Allergic rhinitis is a type I hypersensitivity reaction mediated by IgE antibodies. It has a prevalence of 10-20% in the US and is characterized by symptoms like sneezing, rhinorrhea, nasal congestion and pruritus. Risk factors include family history of atopy, environmental exposures, and lifestyle factors. Treatment involves allergen avoidance, pharmacotherapy with antihistamines, intranasal corticosteroids, leukotriene receptor antagonists and immunotherapy for selected patients.

2. • Allergic rhinitis is a clinical hypersensitivity of
the nasal mucosa to foreign substances
mediated through IgE antibodies .
• type I, IgE-dependent, mast cell–mediated
immune reaction, whereby the release of mast
cell or basophil mediators creates responses to
sensitizing allergens.

3.  Genetics and family history
 The best established is family history
of allergy especially of allergic
rhinitis
(13% , 29% , 47%)
 Environment
 More common in developed
countries
 Pollution (immigrants)
 Hygeine hypothesis (early exposure
to animals and nursery attendance
reduce atopy)
Risk Factors

4. • prevalence of between 10% and 20% and
affects 20 to 40 million individuals in the
United States annually.
• higher in children and adolescents than
in adults.
• In childhood, boys outnumber girls; the
gender ratio becomes approximately
equal in adults.
• In one study, the mean total productivity
losses per employee per year were $593
for allergic rhinitis, which was more
costly than all other prevalent and
chronic disorders.

6. Immunopathology
Immune
system
Adaptive
Humoral
cellular
Innate

7. Hypersensitivity reactions
• Type I :mast cell mediated reactions
• Type II, cytotoxic, antibody-mediated reactions
(IgG-, IgM-mediated , opsonization,
complement activation, penicillin-induced
autoimmune hemolytic anemia).
IgE-dependent IgE-independent

8. • Type III, immune complex–mediated reactions.
(serum sickness)
• Type IV, delayed hypersensitivity (DTH)
reactions (T cell–mediated) (PPD)

9. Pathophysiology of Allergic Rhinitis
 The reaction can be considered in four phase:
1. Sensitization
2. Early phase reaction
3. Late phase reaction
4. Systemic activation
• Initial stage :
low-dose exposure production of specific IgE antibodies.

10. TH2
CD4
IgE ,
Recruitment
and survival of
eosinophils
Antigen-specific IgE then
attaches to high-affinity
receptors on mast cells
and basophils
subsequent exposure
IgE
Mast
cell

11. Early Response to Antigen
• Within minutes after exposure
of an allergic patient to
antigen, an inflammatory
response occurs. The patient
first senses tingling and
pruritus, followed by sneezing,
rhinorrhea, and, last, nasal
congestion.
• increases are noted in the
levels of several mediators,
including histamine, kinins,
tryptase, PGD2, leukotriene C4
(LTC4), leukotriene B4 (LTB4),
major basic protein (MBP) and
platelet-activating factor (PAF).

12. • Histamine is preformed in
Granules
• Histamine causes rhinorrhea
(By action on vascular
endothelial cells and glandular
secretions), sneezing, pruritis
(By action on sensory nerves)
and nasal obstruction (Not
marked and of short duration)
• The major mediator of the
early phase reaction.
• Histamine also possesses
proinflammatory and
immunomodulatory
properties

13. • Prostaglandins are
manufactured by AAA
metabolism by COX pathway
after its break-down form cell
membrane by Ph-Lip-A2.
• PG D2 is the predominant
prostanoid released following
mast cell degranulation.
• It induces a sustained nasal
obstruction and is ten times
more potent than histamine.

14.  Eicosanoids are Manufactured
by AAA metabolism by LOX
pathway after its break-down
form cell membrane by
Phospholipase A2.
 Formally known as the slow
reacting substance of
anaphylaxis (SRS-A), play an
essential role in asthma and
rhinitis.
 They induce vascular
permeability and oedema in
the nose and are also involved
in eosinophil recruitment.
 LTB4 induces neutrophil
recruitment.
Leukotrienes

15. Late phase reaction
• The response to allergen exposure is not
limited to the acute events that occur minutes
after exposure. Hours after antigen challenge,
some patients experience a recurrence of
symptoms, most notably nasal congestion.
• striking characteristic of the late-phase
response is cellular inflammation.

16. • suggesting that nasal secretions and the nasal
mucosa are two separate compartments with
different inflammatory cellular predominance
during allergic inflammation.
• polymorphonuclear cells and eosinophils
predominating in nasal secretions , and
mononuclear cells predominating in the nasal
mucosa.

17. • examination of nasal mucosal scrapings or
biopsy specimens which sample deeper layers,
showed that most metachromatic cells in
these compartments were mast cells.

18. • Langerhans cells : large
mononuclear dendritic
cells that are important in
antige presentation.
• In a study involving
patients with perennial
allergic rhinitis, a
significant decrease in
numbers of Langerhans
cells in the epithelium was
seen after 3 months of
treatment with fluticasone
propionate.

19. Adhesion Molecules and Cellular
Recruitment
• Mechanisms exist for the
migration and accumulation of
these effector cells during
allergic inflammation.
• Recruitment of cells are
mediated, by interactions
between adhesion molecules
on the cells themselves and
those on vascular endothelial
cells.
• Adhesion molecules on the
vascular endothelial cell
surface include ICAM-1
(CD54), ICAM-2, E-selectin, P-
selectin (granule membrane
protein VCAM-1.

21. Neuronal Contribution
• Unilateral intranasal antigen
challenge experiments have
supported the role of the nervous
system in amplifying the allergic
response as challenge.
• an increase in rhinorrhea, secretion
weights, and PGD2 contralateral to
the challenge. The contralateral
secretory response was rich in
glandular markers and was inhibited
by atropine, an anticholinergic,
suggesting that the efferent limb was
cholinergically mediated.
• Histamine’s action on nasal afferent
nerves initiates this reflex.
• increases in the levels of substance P,
calcitonin gene–related peptide, and
vasoactive intestinal peptide
immediately after antigen challenge
in allergic individuals.

22. Hyperresponsiveness
• One of the hallmarks of allergic rhinitis is the
hyperresponsiveness .
Hyperresponsiveness
SpecificHyperresponsiveness(PRIMING ) NonspecificHyperresponsiveness

24. • House dust
mites
• Grass, tree
and weed
pollen
• Pets
• Cockroaches
• Molds

25. History
• The classic symptoms of seasonal allergic rhinitis
are recurrent episodes of sneezing, pruritus,
rhinorrhea, nasal congestion, and lacrimation
that occur after exposure to the offending
allergen.
• Itching is the symptom most suggestive of an
allergic etiology and involves not only the nose
but also the palate, throat, eyes, and ears.
• Systemic symptoms that may accompany allergic
rhinitis include general malaise, fatigue,
irritability, snoring, and sleep problems.
• family history of allergic diseases such as allergic
rhinitis, asthma, and atopic dermatitis.

26. classification of allergic rhinitis
• Classification of allergic rhinitis is
seasonal, perennial, or episodic .
 Seasonal allergic rhinitis is defined by
symptoms that occur during exposure
to seasonal allergens
 Perennial allergic rhinitis, defined as
nasal symptoms for more than 2
hours per day for more than 9 months
of the year.
 Episodic rhinitis refers to symptoms
on exposure to allergens that are not
normally present in the environment.

27. • newer classification was proposed in 1999, during
the ARIA (Allergic Rhinitis and its Impact on Asthma)
Intermittent
Symptoms
• < 4 days / week
• or < 4 weeks
Persistent
Symptoms
• > 4 days / week
• or > 4 weeks
Mild
• Sleep: normal
• Daily activities (incl. sports):
normal
• Work-school activities: normal
• Severe symptoms: no
Moderate- severe
• Sleep: disturbed
• Daily activities: Restricted
• Work and school activities:
disrupted
• Severe symptoms: yes

28. Physical Examination
• A complete ear, nose, and throat examination is
essential in the workup of every patient suspected of
having allergic rhinitis and is useful in identifying other
problems rather than in confirming the diagnosis.
• The patient should be looked at generally to assess any
obvious external features, such as an allergic crease or
allergic salute.
• Atopic dermatitis or conjunctivitis should be sought
and the patient's respiratory state noted.

29. • Examination of the face
:
• allergic shiners .
• Adenoid facies
• allergic salute .
• Dinnie’s lines.
• Injection of bulbar
conjunctiva

30. Nose and throat
• Inferio turbinate Mucosal edema, pale,
bluish, and edematous, and coated with thin,
clear secretions.
2. Cobblestoning of posterior pharyngeal wall

31. Investigations

32. Allergy skin prick testing
(SPT)
• A drop of a standardized allergen extract is
placed on the volar aspect of the forearm
and then pricked into the skin using a
lancet
• A positive control (histamine) and a
negative control (saline or diluent) should
be included
• A separate lancet is used for each test
which is read as the mean wheal diameter
at 15 minutes
• Reactions greater than 2 mm in under fives
and 3 mm in older subjects are regarded as
positive
• Invalid results in +ve negative control and in
–ve positive control (RAST should be
employed)

33. • A positive skin prick test is not indicative of clinical allergy
unless supported by the relevant history.
• Positive skin prick tests occur in 25-30 percent of adults,
only 10-15 percent develop symptoms.
• The risk of clinical allergy increases with the size of the
skin reaction.
• Patients who have positive skin prick tests and no
symptoms are sensitized: approximately half of these will
go on to develop clinical allergic disease.
Sensitivity and specificity of SPT

34. • Skin testing should not routinely be performed in
patients
• 1- who are at high risk for an anaphylactic
reaction to testing (poorly controlled asthma)
• 2- have experienced a recent anaphylactic event
• 3- are taking medications that may interfere with
the treatment of anaphylaxis (TCAs,
Antihistamine) (BBs)
• 4- have certain skin conditions (dermatographism
or skin mastocytosis)

35. • RAST tests are more
expensive, delayed, take
longer and no more
sensitive or specific than
skin prick tests.
• They should be used where
there are contraindications
to skin prick tests, where
skin prick tests are
unavailable or difficult to
interpret. There is usually
good correlation between
RAST and SPT
Specific IgE (RAST study)
Radioallergosorbent Test

37. Immunoassay
• Not influenced by
medication
• Not influenced by
skin disease
• Does not require
expertise
• Quality control
possible
• Expensive
Skin test
• Higher sensitivity
• Immediate results
• Requires expertise
• Cheaper
Immunoassay vs skin test for
diagnosis of allergy

38. • Management of allergic
rhinitis includes allergen
avoidance,
pharmacotherapy,
education and possibly
immunotherapy.
• Treatment strategies
should involve both the
upper and lower airway
where the latter is also
affected.
Treatment

39.  Secondary measures
- Major indoor allergens
include house dust mite,
domestic pets, cockroach and
moulds.
- In sensitized symptomatic
individuals, allergen
avoidance is desirable &
complementary
 However, allergen avoidance
measures are frequently
expensive, time-consuming,
impracticable or, in the case
of pollens, not feasible
 Primary prevention
- Early uses of antibiotics
and vaccinations (↑)
- High allergenic foods
during early life (↑)
- Smoking during
pregnancy (↑)
- Obsessional house dust
mite avoidance (↑)
Allergen avoidance and environmental
control

40. Pharmacotherapy

41.  Antihistamines: These rapidly
relieve running, itching and
sneezing, but have little or no
effect on blockage
 First-generation antihistamines,
should be avoided because of
sedation, psychomotor
retardation and learning (Cross
BBB acting on central H
receptors)
 Cetirizine, fexofenadine and
desloratadine do not appear to
block potassium channels even
at supranormal doses. (No effect
on K+ reuptake and so on
arrhythmias)
Antihistamines

42. • These are the most effective
treatment for rhinitis, especially if
started prior to allergen
exposure. Regular treatment is
necessary.
• Side effects are minor and include
epistaxis and nasal irritation in 5-
10 % patients.
• Nasal steroids reduce
inflammation and consequent
hyperreactivity, reduce nasal
symptoms, eye symptoms and
improve the sense of smell.
Topical Glucocorticosteroids

43. • Their onset of action is slow with
some improvement after 6-12 hours
and maximum effects occurring
only after several days.
• No difference in efficacy between
various preparations, but lowest
bioavailability is seen with
fluticasone and mometasone.
• In three large retrospective studies,
topical corticosteroids reduced the
relative risk of asthma exacerbation
by 50% if used with antihistamines
Topical Glucocorticosteroids

44. • Stabilize mast cell membrane (prophylactic
use)
• This spray is weakly effective against all
rhinitis symptoms.
• Needs to be used three to four times daily
and this limits compliance.
• Its safety means that it is useful for small
children (less than 4 years) for whom a
topical corticosteroid is not available.
Sodium Cromoglicate

45. • Used topically, these reduce
nasal obstruction, but increase
rhinorrhoea.
• Regular use for more than a few
days can result in rhinitis
medicamentosa
• Very short-term use (for flying,
OME, and rhinosinusitis) is
therefore recommended.
• Systemic decongestants are
relatively ineffective and have
side effects such as hyperactivity
and insomnia in children and
hypertension in adults.
Decongestants

46. • This atropine-like nasal spray is
useful against watery rhinorrhoea
and may, if regularly used, be
curative.
• Occasionally it is helpful in patients
with allergic rhinitis who do not
respond to topical corticosteroids
alone.
• Side effects can include worsening of
glaucoma or prostatism and dry
mouth and eyes.
Ipratropium Bromide

47. • These can be used to unblock the
nose at the start of treatment or
provided for very severe symptoms
during the hayfever season.
• Regular use is associated with
significant systemic side effects and
therefore only occasional
intermittent use for a few days at a
time is sensible.
• They should be combined with
topical corticosteroid and the usual
precautions apply.
Systemic Corticosteroids

48. • They are effective against congestion
and mucus production, with efficacy
similar to that of loratadine, but less
than topical corticosteroids.
• Combination of an antileukotriene
plus an antihistamine was superior to
either alone in one study, but in a
second study did not show much
clinically significant added benefit.
Antileukotriens

49.  Allergen immunotherapy involves the
repeated administration of an allergen
extract in order to induce a state of
immunological tolerance, with a reduction
in clinical symptoms and requirements for
medication during subsequent natural
allergen exposure.
 indicated in those patients with allergic
rhinitis with severe symptoms who fail to
respond adequately to usual treatment
with antihistamines and topical nasal
corticosteroids
 Immunotherapy is more effective in
patients with a limited spectrum of
allergies.
Immunotherapy

50. • Up-dosing phase involves weekly injections for 8-16 weeks
followed by Maintence injections at 4-8 weekly intervals for
3-5 years
• Hospital based clinics and full observation for 60 minutes
following injections
• Mechanism is blunting of seasonal increases in allergen
specific IgE by an increase in blocking IgG antibodies and
inhibition of recruitment and activation of inflammatory
cells. (Deviation from Th2-type in favor of protective Th1-
type).
• The sublingual route can be an alternative in view of side
effects of subcutaneous immunothearapy.

52. • Nasal surgery may be needed where
there is a marked septal deviation
or bony turbinate enlargement
which makes topical nasal sprays
usage difficult.
• Mucosal hypertrophy is preferably
dealt with medically if possible,
since after surgery the problem
tends to recur within months.
• Endoscopic sinus surgery may also
be needed to relieve symptoms of
rhino sinusitis
Surgery

53. • Few treatments are available for small children
• Sedating antihistamines should be avoided because they
impair cognitive function.
• The only intranasal formulation licensed for younger children is
sodium cromoglicate.
• Saline drops or spray may also be useful in children under two.
• Topical corticosteroid nasal sprays differ in their lower age
limit.
• Fluticasone propionate is licensed for children from 4 years, for
others the age limit is 5 or 6 years (beclomethasone or
mometasone)
• Budesonide is not licensed for paediatric use
Special Considerations: Pediatric
Rhinitis

54. • Existing rhinitis may be
exacerbated by pregnancy and
rhinitis can occur de novo in
pregnancy, probably due to high
circulating estrogen.
• Usually allergic rhinitis in
pregnancy is resistant to
treatment.
• The least absorbed topical nasal
corticosteroids would seem a
sensible option for the treatment
of existing rhinitis
Special Considerations: Pregnancy

55. • Thank you ..