunotherapy may be considered; however, consultation with an allergy specialist is advised.

TREATMENT

Adjunctive therapy:

• If nasal congestion/obstruction is severe, an oral or intranasal decongestant may be added for

up to 3 to 5 days. Tolerance and rebound nasal congestion (rhinitis medicamentosa) can occur if
intranasal decongestants are used beyond this time. Nasal saline irrigation (also known as saline

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 Allergic rhinitis Treatment
douching) can be used to cleanse the nostrils before administering intranasal sprays. This may help
reduce nasal symptoms and reduce the dosage of intranasal treatment, particularly in children.[64]
If symptoms persist at 2- to 4-week follow-up appointment, treatment options for persistent moderate to
severe symptoms should be considered.

When symptoms improve, decreasing or discontinuing treatment may be considered. Nasal sprays
may be decreased from 2 sprays to 1 spray per nostril once daily as long as symptoms continue to be
controlled. In intermittent disease, medications may be discontinued if a known allergen has ceased to be
present.

Persistent moderate or severe symptoms

Intranasal corticosteroids should be the first consideration if symptoms are persistent and moderate
or severe. They may also provide additional benefit in reducing AR-associated ocular symptoms.[60]
[61] Intranasal antihistamines (e.g., azelastine, olopatadine) are an alternative to intranasal
corticosteroids.

If symptoms persist at 4-week follow-up appointment, accuracy of diagnosis may be re-assessed and
differential diagnoses tested for. If AR remains the diagnosis:

• Intranasal antihistamines can be combined with an intranasal corticosteroid if symptoms are

uncontrolled with intranasal corticosteroid alone. An intranasal preparation containing the
corticosteroid fluticasone in combination with azelastine is available. This combination preparation
has been found to be superior to either agent alone, particularly during the first 2 weeks of use.[65]
[66]
• If the addition of an intranasal antihistamine is not effective, the dose of intranasal corticosteroid
can be increased.
• Intranasal ipratropium can be added to the intranasal corticosteroid for uncontrolled rhinorrhoea.
• An oral antihistamine may be added to the intranasal corticosteroid if there is persistent sneezing,
rhinorrhoea, and itching of the nose, palate, and eyes.
• A nasal decongestant can be added for 3 to 5 days if there are symptoms of severe nasal
congestion/blockage. Nasal saline irrigation can also be used to cleanse the nostrils before
administering intranasal sprays. An oral corticosteroid may be used for up to 7 days if nasal
congestion is persistent and severe.
Immunotherapy may be considered as a second-line option; however, consultation with an allergy
specialist is advised.

When symptoms improve, decreasing or discontinuing treatment may be considered. Nasal sprays
may be decreased from 2 sprays to 1 spray per nostril once daily as long as symptoms continue to be
controlled. If multiple pharmacological agents are used, discontinuation of the medication added to the
intranasal corticosteroid may be considered.

Usual therapy not effective

Evaluation by an allergy consultant is advisable when:
TREATMENT

• The clinician is able to elicit significant impact on quality of life (interference with hobbies, family
life, activities of daily living, sleep, emotional well-being) along with patient's subjective impression
that symptoms are severe

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Allergic rhinitis Treatment
• There is an incomplete response to trial of therapy of environmental and pharmacological
interventions
• There is an inability to adequately control associated conditions such as asthma or sinus disease.

Immunotherapy
After allergy testing, immunotherapy might be considered by an allergy specialist. Immunotherapy is
most commonly reserved for patients not responding to pharmacotherapy, or those either unwilling
to take or unable to tolerate medications. Subcutaneous immunotherapy (SCIT) may alter the natural
history of allergic disease (induce long-term remission after discontinuation of therapy and prevent new
sensitisations), as well as reduce the progression from AR to asthma when given in children aged 6
to 14 years for a minimum of 3 years.[67] Sublingual immunotherapy (SLIT), an alternative to SCIT
depending on the allergen involved, is effective in treating AR in adults and children and may also have
disease-modifying potential.[68] [69] [70] [71] [72] It is considered to be safer than SCIT because side
effects are usually limited to mucosal symptoms, and is easier to administer (patient self-administers);
however, it may be less effective than SCIT.[73] Direct comparisons using standardised and validated
outcome measures between SLIT and SCIT are not available.[74] SLIT is more appropriately used in
monosensitised patients, especially those sensitized to dust mites,[75] grass,[76] [77] [78] or ragweed.[79]
The US Food and Drug Administration has approved a SLIT for the treatment of adults with house dust
mite-associated AR.[75] Immunotherapy should be targeted to include allergens that are clinically relevant
to the geographic locale.

Treatment details overview

Consult your local pharmaceutical database for comprehensive drug information including contraindications,
drug interactions, and alternative dosing. ( see Disclaimer )

Acute ( summary )
Patient group Tx line Treatment

intermit tent mild symptoms 1st oral antihistamine plus allergen

avoidance

intermit tent mild symptoms 1st intranasal antihistamine plus allergen

avoidance

2nd leukotriene receptor antagonist plus

allergen avoidance

persistent mild or intermit tent 1st oral antihistamine plus allergen

TREATMENT

moderate to severe symptoms avoidance

adjunct oral or intranasal decongestant

adjunct nasal saline irrigation (saline douching)

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 Allergic rhinitis Treatment

Acute ( summary )

persistent mild or intermit tent 1st intranasal antihistamine or sodium

moderate to severe symptoms cromoglicate or leukotriene receptor
antagonist plus allergen avoidance

adjunct oral or intranasal decongestant

adjunct nasal saline irrigation (saline douching)

2nd intranasal corticosteroid plus allergen

avoidance

adjunct oral or intranasal decongestant

adjunct nasal saline irrigation (saline douching)

3rd sublingual immunotherapy (SLIT)

3rd subcutaneous immunotherapy (SCIT)

persistent moderate to severe 1st intranasal corticosteroid and/or

symptoms antihistamine

plus allergen avoidance

adjunct intranasal ipratropium

adjunct oral antihistamine

adjunct oral or intranasal decongestant or oral

corticosteroid

adjunct nasal saline irrigation (saline douching)

2nd sublingual immunotherapy (SLIT)

2nd subcutaneous immunotherapy (SCIT)

Ongoing ( summary )
Patient group Tx line Treatment

usual therapy ineffective 1st sublingual immunotherapy (SLIT)

usual therapy ineffective 1st subcutaneous immunotherapy (SCIT)

plus allergen avoidance

TREATMENT

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Allergic rhinitis Treatment

Treatment options

Acute
Patient group Tx line Treatment

intermit tent mild symptoms 1st oral antihistamine plus allergen

avoidance
» Oral antihistamines reduce sneezing,
rhinorrhoea, and itching of the nose, palate, and
eyes. However, they only have a modest effect
on nasal congestion.[47]

» Second-generation oral antihistamines are

preferred to first-generation agents because
they cause less or no sedation. Cetirizine has
been found to be particularly effective in allergic
rhinitis (AR).[59]

» Sedation is possible with cetirizine and

levocetirizine; unlikely with loratadine,
desloratadine, and fexofenadine; and likely with
chlorphenamine and diphenhydramine.

» There is a risk of paradoxical hyperactivity with

use of sedating antihistamines, particularly in
children.

» Allergen avoidance should be attempted by all

patients with AR. Allergy testing can be helpful
in identifying the allergens of concern for a
particular patient.

Primary options

» cetirizine: children >6 months of age: 2.5 to

5 mg orally once daily; children >6 years of
age and adults: 5-10 mg orally once daily

OR
Primary options

» desloratadine: children >6 months of age:

1 to 2.5 mg orally once daily; children >12
years of age and adults: 5 mg orally once
daily

OR
Primary options
TREATMENT

» fexofenadine: children >6 months of age:

15-30 mg orally twice daily; children >12
years of age and adults: 60 mg orally twice
daily or 180 mg once daily

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BMJ Best Practice topics are regularly updated and the most recent version
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 Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
OR
Primary options

» levocetirizine: children >6 months of age:

1.25 to 2.5 mg orally once daily; children
>6-12 years of age: 2.5 mg orally once daily;
children >12 years of age and adults: 2.5 to 5
mg orally once daily

OR
Primary options

» loratadine: children >2 years of age: 5 mg

orally once daily; children >6 years of age
and adults: 10 mg orally once daily

OR
Secondary options

» chlorphenamine: children >2 years of age:

1-2 mg orally (immediate-release) every 4-6
hours when required; children >12 years
of age and adults: 4 mg orally (immediate-
release) every 4-6 hours when required

OR
Secondary options

» diphenhydramine: children >2 years of

age: 6.25 to 25 mg orally every 4-6 hours
when required; children >12 years of age and
adults: 25-50 mg orally every 4-6 hours when
required

intermit tent mild symptoms 1st intranasal antihistamine plus allergen

avoidance
» Intranasal antihistamines (e.g., azelastine,
olopatadine) are particularly effective for
rhinorrhoea and nasal congestion, but they do
not improve symptoms at non-nasal sites.

» They have a fast onset of action after initial

dosing (usually 15 to 30 minutes, and no later
than 3 hours) and are effective over a 12-hour
period, but they may cause sedation
TREATMENT

» Allergen avoidance should be attempted by all

patients with AR. Allergy testing can be helpful
in identifying the allergens of concern for a
particular patient.

Primary options

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BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
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Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
» azelastine nasal: (137 micrograms/spray)
children ≥5 years of age: 137 micrograms (1
spray) in each nostril twice daily; children ≥12
years of age and adults: 137-274 micrograms
(1-2 sprays) in each nostril twice daily; (205.5
micrograms/spray) children ≥12 years of age
and adults: 205.5 to 411 micrograms (1-2
sprays) in each nostril once to twice daily

OR
Primary options

» olopatadine nasal: (665 micrograms/spray)

children ≥6 years of age: 665 micrograms (1
spray) in each nostril twice daily; children ≥12
years of age and adults: 1330 micrograms (2
sprays) in each nostril twice daily
2nd leukotriene receptor antagonist plus
allergen avoidance
» Leukotriene receptor antagonists are an
alternative to antihistamines, especially in those
who also have mild persistent asthma.[58]

» Although effective for nasal congestion,

they are less effective than antihistamines for
rhinorrhoea, sneezing, and itching.

» They may be associated with adverse

neuropsychiatric events (mood changes,
aggression, and depression, among others).

» Allergen avoidance should be attempted by all

patients with AR. Allergy testing can be helpful
in identifying the allergens of concern for a
particular patient.

Primary options

» montelukast: children >6 months of age:

4 mg orally once daily; children >6 years of
age: 5 mg orally once daily; children >15
years of age and adults: 10 mg orally once
daily

persistent mild or intermit tent 1st oral antihistamine plus allergen

moderate to severe symptoms avoidance
TREATMENT

» Oral antihistamines reduce sneezing,

rhinorrhoea, and itching of the nose, palate, and
eyes. However, they only have a modest effect
on nasal congestion.[47]

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jun 13, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
25
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
» Second-generation oral antihistamines are
preferred to first-generation agents because they
cause less or no sedation. Cetirizine has been
found to be particularly effective in AR.[59]

» Sedation is possible with cetirizine and

levocetirizine; unlikely with loratadine,
desloratadine, and fexofenadine; and likely with
chlorphenamine and diphenhydramine.

» There is a risk of paradoxical hyperactivity with

use of sedating antihistamines, particularly in
children.

» Allergen avoidance should be attempted by all

patients with AR. Allergy testing can be helpful
in identifying the allergens of concern for a
particular patient.

Primary options

» cetirizine: children >6 months of age: 2.5 to

5 mg orally once daily; children >6 years of
age and adults: 5-10 mg orally once daily

OR
Primary options

» desloratadine: children >6 months of age:

1 to 2.5 mg orally once daily; children >12
years of age and adults: 5 mg orally once
daily

OR
Primary options

» fexofenadine: children >6 months of age:

15-30 mg orally twice daily; children >12
years of age and adults: 60 mg orally twice
daily or 180 mg once daily

OR
Primary options

» levocetirizine: children >6 months of age:

1.25 to 2.5 mg orally once daily; children
>6-12 years of age: 2.5 mg orally once daily;
children >12 years of age and adults: 2.5 to 5
mg orally once daily
TREATMENT

OR
Primary options

26 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jun 13, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
» loratadine: children >2 years of age: 5 mg
orally once daily; children >6 years of age
and adults: 10 mg orally once daily

OR
Secondary options

» chlorphenamine: children >2 years of age:

1-2 mg orally (immediate-release) every 4-6
hours when required; children >12 years
of age and adults: 4 mg orally (immediate-
release) every 4-6 hours when required

OR
Secondary options

» diphenhydramine: children >2 years of

age: 6.25 to 25 mg orally every 4-6 hours
when required; children >12 years of age and
adults: 25-50 mg orally every 4-6 hours when
required
adjunct oral or intranasal decongestant
» Oral or intranasal decongestants may be used
as a short-term adjunct for 3 to 5 days if nasal
congestion is severe.

» Increased nasal patency typically occurs within

5 to 10 minutes with intranasal decongestants,
or within 30 minutes with oral decongestants.
The decongestive effects may last up to 8 to
12 hours with intranasal decongestants, and
up to 24 hours with extended-release oral
decongestants.

» Oral or intranasal decongestants as

monotherapy have a limited role in the treatment
of AR. However, when combined with an
antihistamine, all cardinal symptoms of AR are
addressed.

» Tolerance and rebound nasal congestion

(rhinitis medicamentosa) can occur if intranasal
decongestants are used for longer than 3 to 5
days.

Primary options

» oxymetazoline nasal: (0.025%) children

TREATMENT

2-5 years of age: 2-3 sprays into each nostril

twice daily; (0.05%) children >6 years of age
and adults: 1-2 sprays in each nostril twice
daily

OR

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27
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 Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
Primary options

» pseudoephedrine: children 2-5 years of

age: 15 mg orally every 4-6 hours when
required, maximum 60 mg/day; children
6-11 years of age: 30 mg orally every 4-6
hours when required, maximum 120 mg/
day; children >12 years of age and adults:
60 mg orally every 4-6 hours when required,
maximum 240 mg/day
adjunct nasal saline irrigation (saline douching)
» Nasal saline irrigation can be used to cleanse
the nostrils before administering intranasal
sprays. This may help reduce nasal symptoms
and reduce the dosage of intranasal treatment,
particularly in children.[64]

» Large volumes (e.g., 4-8 ounces of saline per

session) of isotonic or hypertonic saline solution
are likely to be effective.

» Although the effects are likely to be modest,

there are few adverse effects associated with
this procedure.

persistent mild or intermit tent 1st intranasal antihistamine or sodium

moderate to severe symptoms cromoglicate or leukotriene receptor
antagonist plus allergen avoidance
» Intranasal antihistamines (e.g., azelastine,
olopatadine) are particularly effective for
rhinorrhoea and congestion, but they do not
improve symptoms at non-nasal sites.

» Intranasal sodium cromoglicate is moderately

effective for nasal symptoms, but repeat sprays
may be required.

» Leukotriene receptor antagonists can be used

as an alternative to antihistamines, especially
in those who also have mild persistent asthma.
Although effective for nasal congestion, they
are less effective than antihistamines for
rhinorrhoea, sneezing, and itching. Adverse
neuropsychiatrical events (e.g., mood changes,
aggression, and depression, among others) may
TREATMENT

also occur with these agents.

» Allergen avoidance should be attempted by all

patients with AR. Allergy testing can be helpful
in identifying the allergens of concern for a
particular patient.

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Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
Primary options

» azelastine nasal: (137 micrograms/spray)

children ≥5 years of age: 137 micrograms (1
spray) in each nostril twice daily; children ≥12
years of age and adults: 137-274 micrograms
(1-2 sprays) in each nostril twice daily; (205.5
micrograms/spray) children ≥12 years of age
and adults: 205.5 to 411 micrograms (1-2
sprays) in each nostril once to twice daily

OR
Primary options

» olopatadine nasal: (665 micrograms/spray)

children ≥6 years of age: 665 micrograms (1
spray) in each nostril twice daily; children ≥12
years of age and adults: 1330 micrograms (2
sprays) in each nostril twice daily

OR
Primary options

» sodium cromoglicate nasal: (5.2 mg/spray)

children >2 years of age and adults: 5.2 mg
(1 spray) into both nostrils two to four times
daily

OR
Secondary options

» montelukast: children aged >6 months: 4

mg orally once daily; children aged >6 years:
5 mg orally once daily; children aged >15
years and adults: 10 mg orally once daily
adjunct oral or intranasal decongestant
» Oral or intranasal decongestants may be used
as a short-term adjunct for 3 to 5 days if nasal
congestion is severe.

» Reduction in blood flow to the nasal

vasculature after administration leads to
increased nasal patency in 5 to 10 minutes when
used topically or 30 minutes when used orally.

» Increased nasal patency typically occurs within

5 to 10 minutes with intranasal decongestants,
TREATMENT

or within 30 minutes with oral decongestants.

The decongestive effects may last up to 8 to
12 hours with intranasal decongestants, and
up to 24 hours with extended-release oral
decongestants.

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29
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 Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
» Oral or intranasal decongestants as
monotherapy have a limited role in the treatment
of AR. However, when combined with an
antihistamine, all cardinal symptoms of AR are
addressed.

» Tolerance and rebound congestion (rhinitis

medicamentosa) can occur if intranasal
decongestants are used for longer than 3 to 5
days.

Primary options

» oxymetazoline nasal: (0.025%) children

2-5 years of age: 2-3 sprays into each nostril
twice daily; (0.05%) children >6 years of age
and adults: 1-2 sprays in each nostril twice
daily

OR
Primary options

» pseudoephedrine: children 2-5 years of

age: 15 mg orally every 4-6 hours when
required, maximum 60 mg/day; children
6-11 years of age: 30 mg orally every 4-6
hours when required, maximum 120 mg/
day; children >12 years of age and adults:
60 mg orally every 4-6 hours when required,
maximum 240 mg/day
adjunct nasal saline irrigation (saline douching)
» Nasal saline irrigation can be used to cleanse
the nostrils before administering intranasal
sprays. This may help reduce nasal symptoms
and reduce the dosage of intranasal treatment,
particularly in children.[64]

» Large volumes (e.g., 4-8 ounces of saline per

session) of isotonic or hypertonic saline solution
are likely to be effective.

» Although the effects are likely to be modest,

there are few adverse effects associated with
this procedure.

2nd intranasal corticosteroid plus allergen

avoidance
TREATMENT

» Intranasal corticosteroids are reserved for

second-line use in AR patients with persistent
mild or intermittent moderate or severe
symptoms.

30 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jun 13, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
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Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
» They are the single most effective class
of medications for AR, improving all nasal
symptoms (congestion, rhinorrhoea, itching, and
sneezing), as well as ocular symptoms.[60] [61]
However, delayed onset of action means they
should be used for at least 2 weeks on a daily
basis before any conclusions can be drawn on
their clinical effects. Thus, while being the single
most effective group of pharmacologic agents
for AR, they may not always lend themselves to
treatment of intermittent symptoms.

» Intranasal corticosteroids may not be equally

effective in treating symptoms of AR. Results
from one review found that fluticasone furoate
had the most consistent efficacy data for
managing nasal and ocular symptoms.[80]

» Local atrophy, like the type that occurs

with high-potency local corticosteroids for
dermatological indications, has not been
observed in year-long studies with intranasal
fluticasone and mometasone.

» Laboratory evaluations of the hypothalamic-

pituitary-adrenal (HPA) axis by multiple means
have shown minimal or no suppression.

» Linear growth suppression, a sensitive

marker of HPA suppression in children,
has been shown not to be affected by the
intranasal administration of budesonide,
fluticasone, triamcinolone, and mometasone
at recommended doses in several long-term
studies.

» Finally, no increased risk of bone fractures was

found among older people who used intranasal
corticosteroids, regardless of the dose used.[62]

» One notable exception may be intranasal

dexamethasone, which has significantly higher
systemic bio-availability than other intranasal
corticosteroids and has also been linked to
Cushing's syndrome.[63]

» Allergen avoidance should be attempted by all

patients with AR. Allergy testing can be helpful
in identifying the allergens of concern for a
particular patient.
TREATMENT

Primary options

» beclometasone nasal: (50 micrograms/

spray aqueous) children >6 years of age
and adults: 50-100 micrograms (1-2 sprays)

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 Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
in each nostril twice daily; (40 micrograms/
spray aerosol) children 4-11 years of age:
40 micrograms (1 spray) in each nostril once
daily; (80 micrograms/spray aerosol) children
≥12 years of age and adults: 160 micrograms
(2 sprays) in each nostril once daily

OR
Primary options

» budesonide nasal: (32 micrograms/spray)

children >6 years of age and adults: 32-64
micrograms (1-2 sprays) in each nostril once
daily

OR
Primary options

» flunisolide nasal: (25 micrograms/spray)

children >6 years of age and adults: 50
micrograms (2 sprays) in each nostril twice
daily

OR
Primary options

» fluticasone furoate nasal: (27.5 micrograms/

spray) children 2-11 years of age: 27.5
micrograms (1 spray) in each nostril once
daily, increase to 55 micrograms (2 sprays) in
each nostril if inadequate response; children
≥12 years and adults: 27.5 to 55 micrograms
(1-2 sprays) in each nostril once daily

OR
Primary options

» fluticasone propionate nasal: (50

micrograms/spray) children >4 years of age:
50-100 micrograms (1-2 sprays) in each
nostril once daily; adults: 100 micrograms (2
sprays) in each nostril once daily

OR
Primary options

» mometasone nasal: (50 micrograms/spray)

TREATMENT

children >2 years of age: 50 micrograms (1

spray) in each nostril once daily; adults: 100
micrograms (2 sprays) in each nostril once
daily

OR

32 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jun 13, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
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Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
Primary options

» triamcinolone nasal: (55 micrograms/spray)

children 2-5 years of age: 55 micrograms (1
spray) in each nostril once daily; children 6-11
years of age: 55-110 micrograms (1-2 sprays)
in each nostril once daily; children >11 years
of age and adults: 110 micrograms (2 sprays)
in each nostril once daily

OR
Primary options

» ciclesonide nasal: (nasal spray: 50

micrograms/spray) children ≥6 years of age
and adults: 100 micrograms (2 sprays) in
each nostril once daily; (nasal aerosol: 37
micrograms/spray) children ≥12 years of age
and adults: 37 micrograms (1 spray) in each
nostril once daily
adjunct oral or intranasal decongestant
» Oral or intranasal decongestants may be used
as a short-term adjunct for 3 to 5 days if nasal
congestion is severe.

» Increased nasal patency typically occurs within

5 to 10 minutes with intranasal decongestants,
or within 30 minutes with oral decongestants.
The decongestive effects may last up to 8 to
12 hours with intranasal decongestants, and
up to 24 hours with extended-release oral
decongestants.

» Oral or intranasal decongestants as

monotherapy have a limited role in the treatment
of AR. However, when combined with an
antihistamine, all cardinal symptoms of AR are
addressed.

» Tolerance and rebound nasal congestion

(rhinitis medicamentosa) can occur if intranasal
decongestants are used for longer than 3 to 5
days.

Primary options

» oxymetazoline nasal: (0.025%) children

2-5 years of age: 2-3 sprays into each nostril
TREATMENT

twice daily; (0.05%) children >6 years of age

and adults: 1-2 sprays in each nostril twice
daily

OR

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33
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 Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
Primary options

» pseudoephedrine: children 2-5 years of

age: 15 mg orally every 4-6 hours when
required, maximum 60 mg/day; children
6-11 years of age: 30 mg orally every 4-6
hours when required, maximum 120 mg/
day; children >12 years of age and adults:
60 mg orally every 4-6 hours when required,
maximum 240 mg/day
adjunct nasal saline irrigation (saline douching)
» Nasal saline irrigation can be used to cleanse
the nostrils before administering intranasal
sprays. This may help reduce nasal symptoms
and reduce the dosage of intranasal treatment,
particularly in children.[64]

» Large volumes (e.g., 4-8 ounces of saline per

session) of isotonic or hypertonic saline solution
are likely to be effective.

» Although the effects are likely to be modest,

there are few adverse effects associated with
this procedure.

3rd sublingual immunotherapy (SLIT)

» Immunotherapy is the only treatment modality
to potentially have a disease-modifying
effect.[81] It is most commonly reserved for
patients not responding to pharmacotherapy,
or for those either unwilling to take or unable
to tolerate medications. Consultation with an
allergy specialist is recommended.

» Sublingual immunotherapy (SLIT) is effective

in treating AR in both adults and children.[69]
[70] [71] [73] [82] It is safer than subcutaneous
immunotherapy (SCIT), as side effects are
usually limited to mucosal symptoms, and it is
easier to administer (patient self-administers).
However, it may be less effective than SCIT.[82]
Direct comparisons using standardised and
validated outcome measures between SLIT and
SCIT are not available.[74]

» SLIT is more appropriately used in

monosensitised patients, especially those
TREATMENT

sensitised to dust mites,[75] grass,[76] [77] [78]

or ragweed.[79] However, it may not be available
in all jurisdictions, depending on local regulations
and drug approval processes. The US Food and
Drug Administration has approved a SLIT for

34 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jun 13, 2018.
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Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
the treatment of adults with house dust mite-
associated AR.[75]

» For polysensitised patients, SLIT with multiple

allergens is sometimes employed, although no
commercially available formulations containing
more than one allergen currently exist.

» SLIT formulations can be employed in two

different manners. One involves taking it for
about 12 weeks before and throughout the
pollen season, stopping thereafter. Alternatively,
for more of a disease-modifying effect, it
can be taken daily for 3 years to provide a
sustained effect for a fourth year, even after
discontinuation.[81] [83]

» Immunotherapy should be targeted to include

allergens that are clinically relevant to the
geographic locale.

Primary options

» house dust mite allergen extract: consult

specialist for guidance on dose

OR
Primary options

» mixed grass pollens allergen extract:

consult specialist for guidance on dose

OR
Primary options

» timothy grass pollen allergen extract:

consult specialist for guidance on dose

OR
Primary options

» short ragweed pollen allergen extract:

consult specialist for guidance on dose
3rd subcutaneous immunotherapy (SCIT)
» Immunotherapy is the only treatment modality
to potentially have a disease-modifying
effect.[81] It is most commonly reserved for
patients not responding to pharmacotherapy,
TREATMENT

or those either unwilling to take or unable to

tolerate medications. Consultation with an
allergy specialist is recommended.

» SCIT with dog or mould allergens has not been

uniformly deemed clinically effective in the past;

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35
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 Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
new dog allergens are now available that might
prove more effective.

» Improvement requires several months of

treatment. It is generally accepted that a 1-year
trial will determine who will and who will not
respond to SCIT.

» Adverse reactions occur in both local and

systemic form. Systemic reactions can vary
from mild to life-threatening; fatal reactions after
receiving an allergy vaccine are estimated to
occur at a rate of 1 in 2 to 2.5 million.[84] [85]
SCIT may reduce the progression from AR to
asthma when given in children aged 6 to 14
years for a minimum of 3 years. [67]

» Immunotherapy should be targeted to include

allergens that are clinically relevant to the
geographic locale.

» Various extract manufacturers and dosing

regimens exist.

persistent moderate to severe 1st intranasal corticosteroid and/or

symptoms antihistamine
» Intranasal corticosteroids are the single
most effective class of medications, improving
all nasal symptoms associated with AR
(congestion, rhinorrhoea, itching, and sneezing),
as well as ocular symptoms.[60] [61] However,
delayed onset of action means they should be
used for at least 2 weeks on a daily basis before
any conclusions can be drawn on their clinical
effects.

» Intranasal corticosteroids may not be equally

effective in treating symptoms of AR. Results
from one review found that fluticasone furoate
had the most consistent efficacy data for
managing nasal and ocular symptoms.[80]

» Local atrophy, like the type that occurs

with high-potency local corticosteroids for
dermatological indications, has not been
observed in year-long studies with intranasal
fluticasone and mometasone.
TREATMENT

» Laboratory evaluations of the hypothalamic-

pituitary-adrenal (HPA) axis by multiple means
have shown minimal or no suppression.

36 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jun 13, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
» Linear growth suppression, a sensitive
marker of HPA suppression in children,
has been shown not to be affected by the
intranasal administration of budesonide,
fluticasone, triamcinolone, and mometasone
at recommended doses in several long-term
studies.

» No increased risk of bone fractures was

found among older people who used intranasal
corticosteroids, regardless of the dose used.[62]

» One notable exception may be intranasal

dexamethasone, which has significantly higher
systemic bio-availability than other intranasal
corticosteroids and has also been linked to
Cushing syndrome.[63]

» Intranasal antihistamines (e.g., azelastine,

olopatadine) are an alternative to intranasal
corticosteroids. They can also be combined
with an intranasal corticosteroid if symptoms
are uncontrolled with intranasal corticosteroid
alone. An intranasal preparation containing
the corticosteroid fluticasone in combination
with azelastine is available. This combination
preparation has been found to be superior to
either agent alone, particularly during the first
2 weeks of use.[65] [66] If the addition of an
intranasal antihistamine is not effective, the dose
of intranasal corticosteroid can be increased.

Primary options

» beclometasone nasal: (50 micrograms/

spray aqueous) children >6 years of age
and adults: 50-100 micrograms (1-2 sprays)
in each nostril twice daily; (40 micrograms/
spray aerosol) children 4-11 years of age:
40 micrograms (1 spray) in each nostril once
daily; (80 micrograms/spray aerosol) children
≥12 years of age and adults: 160 micrograms
(2 sprays) in each nostril once daily

OR
Primary options

» budesonide nasal: (32 micrograms/spray)

children >6 years of age and adults: 32-64
TREATMENT

micrograms (1-2 sprays) in each nostril once

daily

OR
Primary options

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jun 13, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
37
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 Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
» flunisolide nasal: (25 micrograms/spray)
children >6 years of age and adults: 50
micrograms (2 sprays) in each nostril twice
daily

OR
Primary options

» fluticasone furoate nasal: (27.5 micrograms/

spray) children 2-11 years of age: 27.5
micrograms (1 spray) in each nostril once
daily, increase to 55 micrograms (2 sprays) in
each nostril if inadequate response; children
≥12 years and adults: 27.5 to 55 micrograms
(1-2 sprays) in each nostril once daily

OR
Primary options

» fluticasone propionate nasal: (50

micrograms/spray) children >4 years of age:
50-100 micrograms (1-2 sprays) in each
nostril once daily; adults: 100 micrograms (2
sprays) in each nostril once daily

OR
Primary options

» mometasone nasal: (50 micrograms/spray)

children >2 years of age: 50 micrograms (1
spray) in each nostril once daily; adults: 100
micrograms (2 sprays) in each nostril once
daily

OR
Primary options

» triamcinolone nasal: (55 micrograms/spray)

children 2-5 years of age: 55 micrograms (1
spray) in each nostril once daily; children 6-11
years of age: 55-110 micrograms (1-2 sprays)
in each nostril once daily; children >11 years
of age and adults: 110 micrograms (2 sprays)
in each nostril once daily

OR
Primary options
TREATMENT

» ciclesonide nasal: (nasal spray: 50

micrograms/spray) children ≥6 years of age
and adults: 100 micrograms (2 sprays) in
each nostril once daily; (nasal aerosol: 37
micrograms/spray) children ≥12 years of age

38 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jun 13, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
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Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
and adults: 37 micrograms (1 spray) in each
nostril once daily

OR
Primary options

» azelastine nasal: (137 micrograms/spray)

children ≥5 years of age: 137 micrograms (1
spray) in each nostril twice daily; children ≥12
years of age and adults: 137-274 micrograms
(1-2 sprays) in each nostril twice daily; (205.5
micrograms/spray) children ≥12 years of age
and adults: 205.5 to 411 micrograms (1-2
sprays) in each nostril once to twice daily

OR
Primary options

» olopatadine nasal: (665 micrograms/spray)

children ≥6 years of age: 665 micrograms (1
spray) in each nostril twice daily; children ≥12
years of age and adults: 1330 micrograms (2
sprays) in each nostril twice daily

OR
Primary options

» azelastine/fluticasone propionate nasal:

(137 micrograms/50 micrograms) children
≥12 years of age and adults: 1 spray in each
nostril twice daily
plus allergen avoidance
» Allergen avoidance should be attempted by all
patients with AR. Allergy testing can be helpful
in identifying the allergens of concern for a
particular patient.

adjunct intranasal ipratropium

» Intranasal ipratropium may be added to
intranasal corticosteroids for uncontrolled
rhinorrhoea.

Primary options

» ipratropium nasal: (0.03%) children >6

years of age and adults: 42 micrograms (2
TREATMENT

sprays) in each nostril two to three times daily

adjunct oral antihistamine
» Oral antihistamines may be added to intranasal
corticosteroids in persistent moderate/severe
symptoms if sneezing, rhinorrhoea, and itching

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 Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
of the nose, palate, and eyes persist. Their effect
on nasal congestion is mild at best. Evidence
for benefit of adding an antihistamine to an
intranasal corticosteroid in paediatric populations
is lacking.[86]

» While oral antihistamines reduce conjunctival

itching, redness, and tearing, they are less
effective than intranasal antihistamines.

» Although there are no data to support

the use of oral antihistamines in addition to
intranasal antihistamines for nasal symptoms,
this combination may be reasonable for the
treatment of oral and/or palatal pruritus as well
as for allergic conjunctivitis if symptoms persist
despite nasal therapy.

» Second-generation oral antihistamines are

preferable to first-generation antihistamines
because they cause less or no sedation.

» Sedation is possible with cetirizine;

unlikely with loratadine, desloratadine, and
fexofenadine; and likely with chlorphenamine
and diphenhydramine.

» There is a risk of paradoxical hyperactivity with

use of sedating antihistamines, particularly in
children.

Primary options

» cetirizine: children >6 months of age: 2.5 to

5 mg orally once daily; children >6 years of
age and adults: 5-10 mg orally once daily

OR
Primary options

» desloratadine: children >6 months of age:

1 to 2.5 mg orally once daily; children >12
years of age and adults: 5 mg orally once
daily

OR
Primary options

» fexofenadine: children >6 months of age:

TREATMENT

15-30 mg orally twice daily; children >12

years of age and adults: 60 mg orally twice
daily or 180 mg orally once daily

OR

40 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jun 13, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
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Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
Primary options

» levocetirizine: children >6 months of age:

1.25 to 2.5 mg orally once daily; children
>6-12 years of age: 2.5 mg orally once daily;
children >12 years of age and adults: 2.5 to 5
mg orally once daily

OR
Primary options

» loratadine: children >2 years of age: 5 mg

orally once daily; children >6 years of age
and adults: 10 mg orally once daily

OR
Secondary options

» chlorphenamine: children >2 years of age:

1-2 mg orally (immediate-release), every
4-6 hours when required; children >12 years
of age and adults: 4 mg orally (immediate-
release) every 4-6 hours when required

OR
Secondary options

» diphenhydramine: children >2 years of

age: 6.25 to 25 mg orally every 4-6 hours
when required; children >12 years of age and
adults: 25-50 mg orally every 4-6 hours when
required
adjunct oral or intranasal decongestant or oral
corticosteroid
» Oral or intranasal decongestants may be used
as a short-term adjunct for 3 to 5 days if nasal
congestion is severe.

» Increased nasal patency typically occurs within

5 to 10 minutes with intranasal decongestants,
or within 30 minutes with oral decongestants.
The decongestive effects may last up to 8 to
12 hours with intranasal decongestants, and
up to 24 hours with extended-release oral
decongestants.

» Oral or intranasal decongestants as

TREATMENT

monotherapy have a limited role in the treatment

of AR. However, when combined with an
antihistamine, all cardinal symptoms of AR are
addressed.

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BMJ Best Practice topics are regularly updated and the most recent version
41
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 Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
» Tolerance and rebound nasal congestion
(rhinitis medicamentosa) can occur if intranasal
decongestants are used for longer than 3 to 5
days.

» An oral corticosteroid may be used for up

to 7 days if nasal congestion is persistent
and severe. Oral corticosteroids should not
be used for persistent mild symptoms. Depot
corticosteroids should be avoided.

Primary options

» oxymetazoline nasal: (0.025%) children

2-5 years of age: 2-3 sprays into each nostril
twice daily; (0.05%) children >6 years of age
and adults: 1-2 sprays in each nostril twice
daily

OR
Primary options

» pseudoephedrine: children 2-5 years of

age: 15 mg orally every 4-6 hours when
required, maximum 60 mg/day; children
6-11 years of age: 30 mg orally every 4-6
hours when required, maximum 120 mg/
day; children >12 years of age and adults:
60 mg orally every 4-6 hours when required,
maximum 240 mg/day

OR
Secondary options

» prednisolone: children: 1-2 mg/kg/day orally

given in 1-2 divided doses, maximum 60 mg/
day; adults: 20-60 mg/day orally given in 1-2
divided doses
adjunct nasal saline irrigation (saline douching)
» Nasal saline irrigation can be used to cleanse
the nostrils before administering intranasal
sprays. This may help reduce nasal symptoms
and reduce the dosage of intranasal treatment,
particularly in children.[64]

» Large volumes (e.g., 4-8 ounces of saline per

session) of isotonic or hypertonic saline solution
are likely to be effective.
TREATMENT

» Although the effects are likely to be modest,

there are few adverse effects associated with
this procedure.

42 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jun 13, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
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Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
2nd sublingual immunotherapy (SLIT)
» Immunotherapy is the only treatment modality
to potentially have a disease-modifying effect.
[81] It is most commonly reserved for patients
not responding to pharmacotherapy, or those
either unwilling to take or unable to tolerate
medications. Consultation with an allergy
specialist is recommended.

» Sublingual immunotherapy (SLIT) is effective

in treating both adults and children.[69] [70]
[71] [73] [72] It is considered to be safer than
SCIT because side effects are usually limited to
mucosal symptoms, and is easier to administer
(patient self-administers). However, it may be
less effective than SCIT.[73] Direct comparisons
using standardised and validated outcome
measures between SLIT and SCIT are not
available.[74]

» SLIT is more appropriately used in

monosensitised patients, especially those
sensitised to dust mites,[75] grass[76] [77] [78]
or ragweed.[79] However, it may not be available
in all jurisdictions, depending on local regulations
and drug approval processes. The US Food and
Drug Administration has approved a SLIT for
the treatment of adults with house dust mite-
associated AR.[75]

» For polysensitised patients, SLIT with multiple

allergens is sometimes employed, although no
commercially available formulations containing
more than one allergen currently exist.

» SLIT formulations can be employed in two

different manners. One involves taking it for
about 12 weeks before and throughout the
pollen season, stopping thereafter. Alternatively,
for more of a disease-modifying effect, it
can be taken daily for 3 years to provide a
sustained effect for a fourth year, even after
discontinuation.[81] [83]

» Immunotherapy should be targeted to include

allergens that are clinically relevant to the
geographic locale.

Primary options
TREATMENT

» house dust mite allergen extract: consult

specialist for guidance on dose

OR

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 Allergic rhinitis Treatment

Acute
Patient group Tx line Treatment
Primary options

» mixed grass pollens allergen extract:

consult specialist for guidance on dose

OR
Primary options

» timothy grass pollen allergen extract:

consult specialist for guidance on dose

OR
Primary options

» short ragweed pollen allergen extract:

consult specialist for guidance on dose
2nd subcutaneous immunotherapy (SCIT)
» Immunotherapy is the only treatment modality
to potentially have a disease-modifying
effect.[81] It is most commonly reserved for
patients not responding to pharmacotherapy,
or those either unwilling to take or unable to
tolerate medications. Consultation with an
allergy specialist is recommended.

» SCIT with dog or mould allergens has not been

uniformly deemed clinically effective in the past;
new dog allergens are now available that might
prove more effective.

» Improvement requires several months of

treatment. It is generally accepted that a 1-year
trial will determine who will and who will not
respond to SCIT.

» Adverse reactions occur in both local and

systemic form. Systemic reactions can vary
from mild to life-threatening; fatal reactions after
receiving an allergy vaccine are estimated to
occur at a rate of 1 in 2 to 2.5 million.[84] [85]
SCIT may reduce the progression from AR to
asthma when given in children aged 6 to 14
years for a minimum of 3 years. [67]

» Immunotherapy should be targeted to include

allergens that are clinically relevant to the
geographic locale.
TREATMENT

» Various extract manufacturers and dosing

regimens exist.

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BMJ Best Practice topics are regularly updated and the most recent version
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Allergic rhinitis Treatment

Ongoing
Patient group Tx line Treatment

usual therapy ineffective 1st sublingual immunotherapy (SLIT)

» Immunotherapy is the only treatment modality
to potentially have a disease-modifying
effect.[81] It is most commonly reserved for
patients not responding to pharmacotherapy,
or those either unwilling to take or unable to
tolerate medications. Consultation with an
allergy specialist is recommended.

» Sublingual immunotherapy (SLIT) is effective

in treating both adults and children.[69] [70]
[71] [73] [72] It is considered to be safer than
SCIT because side effects are usually limited to
mucosal symptoms, and is easier to administer
(patient self-administers). However, it may be
less effective than SCIT.[73] Direct comparisons
using standardised and validated outcome
measures between SLIT and SCIT are not
available.[74]

» SLIT is more appropriately used in

monosensitised patients, especially those
sensitised to dust mites,[75] grass[76] [77] [78]
or ragweed.[79] However, it may not be available
in all jurisdictions, depending on local regulations
and drug approval processes. The US Food and
Drug Administration has approved a SLIT for
the treatment of adults with house dust mite-
associated AR.[75]

» For polysensitised patients, SLIT with multiple

allergens is sometimes employed, although no
commercially available formulations containing
more than one allergen currently exist.

» SLIT formulations can be employed in two

different manners. One involves taking it for
about 12 weeks before and throughout the
pollen season, stopping thereafter. Alternatively,
for more of a disease-modifying effect, it
can be taken daily for 3 years to provide a
sustained effect for a fourth year, even after
discontinuation.[81] [83]

» Immunotherapy should be targeted to include

allergens that are relevant to the geographic
locale.
TREATMENT

Primary options

» house dust mite allergen extract: consult

specialist for guidance on dose

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jun 13, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
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of the topics can be found on [Link] . Use of this content is
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 Allergic rhinitis Treatment

Ongoing
Patient group Tx line Treatment
OR
Primary options

» mixed grass pollens allergen extract:

consult specialist for guidance on dose

OR
Primary options

» timothy grass pollen allergen extract:

consult specialist for guidance on dose

OR
Primary options

» short ragweed pollen allergen extract:

consult specialist for guidance on dose

usual therapy ineffective 1st subcutaneous immunotherapy (SCIT)

» Immunotherapy is the only treatment modality
to potentially have a disease-modifying
effect.[81] It is most commonly reserved for
patients not responding to pharmacotherapy,
or those either unwilling to take or unable to
tolerate medications. Consultation with an
allergy specialist is recommended.

» SCIT with dog or mould allergens has not been

uniformly deemed clinically effective in the past;
new dog allergens are now available that might
prove more effective.

» Improvement requires several months of

treatment. It is generally accepted that a 1-year
trial will determine who will and who will not
respond to SCIT.

» Adverse reactions occur in both local and

systemic form. Systemic reactions can vary
from mild to life-threatening; fatal reactions after
receiving an allergy vaccine are estimated to
occur at a rate of 1 in 2 to 2.5 million.[84] [85]
SCIT may reduce the progression from AR to
asthma when given in children aged 6 to 14
years for a minimum of 3 years.[67]

» Immunotherapy should be targeted to include

TREATMENT

allergens that are relevant to the geographic

locale.

» Various extract manufacturers and dosing

regimens exist.

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Allergic rhinitis Treatment

Ongoing
Patient group Tx line Treatment
plus allergen avoidance
» Allergen avoidance should be attempted by all
patients with AR. Allergy testing can be helpful
in identifying the allergens of concern for a
particular patient.

TREATMENT

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 Allergic rhinitis Treatment

Emerging
Alternative therapies
Alternative therapies such as selected herbal remedies for seasonal allergic rhinitis (SAR), acupuncture for
SAR[87] and perennial allergic rhinitis, and probiotics possibly play a role in reducing symptoms of allergic
rhinitis but, with perhaps the exception of pyrrolizidine-free butterbur, cannot be recommended due to a
scarcity of well-designed studies.[88] [89] [90]
TREATMENT

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Allergic rhinitis Follow up

Recommendations
Monitoring

FOLLOW UP
After a treatment regimen has been initiated, follow-up should take place in approximately 2 to 4 weeks
and therapy stepped up or stepped down as deemed necessary. If sub-optimal control is obtained despite
appropriate pharmacotherapy, determination of specific IgE reactivity using skin-prick testing or in vitro
specific IgE should take place. Results may be used to confirm the presence of allergic disease and help
in directing environmental control interventions.

Patient instructions
An initial official consultation for allergic rhinitis (AR) should include information on allergen avoidance
(if allergy testing has been performed) as well as an action plan detailing various aspects of the chosen
pharmacological agent(s) and expected clinical outcomes. Details on medications should include proper
dosing frequency and technique (including teaching on proper administration of nasal sprays), whether
treatments should be used on a schedule or as needed, expected time to clinical improvement, and
possible side effects (e.g., sedation with first-generation antihistamines). Finally, plans for appropriate
follow-up should be made, usually 2 to 4 weeks after initial assessment.

Complications

Complications Timeframe Likelihood

acute conjunctivitis (allergic) variable medium

Appropriate therapy with oral or ophthalmic antihistamines or ophthalmic sodium cromoglicate may be
required to achieve a successful and comprehensive therapeutic outcome.

asthma variable medium

Poorly controlled allergic rhinitis (AR) may result in the development of lower respiratory tract symptoms or
loss of asthma control in certain individuals. If this occurs, the physician will need to address both airways
equally to gain adequate disease control.

antihistamine-associated sedation variable medium

Use of first-generation antihistamines may result in both drowsiness and a global reduction or impairment
in intellectual and motor performance, such as learning a new task or driving a motor vehicle. This can
also occur with some second-generation antihistamines (e.g., cetirizine and levocetirizine), but is less
common than with first-generation agents.

adverse effects of nasal decongestants variable medium

Include nasal burning, stinging, dryness, and less commonly, mucosal ulceration.

rhinitis medicamentosa (rebound nasal congestion) variable medium

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 Allergic rhinitis Follow up

Complications Timeframe Likelihood

Can occur when intranasal decongestants are used for longer than 3 to 5 days.
FOLLOW UP

adverse effects of oral decongestants variable medium

Adverse effects of oral decongestants include central nervous stimulation such as insomnia, which may
occur in up to one third of people; nervousness; anxiety; tremors; tachycardia; palpitations; and increases
in BP.

chronic sinusitis variable medium

There is considerable epidemiological evidence to support the linkage between sinus disease and AR.
Studies have noted that 40% to 67% of patients with unilateral chronic sinusitis and up to 80% with chronic
bilateral sinusitis have AR.

acute sinusitis variable medium

There is considerable epidemiological evidence to support the linkage between sinus disease and AR.
Studies have noted that 25% to 30% of patients with acute sinusitis have AR.

Prognosis

Natural history of disease

While AR can present in infancy, its prevalence increases in young childhood and peaks in childhood and
adolescence until decreasing with advancing age. In one longitudinal study, 738 former university students
who were evaluated and underwent skin testing during their first year at university completed a 23-year
follow-up questionnaire inquiring into their history of allergies and asthma.[91] The mean age of this group
at the time of the follow-up study was 40 years. During the 23 years subsequent to the original study, 131
developed new allergy symptoms in addition to the 175 individuals already diagnosed when they were first-
year university students, totalling 306. At the time of the 23-year follow-up, improvement was noted by 54.9%
(168/306) of those affected, with a trend of increasing percentage of improvement with younger age of onset
of allergy symptoms. Among those who improved, 41.6% (70/168) described themselves as symptom-free,
while the remaining 58.3% (98/168) were better, if not symptom-free.[91]

This suggests that in the long term, AR symptoms improve in at least one half of affected individuals.

Variability of severity
Similarly to other chronic diseases, AR can vary in severity over time. While a long-term trend for the
improvement or resolution of symptoms exists, the perceived severity of disease can increase or decrease,
wax and wane, or even change unpredictably over a short time span. Possible factors explaining severity
variability may be divided into being external or internal. External factors include time of the day, location,
and season, because they all affect pollen counts. Internal factors may include circadian rhythms, mood, and
affect, as well as immunological changes that occur over time.

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Allergic rhinitis Follow up

Immunotherapy outcomes
In patients receiving grass allergen immunotherapy for a period of 3 to 4 years, approximately 50% of
patients continued to derive clinical benefits 3 years after immunotherapy had been discontinued.[81] [83]

FOLLOW UP

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 Allergic rhinitis Guidelines

Diagnostic guidelines

Europe

BSACI guidelines for the management of allergic and non-allergic rhinitis

(revised ed)
Published by: British Society for Allergy and Clinical Immunology Last published: 2017

Practical guide to skin prick tests in allergy to aeroallergens

Published by: Global Allergy and Asthma European Network Last published: 2012
(GA(2)LEN)

North America

Clinical practice guideline: allergic rhinitis

GUIDELINES

Published by: American Academy of Otolaryngology; Head & Neck Last published: 2015
Surgery Foundation

Consultation and referral guidelines citing the evidence: how the allergist/
immunologist can help
Published by: American Academy of Allergy, Asthma & Immunology Last published: 2014

The diagnosis and management of rhinitis

Published by: Joint Task Force on Practice; American Academy of Last published: 2008
Allergy, Asthma & Immunology; American College of Allergy, Asthma and
Immunology; Joint Council of Allergy, Asthma and Immunology

Treatment guidelines

Europe

Treatment of seasonal allergic rhinitis: an evidence-based focused 2017

guideline update
Published by: Joint Task Force on Practice; American Academy of Last published: 2017
Allergy, Asthma & Immunology; American College of Allergy, Asthma and
Immunology

BSACI guidelines for the management of allergic and non-allergic rhinitis (rev
ed)
Published by: British Society for Allergy and Clinical Immunology Last published: 2017

National clinical guideline for the treatment of hay fever (allergic

rhinoconjunctivitis)
Published by: Danish Health Authority Last published: 2016

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Allergic rhinitis Guidelines

Europe

Immunotherapy for allergic rhinitis

Published by: British Society for Allergy and Clinical Immunology Last published: 2011

International

Allergic rhinitis and its impact on asthma (ARIA) guidelines: 2016 revision
Published by: Global Allergy and Asthma European Network Last published: 2016
(GA(2)LEN); Grading of Recommendations Assessment, Development
and Evaluation Working Group; American Academy of Allergy, Asthma &
Immunology

North America

GUIDELINES
Treatment of seasonal allergic rhinitis: an evidence-based focused 2017
guideline update
Published by: Joint Task Force on Practice; American Academy of Last published: 2017
Allergy, Asthma & Immunology; American College of Allergy, Asthma and
Immunology

Clinical practice guideline: allergic rhinitis

Published by: American Academy of Otolaryngology; Head & Neck Last published: 2015
Surgery Foundation

The diagnosis and management of rhinitis

Published by: Joint Task Force on Practice; American Academy of Last published: 2008
Allergy, Asthma & Immunology; American College of Allergy, Asthma and
Immunology; Joint Council of Allergy, Asthma and Immunology

Spectrum of noninfectious health effects from molds

Published by: American Academy of Pediatrics Last published: 2006

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 Allergic rhinitis Evidence scores

Evidence scores
1. Symptom relief: there is poor-quality evidence from one small randomised controlled trial of 76
households, randomised to behavioural programme, receipt of a dehumidifier, or no intervention, that
showed no major effect on dust mite counts or allergen counts.[51]
Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomized
controlled trials (RCTs) of <200 participants.
EVIDENCE SCORES

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Allergic rhinitis References

Key articles
• Bousquet J, Khaltaev N, Cruz AA, et al. Allergic rhinitis and its impact on asthma (ARIA) 2008. Allergy.

REFERENCES
2008;63(suppl s86):8-160. Full text Abstract

• Scadding GK, Kariyawasam HH, Scadding G, et al. BSACI guideline for the diagnosis and
management of allergic and non-allergic rhinitis (rev ed 2017). Clin Exp Allergy. 2017;47:856-89. Full
text

• Nurmatov U, van Schayck CP, Hurwitz B, et al. House dust mite avoidance measures for perennial
allergic rhinitis: an updated Cochrane systematic review. Allergy. 2012 Feb;67(2):158-65. Full text
Abstract

References
1. Bousquet J, Khaltaev N, Cruz AA, et al. Allergic rhinitis and its impact on asthma (ARIA) 2008. Allergy.
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2. European Academy of Allergy and Clinical Immunology. Global atlas of allergic rhinitis and chronic
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 Allergic rhinitis References
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19. Cuello-Garcia CA, Fiocchi A, Pawankar R, et al. World Allergy Organization-McMaster University
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21. Riedler J, Braun-Fahrlander C, Eder W, et al. Exposure to farming in early life and development of
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subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
Allergic rhinitis References
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population. J Allergy Clin Immunol. 2016 Dec;138(6):1556-8. Full text Abstract

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allergic sensitization at 6 to 7 years of age. JAMA. 2002 Aug 28;288(8):963-72. Abstract

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risk factors for positive allergy skin test responses in the Childhood Asthma Management Program. J
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36. Giwercman C, Halkjaer LB, Jensen SM, et al. Increased risk of eczema but reduced risk of early
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37. Wright AL, Holberg CJ, Taussig LM, et al. Factors influencing the relation of infant feeding to asthma
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 Allergic rhinitis References
38. Wright AL, Sherrill D, Holberg CJ, et al. Breast-feeding, maternal IgE, and total serum IgE in
childhood. J Allergy Clin Immunol. 1999 Sep;104(3 Pt 1):589-94. Abstract
REFERENCES

39. Cuello-Garcia CA, Brożek JL, Fiocchi A, et al. Probiotics for the prevention of allergy: A
systematic review and meta-analysis of randomized controlled trials. J Allergy Clin Immunol. 2015
Oct;136(4):952-61. Full text Abstract

40. Schindler T, Sinn JK, Osborn DA. Polyunsaturated fatty acid supplementation in infancy for the
prevention of allergy. Cochrane Database Syst Rev. 2016 Oct 28;10:CD010112. Full text Abstract

41. Meltzer EO, Schatz M, Nathan R, et al. Reliability, validity, and responsiveness of the Rhinitis Control
Assessment Test in patients with rhinitis. J Allergy Clin Immunol. 2013 Feb;131(2):379-86. Full text
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42. Juniper EF, Thompson AK, Ferrie PJ, Roberts JN. Validation of the standardized version of the
Rhinoconjunctivitis Quality of Life Questionnaire. J Allergy Clin Immunol. 1999 Aug;104(2 Pt 1):364-9.
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43. Juniper EF, Riis B, Juniper BA. Development and validation of an electronic version of the
Rhinoconjunctivitis Quality of Life Questionnaire. Allergy. 2007 Sep;62(9):1091-3. Full text Abstract

44. Bousquet J, Heinzerling L, Bachert C, et al. Practical guide to skin prick tests in allergy to
aeroallergens. Allergy. 2012;67:18-24. Full text Abstract

45. Lindberg S, Malm L. Comparison of allergic rhinitis and vasomotor rhinitis patients on the basis of a
computer questionnaire. Allergy. 1993 Nov;48(8):602-7. Abstract

46. Meltzer EO, Hamilos DL, Hadley JA, et al. Rhinosinusitis: establishing definitions for clinical research
and patient care. J Allergy Clin Immunol. 2004;114:155-212. Abstract

47. Scadding GK, Kariyawasam HH, Scadding G, et al. BSACI guideline for the diagnosis and
management of allergic and non-allergic rhinitis (rev ed 2017). Clin Exp Allergy. 2017;47:856-89. Full
text

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Contributors:

// Authors:

Alexander Greiner, MD
Co-Director
Allergy and Asthma Medical Group and Research Center, Rady Children’s Hospital, University of California
at San Diego School of Medicine, La Jolla, CA
DISCLOSURES: AG has received grant/research support from: Astra Zeneca; Boehringer Ingelheim;
Cephalon Circassia Ltd; Clement Clarke Cytos biotechnology; GlaxoSmithKline; Glenmark Specialty,
S.A.; Hoffman-LaRoche/Genentech; HRA/Novartis; Janssen Research & Development; Kalypsys , Inc.;
Lupin; Merck; Mylan Pharmaceuticals, Inc.; Nestle (Nestec Ltd); Novartis Ono Pharmaceutical Co., Ltd.;
Perrigo; Rigel Pharmaceuticals, Inc.; Roxane Laboratories Inc.; Shionogi Inc.; Sunovion TEVA Branded
Pharmaceutical Products; UBC (United Biosource Corporation)/Amgen Pharmaceuticals; and sponsorship
for pharmaceutical trials from Allergen Research Corporation/Aimmune Therapeutics, Inc. and Astra
Zeneca.

// Peer Reviewers:

Mark Davis-Lorton, MD
Clinical Immunology Coordinator
Division of Rheumatology, Immunology and Allergy, Winthrop-University Hospital, Mineola, NY
DISCLOSURES: MDL declares that he has no competing interests.

Glenis Scadding, MD
Consultant Allergist/Rhinologist
Allergy & Rhinology Department, Royal National TNE Hospital, London, UK
DISCLOSURES: GS is a consultant/advisory board member for ALK, Britannia Pharmaceuticals, CMP
Therapeutics, Groupo Uriach, GSK, Merck, Sanofi-Aventis, Schering Plough, and UCB. She has received
research funds from ALK, GSK, UCB, and Schering Plough. She has given talks for ALK, GSK, Merck,
Schering Plough, and UCB and has co-written articles for Schering Plough and GSK.