Coass II-Allergy Rhinitis

Allergic Rhinitis
Third Edition
James A. Hadley, M.D. and

J. David Osguthorpe, M.D.
2003 The American Academy of Otolaryngology Head and Neck Surgery Foundation
Nasal Airway Insufficiency

(the stuffy nose)
ALLERGY (medically reported as 17 - 22% of population)
ANATOMIC OBSTRUCTION (septum, turbinate)
RHINOSINUSITIS (self reported by 10 -13.5% of population)
NON-ALLERGIC RHINITIS (vasomotor, gustatory, etc.)
MEDICATION SIDE EFFECT (rhinitis medicamentosa,
anti-HTN, birth control pills, estrogen, etc.)
PREGNANCY or OTHER ENDOCRINE

SOURCE, FLUID RETENTION
NEOPLASM, FOREIGN BODY, ETC.
Nasal Insufficienty can be multifactorial.
Nasal
insufficiency
can be
multifactorial
This cigarette
smoker has a
septal deviation,
turbinate
hypertrophy
from allergies,
polyps, &
rhinosinusitis.
Allergic and Non- Allergic Rhinitis

This educational slide series
will review the
pathophysiology, impact,
diagnosis and management
scenarios of both allergic and
non-allergic rhinitis.
A summary of the
otolaryngolgists perspective
and treatment paradigms.
Impact of Allergic Rhinitis

6th most prevalent chronic, & most common
respiratory, disease (most prevalent chronic
condition in those < 18 y/o)
2.5% physician office visits, common reason for
both OTC & physician prescriptions
Diminished QOL (irritability, fatigue, sleep
disturbance, depression)
Direct costs to US economy of approximately $4.5
billion/year, plus 3.8 million lost work & school days annually
Allergic Rhinitis : Associated Diseases

Otitis
Media
Laryngitis,
Pharyngitis
Asthma
Allergic
Rhinitis
Rhinosinusitis
Chronic
Rhinitis
Complications of Allergic Rhinitis
Rhinosinusitis, Nasal Polyps

Pharyngitis, Laryngitis
Otitis Media, Otitis Externa
Conjunctivitis
Exacerbation of Asthma, Bronchitis, Vertigo,
Migraine, Eczema
Impaired Olfaction / Taste, Sleep Apnea,
Facial Growth Abnormalities in Children (all
from nasal obstruction)
Allergic Rhinitis
Provoked by exposure to antigens
(allergens) in the environment and food
Symptoms:
Nasal congestion with nasal mucosal edema or
obstruction (mouth breathing, midfacial
fullness / pressure or headache.)
Sneezing, nasal, conjunctival and/or palatal
pruritis
Watery rhinorrhea, post nasal drip, lacrimation
Diminished sense of smell, Eustachian tube
dysfunction
Definition of Allergy
Von Pirquet 1906 Allergy
An altered reactivity to a foreign substance
after prior exposure to the same material
Allergy & Hypersensitivity are used
interchangeably to describe an adverse
clinical reaction to an environmental agent
caused by an immunological reaction
(Antigen-Antibody reaction).
Hypersensitivity Reactions
(Allergic Rhinitis is primarily a Type I,
IgE mediated reaction)
Type I
Immediate (allergic rhinitis, asthma,
immediate onset food reactions)
Type II Cytotoxic (hemolytic anemia, Hashimotos)
Type III Immune Complex (serum sicknesss,
delayed onset food reactions,
glomerulonephritis)
Type IV Delayed, Cell Mediated (TB, poison ivy)
Type V Stimulating Antibody Reaction (Graves)
Type VI Antibody Dependent Cell Cytoxicity
(transplant rejection)
Definitions Relevant to Allergic Rhinitis

Hypersensitivity
A heightened or exaggerated immune response
that develops after >1 exposure to a specific
antigen.
Allergen (Antigen):
A foreign substance that when introduced into the
body elicits a specific immunologic response.
Antibody:
A protein (immunoglobulin) that selectively binds
to a specific allergen.
Pathophysiology of Allergic Disease

1.
2.
3.
4.
Host sensitization to allergen

IgE production by host
Mast cell sensitization
Allergen provocation by further
exposure after sensitizing event
5. Mediator release:
Histamine, kinins, leukotrienes, cytokines
6. End-organ response
Pathophysiology of Allergic
Inflammation: Sensitization
Phase 1 :
Sensitization
Allergens
Antigen-presenting
cell
Processed
allergens
B cell
CD4
T cell
IgE antibodies
Plasma cell
Naclerio, RM. New Engl J Med 1991:325; 860-9
Pathophysiology of Allergic
Inflammation: Clinical Disease
Phase 2 :
Clinical Disease
Early
Inflammation
Late
Inflammation
Allergens
Cellular
infiltration
Mast
cell
Mediator release
Nerves
Blood
vessels
Glands
Resolution
Late-phase
reaction
IgE antibodies
Eosinophils
Basophils
Monocytes
Lymphocytes
Hyperresponsiveness
Complications
Priming
Sneezing
Rhinorrhea
Congestion
Irreversible
disease (?)
Mast Cells / Basophils and

Inflammatory Cascade
Antigen
Lipid
Mediators
PGs
LTs
Cytokines
IL4,5,6,8
Nucleus
Nucleus
Preformed
Mediators
Histamine
Heparin
Tryptase(MastCells)
Chemical Mediators of Allergic, and Some

Non-Allergic, Rhinitis
(principally from Mast cells & Basophils)
Pre-formed (stored) Newly formed mediators

(created by & after reaction)
mediators
Leukotrienes
Histamine
LTB4, LTC4, LTD4
Kinins
Cytokines
Heparin
ECF-A,
Prostaglandins
Platelet activating
PGD2
factor (PAF)
Interleukins
Basic Immunology:
Sensitization vs. Subsequent
Exposure
I
Antigen
II
Macrophage
Cytokines
T-cell
TH2
IgE
B-cell
Sensitization
Mast Cell
IgE presentation
Degranulation
IgE bridging
Consequences of Mediator Release

Atg
Mast Cell
Mediators
Early Phase Reaction

(maximum 10-30 minutes)
Pruritis, Sneezing
Smooth muscle contraction
Flush, Vascular leakage with
Rhinorrhea
Nasal congestion
Mucous Secretion
Late Phase Reaction

(maximum at 10-12 hours)
Infiltration with Eosinophils
Fibrin deposition
Infiltration with Monocytes
Tissue destruction
Nasal Response to Inhaled Allergen

S
y
m
p
t
o
m
s
Early Phase
Response
Late Phase
Response
Time in Hours from Initial

Challenge
Types of Rhinitis - 1
Seasonal allergic rhinitis (classic hayfever with
spring, summer &/or fall symptoms)
Perennial allergic rhinitis (mite, mold,

cockroach, animal dander)
Infectious rhinitis (virus, bacteria, fungi)

Occupational rhinitis (latex)
Chemical / irritative rhinitis (perfumes,
strong odors, fine particles)
Anatomic rhinitis (nasal drainage obstruction

by septum, etc.)
Turbinate Hypertrophy/Rhinitis of Pregnancy
Types of Rhinitis - 2
Vasomotor rhinitis (temperature variation
induced, either inhaled or with food intake)
Non-allergic rhinitis with eosinophilia

Medication-induced rhinitis (rhinitis
medicamentosa, oral contraceptives, antihypertensives)
Hormonal rhinitis (pregnancy, menopause,

hypothyroidism)
Atrophic rhinitis (ageing, surgery, infection)

Gustatory rhinitis (food allergy induced)
ARIA Classification & Allergic Rhinitis

Intermittent
Intermittent
Symptoms
Symptoms<<44days
daysper
perweek
week
or
orSymptoms
Symptoms<<44weeks
weeks
Mild
Mild
Normal
Normalsleep
sleep
&&no
noimpairment
impairmentof
ofdaily
daily
activities,
activities,sport,
sport,leisure
leisure
&&normal
normalwork
workand
andschool
school
&&no
notroublesome
troublesomesymptoms
symptoms
Persistent
Persistent
>>44days
daysper
perweek
week
and
and>>44weeks
weeks
Moderatesevere
Moderatesevere
One
Oneor
ormore
moreitems
items
Abnormal
Abnormalsleep
sleep
Impairment
Impairmentof
ofdaily
daily
activities,
activities,sport,
sport,leisure
leisure
Abnormal
Abnormalwork
workand
andschool
school
Troublesome
Troublesomesymptoms
symptoms
Symptoms of Allergic Rhinitis

Provoked by exposure to Antigens (in atopic context,
called Allergens) in environment & food
Common Symptoms:
Nasal, conjunctival &/or palatal pruritis
Sneezing, watery rhinorrhea, post nasal drip,
lacrimation
Mucosal edema with nasal congestion /
obstruction (mouth breathing, sleep disturbances),
sinus ostial &/or eustachian tube dysfunction
(midfacial pressure/pain, headache, ear pressure &
occasional mild dizzyness), & diminished olfaction
Diagnosis and the Allergic Patient

Diagnosis based on:
1. History
2. Physical Examination
3. Laboratory &/or Skin Testing
Note: # 1 & #2 suffice for initiation of
Environmental Measures & Pharmacotherapy,
and may be all that is necessary in mild to
moderate cases; #3 affords definitive diagnosis
& is required prior to Immunotherapy
Allergies & Past Medical History

Childhood allergy / asthma Surgery
T &/or A
Recurrent OM, recurrent
P E Tubes
acute or chronic RS
Sinus
Eczema
Colic / formula intolerance OTC or Rx
medications with
Anaphylactic reaction (food
anti-allergy, cold
or drug)
or decongestant
Seasonal colds (spring,
effects
fall)
Allergies & Family History
Chance of
having
atopy
based on
family
history
Physical Examination of Allergy Patient

Eyes: conjunctivitis, Dennies lines, shiners
Ears: otitis media or externa, retracted
tympanic membrane from ET dysfunction
Nose: boggy / pale nasal mucosa, clear / thin
mucoid rhinitis, turbinate hypertrophy, polyps,
transverse nasal crease from allergic salute
Throat: prominent lymphoid patches
(cobblestoning), lateral pharyngeal bands
R = Shiners & nasal obstruction (mouth

breather) from nasal edema & venous congestion ,
L = Dennies Lines
L
R = turbinate congestion & hypertrophy from

allergies;
L = allergic conjunctivitis
R
2003 The American Academy of Otolaryngology
Head and Neck Surgery Foundation
.
Posterior Pharyngeal Cobblestoning (submucosal

lymphoid hyperplasia from chronic post-nasal drip
of inhalant allergies)
Physical Examination
of Allergy Patient
Dental: crowded teeth, high arched palate
Nasopharynx: hypertrophic adenoids
(adenoid facies), lateral pharyngeal bands
Larynx: edematous / polypoid vocal cords
Lungs: sibilant rales, wheezing suggestive of
bronchospasm
Skin: eczema or other pruritic rashes
(especially if food allergic)
L = Rash from Birch Containing Shampoo;

R = Atopic Eczema from Food Sensitivities
L
Testing for Allergic Rhinitis
IgE testing
Skin In vivo (prick or intradermal tests)
Laboratory In vitro antigen specific assay
(radioallergosorbent / RAST Test or enzyme linked
immunosorbent / ELISA Test)
Other Laboratory testing:
Eosinophil count (also may be elevated in asthma,
NARES, parasitic infection, etc.)
Nasal cytology
Dietary Elimination and Challenge Feeding tests
In Vivo or In Vitro Allergy Screens

Test Battery of 8 - 12 common Allergens in patients
geographic region is 96% efficient & 94.2%
sensitive in detecting those with clinically
significant sensitivities (unless there is an unusual
or occupational exposure, e.g. latex in health care
worker, mice in laboratory worker)
Example of common inhalant screen: 2 trees, 1-2
weeds, 1-2 grasses, 1 mite, cockroach, 2 molds,
cat dander
In children with eczema, colic, etc., common foods
can be added to screen, such as milk, soybean,
peanut, egg, wheat, corn
Nasal Cytogram - mucous, epithelial cells and some bacteria,

with leukocytes (& more bacteria) in infection, & eosinophils in allergy
(most of the time)
Clinical Approach to the Allergic Patient

Classic Quartet of Treatment Approaches:
1. Avoidance & Environmental Measures
2. Counseling of Patient & Family
(home, vocation, avocation, school )
3. Physical fitness
4. Pharmacotherapy (e.g., steroids, antihistamines)
5. Eradicate comorbidity
6. Immunotherapy
[if warranted by skin or in vitro testing that confirms IgE to
offending Allergens, plus inadequate (or unrealistic) control
by both #2 & # 3]
Diagnosis and Treatment of Inhalant Allergy

History and Physical Examination
Seasonal pollens
Perennial dust, mold, danders
Education, Environmental Control,

Pharmacotherapy
If Failure
Allergy Testing : Consider screen, then if positive, full battery of tests
Immunotherapy
Air Filtration: Personal, Room, House, Car

Air Filters, in
Consumer
Reports of
1/2002
Indoor Environmental Allergen Control:

Example for Allergic (Extrinsic) Asthma
60-80% with asthma have IgE sensitivities, commonly mite,

cockroach, cat &/or Alternaria species
Indoor allergen reduction decreases severity of asthma:
Mite allergen : mite impermeable mattress & pillow
covers; wash comforters, bedding, etc at >130F; mite
killing powders (acaricides) on rugs, upholstered
furniture, drapes; house humidity < 50%
Cockroach allergen : extermination, cleaning
Mold : house humidity < 50%; clean bathrooms,
kitchens, laundry rooms; vent moist areas
High efficiency air filtration & vacuum cleaner bags
Treatment Considerations in
Allergic Rhinitis
Pharmacotherapy Factors :
Effectiveness
Side effect profile
Dosing schedule
Affordability
Immunotherapy Factors (Allergy shots) :

Effective in 70-80% with allergic rhinitis, must be continued
for 3-5 years in most (seems to require such for sustainable
levels of blocking antibodies & the like; some require
lifelong therapy)
Treatment of Allergic Rhinitis

Type of Drug
Action
Antihistamines
Intranasal Steroids
Cromolyn sodium
Decongestants
Leukotrienes
Immunotherapy
IgE specific agents
Block histamine
Local anti-inflammatory
Stabilizes mast cells
Vasoconstriction
Block cytokine action
Competing antibodies, etc.
Bind IgE, block receptor
sites, etc.
Effects of Various Pharmacotherapies

Therapy0
Sneezing Rhinorrhea
Nasal
obstruction
Nasal itch
Eye
symptoms
H1-antihistamines
Oral
Intranasal
Intraocular
Corticosteroids
Intranasal
Cromolyn sodium
Intranasal
Intraocular
Decongestants
Intranasal
Oral
Anticholinergics
Antileukotrienes
++
++
0
++
++
0
+
+
0
+++
++
0
++
0
+++
+++
+++
+++
++
++
+
0
+
0
+
0
+
0
0
++
0
0
0
++
0
0
++
++
++++
+
0
+
0
0
0
++
0
0
0
++
Adapted from van Cauwenberge P, et al. Allergy. 2000;55:116-134 and Nayak AS, et al.
Ann Allergy Asthma Immunol. 2002;88:592-600.
Management of Allergic Rhinitis

Options Common in a Stepwise Approach
Mild
intermittent
Moderatesevere
intermittent
Mild
persistent
Moderatesevere
persistent
Intranasal corticosteroid
Cromolyn Sodium
Patient
education
and
allergen
and irritant avoidance
Patient
education
and
allergen
avoidance
Intranasal decongestant (<10 days) or oral decongestant

Oral or local nonsedating
antihistamine
Immunotherapy, if other therapies fail
Traditional Drug Therapies
Over the Counter (OTC) Allergy Medications:

Accessible, at modest cost in most cases
Most current OTC antihistamines, may cause
drowsiness, dry mouth, blurry vision,
constipation & urinary retention
Oral decongestants may cause agitation &
sleeplessness, or elevate blood pressure
Topical decongestants can lead to rebound
congestion or rhinitis medicamentosa
Cromolyn requires frequent dosing prior to &
during exposure
Topical & Oral Decongestants

(action per alpha adrenergic receptors, do not relieve
rhinitis, pruritis, sneezing)
Topical Decongestants (neosynephrine, oxymetazoline)

Shrink inflamed & swollen mucosa through local
vasoconstriction
Use no longer than 4 - 7 days to avoid rebound
Oral Decongestants (pseudoephedrine)

Reduce nasal blood flow (hence, edema &
hyperemia) & may improve sinus ostial patency
May be used indefinitely (watch BP, sleep, anxiety, & use
with caution if diabetes, glaucoma, prostatic hypertrophy,
ASVD, etc.)
Prescription Antihistamines
Relieves rhinitis, excess mucous production, as well
as most ocular & non-nasal manifestions, but not

nasal congestion with short term therapy
Minimal to no sedation (mental alertness &
coordination usually intact)
Mucosal drying variably present (much less among
than older antihistamines); consider topical
antihistamine alternative in those with severe asthma
or bronchitis
Costlier than OTC / older generation antihistamines
(though most sedate to varying degrees)
Topical Nasal Steroids

Topically effective in relieving sneezing, nasal
pruritis, rhinorrhea & reactive mucosal edema
Minimal systemic absorption for most
(in younger
children, use drugs least absorbed & effective with once
daily dosing, particularly if also on steroids for asthma)
Effectiveness depends on regular use & adequate
nasal airway for delivery; requires at least day or

two before clinical onset of action (may need oral
decongestant for first week to aid penetration); can irritate
nasal mucosa; modest effect on ocular symptoms
Leukotriene Suppressors
Leukotriene synthesis inhibitors or receptor
antagonists commonly used for asthma (after
therapies with inhaled steroids & B-agonists fail)
Consider in patients with persisting symptoms
despite topical steroids &/or antihistamines,
especially in asthmatics or those with ASA triad
May be useful (variable effect) on polyps or
hyperplastic nasal / sinus mucosa
Few side effects, safe in children > 2y/o
Other Therapies for Inhalant Allergies
Mast Cell Stabilizers: cromolyn or

nedocromil in nasal, ophthalmic or inhaled
preparations
Anticholinergics: topical atropine or
ipratropium
IgE Blockers / Binders: omalizumab (as a
periodic shot), many in pipeline for release
in next few years
Saline: saline sprays, pumped irrigations
Types of Skin Testing

Patch test
(derm use only)
Scratch Test
(poor
reproducibility)
Prick Test
single prick test
multi-test devices
Intradermal Tests
single intradermal
skin endpoint
titration (serial
dilutions, multiple
tests to quantitate
sensitivity)
Selection of Antigens for Skin or

Laboratory Testing
Identify antigens in patients environment

(regional, work & home)
Successful immunotherapy, &

environmental modification, depends upon
accurate determination of all (or at least the
majority) of clinically significant allergens
Prick Testing
Strength of antigen predetermined
usually 1:10 or 1:20 antigen weight to volume of liquid
Antigen placed on skin (back or arm) prior to

prick, skin is tented up with sharp instrument &
then pricked
Reactions are determined after 20 minutes
Grading system 1+ to 4+, measuring both wheal
and erythema flare responses
Designed to detect major sensitivities, without
quantitation as to degree; can miss low grade
sensitivities such as molds
Skin Prick Techniques
Single Prick Options
Multi Prick (various devices, all of which accomplish

simultaneous punctures with different antigens)
Intradermal Testing : Single Antigen

Concentration Tests
Strength of antigen predetermined
usually 0.01 0.04cc of 1:500 to 1:1000 antigen weight to
volume injected subcutaneously
Reaction read after 10-20 minutes

Grading system 1+ to 4+ , measure both wheal size
& erythema flare responses
Detects major sensitivities but without quantitative
information; can detect most low grade
sensitivities if 1:500 antigen solution utilized
Skin Endpoint (Dilutional) Titration

or SET
Intradermal injection of 0.01-0.02 cc of serially
diluted antigen (usually 1:5, starting with the antigen
concentrate) to produce a 4mm wheal
Reaction read per wheal growth by 10-15 minutes
If no reaction is detected, progressively more
concentrated antigen solutions are injected until a
2mm or more growth in wheal size occurs or the
highest concentration of antigen (usually 1:100
weight per volume) dilution is reached, signaling no
significant sensitivity to the antigen
SET Diagram
0.01-.02cc intradermal test

produces 4 mm wheal
Spreads to 5mm by diffusion
If it further enlarges >2mm after
10-15 minutes, test is likely
positive (i.e., patient sensitive to the antigen,
but such must be confirmed by yet another 2mm

wheal growth when the next stronger antigen is
injected)
5
7
Serial Endpoint (Dilutional) Skin Testing

for Identification and Quantification of
Inhalant Sensitivities
Skin Endpoint (Dilutional) Titration

Advantages:
Very safe, and can detect low levels of patient
sensitivity to an antigen
Few false positives or false negatives
Both quantitative and qualitative (i.e., identifies
not only patient sensitivities, but magnitude of
those sensitivities)
Safe guide to starting therapy
Antigen Dose
Comparisons among
Skin Testing
Techniques
Prick 1:10 w/v = .30 g
0.01 ml of
various antigen
dilutions
delivered by SET
#6 = 0.03 g
#5 = 0.16 g
#4 = 0.80 g
0.02ml
Single ID 1:1000 w/v = 20 g
0.02ml
Single ID 1:500 w/v = 40 g
#3 = 4.0 g
#2 = 20 g
#1 = 100 g
In Vitro Testing Procedure

Sandwich Assay Technique
Allergen coupled to a solid phase : Paper disk

(RAST), Cellulose sponge (ImmunoCAP, etc.)
Add patients serum
Antigen-Antibody complex formed
Anti- IgE added
Anti-IgE Antibody-Allergen complex formed
Computerized reading of different tags
(radioactive, fluorescence, colorimetric,
enzymatic)
In Vitro Methodology
Courtesy Scientific American
Allergen coupled to a solid phase : paper disk or cellulose sponge

Add patients serum, & IgE Antibody-Allergen complexes formed
(& possibly some IgG Antibody-Allergen complexes)
Add Anti-IgE, & Anti-IgE Antibody-IgE Antibody-Allergen complexes formed
Computerized reading of different tags (radioactive, fluorescence,
colorimetric, enzymatic)
Modified In Vitro Scoring

(quantifies patient sensitivity per scale that reflects
amount of specific IgE and correlates with SET results;
RAST-specific scale shown )
Class 0
Class 1/0
Class 1
Class 2
Class 3
Class 4
Class 5
250 - 500 (Not sensitive)

501 - 750 (Marginally sensitive)
751 - 1600 (Low sensitivity)
1601 - 3600
3601 - 8000
8001 - 18000
18001 - 40000 (Very sensitive)
Comparison of
Scoring
Systems
Relative Advantages:
In Vivo vs. In Vitro Testing
In Vitro (immunoassay)
No risk of allergic reaction
Not affected by drugs or
skin conditions
Patient convenience
(single venipuncture)
Easy to document quality
control, reproducibility
Most convenient for allergy
screen
In Vivo (skin tests)

Greater sensitivity (e.g.,
molds)
Larger availability of
antigens
Immediate test results
Moderately less expense
No laboratory certification
paperwork
Principles Common to SET

In Vivo & In Vitro Methods of Testing
Testing
Screens of 8 - 10 antigens can precede full battery

Testing with individual antigens rather than antigen mixes
Treatment
Decision to treat rests on clinical judgement, NOT just + results

ENDPOINT, a quantification of patient sensitivity, via SET or
Modified RAST score, indicates safe immunotherapy starting
dose
When enough sensitivities necessitate 2 different treatment
vials, high & low sensitivities are separated & different speeds
of dose escalation are possible (faster with low sensitivity
antigens)
Food Allergy
(2 basic types : Fixed and Cyclic)
May cause nasal congestion & rhinitis, in
addition to more common food sensitivity
manifestations: GI disturbance, rash,
headache, vertigo
Consider evaluation if patient has positive
history for food reactions (or colic/eczema
as child), inhalant allergy workup is
unimpressive, or therapy (environmental
modification, pharmacotherapy,
immunotherapy) fails to bring expected relief
Food Reactions
Prevalence greatest < 3 years of age, & declines
over next decade
90% of food allergy reactions in children are
caused by 6 foods : milk, egg, soy (all of which can
be outgrown), & wheat, peanut, tree nuts
90% of food allergy reactions in adults are caused
by 4 foods: peanut, tree nuts, fish, shellfish
Common cross reactions between inhalants &
foods: ragweed & melon / banana; birch &
apple / carrot / potato / hazelnut / almond
Fixed Food Allergies

IgE mediated with immediate clinical reaction to
ingestion, frequently angioedema or anaphylaxis
(most frequently shellfish or peanut)
Diagnosis usually made from patient history
specific IgE assay will confirm if needed (do NOT skin
test for the food)
Treatment is avoidance of offending food,

patient should be instructed in use of self
administered, injectable epinephrine
Cyclic Food Allergies

Most common type of food sensitivity, with
delayed onset of symptoms (up to 24 hours)
Mediated by any of the Gell & Coombs
reactions
Most are immune complex reactions
Diet and symptom diary identify likely offending foods
4 day elimination of the particular food, and then a Challenge
feeding test of that food on 5th day
In vitro tests are alternative in young children (higher frequency
of IgE-mediated food reactions)
Elimination Diet and Challenge Food Test

Eliminate suspect food, in all
products, based on patient history
Patient improves
Reintroduce suspect
food into diet
Symptoms recur
Patient unchanged
Evaluate other food(s),

consider other origins to
symptoms
Eliminate food for 4-5 days,

then Challenge Food Test
Indications for Immunotherapy

Avoidance & Environmental Measures fail to control
symptoms, or are impractical (e.g., teacher in moldy
school building, florist sensitive to plant pollens or
veterinarian sensitive to cats)
Pharmacotherapy fails to fully control symptoms, or
produces bothersome side-effects
Moderate to severe symptoms in 2 or more seasons, &
Skin or In Vitro tests document IgE mediated
sensitivity
Contraindications : -blocker or potential problem with
epinephrine, poorly controlled asthma, autoimmune or
immunodeficiency disease, unreliable patient
Immunotherapy for Allergic Rhinitis

Regular injections of increasing amounts of Allergen
administered every 5-7 days until symptom relieving
dose or maximum tolerated dose reached, then
maintenance dose q 2-4 weeks, based on symptoms
Continue maintenance dose until symptoms are
controlled for 3 -5 years, then can discontinue
Immunotherapy in about 75%
Injections during dose escalation under direct
supervision of physician trained to manage
anaphylaxis
Immunotherapy Failure:
Common Reasons
Patient failure to regularly comply with the
immunotherapy regimen
Incorrect antigen dosing &/or too infrequent shot
intervals
Food or chemical sensitivities, or inhalants to
which patient was not tested or for which
commercial antigens are unavailable
Non-allergic rhinitis (vasomotor, occupational,
atrophic, medication-induced)
Rhinosinusitis, Anatomic airway obstruction
Allergic Fungal Pansinusitis
Summary : Allergic Rhinitis

Affects 17-25% of US population
Symptoms / related diseases very relevant to the
otolaryngologists (e.g., nasal congestion,
rhinitis, rhinosinusitis, otitis media,
pharyngitis, laryngitis)
Initial diagnosis by H & P, with skin or in vitro tests
as needed
Treatments available : avoidance &/or environmental
measures, patient counseling, physical fitness,
pharmacotherapy, eradicate comorbidity,
immunotherapy
References
Fornadley J, Corey J, Osguthorpe J, et al: Allergic
Rhinitis: Clinical Practice Guidelines. Otolaryngol
Head Neck Surg 115:115, 1996 (consensus of American
Academy of Otolaryngology - Head and Neck Surgery & American
Academy of Otolaryngic Allergy).
Osguthorpe J, Derebery J (guest editors):

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Coass II-Allergy Rhinitis

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Coass II-Allergy Rhinitis

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Allergic Rhinitis

James A. Hadley, M.D. and

Nasal Airway Insufficiency

PREGNANCY or OTHER ENDOCRINE

Nasal Insufficienty can be multifactorial.

Allergic and Non- Allergic Rhinitis

Impact of Allergic Rhinitis

Allergic Rhinitis : Associated Diseases

Complications of Allergic Rhinitis

Rhinosinusitis, Nasal Polyps

Definitions Relevant to Allergic Rhinitis

Pathophysiology of Allergic Disease

Host sensitization to allergen

Mast Cells / Basophils and

Chemical Mediators of Allergic, and Some

Pre-formed (stored) Newly formed mediators

Consequences of Mediator Release

Early Phase Reaction

Late Phase Reaction

Nasal Response to Inhaled Allergen

Time in Hours from Initial

Perennial allergic rhinitis (mite, mold,

Infectious rhinitis (virus, bacteria, fungi)

Anatomic rhinitis (nasal drainage obstruction

Turbinate Hypertrophy/Rhinitis of Pregnancy

Non-allergic rhinitis with eosinophilia

Hormonal rhinitis (pregnancy, menopause,

Atrophic rhinitis (ageing, surgery, infection)

ARIA Classification & Allergic Rhinitis

Symptoms of Allergic Rhinitis

Diagnosis and the Allergic Patient

Allergies & Past Medical History

Allergies & Family History

Physical Examination of Allergy Patient

R = Shiners & nasal obstruction (mouth

R = turbinate congestion & hypertrophy from

Posterior Pharyngeal Cobblestoning (submucosal

L = Rash from Birch Containing Shampoo;

Testing for Allergic Rhinitis

In Vivo or In Vitro Allergy Screens

Nasal Cytogram - mucous, epithelial cells and some bacteria,

Clinical Approach to the Allergic Patient

Diagnosis and Treatment of Inhalant Allergy

Perennial dust, mold, danders

Education, Environmental Control,

Air Filtration: Personal, Room, House, Car

Indoor Environmental Allergen Control:

60-80% with asthma have IgE sensitivities, commonly mite,

Immunotherapy Factors (Allergy shots) :

Treatment of Allergic Rhinitis

Effects of Various Pharmacotherapies

Management of Allergic Rhinitis

Intranasal decongestant (<10 days) or oral decongestant

Immunotherapy, if other therapies fail

Traditional Drug Therapies

Over the Counter (OTC) Allergy Medications:

Topical & Oral Decongestants

Topical Decongestants (neosynephrine, oxymetazoline)

Oral Decongestants (pseudoephedrine)

as most ocular & non-nasal manifestions, but not

Topical Nasal Steroids

pruritis, rhinorrhea & reactive mucosal edema

Minimal systemic absorption for most

Effectiveness depends on regular use & adequate