Allergic Rhinitis

1. Allergic Rhinitis
-Dr. Richa (MS-ENT)
PMCH, Patna
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2. Introduction
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3. Definition
 An inflammatory disorder of the nasal mucosa initiated by an IgE-mediated
hypersensitivity.
 characterized by a symptom complex that consists of a combination of two or more
of the following:
 sneezing,
 nasal congestion,
 nasal itching, and
 rhinorrhea
3

4. Epidemiology
 Allergic rhinitis is a global health problem and is increasing in prevalence.
 incidence: most common chronic disease of the respiratory tract affecting 10% of
children and 20% of adolescents and young adults
 The International Study of Asthma and Allergies in Childhood noted the prevalence
of rhinitis with itchy watery eyes, in six to seven year olds as 0.8 to 14.9 percent and
in 13-14 year olds from 1.4 to 39.7 %.
 A recent survey carried out in India shows that 20–30% of the population suffer from
allergic rhinitis and that 15% develop asthma.#
4
#Chhabra SK, Gupta CK, Chhabra P, Rajpal S: Prevalence of bronchial asthma in schoolchildren in Delhi. J Asthma 1998, 35, 291-296

5.  Age:
 Onset is common in childhood, adolescence and early Adulthood.
 Symptoms often wane in older adults, but may develop or persist at any age
 Sex:
 In childhood, boys with allergic rhinitis outnumber girls.
 The gender ratio becomes approximately equal in adults.
 Family history:
 Children with parents who have allergies or asthma are more likely to be affected. If a
child has one parent with allergies, chances are 30% that a child will have allergic
rhinitis. This increases to 50-70% if both parents have allergies or atopic asthma.
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6. Classification
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7. Allergic Rhinitis
 Traditionally, allergic rhinitis has been categorized as seasonal (occurs during a
specific season) or perennial (occurs throughout the year).
 However this classification is not accurate because :
– Some pollens had perennial pollination
– Perennial allergic symptoms are not persistent all over the year
– Polysensitized patients are often symptomatic all over the year
 It is now classified according to symptom duration (intermittent or persistent) and
severity (mild, moderate or severe)
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8. 8
Classification based on ARIA guidelines
Intermittent
. < 4 days per week
. or < 4 weeks
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
Moderate-
severe
one or more of
following
. abnormal sleep
. impairment of daily
activities, sport,
leisure
. abnormal work and
school
. troublesome
symptoms

9. Pathophysiology
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10. Risk factors
Genetics and family history
 The best established risk factor for allergic rhinitis is a family history of allergy,
especially of allergic rhinitis.
 Genes which appear to be involved in atopy include an area on the 5q
chromosome.
 Other possible susceptibility loci exist on chromosome 11q, chromosome 13 in the
Japanese population and chromosome 12q.
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11. Risk Factors
Environment-
 more common in developed countries
 Lifestyle changes, increased exposure to allergen, pollution and irritants, dietary
modifications responsible for diminution of protective nutrients, decrease in
infections, leading to a reduction in Th 1-type immune response and stress.
Co-morbidities-
 Conditions associated with allergic rhinitis are asthma, sinusitis, otitis media,
sleep disorders, LRTI & dental occlusion.
 Rhinitis is a risk factor for the development of subsequent asthma, is a frequent
cause of asthma exacerbations and there is evidence that effective rhinitis
treatment reduces asthma.
 We now recognize that sensitization affects nose and the lungs together, giving
rise to concept of “unified allergic airway”.
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12. PATHOPHYSIOLOGY
 Allergic reaction occurs in four phases-
1. Sensitization
2. Subsequent reaction to allergen-early phase.
3. Late phase reaction.
4. Systemic activation.
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13. Sensitization
 In atopies, allergen molecules are inhaled and presumably not completely cleared by the mucociliary
system.
 They reach antigen presenting cells in the nose, the most important of which are dendritic cells /
Langerhans cells.
 They capture antigen, process it and present it to naive T cells in the local lymph nodes.
 In atopic individuals, Th2 cells predominate at the sites of allergic response.
 Activated, Th2 cells secrete cytokines, (IL-4, IL- 13 , IL-5).
 They also activate B lymphocytes in the local lymphoid tissues, encouraging them to proliferate,
migrate to the nasal lining and produce IgE antibody.
 Once produced, the IgE is very rapidly taken up by local cells possessing FcER1, i.e. mainly mast cells.
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14. Sensitization
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15. Early phase response
 Within 5-30 min.
 Mast cells are encouraged to degranulate once their cell-bound IgE has
been cross-linked by allergen.
 Secretion of histamine, leukotriene C4 & prostaglandin D2 in nasal mucus.
 Histamine & cytokines are preformed while leukotriene and PGs are
manufactured from membrane arachidonic acid.
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16.  Histamine causes
 Rhinorrhoea, sneezing, pruritis and nasal obstruction.
 Action on sensory nerves induces itching and sneezing.
 Prostaglandins induces
 Sustained nasal obstruction and is ten times more potent than
histamine.
 Leukotrienes induce
 Vascular permeability and oedema in the nose
 Involved in eosinophil and neutrophil recruitment.
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17. Late phase response
 2-8 hours after exposure to allergen without additional exposure
 Involves the ingress of cells such as eosinophils, basophils, mast cells, T
lymphocytes, neutrophils and macrophages into the local reaction site.
 The main symptoms are nasal obstruction and hyper-reactivity.
 Eosinophil products increase local vascular permeability and mucus secretion and
cause further inflammatory cell influx.
 Thus, the allergic nasal mucosa is oedematous, cellular and contains many
proinflammatory molecules.
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18. 18

19. Systemic activation
 Upregulation of production and release of eosinophil and basophil
precursors from the bone marrow occurs in response to allergen contact in
the nose or lung.
 The resultant circulating precursors are attracted to the reaction site & other
parts of respiratory tract.
Ig E-INDEPENDENT RESPONSES
 Certain drugs, e,g. morphine, codeine and aspirin, can act directly on the
mast cell membrane causing degranulation.
 House dust mite allergen is able to alter epithelial tight junctions therefore
increasing permeability.
 Some allergens may produce direct response via enzymatic proteolytic
activity.
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20. 20

21. Allergic Rhinitis - Causes
Seasonal/ Intermittent
Pollen from trees,
grasses, and weeds
Perennial/ Persistent
House dust, mites
Mold and fungus spores
Cockroaches
Animal danders
Food
chemicals
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22. Diagnosis
22

23. Diagnosis of Allergic Rhinitis
 Most allergic rhinitis patients can be diagnosed by a combination of
 History,
 Examination
 Diagnostic Tests
 Demonstration of Ig E
 SPT (Skin Prick Test )
 Radioallergoabsorbent tests (RAST) for specific IgE.
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24. Symptoms
 sneezing,
 itching (of nose, eyes, ears, palate),
 rhinorrhea,
 Nasal obstruction,
 Anosmia,
 postnasal drip,
 headache,
 earache,
 tearing, red eyes, eye swelling,
 fatigue, drowsiness, and malaise.
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25. Examination
 Signs
• Mouth breathing
• Rubbing the nose/transverse nasal crease
• Frequent sniffing and/or throat clearing
• Allergic shiners (dark circles under eyes)
 Nose
• Mucosal edema, bleeding
• Mucoid/watery thin secretions
• Polyps
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26.  Ears
• Generally normal
• Pneumatic otoscopy to assess for Eustachian tube dysfunction
• Middle ear effusion may be present
•Conductive hearing loss
 Posterior oropharynx
• Postnasal drip
• Lymphoid hyperplasia (“cobblestoning”)
• Tonsillar hypertrophy
 Chest and skin
• Atopic disease
• Wheezing
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27. Diagnostic tests
 Demonstration of IgE allergy
 Nasal Secretion
 for eosinophilia (>10-20%) with Wright or Eosin/
Methylene Blue stains
 Serum
 eosinophilia
 elevated IgE
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Eosinophilia on nasal smear from a patient
with allergic rhinitis

28. SPT(SKIN PRICK TEST)
 Goal is to identify antigens to which patients are symptomatically
reactive
 Allergen introduced into the skin causes degranulation of IgE-sensitized
mast cells with mediator release and formation of a wheal and flare.
 Simple, cheap & safe.
 Low risk of systemic reactions.
 The wheal size relates to the amount of IgE.
 Should not be performed in pts on antihistamines or with severe
eczema, previous anaphylaxis.
 Positive results- reaction >2mm in under fives
>3mm in adults.
 Positive SPT occurs in 20-30% of adults but only 10-15% develop
symptoms.
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29. BLOOD TESTS FOR ALLERGY
 Stabilized allergen is incubated with the patient's serum, any specific IgE
binds to allergen and is identified by a second incubation with labelled anti-
IgE.
 This can be undertaken by RASTs or by fluorescent assays and enzyme-
linked immunosorbent assays (ELISA).
 RAST involves
 allergen bound to a solid phase, &
 incubated with the patient's serum
 After washing, radio labelled anti-IgE is added
 the radioactivity is measured.
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30.  CAP RAST is a recent improvement in which
 the allergen is coupled to a cellulose carrier
 anti-IgE is enzyme-labelled with a fluorescent substrate acting as the developing agent.
 This system has a higher sensitivity and specificity than RAST test
 ELISA test
 allergen is in the fluid phase
 IgE is enzyme-labelled.
 The substrate for the enzyme is added and
 the resulted colour change is detected photometrically.
 These are expensive, takes longer and is no more sensitive and specific than skin prick testing.
They should be used when there are contraindications to skin prick testing or where they are
unavailable or difficult to interpret.
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31. Immunoassay vs Skin Test for Diagnosis of Allergy
Immunoassay
 Not influenced by medication
 Quality control possible
 Results take time
 Does not require expertise
 Expensive
Skin test
 Influenced by medication
 Higher sensitivity
 Immediate results
 Requires expertise
 Cheaper
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32. NASAL ALLERGEN CHALLENGE
 Allergen is introduced into the nose and any reaction is measured and compared
to placebo.
 This is the gold standard of allergy diagnosis, but is rarely necessary.
 Nasal challenge testing is time-consuming, difficult and requires extensive
laboratory facilities.
 Useful for diagnosis of local allergic rhinitis (LAR).
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33. Management
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34. Management of allergic rhinitis
The management of allergic rhinitis involves the
following components:
 Allergen avoidance
 Pharmacotherapy.
 Allergen immunotherapy
 Surgery is rarely needed
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35. Allergen Avoidance
 Pets
 Remove pets from bedrooms and, even better, from the entire home
 Vacuum carpets, mattresses and curtains regularly
 Wash pets regularly
 Moulds
 Ensure dry indoor conditions
 Use ammonia to remove mold from bathrooms and other wet spaces
 Cockroaches
 Eradicate cockroaches with insecticides
 Eliminate dampness, cracks in floors, ceilings; cover food; wash surfaces, fabrics
to remove allergen
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36.  House Dust Mite
 Provide adequate ventilation to decrease
humidity
 Wash bedding regularly
 Encase pillow, mattress and quilt in allergen
impermeable covers
 Use vacuum cleaner with HEPA filter
 Dispose of feather bedding
 Remove carpets
 Remove curtains, pets and stuffed toys from
bedroom
 replace or wash air filters on air conditioners
every month to remove debris.
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 Pollen
• Remain indoors with windows closed at
peak pollen times
• avoid grassy open spaces
• Wear sunglasses
• Use air-conditioning, where possible
• Install car pollen filter

37. Basic treatment plan for allergic
rhinitis according to severity and duration.
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38. 1.Oral Antihistamines
 First generation agents
Diphenydramine
Promethazine
Hydroxyzine
Pheniramine
Chlorpheniramine
 Newer agents
Azelastine (Topical)
Olopatadine(Topical)
Cetirizine
Fexofenadine
Levocetirizine
Loratadine
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39. Newer Generation Oral Antihistamines
 First line treatment for mild allergic rhinitis
 Effective for
 Rhinorrhea
 Nasal pruritus
 Sneezing
 Less effective for
 Nasal blockage
 Minimal or no sedative effects
 Rapid onset and 24 hour duration of action
 Once daily administration
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40. 2.Decongestants: Alpha
Adrenergic Agonists
Oral
 Pseudoephedrine
Nasal
 Phenylephrine
 Oxymetazoline
 Xylometazoline
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41.  EFFICACY:
• Oral decongestants: moderate
• Nasal decongestants: high
 ADVERSE EFFECTS:
• Oral decongestants: insomnia, tachycardia, tremor, increased blood pressure, stroke (?)
• Nasal decongestants: tachyphylaxis, rebound congestion, rhinitis medicamentosa(>10 days
use)
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42. 3. Anti-leukotriene agents
a. CysLT1 Receptor Antagonists
 Montelukast
 Pranlukast
 Zafirlukast
b. 5-Lipoxygenase Inhibitors
 Zileuton
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Efficacy
• Equipotent to H1 receptor antagonists but with onset of action after 2 days
• Reduce nasal and systemic eosinophilia

43. 4. Nasal Corticosteroids
• Most potent anti-inflammatory agents
• First line drug for persistent allergic rhinitis
• Effective in treatment of all nasal symptoms including obstruction
• Superior to anti-histamines and anti-leukotienes
• onset of action is slow with some improvement after 6–12 hours and
maximum effects occurring only after several days
• Adverse Effects
– Nasal irritation
– Epistaxis
– Septal perforation (extremely rare)
– HPA axis suppression
– Suppressed growth
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44. Others
5. Intranasal sodium cromoglycate
 Mast cell stabiliser
 Prevents release of chemical mediators
6. Anticholinergics  ↓rhinorrhea
 Ipratropium bromide
7. Systemic corticosteroids
 only in exceptional circumstances, where there is intense irritability of the nose or severe obstruction.
 They should only be used short-term under medical supervision
8.Omalizumab(Anti-Ig E)
 Could be considered in severe cases unresponsive to conventional treatment
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45. 45TREATMENT
Pharmacotherapy. Itching/sneezing discharge blockage impaired smell
Sodium cromoglycate + + +/- +
Oral Antihistamines +++ ++ +/- -
Ipratropium bromide - +++ - -
Topical Decongestants - - +++ -
Topical glucocorticoids +++ +++ ++ +
Antileukotrienes. - ++ + +/-

46. Indications for immunotherapy in AR
 IgE mediated disease(+SPT/RAST)
 Inability to avoid allergen.
 Inadequacy of drug treatment.
 patients need medication most days.
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47. IMMUNOTHERAPY
 Repeated administration of an allergen extract in order to induce immunological
tolerance.
 This lead to a reduction in clinical symptoms & requirements for medication during
subsequent natural allergen exposure.
 Routes-Subcutaneous or Sublingual
 T/t involves updosing phase over several weeks followed by a maintenance phase of 3
years.
 The sublingual route involves application of allergen as drops or tablets under the
tongue where they are retained for several minutes.
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48. Surgery
 Role in selected cases where nasal obstruction has any structural element.
 Inferior turbinate reduction -chronic cases with irreversible turbinate
engorgement.
 Septoplasty – correction of deviation of septum
 Sinus surgery – clearance of sinuses if sinusitis is present
 Polypectomy
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49. To Conclude…
 Allergic rhinitis is very common and causes considerable morbidity.
 Co-morbid conditions are common and warrants special attention and treatment
for optimal results.
 Diagnosis is usually clinical supported by various tests
 Topical corticosteroids and oral antihistamines form the mainstay of allergic
rhinitis treatment
 Environmental manipulations is also important in the control of disease
 Adequate and appropriate treatment leads to significant improvement in quality
of life.
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50. Bibliography
 Cummings Otolaryngology, Head and Neck Surgery, 6th Edition, 2015
 Scott-Brown’s Otorhinolaryngology, Head and Neck Surgery, 7th Edition, 2008
 Logan Turner’s Diseases of the Nose , Throat and Ear, 8th Edition
 Diseases of Ear, Nose and Throat, P. L. Dhingra, 5th Edition, 2012
 Management of allergic rhinitis; ASCIA Education Resources
 Internet
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51. THANK
YOU
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