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Allergic Rhinitis
1. Allergic rhinitis
Ramesh Parajuli MS
Lecturer, Department of Otorhinolaryngology, Head & Neck Surgery
Chitwan Medical College Teaching Hospital
Bharatpur-10, Fax: 977-56-532937, Chitwan, Nepal
drrameshparajuli@gmail.com
2. Definition
“IgE mediated hypersensitivity disease of mucous membranes of
nasal airways characterized by sneezing, watery nasal discharge ,
itching and nasal obstruction” (Durham, 1999)
3. Prevalence
• Global health problem
• Prevalence - 15% and 20% (Nathan et al.,1999)
• Higher in pediatric age group(Wright et al.,1994)
• Approx. 80% develop symptoms before age of 20
(Skoner et al., 2001)
4. • Not a severe disorder but significantly
alters patient’s social life
-school performance
-work productivity
• Substantial cost
Impact on quality of life
5. Risk factors
1. Genetic susceptibility:
2. Family history of atopy: e.g. asthma,eczema,hay
fever,urticaria
(Genes involved in atopy - loci on 5q,11q and 12q
chromosomes)
3. Environmental factors:
• Pollution-climate interaction
• Irritants
eg. fumes, tobacco smoke, diesel exhaust,
mosquito repellents, perfumes, scented sticks,
domestic sprays, bleaches
4. Exposure to allergens:
• Seasonal : Pollen, Fungus
• Perennial: Dust mite, domestic pets, cockroaches
6. 5.Hygiene hypothesis
• Increased exposure to various allergensimmune maturationhelp decrease
the incidence of allergic diseases and asthma (Svanes C et al., 2003)
• Early environmental exposure to infectious agents, protects against
development of atopy (Tulic MK et al.,2003)
• Early nursery attendance also reduces subsequent atopy (Kramer et al.,2003)
• Lack of immune maturation (understimulated immune system) in
infancyallergic responses (Liu A,2007)
7. Pathogenesis
• Sensitization & Priming to specific antigen:
Inhaled allergen produces specific IgE antibody
which gets attached to mast cells
• Subsequent exposure to same antigen:
Allergen combines with specific IgE antibody ®
degranulation of mast cells ® chemical mediators
released
8.
9. Acute or early phase response
• Occurs 5–30 min after antigen exposure
• Release of inflammatory mediators
· Increased nasal gland secretion ® runny nose
· Mucosal edema & Vasodilation ® nose block
· Nerve irritation ® sneezing & itching
10. Late or delayed phase response
• Occurs 2-8 hours after antigen exposure
• Infiltration by inflammatory cells
(eosinophils, neutrophils, basophils,
monocytes & CD4+ T lymphocytes)
• Edema, congestion & thick nasal secretion
• Sneezing & itching decreases
16. Seasonal allergic rhinitis
Pollen:
Spring (March-June) = Tree pollen
Summer (May-August) = Grass
Fall (August-October) = Weeds
Mold:
Spores in outdoors have seasonal
variation (reduced in winter, increased in
summer/fall due to humidity)
House dust mites:
Generally “perennial” allergen,
but increased in damp autumn months
17. Perennial allergic rhinitis
Fungi/mold:
Exposure peaks accompany activities
such as harvesting & cutting grass
Pet dander (cats, dogs):
up to 4 months after pet removal
House dust mites:
Live in bedding & carpets
Cockroaches:
Respiratory allergy
Important allergen
18. Diagnosis
1.History
2.Physical exam
3.Allergy diagnosis
(I) Skin prick test (SPT)
(II) Blood tests for allergy: Total IgE, Specific IgE
(III) Nasal allergen challenge test
21. Skin Prick test
Advantages:
1. Cheap
2. Immediate result
3. Sensitive
Contraindications:
1. Patients on antihistamines
2. Severe eczema
3. Previous anaphylaxis
4. Dermagraphism
22. (II) Blood tests for allergy
1.Total IgE:
Rarely helpful as 50% pts have IgE levels within normal range
2.Specific IgE:
(i) Radio-allergosorbent test (RAST) (ii)Modified RAST
Stabilized allergen is incubated with patient’s serumany specific IgE binds to
allergen identified by a second incubation with labelled anti-IgE.
23. Radio-allergosorbent test (RAST)
Indications:
1. When there is C/I to SPT
2. Where SPT unavailable
3. When SPT difficult to interpret
Disadvantages:
More expensive
Delayed(takes longer)
No more sensitive or specific to SPT
27. • Nasal symptoms -noted 80% of
asthmatics
• Adults-Asthma present in 22.5% of
adults with AR, Vs 7.2% in general
population (Laynaert, 1999 )
• Children-Ratio of asthmatics with AR to
asthmatics without AR is even higher
(Wright et al.,1996)
• Effective treatment of allergic rhinitis
reduces development of subsequent
asthma (Ragab et al., 2006)
28. Differential diagnosis
1.Vasomotor rhinitis (Intrinsic rhinitis/NANIPER)
2.Sinonasal polyposis
3.Rhinitis medicamentosa
4.Hormonal rhinitis
(Pregnancy, Hypothyroidism, OCP use )
5.CSF leak
Take a moment to consider
differential diagnosis
29.
30. Management of allergic rhinitis
1. Environmental control measures (Avoidance of allergens)
2. Patient education
3. Nasal douching
4.Medical therapy
5.Immunotherapy
6.Surgery
31. (I) Avoidance of allergens
• Best treatment method
• Not always practical
• Indoor allergens: Removing allergen from the indoor
environment should be a primary strategy for the management
and treatment of allergic disease
• Outdoor allergens:
32. General advice
• Avoid irritants: smoke, dust, vehicular & other atmospheric pollutants,
• Physical factors – extreme changes in temperature can produce symptoms
like allergic rhinitis but are non-IgE mediated responses
• Avoid foods & drugs to which you are allergic
• Avoid occupational irritants or change profession
34. Avoidance of animal allergen
• Remove pet animals (cats, dogs)
from bedroom
• Wash the pet weekly
35. Measures to avoid house dust mite
• Mattress covers
• Covers for pillows & bedding
• Vacuuming
• Regulation of ventilation & humidity at home
• Liquid nitrogen
• Acaricides
• Protein denaturating agents- Tannic acid
36. Pollen avoidance measures
• Avoid walking in open grassy spaces
during hot, dry days
• Keep windows closed
• Wear facemask & sunglasses when
moving out
37. (II) Patient education
Educate patients on environmental control measures,
which involve both the avoidance of known allergens
(substances to which the patient has IgE-mediated
hypersensitivity) & the avoidance of nonspecific, or
irritant, triggers
38. (III) Nasal douching
•Saline irrigation
•Improves quality of life
Neti Pot: Home remedy to clean nasal passages
42. Steroid
• Most effective treatment for Allergic rhinitis(AR)
-Topical: Nasal spray or nasal drop
-Systemic:Oral, extremely effective
• Reduces inflammation & consequent
hyperreacitvityreduce nasal symptoms, eye
symptoms, improve smell sense
• Topical steroid when combined with antihistamines
reduces risk of asthma exacerbation and hospitalization
by 50% or more (Adams et al., 2002, Crystal peters et
al., 2002)
• Fluticasone and mometasone have low systemic
bioavailabilitylower risk
43. Antihistamines
• Adverse effects of first generation antihistamines
“First-generation oral H1-antihistamines are not recommended when second-generation
ones are available, due to safety concerns”
(Allergy. 2008 Apr;63 Suppl 86:8-160)
47. Decongestants
• Topical vasoconstrictor:
-imidazoline (eg, oxymetazoline)
• systemic (oral) vasocontrictor
-Phenylephrine
- Pseudoephedrine.
• Monotherapy with vasoconstrictors has limited role
• Oral decongestants + Antihistamineall cardinal
symptoms of allergic rhinitis targeted
48. Mast cell stabilizer
• Sodium cromoglycate inhibits degranulation of
sensitized mast cells
• 2% Nasal drop: Use 3 to 4 times daily limits
compliance
• Poorly absorbed systemically excellent safety
record
• Used before the onset of symptoms
• Can be used in younger children < 2 years of age
Ipratropium Bromide
• Useful against nasal discharge
• Occasionally helpful in pts with AR who do not
respond to topical steroid(Dockhorn et al., 1999)
49. Antilukotrienes
Zafirlukast performed no better than placebo - seasonal alllergic
rhinitis ( Pullerits T et al., 1999)
• Montelukast clinical efficacy seasonal Allergic rhinitis
(Chervinsky P et al., 2004)
• Montelukast + loratadine -superior reducing day time nasal
symptoms in seasonal Allergic rhinitis. (Meltzer EO et al., 2000)
• Montelukast + ebastine- better symptomatic control in allergic rhinitis.
• Montelukast -less effective than Intranasal steroid (Ratner PH et al.,
2003)
• Leukotriene antagonist (Montelukast) doesn’t appear more effective
than nonsedating antihistamines (Fexofenadine) (Wilson AM et al., 2004)
50. (V) Immunotherapy
• Repeated administration of allergen extract
induce state of immunological tolerance
• Render an allergy patient less symptomatic
when exposed to the offending antigen
• Desensitization or Hyposensitization:
because complete elimination of the allergic
reaction is seldom achieved
• Subcutaneous injection or sublingual route
51. Contraindications
• Asthma(severe)
• Autoimmune diseases
• Beta-blockers or Anti-adrenergic medicines
• Children less than < 5 yrs
• Pregnancy (induction but not maintenance)
• Efficacy:
• Highly effective -selected patients (Grade A)
• Treatment for 3 to 4 yrs –improvement for 3 yrs following discontinuation
(Durham SR et al.,1999)
• Children –seasonal rhinitis-ITX for 3 yrs-2 to 3 fold reduction –developing
asthma (Moller et al.,2002)
• Offers long term disease modification & prophylaxis
52. Side effects of Immunotherapy
Local reactions - trivial
Systemic reactions-10%-up dosing phase
Occasionally – severe systemic reactions-general
urticaria , severe asthma or
anaphylaxis
53. (VI) Surgery
• Usually not indicated
• Not last resort but complementary
• Comorbid or complicating conditions eg
Marked DNS, Turbinate hypertrophy, CRS
54. (VII) Complementary and integrative medicine(CIM) therapies
• Honey – For seasonal AR caused by pollen
• Chinese herbal medicine
• Acupuncture
55. Recent advances
(VIII) Human monoclonal antibody(Anti-IgE)
• Omalizumab - recent developments in the treatment of atopic
diseases
first of several monoclonal antibodies (anti IgE antibody)
Modulation of allergic inflammation
expensive for routine treatment of AR primarily indicated -severe
asthma
• Multiple randomized, double-blind, placebo-controlled studies
-efficacy in seasonal and perennial AR (Vignola AM et al.,2004)
Continued research on the molecular mechanism of
allergic disease will inevitably generate new forms of
therapy.
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Hinweis der Redaktion
Furthermore, the GA2 LEN (Global Allergy and Asthma European Network) task force assessed the unwanted side-effects and potential dangers of first-generation H1-antihistamines by reviewing the literature.
The therapeutic window of H1 antihistamine is the dose range over which it is efficacious and also free from unwanted side effects. The lower limit of the therapeutic window is set by the lowest clinically effective dose for the disease condition whereas the upper limit is set by the highest dose tolerated without adverse effect.
As an example, fexofenadine has a wide therapeutic window. It is effective at a dose of 60 mg and is free from sedation at 690 mg twice daily (1380 mg).