CASE REPORT

ALLERGIC RHINITIS

Presented by : dr. Seno Aji Saputro

Moderator : dr. Agus Surono, Ph.D, Sp.T.H.T.K.L., M. Kes

Department of Otorhinolaringology Head and Neck Surgery

Faculty of Medicine University of Gadjah Mada-dr. Sardjito General Hospital

2017
 Allergic rhinitis is defined as
symptoms of sneezing, nasal pruritus,
airflow obstruction, and mostly clear nasal
discharge caused by IgE-mediated reactions
against inhaled allergens and involving
mucosal inflammation driven by type 2
helper T (Th2) cells.1 Allergens of
importance include seasonal pollens and
molds, as well as perennial indoor allergens,
such as dust mites, pets, pests, and some
molds. The pattern of dominant allergens
depends on the geographic region and the
degree of urbanization, but the overall
prevalence of sensitization to allergens does
not vary across census tracts in the United
States.2 [1] Although allergic rhinitis itself is
not life-threatening (unless accompanied by
severe asthma or anaphylaxis), morbidity
from the condition can be significant.
The frequency of sensitization to
inhalant allergens is increasing and is now
more than 40% in many populations in the
United States and Europe.2,5,6 The
prevalence of allergic rhinitis in the United
States is approximately 15% on the basis of
physician diagnoses7 and as high as 30% on
the basis of self-reported nasal symptoms.3
Allergic rhinitis contributes to missed or
unproductive time at work and school, sleep
problems, and among affected children,
decreased involvement in outdoor
activities.7 In addition, children with
allergic rhinitis are more likely than
unaffected children to have myringotomy
tubes placed and to have their tonsils and
adenoids removed.
Most people with asthma have
rhinitis. The presence of allergic rhinitis
increases the probability of asthma: up to
40% of people with allergic rhinitis have or
will have asthma.9,10 Atopic eczema
frequently precedes allergic rhinitis.11
Patients with allergic rhinitis usually have
allergic conjunctivitis as well.12 The factors
determining which atopic disease will
develop.
According to International Study of
Asthma and Allergies in Children (ISAAC,
2006), Indonesia along with Albania,
Rumania, Georgia dan Yunani are the
lowest allergic rhinitis country less than 5%
of total population.
in an individual person and the
reasons why some people have only rhinitis
and others have
rhinitis after eczema or with asthma remain
unclear. Having a parent with allergic
rhinitis more than doubles the risk.13
Having multiple older siblings and growing
up in a farming environment are associated
with a reduced risk of allergic rhinitis14,15;
it is hypothesized that these apparently
protective factors may reflect microbial Meanwhile, the late response which
exposures early in life that shift the immune occurs within hours after the early
system away from Th2 polarization and response, involve recruitment and
allergy.14,15 interaction of numerous cells. These
The development of allergic rhinitis symptoms mainly lead to congestion and
starts with sensitization. Deposition of production of additional allergen-specific
allergens leads to migration of sample IgE and contribute to development of
antigen to the lymph nodes where the increased responsiveness to allergen
presentation to sensitize T cells occurs. (priming) and exposure to irritants
Binding of the allergen to a specific IgM on (hyperresponsiveness). Hyperactive nasal
an APC causes endocytosis and breaking mucosa to normal stimuli such as tobacco,
down of the allergen in lysosomes. The cold air, or dry air or simply termed as
allergen is then presented as small nonspecific hyperresponsiveness is
fragments of MHC-11 complexes to Th mediated by eosinophil infiltration
cells in lymphoid tissue. Secretion of (Johnson & Rosen, 2014).
cytokines such as IL-4 triggers IgE In the late response, T cells
production through the binding of IL-4 facilitated the cascade of events that leads to
from T cells to its receptor on B inflammatory reactions and induce
lymphocytes (Johnson & Rosen, 2014). eosinophil response through IL-5
Nasal mucosa may respond to allergen in 2 production. T helper and mast cells also
distinct ways, which are early response and produce IL-4 that contributes in the cascade
late response. Symptoms of sneezing, of events. Local epithelia recruit basophils,
itching, rhinorrhea, and congestion are T cells, monocytes and eosinophils to the
manifestations of mast cell predominance site of inflammation through VCAM-1, and
in early response phase which appear upregulate antigen 4 and ICAM-1 in
within minutes after exposure to specific response to IL-4, IL-1β or TNF-α. RANTES
antigen. Excluding congestion, these and eotaxin act to recruit mast cells and
responses are mediated by histamine eosinophils whereas TGF-β appears to be
release which lead to vasodilation, vascular recruiting mast cells in epithelia of inferior
leakage, and stimulation of glands turbinate. Transcellular migration of cells on
and neurons. endothelium is facilitated by changes in
intracellular and cell-surface. Platelet chemokines, and cytokines which then
endothelial cell adhesion molecule 1 allows the recruitment of other leukocytes,
(PECAM-1) and vascular endothelial basophils, eosinophils, and Th2
cadherin are known to be molecule lymphocytes to the site of inflammation.
associated with delayed resolution of This response is known as late reaction.
vascular permeability and modulation of Antihistamines, corticoids, and other anti-
endothelial permeability, respectively. inflammatory medications had classically
Interaction between leukocytes and been used to treat the allergic symptoms
endothelial ligands facilitate cells due to this Ig-E mediated chronic disease,
recruitment. Those cells thus roll along the including wheezing, cough, urticaria,
endothelial surface, adhere, and transmigrate diarrhea, and bronchospasm, although
through gap junctions of endothelial cells some of the patients have no response to
called paracellular pathway. Another known these treatment (Ferrer et al, 2016).
theory of the migration of leukocytes is Problems which may arise as
through transcellular pathway (Johnson & complications of allergic rhinitis are
Rosen, 2014). rhinosinusitis, asthma, COPD (chronic
In the initial phase of type 1 obstructive pulmonary disease), sleep
hypersensitivity, an antigen (the allergen) disturbance, otitis media, learning
is presented to antigen-spesific CD4+ Th2 impairment, and lower quality of life.
cells, which then stimulate B-cell to Rhinosinusitis has been discussed to have
produce IgE. The IgE antibodies bind to relationship with allergic rhinitis,
Fc RI on the surface of tissue membrane especially chronic rhinosinusitis. Given
cell and blood BS during sensitization. Re- the high prevalence of atopy in patients
exposure to the same allergen will cross- with chronic rhinosinusitis, it has been
links the bound IgE on sensitized cells, postulated that atopy and allergic rhinitis
which leads to degranulation and secretion contribute to the severity of chronic
of preformed pharmacologically active rhinosinusitis. Asthma is present in 78%
mediators such as histamines. This reaction of patient with both allergic and non
starts within seconds as an immediate allergic rhinitis. In a study by Guerra et
response. Activated mast cells will induce al. (2002) in subjects with rhinitis, both
synthesis and releases of leukotrienes, allergic and non allergic rhinitis had a 3-
fold increase in the development of
asthma compared with individuals without
rhinitis. The presence of allergic rhinitis in
individuals with COPD has been
associated with an increased risk of COPD
exacerbations and increased respiratory
symptoms, such as wheeze, cough, and
phlegm production. Inflammatory
mediators and cytokines in allergic rhinitis
have been shown to contribute to sleep
disturbance and fatigue by increasing
latency to REM (rapid eye movement)
sleep, decreasing time in REM sleep, and
decreasing latency to sleep onset. The
decrease in REM sleep in the subjects
with allergic rhinitis may have contributed
to daytime sleepiness and fatigue. Nasal
congestion is frequently accompanied with
mouth breathing, both of them reducing
respiratory tract diameter that can lead to
OSA (obstructive sleep apnea) which may
cause frequent arousals and lead to
daytime somnolence. Allergic
inflammation may contribute to the
pathogenesis of otitis media with effusion
by swelling and blockage of the entrance
to the Eustachian tube, causing
dysfunction and secondary inflammation
of the middle ear in addition to a reduction
in the lumen size of the inflamed
Eustachian tube which may impede
mucociliary clearance and leading to
delayed clearance of middle ear effusions
and resultant otitis media.
Moreover, allergic rhinitis can
significantly affect cognition, fatigue, and
memory in children, which can, therefore,
have an impact on learning and school
performance. Chronic rhinitis has also
been associated with reduced quality of
life. Additionally, recreational activities of
children with allergic rhinitis are often
limited by the disease and can lead to
diminished social interactions (Keswani &
Peter, 2016).
The diagnosis of allergic rhinitis
requires detailed history taking, physical
examination, and either skin prick testing
or allergen-specific IgE serum testing
(Scadding & Scadding, 2016). Presence of
2 or more symptoms out of watery
rhinorrhea, sneezing, nasal obstruction, and
nasal pruritus for 1 hour or more on most
days raises the suspicion of allergic rhinitis
(Min, 2010). Unilateral symptoms, nasal
obstruction without other symptoms,
mucopurulent rhinorrhea, post nasal drip
with thick mucous, pain, recurrent
epistaxis, and anosmia are usually not
associated with allergic rhinitis (Nonikov,
2008). On inspection, Dennie-Morgan lines
described as folds of the lower eyelid,
 allergic shiners (i.e., dark areas under the physical examination confirmed by
eyes as a result of venous congestion), red diagnostic testings are needed to exclude
watery eyes suggesting allergic those conditions (Akdis et al, 2015).
conjunctivitis, frequent sniffing, use of The primary goal of allergic rhinitis
tissues, nasal rubbing (allergic salute), treatment is to restore and permit
nasal speech, allergic crease, mouth the achievement of normal social, olfaction,
breathing, presence of asthmatic symptoms, and gustatory function as well as good
and allergic or atopic manifestation in the sleep quality (Akdis et al, 2015). Principles
skin (i.e., eczema) are suggestive of allergic of allergic rhinitis management are
rhinitis (Akdis et al, 2015; Quillen & included in 3 key elements which are
Feller, 2006; Scadding & Scadding, 2016). reduction of the sensitisizing
Examination for nasal obstruction is allergenexposure encompassing
performed to assess nasal airflow by simple environmental avoidance of the inciting
method such as observing for the misting allergens, targeted pharmacotherapy, and
area of the cold metal object held beneath subcutaneous or sublingual immunotherapy
both nostrils or by other methods such as (Bernstein et al., 2016). Elimination of the
inspiratory peak flow, acoustic rhinometry, offending allergens is also included in
and rhinomanometry. On anterior environmental control in management of
rhinoscopy, classic demonstration of allergic rhinitis. Pharmacotherapy
edematous, pale, boggy inferior and/or embraces the choices between some
middle turbinates with clear and medications used to control the symptoms
seromucous secretrions is indicative of of allergic rhinitis. Topical or oral
allergic mucosa (Scadding & Scadding, antihistamines of first or second generation,
2016). intranasal or systemic glucocorticosteroids,
Differential diagnosis of allergic leukotriene inhibitors and blockers, oral
rhinitis include idiopathic rhinitis, NARES sympathomimetics, and intranasal saline
(nonallergic rhinitis and eosinophilia are the modalities of treatment which can
syndrome), rhinosinusitis, atrophic rhinitis, be used to control allergic rhitinis. A
gustatory rhinitis, rhinitis of pregnancy, and strategy of treatment using allergen-
AERD (aspirin exacerbated respiratory specific subcutaneous or sublingual
disease). Thorough history taking and allergen immunotherapy may also be
 performed to induce tolerance to the
allergens leading to the resolution of
inflammatory symptoms (Akdis et al,
2015).
CASE REPORT
A 52 years old woman presented to
ENT clinic with itchy nose, clear nasal
discharge and continuous sneezing. She
complained that her nose was itchy and
sometimes obstructed. The simptoms started
since 10 years ago, the simptoms usually
occurs 2 to 3 days a week. The nasal
discharge is serous, clear and not smelly.
Despite of that she said that she still can do
the daily routine and she sleep well at night
She denied about fever, facial pain,
tinnitus, dizziness, sore thorat. On
examination the patient generally in good
condition, afebrile and normal vital signs.
The nose were morphologically normal and
there was no deformity. On Rhinoscopy
anterior the mucous layer was livid, the
septum was straight and no deformity
founded, the turbinate on right nosetrill was
hypertrophy and serous clear nasal discharge
found on both nosetrills. No foreign body
was detected. Examination of the ear,
mouth, and throat within normal limit
The patient is diagnosed with
Allergic Rhinitis Mild Intermitten and was
advised to avoid the allergens and given
Avamys nasal spray twice a day and Aldisa
twice a day. The medication was given for 5
days
DISCUSSION
Treatment for allergic rhinitis is
divided according to patient’s symptom
severity and persistency. Spectrum of
allergic rhinitis severity ranges from mild
and moderate severe while spectrum of the
persistency encompasses intermittent and
persistent symptoms.
For mild intermittent symptoms, ARIA
recommends usage of oral/intranasal H1-
antihistamine and/or decongestant or
LTRA (leukotriene receptor antagonists)
(not on preferred order). For moderate-
severe intermittent and mild persistent
symptoms, medications used are
oral/intranasal H1-antihistamine and/or
decongestant or LTRA (not on preferred
order) also patient response review after 2-
4 weeks. If patient symptoms improved,
continue the therapy for 1 month. If patient
symptoms are stagnating, step up the dose.
Patient with moderate-severe
persistent symptoms need more specified
treatment and observation. First preferred
medication is intranasal corticosteroid, H1-
antihistamine or LTRA (in preferred order).
Review of patient’s response is carried out
after 2–4 weeks, and if it improves, dose
needs to be tappered off and the treatment is
continued for 1 month. If patient’s
symptoms still persist, review of diagnosis
and patient’s compliance is necessary.
Consideration of possible infection or other
causes for patient’s symptoms is suggested.
Medications are increased according to
patient’s specific symptoms, in example:
CONCLUSION
We have reported a 20 year old
female with Allergic Rhinitis Mild
Intermitten . She has been treated with
Avamys spray twice a day and Aldisa twice
a day and she has showed an improvement
with the decrease of itchy nose, clear nasal
discharge and sneezing both on frequency or
severity
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