Allergic rhinitis

Dr Utsav Shrestha
Lecturer
ENT
Rhinitis
Clinically combination of two or more symptoms :
 Runny nose
 Blocking
 Itching
 Sneezing

Allergic rhinitis
When symptoms occur due to IgE mediated reaction following
exposure to allergen
• Allergic rhinitis is an IgE-mediated immunologic response of nasal
mucosa to airborne allergens and is characterized by watery nasal
discharge, nasal obstruction, sneezing and itching in the nose.

• Other associated symptoms are itching in the eyes, palate and

pharynx
AETIOLOGY
1)Inhalant allergens:
• may be seasonal or perenial.
• Seasonal allergens include pollens from trees, grasses and weeds.
They vary geographically.
• Perennial allergens are present throughout the year They in molds,
dust mites, cockroaches and dander from animals. Dust includes dust
mite, insect parts, fibres and animal danders.
2) Genetic predisposition.
• plays an important part.
• Chances of children developing allergy are 20 and 47%, respectively, if one
or both parents suffer from allergic diathesis.

3) Hygiene hypothesis
reduced exposure to microbes in early childhood due to modern hygiene
practices, antibiotics, smaller family sizes, and urban living leads to an
under-stimulated immune system.
This immune system may then overreact to harmless substances like pollen,
dust mites, or pet dander, resulting in allergies.
PATHOGENESIS
Reaction can be considered in four phases
• Sensitization
• Early phase reaction
• Late phase reaction
• Systemic activation
• Inhaled allergens produce specific IgE antibody in the genetically
predisposed individuals

• This antibody becomes fixed to the blood basophils or tissue mast

cells by its Fc end ( sensitization)

• On subsequent exposure, antigen combines with IgE antibody at its

Fab end.
• “priming affect” - mucosa earlier sensitized to an allergen will react
to smaller doses of subsequent specific allergen

• Also gets “primed” to other nonspecific antigens to which patient was

not exposed
Allergic response occurs in two
phases:
1) Acute or early phase: It occurs immediately within 5–30 min, after
exposure to the specific allergen and consists of sneezing, rhinorrhoea
nasal blockage and/ or bronchospasm.
It is due to release of vasoactive amines like histamine.

2. Late or delayed phase: It occurs 2–8 h after exposure to allergen

without additional exposure.
It is due to infiltration of inflammatory cells—eosinophils, neutrophils,
basophil, monocytes and CD4 + T cells at the site of antigen deposition
causing swelling, congestion and thick secretion.
Early phase reaction :
Mast cell degranulation
 Histamine
Tryptase, Chymase
 PG D2
 LT B4, C4
 IL – 4, 5, 6, 8, 10, 13, TNF-a, GM-CSF
 Bradykinin
 PAF
Pathophysiology

Sneezing, itching

Histamine Rhinorrhoea

Nasal obstruction
Pathophysiology

Nasal obstruction

PG D2

10 times more
potent than
histamine
Pathophysiology
Eicosanoids

Lipooxygena Increased vascular

se pathway permeability and
edema

Lt B4, C4 Eosinophil &

(SRS-A) neutrophil
recruitment
Pathophysiology
Rhinorrhoea

Kinins

Sneezing

Nasal obstruction
and pain
Pathophysiology
Late phase reaction
 High doses allergen
 Involves the ingress of :
a) eosinophils,
b) basophils,
c) mast cells,
d) T lymphocytes,
e) neutrophils and
f) macrophages
 Main symptoms are nasal obstruction and
hyperreactivity
Pathophysiology

Eosinophil's
• < 1 percent of circulating cells
• Migrate into the tissue upon an appropriate
signal (cytokines, chemokines and
adhesion molecules, GMCSF, IL-5, RANTES
and eotaxin )
• In tissue, mature and remain alive for days
or weeks
Pathophysiology
Eosinophil content and secretion products
• Major basic protein (MBP)
• Eosinophil cationic protein (ECP)
• Eosinophil-derived neurotoxin (EDN)
• Eosinophil peroxidase and beta glucuronidase
• Enzyme-containing granules (arylsulphatase B)
• Cytokines, such as IL-3, IL-5 and GMCSF, IL-8, MIP I-alpha, TGF
beta-l
• Cysteinyl leukotrienes
• PG EI
• Thomboxane B2 and PAF
• Reactive oxygen intermediates
• Histaminase
Pathophysiology

Increase
vascular
permeability

Activated
eosinophils
Increase mucus
secretion

Alteration in
nasal
mucosa
Pathophysiology
Allergen Ig E

B
Antigen Mast Lymphocytes
presenting cells
cells

TH2 cells IL-4, IL-5, IL-13

CLINICAL FEATURES
• no age or sex predilection

• may start in infants as young as 6 months or older people.

• Usually the onset is at 12–16 years of age.

• cardinal symptoms of seasonal nasal allergy include paroxysmal
sneezing, 10–20 sneezes at a time, nasal obstruction, watery nasal
discharge and itching in the nose.

• duration and severity of symptoms may vary with the season.

• Symptoms of perennial allergy are not so severe as that of the

seasonal type.

• include frequent colds, persistently stuffy nose, loss of sense of smell

due to mucosal oedema, postnasal drip, chronic cough and hearing
impairment due to eustachian tube blockage or fluid in the middle ear.
Signs of allergic rhinitis
1) Nasal signs:
• transverse nasal crease—a black line across the middle of dorsum of
nose due to constant upward rubbing of nose simulating a salute
(allergic salute)
• pale and oedematous nasal mucosa which may appear bluish.
• Turbinates are swollen.
• Thin, watery or mucoid discharge is usually present.
2) Ocular signs:
• oedema of lids
• congestion and cobble-stone appearance of the conjunctiva
• dark circles under the eyes (allergic shiners).

3) Otologic signs:
• retracted tympanic membrane or serous otitis media as a result of
eustachian tube blockage.
4) Pharyngeal signs:
• granular pharyngitis due to hyperplasia of submucosal lymphoid
tissue.
• mouth breathing as seen in adenoid hyperplasia in child

5) Laryngeal signs:
• hoarseness and oedema of the vocal cords.
• Allergic rhinitis is subdivided into intermittent (IAR) or persistent (PER)
disease and the severity into mild or moderate/severe
INVESTIGATIONS

1. Total and differential count. Peripheral eosinophilia.

2. Nasal smear. It shows large number of eosinophils in allergic

rhinitis. Nasal smear should be taken at the time of clinically active
disease or after nasal challenge test.
Nasal eosinophilia is also seen in certain nonallergic rhinitis, e.g.
NARES (nonallergic rhinitis with eosinophilia syndrome).
3. Skin prick test
• Simple, cheap and safe

• Must be undertaken with emergency

equipment

• Staff training
These tests help to identify specific allergen.

This is an excellent method to demonstrate the allergen

A drop of concentrated allergen solution is placed on the volar surface

of the forearm or back and a sharp needle pricked into the dermis
through the drop.

It introduces the allergen into the dermis.

• A positive reaction - formation of a central wheal and a surrounding zone
of erythema (flare) within 15 min.
>= 3 mm wheal larger than negative control : + ve

Negative control with positive reaction : invalid

RAST testing should be employed

• Simultaneously a positive control test is performed with

histamine(10mg/ml).
Disadvantages
• Skin reactivity might be affected by previous ingestion of
antihistamines or other drugs

• Children often do not tolerate multiple skin needle pricks

• Prior or coexisting dermatologic conditions (eczema or

dermatographism) may preclude the performance of skin tests

• Potency of antigen extracts needs to be maintained

• Systemic reactions may occur

Contraindications

• Antihistamines
• Severe eczema
• Previous life-threatening anaphylaxis or has
dermagraphissm
• Severe asthma
4. Total serum IgE
• Rarely helpful in uncomplicated rhinitis
• 50 percent of patients : IgE levels within normal range
Phadiatop test
• Use of several common allergens in a single test
• Flouresence labelled anti IgE AB
• Reported as either positive
or negative
• More sensitive and specific in the identification of atopy
than is total IgE
• 4. Specific IgE measurements.

It is an in vitro test to find the specific allergen. There is a good correlation

between the skin tests and specific IgE measurements. It is therefore
recommended to correlate the two tests with clinical symptoms.

a. RAST
b. ELISA
a. Radioallergosorbent test (RAST).

It is an in vitro test and measures specific IgE antibody concentration in

the patient’s serum.
RAST

Ag in
Incubation Patient’s
solid
serum
phase

Ag + IgE Radio Radioactivity

labelled Anti
IgE
ELISA

Ag in solid Incubation Patient’s

phase serum

Ag + IgE
Colour change
by
Enzyme linked Anti IgE + photometric
Substrate of enzyme analysis
SPT Vs RAST
SPT RAST

Time for results Immediate result Days to weeks

Safety Safe Very safe
Sensitivity Sensitive Slightly less
sensitive

Affected by therapy Yes No

Other requirements Training for Trained operator and
performance and interpreter
interpretation required
5. Nasal provocation test:
• Challenge the nasal mucosa with a small amount of allergen placed at
the end of a toothpick and asking the patient to sniff into each nostril
and to observe if allergic symptoms are reproduced.

• (Gold standard of allergy diagnosis, but rarely

necessary)

Indications
• Positive history is accompanied by a negative SPT
TREATMENT
Treatment can be divided into:

• 1. Avoidance of allergen.
• 2. Treatment with drugs.
• 3. Immunotherapy.
• 1. Avoidance of allergen.

This is most successful if the antigen involved is single.

Removal of a pet from the house,
Encasing the pillow or mattress with plastic sheet,
Change of place of work or sometimes change of job may be required.
A particular food article to which the patient is found allergic can be
eliminated from the diet
• Treatment with drugs

1. Antihistaminics:

• Blocks H1 receptor.
• They control rhinorrhoea, sneezing and nasal itch.
• most antihistaminics have the side effect of drowsiness
2. Sympathomimetic drugs (oral or topical) ( Decongestants)

• Alpha-adrenergic drugs constrict blood vessels and reduce nasal

congestion and oedema.
• They also cause central nervous system stimulation and are often
given in combination with antihistaminics to counteract drowsiness.
• Pseudoephedrine and phenylephrine are often combined with
antihistaminics for oral administration.
3. Corticosteroids.
• corticosteroids are very effective in controlling the symptoms of
allergic rhinitis but their use should be limited to acute episodes
which have not been controlled by other measures.
• Anti-inflammatory
• Intra nasal or oral steroids
4. Sodium cromoglycate.
• It stabilizes the mast cells and prevents them from degranulation
despite the formation of IgE-antigen complex.
• It is used as 2% solution for nasal drops or spray or as an aerosol
powder.
• It is useful both in seasonal and perennial allergic rhinitis.
• Good control of sneezing, itching, and rhinorrhea
and less effective in relieving nasal congestion
5. Anticholinergics.

• They block rhinorrhoea both of the allergic and nonallergic rhinitis.

• Ipratropium bromide has been used as nasal spray to control rhinorrhoea. There are no
systemic side effects.

6. Leukotriene receptor antagonists.

• They include montelukast, pranlukast and zafirlukast.

• They are well-tolerated and have few side effects.
• Combination of an antileukotriene plus an antihistamine superior to either
alone
(Meltzer et al, 2000)
7. Anti-IgE.

• It reduces the IgE level and has an anti inflammatory effect.

• Omalizumab is such a drug.
• It is indicated in children above 12 years who have moderate to
severe asthma.
• It is not yet approved for allergic rhinitis.
• Nasal douching
Improves quality of life and endoscopic appearances
Immunotherapy.
• Immunotherapy or hyposensitization is used when drug treatment
fails to control symptoms or produces intolerable side effects.
• Allergen is given in gradually increasing doses till the maintenance
dose is reached.
• Immunotherapy suppresses the formation of IgE. It also raises the
titre of specific IgG antibody.
• Immunotherapy has to be given for a year or so before significant
improvement of symptoms can be noticed.
• It is discontinued if uninterrupted treatment for 3 years shows no
clinical improvement.

• Subcutaneous immunotherapy is often used but now sublingual and

nasal routes are also being employed.
• The latter can be used with doses 20–100 times greater than used by
the subcutaneous route.

• Limited spectrum of allergies (one or two)

A step-care approach is recommended by ARIA for allergic rhinitis
treatment.

• for mild intermittent disease: Oral antihistamines or intranasal

cromolyn sodium is recommended
• For moderate severity or for persistent disease: intranasal
corticosteroids can be used as monotherapy.
• For severe intermittent symptoms: combination therapy with oral
nonsedating antihistamines and intranasal steroids is used.
• For severe and persistent symptoms inspite of the above treatment a
short course of oral steroids and immunotherapy is recommended.
• If nasal obstruction persists a short course of intranasal decongestant
can be used. Oral decongestant can be combined with antihistamines

• Avoid allergen and irritants in all forms of disease.

• Nonallergic rhinitis can coexist with allergic rhinitis. Nonspecific

stimuli produce allergic rhinitis-like symptoms due to hyper-reactivity
of nasal mucosa.
Thank you