CASE REPORT

ALLERGIC RHINITIS

Presented by : dr. Seno Aji Saputro

Moderator : dr. Ashadi Prasetyo, M.Sc, Sp.T.H.T.K.L

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.1
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 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.1 Allergic rhinitis contributes to
missed or unproductive time at work and
school, sleep problems, and among affected
children, decreased involvement in outdoor
activities.2 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.1,2 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.2
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.3 Having multiple older
siblings and growing up in a farming
environment are associated with a reduced
risk of allergic rhinitis3 it is hypothesized
that these apparently protective factors may
reflect microbial exposures early in life that
shift the immune system away from Th2
polarization and allergy.2,3
The development of allergic
rhinitis starts with sensitization.
 Deposition of allergens leads to migration
of sample antigen to the lymph nodes
where the presentation to sensitize T cells
occurs. Binding of the allergen to a
specific IgM on an APC causes
endocytosis and breaking down of the
allergen in lysosomes. The allergen is then
presented as small fragments of MHC-11
complexes to Th cells in lymphoid tissue.
Secretion of cytokines such as IL-4
triggers IgE production through the
binding of IL-4 from T cells to its receptor
on B lymphocytes (Johnson & Rosen,
2014). Nasal mucosa may respond to
allergen in 2 distinct ways, which are early
response and late response. Symptoms of
sneezing, itching, rhinorrhea,
congestion are manifestations of mast cell
predominance in early response phase
which appear within minutes after
exposure to specific antigen. Excluding
congestion, these responses are mediated
by histamine release which lead to
vasodilation, vascular leakage,
stimulation of glands
3,4
neurons.
Meanwhile, the late response
which occurs within hours after the early
response, involve recruitment and
interaction of numerous cells. These
symptoms mainly lead to congestion and
production of additional allergen-specific
IgE and contribute to development of
increased responsiveness to allergen
(priming) and exposure to irritants
(hyperresponsiveness). Hyperactive nasal
mucosa to normal stimuli such as tobacco,
cold air, or dry air or simply termed as
nonspecific hyperresponsiveness is
mediated by eosinophil infiltration 3,4
In the late response, T cells
facilitated the cascade of events that leads
to inflammatory reactions and induce
eosinophil response through IL-5
production. T helper and mast cells also
produce IL-4 that contributes in the cascade
of events. Local epithelia recruit basophils,
T cells, monocytes and eosinophils to the
site of inflammation through VCAM-1, and
and upregulate antigen 4 and ICAM-1 in
response to IL-4, IL-1β or TNF-α.
RANTES and eotaxin act to recruit mast
cells and eosinophils whereas TGF-β
appears to be recruiting mast cells in
epithelia of inferior turbinate. Transcellular
migration of cells on endothelium is
and facilitated by changes in intracellular and
and cell-surface. Platelet endothelial cell
adhesion molecule 1 (PECAM-1) and
vascular endothelial cadherin are known to
be molecule associated with delayed
resolution of vascular permeability and
modulation of endothelial permeability,
respectively. Interaction between
leukocytes and endothelial ligands facilitate
cells recruitment. Those cells thus roll
along the endothelial surface, adhere, and patients have no response to these
transmigrate through gap junctions of treatment 4,5
endothelial cells called paracellular Problems which may arise as
pathway. Another known theory of the complications of allergic rhinitis are
migration of leukocytes is through rhinosinusitis, asthma, COPD (chronic
4
transcellular pathway obstructive pulmonary disease), sleep
In the initial phase of type 1 disturbance, otitis media, learning
hypersensitivity, an antigen (the allergen) impairment, and lower quality of life.
is presented to antigen-spesific CD4+ Th2 Rhinosinusitis has been discussed to have
cells, which then stimulate B-cell to relationship with allergic rhinitis,
produce IgE. The IgE antibodies bind to especially chronic rhinosinusitis. Given
Fc RI on the surface of tissue membrane the high prevalence of atopy in patients
cell and blood BS during sensitization. with chronic rhinosinusitis, it has been
Re-exposure to the same allergen will postulated that atopy and allergic rhinitis
cross-links the bound IgE on sensitized contribute to the severity of chronic
cells, which leads to degranulation and rhinosinusitis. Asthma is present in 78% of
secretion of preformed pharmacologically patient with both allergic and non allergic
active mediators such as histamines. This rhinitis.5,6
reaction starts within seconds as an In a study by Guerra et al. (2002)
immediate response. Activated mast cells in subjects with rhinitis, both allergic and
will induce synthesis and releases of non allergic rhinitis had a 3-fold increase
leukotrienes, chemokines, and cytokines in the development of asthma
which then allows the recruitment of other compared with individuals without
leukocytes, basophils, eosinophils, and rhinitis. The presence of allergic rhinitis in
Th2 lymphocytes to the site of individuals with COPD has been
inflammation. This response is known as associated with an increased risk of COPD
late reaction. Antihistamines, corticoids, exacerbations and increased respiratory
and other anti-inflammatory medications symptoms, such as wheeze, cough, and
had classically been used to treat the phlegm production. Inflammatory
allergic symptoms due to this Ig-E mediators and cytokines in allergic rhinitis
mediated chronic disease, including have been shown to contribute to sleep
wheezing, cough, urticaria, diarrhea, and disturbance and fatigue by increasing
bronchospasm, although some of the latency to REM (rapid eye movement)
sleep, decreasing time in REM sleep, and requires detailed history taking, physical
decreasing latency to sleep onset. The examination, and either skin prick testing
decrease in REM sleep in the subjects with or allergen-specific IgE serum testing.7,8
allergic rhinitis may have contributed to Presence of 2 or more symptoms out of
daytime sleepiness and fatigue. Nasal watery rhinorrhea, sneezing, nasal
congestion is frequently accompanied obstruction, and nasal pruritus for 1 hour
with mouth breathing, both of them or more on most days raises the suspicion
reducing respiratory tract diameter that of allergic rhinitis9. Unilateral symptoms,
can lead to OSA (obstructive sleep apnea) nasal obstruction without other symptoms,
which may cause frequent arousals and mucopurulent rhinorrhea, post nasal drip
lead to daytime somnolence.6,7 with thick mucous, pain, recurrent
Allergic inflammation may epistaxis, and anosmia are usually not
contribute to the pathogenesis of otitis associated with allergic rhinitis8,9. On
media with effusion by swelling and inspection, Dennie-Morgan lines
blockage of the entrance to the Eustachian described as folds of the lower eyelid,
tube, causing dysfunction and secondary allergic shiners (i.e., dark areas under the
inflammation of the middle ear in addition eyes as a result of venous congestion), red
to a reduction in the lumen size of the watery eyes suggesting allergic
inflamed Eustachian tube which may conjunctivitis, frequent sniffing, use of
impede mucociliary clearance and leading tissues, nasal rubbing (allergic salute),
to delayed clearance of middle ear nasal speech, allergic crease, mouth
effusions and resultant otitis media. breathing, presence of asthmatic
Moreover, allergic rhinitis can symptoms, and allergic or atopic
significantly affect cognition, fatigue, and manifestation in the skin (i.e., eczema) are
memory in children, which can, therefore, suggestive of allergic rhinitis
9,10
have an impact on learning and school Examination for nasal obstruction is
performance. Chronic rhinitis has also performed to assess nasal airflow by
been associated with reduced quality of simple method such as observing for the
life. Additionally, recreational activities of misting area of the cold metal object held
children with allergic rhinitis are often beneath both nostrils or by other methods
limited by the disease and can lead to such as inspiratory peak flow, acoustic
diminished social interactions. 7 rhinometry, and rhinomanometry. On

The diagnosis of allergic rhinitis anterior rhinoscopy, classic demonstration

of edematous, pale, boggy inferior and/or
 middle turbinates with clear and inhibitors and blockers, oral
seromucous secretrions is indicative of sympathomimetics, and intranasal saline
allergic mucosa10 are the modalities of treatment which can
Differential diagnosis of allergic be used to control allergic rhitinis. A
rhinitis include idiopathic rhinitis, NARES strategy of treatment using allergen-
(nonallergic rhinitis and eosinophilia specific subcutaneous or sublingual
syndrome), rhinosinusitis, atrophic rhinitis, allergen immunotherapy may also be
gustatory rhinitis, rhinitis of pregnancy, and performed to induce tolerance to the
AERD (aspirin exacerbated respiratory allergens leading to the resolution of
disease). Thorough history taking and inflammatory symptoms 11
physical examination confirmed by CASE REPORT
diagnostic testings are needed to exclude A 52 years old woman presented to
those conditions 10,11 ENT clinic with itchy nose, clear nasal
The primary goal of allergic discharge and continuous sneezing. She
rhinitis treatment is to restore and complained that her nose was itchy and
permit the achievement of normal social, sometimes obstructed. The simptoms
olfaction, and gustatory function as well as started since 10 years ago, the simptoms
good sleep quality 10Principles of allergic usually occurs 4 to 5 days a week. The nasal
rhinitis management are included in 3 key discharge is serous, clear and not smelly.
elements which are reduction of the The simptomps worsen during morning and
sensitisizing allergenexposure night, and sometimes bother her sleep at
encompassing environmental avoidance night and her daily routines
of the inciting allergens, targeted She denied about fever, facial pain,
pharmacotherapy, and subcutaneous or tinnitus, dizziness, sore thorat. On
sublingual immunotherapy 11 examination the patient generally in good
Elimination of the offending condition, afebrile and normal vital signs.
allergens is also included in environmental The nose were morphologically normal and
control in management of allergic rhinitis. there was no deformity. On Rhinoscopy
Pharmacotherapy embraces the choices anterior the mucous layer was livid, the
between some medications used to control septum was straight and no deformity
the symptoms of allergic rhinitis. Topical founded, the turbinate on right nosetrill was
or oral antihistamines of first or second hypertrophy and serous clear nasal
generation, intranasal or systemic discharge found on both nosetrills. No
glucocorticosteroids, leukotriene foreign body was detected. Examination of
the ear, mouth, and throat within normal
limit
The patient was tested for the
allergens in 2010, Ingestan allergens were
tested positive to house dust, particle of
human skin, particle of dog skin, particle of
horse skin, tepung sari padi (pollen), tepung
sari jagung
And for the food Allergens were
tested Positive to Crab, Bandeng,
Swordfish, Soy, Chocolate
The patient is diagnosed with
Allergic Rhinitis Moderate-Severe
Persistent and was advised to avoid the
allergens and given Fluticasone nasal spray
twice a day and Pseudoefedrine tablet per
oral 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:
increasing nasal corticosteroid dose,
addition of H1-antihistamine dose for
itch/sneeze, addition of ipratropoium for
rhinorrhea, addition of short term
decongestant or oral corticosteroid for
blockage, and if it is all failed, the patient is
considered to get surgical referral.
CONCLUSION
We have reported a 52 year old 2016, ID 8163803.
female with Allergic Rhinitis Moderate- 5. Guerra, S., Sherrill, D.L., Martinez,
Severe Persistent . She has been treated F.D., Barbee, R.A., 2002, Rhinitis as
with Fluticasone nasal spray twice a day an independent risk factor for adult-
and Pseudoefedrine tablet per oral twice a onset asthma, J Allergy Clin
day and she has showed an improvement Immunol, 109:419-425.
with the decrease of itchy nose, clear nasal 6. Johnson, J.T. and Rosen, C.A., 2014,
discharge and sneezing both on frequency Bailey’s Head and Neck Surgery –
or severity for 5 days treatment Otolaryngology, 5th ed., Lippincott
Williams & Wilkins, Baltimore.
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