ALLERGIC RHINITIS

1. DR. VIJAY KUMAR

2. Allergic Rhinitis: Definition
Allergic rhinitis is clinically defined as a
symptomatic disorder of the nose induced by
an IgE-mediated inflammation after allergen
exposure of the membranes lining the nose
ARIA Report 2001

3. DEFINITION:
 Inflammation of the nasal membranes and
is characterized by a symptom complex that
consists of any combination of the following:
sneezing, nasal congestion, nasal itching,
and rhinorrhea.
# Allergic rhinitis is the most common cause
of rhinitis.

4. Ages affected
 Childhood ( usually after 5yrs).
 10-15% in adolescents (adolescents and young
adults).
 Peak age 30 (decades 2, 3 and 4).
 Elderly

5. Predisposition
 Genetic:
 Positive family history (polygenic inheritance)
 Atopic dermatitis:
 Early sign of predisposition to allergy.
 Previous exposure/environmental factors

7. Comorbidities ass’d with AR
 Asthma
 Sinusitis
 Otitis Media (OME)
 Atopic Dermatitis

8. 8
Classification of Rhinitis
 Allergic Rhinitis
 Seasonal allergic rhinitis (SAR)
 Perennial allergic rhinitis (PAR)
 Nonallergic Rhinitis
 Infectious
 Idiopathic or vasomotor
 Drug-induced
 Rhinitis medicamentosa
 Hormonal
 Anatomical

9. Pathophysiology
 Type I immediate hypersensitivity reaction
mediated by IgE antibodies, which trigger
the mast cells and basophils to release
pharmacologically active agents.

10. ATOPY
 It’s the tendency of an individual to develop an
exaggerated IgE antibody response.
 Reflected by positive skin test to one or more common
aero-allergens.
 Genetically inherited
- Autosomal
- Mixed multifactorial influence.

11. Allergy
 Allergic reaction is an exaggerated or inappropriate
immune reaction and causes damage to the host
 Hypersensitivity:
 Type I: anaphylactic reaction: mediated by IgE
antibodies, which trigger the mast cells and
basophils to release pharmacologically active
agents.
 Type II: cytotoxic reaction: IgM or IgG
antibodies bind to antigen on the surface of cells
and activate complement cascade.

12. Hypersensitivity
 Type III: Immune complex reaction: complexes of antigen
and IgM or IgG antibodies accumulate in the circulation or
in tissue and activate the complement cascade.
Granulocytes are attracted to the site of activation and
release lytic enzymes
 Type IV: cell-mediated immunity reaction: mediated by T
cells, which release cytokines upon activation to cause
accumulation and activation of macrophages.

13. Antigen presenting cells
 Function: take up antigen, process and present antigen
to T cells
 Including: macrophage, dendritic cell, B lymphocyte
and activated T lymphocyte
 Major histocompatibility complex (MHC)
 class I: binds with CD8+ T cell only
 Class II: binds with CD4+ T cell only

14. T lymphocyte: Allergic Reaction
 Th2:
 produce IL-4, IL-5, IL-10
 activate B cells and switch antibody synthesis to IgE
 mediate allergic inflammation
 Active Th2 cells leadS to development of allergic
disease.

16. Seasonal Rhinitis
 Pollen:
 Spring (March-June) = Trees
 Summer (May-August) = Grass
 Fall (August-October) = Weeds
 Mold:
 Spores in outdoors have seasonal variation (reduced
#’s in winter, increased in summer/fall due to
humidity).
 House dust mites:
 Generally a “perennial” allergen, but may be
increased in damp autumn months.

17. Perennial Rhinitis
 Fungi/mold:
 Exposure peaks accompany activities such as
harvesting, cutting grass and leaf raking.
 Pet Dander (cats, dogs):
 Can linger up to 4 months after pet removal.
 House dust mites:
 Live in bedding, carpets and upholstery.
 Cockroaches:
 Respiratory allergy.

18. Causes of AR

19. 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
ARIA Classification
ARIA Report 2001

20. Diagnosis of AR
 History
 Physical / Nasal Examination
 Laboratory Testing
- Skin Prick Test
- Peak Nasal Inspiratory Flow Rate
- Rhinomanometry
- RAST / cap RAST
- Nasal smear / Nasal challenge test

21. HISTORY
 History: Obtaining a detailed history is important in
the evaluation of allergic rhinitis.
Allergy history
environmental exposures
occupational exposures
effects on quality of life
Duration and Frequency history
Family history
Past medical history

22. PHYSICAL EXAMINATION
 EYE
 NOSE
 EAR
 MOUTH
 NASOPHARYNX
 OROPHARYNX
 LUNGS

28. Skin Prick Testing
 IgE-mediated rxn (Type I).
 Small, but significant potentail for anaphylactic rxn.
 Wheal & flare response (15-20 minutes)
 Includes a “positive” and “control” soln.
 Positive rxn = over 3cm wheal with ass’d flare and
pruritis (no rxn to neg control).

29. In vitro serum test (RAST)
 Serum levels of specific IgE antibodies.
 Consider in rare pts who:
 have extensive skin disease.
 must take medication that interferes with skin testing
 children may prefer blood draw to skin test

30. Nasal smears
 Eosinophils may help differentiate “allergic” from
“infectious” rhinitis (neutrophils).

31. Management of AR
 Allergen Avoidance
 Pharmacotherapy
 Immunotherapy

32. Pharmacotherapy
Medications used to treat allergic rhinits:
 Antihistamines
 Decongestants
 AH-D combinations
 Corticosteroids
 Mast Cell stabilizers
 Anticholinergics
 Antileukotrienes

33. Actions of Various Nasal Preparations in the
Treatment of Rhinitis
Nasal
Preparation
Sneezing Itching Rhinorrhoea Congestion
Antihistamines +++++ ++++ +++ 0
Anticholinergics 0 0 +++++ 0
Corticosteroids +++++ +++++ +++ +++
Decongestants 0 0 + +++++
Mast cell
stabiliser
+++++ +++ + 0
ATL +++ ++ 0 ++++

34. Anti-Histamines
 Act by preventing histamine from binding to the H1-
receptors
 Primarily helpful in controlling Sneezing, itching &
rhinorrhoea; ineffective in releiving nasal blockage
 1st generation anti-histamines
- chlorpheniramine
- diphenylhydramine
 2nd generation anti-histamines
- cetrizine
- azelastine
- fexofenadine
- loratadine

36. The “Ideal” Drug For Allergic Rhinitis Should
Have The Following Features:
 Inhibit both early and late phases
 Be an H1 blocker
 Counter effects of other mediators
 Fast-acting, to control the early phase
 Dosing-od or bd for compliance
 No side effects
 Manage all symptoms
 Intranasal administration

37. “Corticosteroids are undoubtedly the
pharmacotherapeutic agents with the broadest
application for the treatment of many types of
rhinitis.

38. Corticosteroids
 Mechanism:
 reduce inflammation
 suppress neutrophil chemotaxis
 mildly vasoconstrictive
 reduce intracellular edema
 Effect: reduce nasal blockage, pruritis, sneezing
and rhinirrhea.

39. Decongestants
 Mechanism: alpha-adrenergic agonist.
 Effect: vasoconstriction restricts blood flow to
nasal mucosa decreasing nasal obstruction (no
influence on pruritis, sneezing or nasal secretion).
 Side effects:
 Oral: HA, nervousness, irritability, tachycardia,
palpitations, insomnia.
 Topical(nasal): prolonged use (>5-7 days) leads to
rhinitis medicamentosa

40. Cromolyn Sodium (intranasal)
 Mechanism: mast cell stabilizing agent ; reduces
release of histamine and other mediators.
 Effects: reduces nasal pruritis, sneezing, rhinorrhea
and congestion.
 Note:
 prophylactic use: start before pollinosis sx or
unavoidable/predictable exposures.
 disadvantage: frequent dosing (q4hrs).
 Side effects: locally, <10% of pts (sneezing, nasal
stinging, burning, irritation).

41. Ipratropium (intranasal)
 Mechanism: inhibits muscarinic cholinergic
receptors.
 Effect: reduces watery rhinorrhea (no effect on
nasal itching, sneezing or nasal congestion).
 Note:
 limited to control of watery secretions.
 Side effects: irritation, crusting, epistaxis.

42. Mild intermittent rhinitis
ARIA
Options (not in preferred order)
- oral or intranasal anti-H1
- intranasal decongestants
- oral decongestants (not in children)

43. Moderate-severe intermittent rhinitis
Mild persistent rhinitis
ARIA
Options (not in preferred order)
- oral or intranasal anti-H1
- oral anti-H1 + decongestant
- intranasal CS
- (chromones)
Patient should be re-assessed after 2-4 wks

44. Moderate-severe persistent rhinitis
ARIA
Step-wise approach
- intranasal CS as a first line treatment
- if major blockage: add short course of
oral CS or decongestant
Re-assess after 2-4 weeks
- if symptoms present add:
- oral anti-H1 (± decongestants)
- ipratropium

45. Treatment of allergic rhinitis (ARIA)
Allergic Rhinitis and its Impact on Asthma
Mild
intermittent
mild
persistent
moderate
severe
intermittent
moderate
severe
persistent
allergen and irritant avoidance
immunotherapy
intra-nasal decongestant (<10 days) or oral decongestant
local chromone
intra-nasal steroid
oral or local non-sedative H1-blocker

46. Management of Allergic Rhinitis
Allergen Avoidance
Intermittent Symptoms Persistent Symptoms
Mild Moderate-severe Mild Moderate-severe
Oral H1 blocker
Intranasal H1blocker
and/or decongestant
No Improvement :
switch or add
LTRA
Oral H1 blocker
and/or LTRA
Intranasal H1
blocker and/or
decongestant
Intranasal CS
Oral H1 blocker
and/or LTRA
Intranasal H1 blocker and/or
decongestant
Intranasal CS
Review patient
after 2-4 weeks
No improvement
step up
Improved: continue for
1 month
If intranasal CS
reduced by1/2
Intranasal CS
If nose very blocked
add oral CS or decongestant
or LTRA
Improved Not improved
Step-down and
continue
treatment for
> 3 month
Review diagnosis,
compliance, or
other causes
Blockage: add LTRA or decongestant or
oral CS (short term) or increase INCS
Rhinorrhea:
add ipratropium
Itch/sneeze/rhinorrhea
add H1 blocker
No improvement: refer to specialist

47. IMMUNOTHERAPY:
 Proven allergy with skin test or RAST
 With allergic symptoms that are significant to the
patient
 Attempts to avoid allergens fail or impractical
 Treatment with medicine is not fully successful or when
medication is not well tolerated.
 Young patients without chronic irreversible changes in
the upper airways
 Patient needs to be motivated and compliant with
treatment

48. Immunotherapy
 Subcutaneous immunotherapy is the only approved route.
 Subcutaneous immunotherapy normally involves a weekly injection of
an extract of the allergen, in solution, in increasing doses until a
standard maintenance dose is reached.
 This dose is then injected subcutaneously on a regular basis (at
intervals of approximately 20 days) for not less than 3 years for
perennial allergens.
 Short term immunotherapy does not affect the cytokine profile and do
not have long-term efficacy after discontinuation
 start at an earlier age, so that adverse changes to the immune system
can be prevented before they become irreversible

49.  THANK YOU