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Allergic Rhinitis
Chapter · January 2010
DOI: 10.1007/978-3-540-68940-9_18
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2. 151
2.8 Allergic Rhinitis
Joaquim Mullol and Antonio Valero
2.8.1 Introduction
Allergic rhinitis is a symptomatic disorder of the nose, in-
duced after allergen exposure by an IgE-mediated inflam-
mation of the nasal mucosa. Allergic rhinitis represents a
global health problem. It is a worldwide disease affecting
at least 10–25% of the population [1], and its prevalence
is increasing. In European countries the prevalence of al-
lergic rhinitis has been estimated from 17 to 29% [2]. An
increase in this prevalence has been observed in the past
40 years [3]. Allergic rhinitis is not a severe disease but it
alters a patient’s social life, affecting school performance
and work productivity [4]; the costs incurred by rhinitis
are substantial [5]. Asthma and rhinitis are common co-
morbidities, suggesting the concept of “one airway, one
disease” [6].
Guidelines for the diagnosis and treatment of allergic
rhinitis have already been published [7], but some were
not predicated on evidence-based medicine and few, if
any, considered the patients globally in terms of comor-
bidities. The ARIA (Allergic Rhinitis and Its Impact on
Asthma) initiative [8, 9] has developed a document that
is the state of the art, for the specialist as well as for the
general practitioner to:
Update his/her knowledge of allergic rhinitis
•
Highlight the impact of allergic rhinitis on asthma
•
Provide an evidence-based documented revision on
•
the diagnosis methods and on the treatments avail-
able
Propose a stepwise approach to the management of
•
the disease
2.8.2 Definition and Classification
Symptoms of allergic rhinitis include rhinorrhea, nasal
obstruction, nasal itching, and sneezing, which are re-
versible spontaneously or with treatment. Allergic rhini-
tis was previously classified as seasonal and perennial.
The new ARIA classification of allergic rhinitis is based
on symptoms and quality-of-life parameters. Duration of
symptoms is subdivided into “intermittent” or “persis-
tent” disease, while severity is subdivided into “mild” or
“moderate-severe”, depending on symptoms and quality
of life (Fig. 2.8.1). This classification has been recently
validated [10, 11].
2.8.3 Aetiology and Triggers
2.8.3.1 Allergens
Aeroallergens are very often involved in allergic rhinitis
[12]. The increase in domestic allergens is responsible in
part for the increase in the prevalence of rhinitis, asthma
and allergic respiratory diseases. In the home, the main
allergens are mites, domestic animals, insects or those
derived from plant origin. Outdoor allergens include pol-
lens and moulds.
Occupational rhinitis is less well documented than oc-
cupational asthma is but is often associated with asthma.
Latex allergy has become an increasing concern to pa-
tients and health professionals, who should be aware of
the problem and develop strategies for prevention and
treatment.
2.8.3.2 Pollutants
Pollutants are involved in the aggravation of nasal symp-
toms in patients with allergic and nonallergic rhinitis. The
Moderate-severe
one or more items
- abnormal sleep
- impairment of daily
activities, sport, leisure
- abnormal work and
school
- troublesome symptoms
Persistent
> 4 days per week
and > 4 weeks
Mild
- normal sleep
- no impairment of daily
activities, sport, leisure
- normal work and
school
- no troublesome
symptoms
Intermittent
≤ 4 days per week
or ≤ 4 weeks
Moderate-severe
one or more items
- abnormal sleep
- impairment of daily
activities, sport, leisure
- abnormal work and
school
- troublesome symptoms
Persistent
> 4 days per week
and > 4 weeks
Mild
- normal sleep
- no impairment of daily
activities, sport, leisure
- normal work and
school
- no troublesome
symptoms
Intermittent
≤ 4 days per week
or ≤ 4 weeks
Fig. 2.8.1 Classification of allergic rhinitis (ARIA)

3. 152 2 Nose and Paranasal Sinuses
2.8.5 Comorbidities
Allergic inflammation does not limit itself to the nasal
airway. Multiple comorbidities have been associated with
rhinitis such as asthma [6], rhinosinusitis and conjunc-
tivitis.
2.8.5.1 Asthma
Nasal and bronchial mucosa share many similarities.
Epidemiological studies have shown that asthma and
rhinitis often coexist in the same patients. Most patients
with allergic (80%) and nonallergic (50%) asthma have
rhinitis, while many patients with rhinitis (20–30%) have
also asthma. Allergic rhinitis constitutes a risk factor for
asthma, and many allergic rhinitis patients have bronchi-
al hyperreactivity [18].
Pathophysiological studies also suggest that a strong
relationship exists between rhinitis and asthma. Al-
though differences exist between rhinitis and asthma,
upper and lower airways may be considered as a unique
entity influenced by a common inflammatory process.
Since bronchial challenge leads to nasal inflammation
and nasal challenge leads to bronchial inflammation, al-
lergic diseases may be considered systemic. Consequent-
ly, when considering a diagnosis of rhinitis or asthma, an
evaluation of both the lower and upper airways should
be made.
2.8.5.2 Other Comorbidities
Other comorbidities include rhinosinusitis and conjunc-
tivitis, and the associations between allergic rhinitis, na-
sal polyposis, and otitis media are poorly understood.
2.8.6 Diagnosis
The diagnosis of allergic rhinitis is based on the coordina-
tion between a clinical history (allergic symptoms), nasal
examination and diagnostic tests.
2.8.6.1 Clinical History
It is essential for an accurate diagnosis of rhinitis to assess
its severity and response to treatment. Although not nec-
essarily of allergic origin, the main nasal symptoms are
obstruction, sneezing, itching and rhinorrhea.
interaction between pollutants and rhinitis is suggested
by epidemiological evidence, although the mechanism is
not well understood. Indoor pollution, including domes-
tic allergens and indoor gas pollutants (tobacco smoke),
is of great importance, since in industrialised countries
people spend over 80% of their time indoors.
Urban-type pollution is in many countries primarily
of automobile origin [13], and the principal atmospheric
oxidant pollutants include ozone, nitric oxides, and sul-
phur dioxide. Diesel exhaust fumes may also enhance IgE
formation and allergic inflammation.
2.8.3.3 Aspirin and Nonsteroidal
Anti-inflammatory Drugs
NSAIDs commonly induce rhinitis and asthma [14].
2.8.4 Mechanisms of Action
In allergic rhinitis, the understanding of the mechanisms
of the disease provides a framework for its rational ther-
apy, based on the complex inflammatory reaction rather
than on the symptoms alone. Allergy is classically con-
sidered to result from an IgE-mediated allergy associated
with nasal inflammation of variable intensity [15]. Aller-
gic rhinitis is characterised by an inflammatory infiltrate
made up of different cells, including:
Chemotaxis, activation, differentiation, and survival
•
prolongation of various cell types including eosino-
phils, T cells, mast cells and epithelial cells
Release of mediators by these activated cells: cytok-
•
ines, chemokines, histamine and cysteinyl leukot-
rienes (cys-LT) as the major mediators
Communication with the immune system and the
•
bone marrow
Nonspecific nasal hyperreactivity [16] is an important
feature of allergic rhinitis and is defined as an increased
nasal response to normal stimuli, resulting in sneezing,
nasal congestion and/or secretion. Intermittent rhinitis
can be mimicked by nasal challenge with pollen aller-
gens, and an inflammatory reaction occurs during the
late-phase reaction. In persistent allergic rhinitis, allergic
triggers interact with an ongoing inflammatory reaction,
and symptoms are due to this complex interaction.
The concept of “minimal persistent inflammation”
[17] has been confirmed in perennial allergic rhinitis.
In patients with persistent allergic rhinitis, allergen ex-
posure varies throughout the year, and there are periods
in which there is little exposure. Although symptom free,
these patients still present with nasal inflammation.

4. 153
2.8.7 Management and Treatment
2.8.6.2 Nasal Examination
In patients with mild, intermittent allergic rhinitis, a na-
sal examination is optimal, but all patients with persis-
tent allergic rhinitis need a nasal examination. Anterior
rhinoscopy, using a speculum and mirror, gives limited
information. Nasal endoscopy, which can be performed
only by specialists, is more useful.
2.8.6.3 Diagnostic Tests
In vivo and in vitro tests used to diagnose allergic dis-
eases are directed towards the detection of free or cell-
bound IgE. The diagnosis of allergy has been improved
by allergen standardisation (Table 2.8.1).
2.8.6.3.1 Skin-prick Test
The skin-prick test is used to demonstrate an IgE-medi-
ated allergic reaction and represents a major diagnostic
tool in the field of allergy. If properly performed, it gives
confirmatory evidence for the diagnosis of a specific al-
lergy. Due to the complexity in performance and inter-
pretation of the test, it is recommended that it be carried
out by trained health care professionals [19].
2.8.6.3.2 Serum-specific IgE
Serum-specific IgE has a similar value to that of skin tests
[20].
2.8.6.3.3 Allergen Nasal Challenge
The allergen nasal challenge is mainly used in research
and, to a lesser extent, in clinical practice. It is especially
useful in the diagnosis of occupational rhinitis [21].
2.8.6.3.4 Imaging
Imaging is not usually necessary.
2.8.6.3.5 Diagnosis of Asthma
Guidelines for recognising and diagnosing asthma have
been published by the Global Initiative for Asthma
(GINA) [22] and are recommended. Measurement of
lung function and confirmation of the reversibility of
airflow obstruction are essential steps in the diagnosis of
asthma.
2.8.7 Management and Treatment
The management of allergic rhinitis is based on allergen
avoidance, pharmacological treatment, specific immuno-
therapy, and, when possible, patient education [8, 9, 23].
2.8.7.1 Allergen Avoidance
Most allergen-avoidance studies have dealt with asthma
symptoms, and very few have studied rhinitis symp-
Table 2.8.1 Diagnostic tests for allergic rhinitis
Category of test Specific test
Routine History
Clinical
–
–
Family
–
–
General ENT examination (rhinoscopy)
Nasal airway assessment
Peak nasal inspiratory flow (PNIF)
–
–
Allergy tests
Skin
–
–
Serum-specific IgE
–
–
Additional Endoscopy
Rigid
–
–
Flexible
–
–
Radiology
CT scan
–
–
Optional Nasal challenge
Allergen
–
–
Lysine aspirin
–
–
Nasal samples
Cytology/nasal secretions
–
–
Nasal biopsy
–
–
Nasal swab
–
–
Radiology
MRI
–
–
Mucociliary function
Nasal mucociliary clearance
–
–
(NMCC)
Ciliary beat frequency (CBF)
–
–
Electron microscopy
–
–
Nasal airway assessment
Rhinomanometry (anterior, pos-
–
–
terior)
Acoustic rhinometry
–
–
Smell test (University of Pennsylvania
smell identification test [UPSIT], ZOST,
Barcelona smell test [BAST]-24)
Nitric oxide measurement

5. 154 2 Nose and Paranasal Sinuses
2.8.7.2.1 H1-Antihistamines
Drugs
Old generation: Chlorpheniramine, clemastine,
diphenhydramine, hydroxyzine, keto-
tifen, mequitazine, oxatomide
New generation: Acrivastine, azelastine, cetirizine,
desloratadine, ebastine, fexofenadine,
levocetirizine, loratadine, mizolastine,
rupatadine
Cardiotoxic drugs: Astemizole, terfenadine
Mechanism of Action
The mechanism of action is via blockage of H1 receptor
and some anti-allergic activity. New generation drugs can
be used once daily. There is no development of tachyphy-
laxis is usually noted.
Side Effects
Old generation: Sedation and/or anticholinergic effect
is common
New generation: No sedation for most drugs, no
anticholinergic effect, no cardiotoxic-
ity. Acrivastine has sedative effects,
mequitazine has anticholinergic
effects, and oral azelastine may induce
sedation and has a bitter taste
toms. A single intervention may be insufficient to control
symptoms of rhinitis or asthma. Although more data are
needed to appreciate fully the clinical value of allergens,
allergen avoidance, including house dust mites, should be
an integral part of a management strategy [24, 25].
2.8.7.2 Pharmacological Treatment
Pharmacological management for treatment of allergic
rhinitis involves several classes of drugs (Figs. 2.8.2 and
2.8.3).
sneezing rhinorrhea nasal nasal eye
obstruction itch symptoms
H1-antihistamines
oral +++ +++ 0 to + +++ ++
intranasal ++ +++ + ++ 0
intraocular 0 0 0 0 +++
Corticosteroids
intranasal +++ +++ ++ ++ +
Chromones
intranasal + + + + 0
intraocular 0 0 0 0 ++
Decongestants
intranasal 0 0 ++ 0 0
oral 0 0 + 0 0
Anti-cholinergics 0 +++ 0 0 0
Anti-leukotrienes 0 + ++ 0 ++
Fig. 2.8.2 Pharmacological
management and drug effects on
the symptoms of allergic rhinitis.
0 no effect, + mild, ++ moderate,
+++ intense
intervention SAR
adult children adult children
oral anti -H1 A A A A
intranasal anti -H1 A A A A
intranasal CS A A A A
intranasal chromone A A A A
subcutaneous SIT A A A A
sublingual A A
nasal SIT A A A
allergen avoidance D D D D
intervention SAR PAR
adult children adult children
oral anti-H1 A A A A
intranasal anti-H1 A A A A
intranasal CS A A A A
intranasal chromone A A A A
subcutaneous SIT A A A A
sublingual A A
nasal SIT A A A
allergen avoidance D D D D
Fig. 2.8.3 Strength of evidence for the treatment of allergic
rhinitis. Recommendations are evidence-based on randomised-
controlled trials (RCT) carried out on studies performed with
the previous classification of rhinitis: seasonal (SAR) and pe-
rennial (PAR) allergic rhinitis. Strength of recommendation: A
based on RCT or meta-analysis, D based on the clinical experi-
ence of experts

6. 155
2.8.7 Management and Treatment
Comments
New generation oral H1-antihistamines should be prefer­
red for their favourable efficacy/safety ratio and pharma-
cokinetics.Theyarerapidlyeffective(lessthan1h)onnasal
and ocular symptoms and poorly effective on nasal con-
gestion. Cardiotoxic drugs should be avoided [23, 26].
Local Antihistamines
Local antihistamines include Azelastine and levocabas-
tine. They are rapidly effective (less than 30 min) on nasal
or ocular symptoms. Minor local side effects: azelastine
has a bitter taste.
2.8.7.2.2 Corticosteroids
Drugs
Intranasal: Beclomethasone, budesonide, fluni-
solide, fluticasone, momethasone,
triamcinolone
Oral/intramuscular
(IM):
Dexamethasone, hydrocortisone,
methylprednisolone, prednisolone,
prednisone, triamcinolone, betame-
thasone, deflazacort
Mechanism of Action
The mechanism of action is via potent reduction of nasal
inflammation and nasal hyperreactivity.
Side Effects
Intranasal: Minor local side effects, wide margin
for systemic side effects, growth
concerns with some molecules only.
In young children the combination of
intranasal and inhaled drugs should
be considered
Oral/IM: Systemic side effects common in par-
ticular for IM drugs. Depot injections
may cause local tissue atrophy
Comments
Intranasal: The most effective pharmacological
treatment of allergic rhinitis. Effec-
tive on nasal congestion and loss of
smell. Effect observed after 12 h but
maximal effect after a few days
Oral: When possible, intranasal corticoster-
oids should replace oral or IM drugs.
A short course of oral corticosteroids
may be needed with severe symptoms
[23]
2.8.7.2.3 Chromones (Intranasal, Ocular)
Drugs
Drugs used include cromoglycate and nedocromil.
Mechanism of Action
The mechanism of action is not well known.
Side Effects
Side effects are minor and local in nature.
Comments
Intraocular chromones are very effective. Intranasal
chromones are less effective, and their effect is short last-
ing. Overall they have an excellent safety record.
2.8.7.2.4. Nasal Decongestants
Drugs
Oral: Ephedrine, phenylephrine, phenylpro-
panolamine, pseudoephedrine
Intranasal: Oxymethazoline, naphazoline, xylom-
etazoline, and others
Mechanism of Action
Sympathomimetic drugs relieve symptoms of nasal con-
gestion by acting on alpha-adrenergic receptors.
Side Effects
Oral: Hypertension, palpitations, restless-
ness, agitation, tremor, insomnia,
headache, dry mucous membranes,
urinary retention, exacerbation of
glaucoma or thyrotoxicosis
Intranasal: Same side effects as oral deconges-
tants but less intense. Rhinitis medica-
mentosa is a rebound phenomenon
occurring with prolonged use (over
10 days)

7. 156 2 Nose and Paranasal Sinuses
2.8.7.3 Specific Immunotherapy
Specific immunotherapy is effective when optimally
administered. Standardised therapeutic vaccines are fa-
voured when available. Subcutaneous immunotherapy
raises contrasting efficacy and safety issues [29, 30]. The
use of optimal doses of vaccines either labelled in biologi-
cal units or labelled in mass of major allergens has been
proposed. Doses of 5–20 µg of the major allergen are op-
timal doses for most allergen vaccines.
2.8.7.3.1 Subcutaneous Immunotherapy
Subcutaneous immunotherapy (SIT) alters the natural
course of allergic diseases [31]. SIT should be performed
by trained personnel, and patients should be monitored
for 30 min after injection. SIT is indicated in patients in-
sufficiently controlled by conventional pharmacotherapy,
in whom oral H1-antihistamines and intranasal pharma-
cotherapy insufficiently control symptoms, who do not
wish to be on pharmacotherapy, in whom pharmaco-
therapy produces undesirable side effects and who do not
want to receive long-term pharmacological treatment.
2.8.7.3.2 Nasal and Sublingual-swallow
Specific Immunotherapy
Nasal and sublingual-swallow specific immunotherapy
may be used with doses at least 20–100 times greater than
those used for SIT, or in patients who had side effects or
refused SIT. The indications follow those of subcutaneous
injections.
2.8.7.3.3 Immunotherapy in Children
Specific immunotherapy is effective. It is recommended
to start this treatment after the child reaches 5 years of
age.
2.8.7.4 Education
When possible, education is always recommended.
2.8.7.5 Surgery
Surgical intervention may be used as an adjunctive inter-
vention in few and selected patients (e. g. turbinate hyper-
trophy, septal deviation).
Comments
Oral: Oral decongestants should be used
with caution in patients with heart dis-
ease. Oral H1-antihistamine combined
with decongestant may be more ef-
fective than either product alone, but
side effects are combined
Intranasal: Act more rapidly and more effectively
than oral decongestants. Limit dura-
tion of treatment to less than 10 days
to avoid rhinitis medicamentosa [27]
2.8.7.2.5 Anticholinergics
Drug
Ipratropium is the drug of choice.
Mechanism of Action
Anticholinergic drugs block almost exclusively rhinor-
rhea.
Side Effects
There are minor, local side effects; there is virtually no
systemic anticholinergic activity.
Comments
Ipratropium is effective in allergic and nonallergic pa-
tients with rhinorrhea.
2.8.7.2.6 Leukotriene-receptor Antagonists
Drugs
This class of drugs includes montelukast, pranlukast and
zafirlukast.
Mechanism of Action
This class of drugs works by way of blockage of cys-LT
receptor.
Side Effects
Patients are found to have excellent tolerance of these
drugs.
Comments
These drugs are promising used alone or in combination
with oral H1-antihistamines, but more data are needed to
categorize better these drugs [28].

8. 157
2.8.8 Special Considerations
2.8.7.6 Selection of Medications
Medications have no long-lasting effect when stopped.
Therefore, in persistent disease, maintenance treatment is
required (Fig. 2.8.4).
Tachyphylaxis does not usually occur with prolonged
•
treatment.
Medications used for rhinitis are most commonly ad-
•
ministered intranasally or orally.
Some studies have compared the relative efficacy of
•
these medications, of which intranasal corticosteroids
are the most effective. However, the choice of treat-
ment also depends on many other criteria.
The use of alternative care (e. g. homeopathy, herbal-
•
ism, acupuncture) for the treatment of rhinitis is in-
creasing. Scientific and clinical supports are lacking
for these therapies. There is an urgent need for large,
randomised and controlled clinical trials for alterna-
tive therapies of allergic diseases and rhinitis.
IM injection of glucocorticosteroids is not usually rec-
•
ommended due to the possible occurrence of systemic
side effects.
Intranasal injection of glucocorticosteroids is not usu-
•
ally recommended due to the possible occurrence of
severe side effects.
2.8.7.7 Treatment of Concomitant
Rhinitis and Asthma
Treatment of asthma should follow the GINA guidelines
[22]. Some drugs are effective in the treatment of both
rhinitis and asthma (e. g. glucocorticoids, antileukot-
rienes), while others are only effective in the treatment
of either rhinitis or asthma (e. g. α- and β-adrenergic ago-
nists, respectively). Some drugs are more effective in rhin-
itis than in asthma (e. g. H1-antihistamines). Although
more studies are needed, optimal management of rhinitis
may improve coexisting asthma [32]. Drugs administered
by the oral route may affect both nasal and bronchial
symptoms. The safety of intranasal glucocorticoids is well
established. Large doses of inhaled (intrabronchial) glu-
cocorticoids can induce side effects [33]. One of the prob-
lems of dual administration may be the possible additive
side effects. Although the addition of intranasal formu-
lations to inhaled formulations does not produce any
further significant suppression, more data are needed. It
has been proposed that the prevention or early treatment
of allergic rhinitis may help to prevent the occurrence of
asthma or the severity of bronchial symptoms but more
data are also needed.
2.8.7.8 Treatment of Conjunctivitis
The options of treatment are oral and/or ocular H1-anti-
histamines, ocular chromones and saline. Administration
of ocular corticosteroids is not recommended.
2.8.8 Special Considerations
2.8.8.1 Pregnancy
Rhinitis is often a problem during pregnancy since nasal
obstruction may be aggravated by pregnancy itself [34].
Caution must be taken when administering any medi-
cation during pregnancy, as most medications cross the
placenta. For most drugs, limited studies have been done
only on small groups, with no long-term analysis.
2.8.8.2 Paediatric Aspects
Allergic rhinitis is part of the “allergic march” during
•
childhood, but intermittent allergic rhinitis is unusual
before 2 years of age. Allergic rhinitis is most prevalent
during the school-age years [35].
Allergy tests can be done at any age, and they may
•
yield important information. The principles of treat-
ment for children are the same as for adults. Special
care must be taken to avoid the side effects typical of
this age group.
Doses of medication have to be adjusted and must fol-
•
low special considerations. Few medications have been
tested in children younger than 2 years of age.
In children, symptoms of allergic rhinitis can impair
•
cognitive functioning and school performance, which
can be further impaired by the use of sedating oral H1-
antihistamines.
mild
intermittent
mild
persistent
moderate
severe
intermittent
moderate
severe
persistent
immunotherapy
local chromone
oral or local non-sedative H -blocker
1
allergen and irritant avoidance
oral / topical (<10 days) nasal decongestant
intranasal steroid
Fig. 2.8.4 Treatment of allergic rhinitis (ARIA)

9. 158 2 Nose and Paranasal Sinuses
8. Environmental and social factors should be optimised
to allow the patient to lead a normal life.
9. Asthmatic patients should be evaluated (history and
physical examination) for rhinitis.
10. In terms of efficacy and safety, a combined strategy
should be used to treat the upper and lower airway
diseases.
11. In developing countries, a specific strategy may be
needed depending on the availability and affordability
of interventions.
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sensus statement on the treatment of allergic rhinitis. Eu-
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Allergy 55:116–134
8. Bousquet J, van Cauwenberge P, Khaltaev N, ARIA Work-
shop Group (2001) Allergic rhinitis and its impact on
asthma. ARIA Workshop Report. J Allergy Clin Immunol
108:S147–S334
9. Bousquet J, van Cauwenberge P, Khaltaev N, ARIA Work-
shop Expert Panel (2002) Allergic rhinitis and its impact
on asthma (ARIA). Executive Summary of the Workshop
Report. Allergy 57:841–55
10. Demoly P, Allaert FA, Lecasble M, Bousquet J (2003) Vali-
dation of the classification of ARIA (allergic rhinitis and its
impact on asthma). Allergy 58:672–675
11. Bauchau V, Durham SR (2005) Epidemiological character-
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Intranasal glucocorticosteroids are an effective treat-
•
ment for allergic rhinoconjunctivitis. Their possible
effect on growth for some but not all intranasal glu-
cocorticoids is of concern. Recommended doses of
intranasal momethasone and fluticasone did not affect
growth in children with allergic rhinoconjunctivitis.
Oral and IM glucocorticosteroids should be avoided
•
in the treatment of rhinitis in young children.
Disodium cromoglycate is commonly used to treat al-
•
lergic rhinoconjunctivitis in children because of the
safety of the drug.
2.8.8.3 Ageing
With ageing, various physiological changes occur in the
connective tissue and vasculature of the nose, which may
predispose or contribute to chronic rhinitis [36]. Allergy
is a less common cause of persistent rhinitis in subjects
older than 65 years of age. Atrophic rhinitis is common
and difficult to control. Rhinorrhea can be controlled with
anticholinergics. Some drugs (reserpine, guanethidine,
phentolamine, methyldopa, prazosin, chlorpromazine
or ACE inhibitors) can cause rhinitis. Some drugs may
induce specific side effects in elderly patients. Deconges-
tants and drugs with anticholinergic activity may cause
urinary retention in patients with prostatic hypertrophy.
Sedative drugs can have greater side effects.
2.8.9 Key Guidance
Key guidance includes the following [8, 9]:
1. Allergic rhinitis is a major chronic respiratory disease
due to its prevalence, impact on quality of life, impact
on work/school performance and productivity, eco-
nomic burden, and links with asthma, rhinosinusitis
and conjunctivitis.
2. Allergic rhinitis is a risk factor for asthma.
3. A new classification of allergic rhinitis has been pro-
posed: intermittent and persistent.
4. The severity of allergic rhinitis has been classified as
“mild” and “moderate/severe” depending on symptom
severity and quality of life outcomes.
5. Depending on the subdivision and severity of allergic
rhinitis, a stepwise therapeutic approach has been pro-
posed that should be used.
6. The treatment of allergic rhinitis combines allergen
avoidance (when possible), pharmacotherapy, and im-
munotherapy.
7. Patients with persistent allergic rhinitis should be
evaluated for asthma by history, chest examination,
and assessment of lung function (before and after
bronchodilator).

10. 159
2.8.9 Key Guidance
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