Allergic Rhinitis: James A. Hadley, M.D. and J. David Osguthorpe, M.D

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 Asthma
Laryngitis, Pharyngitis
Allergic Rhinitis
Chronic Rhinitis
Rhinosinusitis
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 :
Allergens
Sensitization
Antigen-presenting cell
Processed allergens CD4 T cell
B cell IgE antibodies Plasma cell

Naclerio, RM. New Engl J Med 1991:325; 860-9
Pathophysiology of Allergic Inflammation: Clinical Disease

Phase 2 :
Early Inflammation
Allergens
Late-phase reaction Cellular infiltration Mast cell Mediator release Nerves Blood vessels Glands Sneezing Rhinorrhea Congestion 2003 The American Academy of Otolaryngology Head and Neck Surgery Foundation Eosinophils Basophils Monocytes Lymphocytes Hyperresponsiveness Priming
Clinical Disease
Late Inflammation
Resolution
IgE antibodies
Complications
Irreversible disease (?)
Mast Cells / Basophils and Inflammatory Cascade

Antigen Cytokines
-IL-4,5,6,8 Nucleus
Lipid Mediators
-PGs -LTs
Preformed Mediators
-Histamine -Heparin -Tryptase (Mast Cells)
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 Mast Cell Degranulation
Sensitization
IgE presentation
IgE bridging
Consequences of Mediator Release

Atg
Mast Cell
Mediators
Late Phase Reaction (maximum at 10-12 hours) Infiltration with Eosinophils Fibrin deposition Infiltration with Monocytes Tissue destruction
Early Phase Reaction (maximum 10-30 minutes) Pruritis, Sneezing Smooth muscle contraction Flush, Vascular leakage with Rhinorrhea Nasal congestion Mucous Secretion
Nasal Response to Inhaled Allergen

S y m p t o m s
Early Phase Response
Late Phase Response
3-4
24
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
Symptoms < 4 days per week or Symptoms < 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
Moderatesevere
One or more items Abnormal sleep Impairment of daily activities, sport, leisure Abnormal work and school Troublesome 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 acute or chronic RS P E Tubes 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

50 40 30
%
20 10 0 None One Two
Chance of having atopy based on family history
Number of parents allergic

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. Counseling of Patient & Family 2. Avoidance & Environmental Measures (home, vocation, avocation, school) 3. Pharmacotherapy (e.g., steroids, antihistamines) 4. 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
Antihistamines Intranasal Steroids Cromolyn sodium Decongestants Leukotrienes Immunotherapy IgE specific agents
Action
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)
Intradermal Tests
titration (serial dilutions, multiple tests to quantitate sensitivity)
Scratch Test
(poor reproducibility)
single intradermal skin endpoint
Prick Test
single prick test multi-test devices
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)
4 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 #3 = 4.0 g #2 = 20 g
0.02ml Single ID 1:1000 w/v = 20 g
0.02ml Single ID 1:500 w/v = 40 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 Eliminate food for 4-5 days, then Challenge Food Test
Patient unchanged
Evaluate other food(s), consider other origins to symptoms
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 : patient counseling, avoidance &/or environmental measures, pharmacotherapy, 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): Otolaryngic Allergy. Otolaryngol Clin N Am 36(4), 2003. Krouse J, Chadwick S, Gordon B, Derebery J: Allergy and Immunology: An Otolaryngic Approach. Lippincott Williams & Wilkins. Phil. 2002.

Allergic Rhinitis: James A. Hadley, M.D. and J. David Osguthorpe, M.D

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Allergic Rhinitis

James A. Hadley, M.D. and J. David Osguthorpe, M.D.

Nasal Airway Insufficiency

ANATOMIC OBSTRUCTION (septum, turbinate) RHINOSINUSITIS (self reported by 10 -13.5% of population)

MEDICATION SIDE EFFECT (rhinitis medicamentosa,

Nasal Insufficienty can be multifactorial.

Nasal insufficiency can be multifactorial

Allergic and Non- Allergic Rhinitis

Impact of Allergic Rhinitis

Allergic Rhinitis : Associated Diseases

Complications of Allergic Rhinitis

Definitions Relevant to Allergic Rhinitis

Pathophysiology of Allergic Disease

Pathophysiology of Allergic Inflammation: Sensitization

B cell IgE antibodies Plasma cell

Pathophysiology of Allergic Inflammation: Clinical Disease

Irreversible disease (?)

Mast Cells / Basophils and Inflammatory Cascade

Chemical Mediators of Allergic, and Some Non-Allergic, Rhinitis

Basic Immunology: Sensitization vs. Subsequent Exposure

Consequences of Mediator Release

Nasal Response to Inhaled Allergen

Early Phase Response

Late Phase Response

Time in Hours from Initial Challenge

Perennial allergic rhinitis (mite, mold,

Anatomic rhinitis (nasal drainage obstruction

Turbinate Hypertrophy/Rhinitis of Pregnancy

Non-allergic rhinitis with eosinophilia Medication-induced rhinitis (rhinitis

Hormonal rhinitis (pregnancy, menopause,

ARIA Classification & Allergic Rhinitis

Symptoms of Allergic Rhinitis

Diagnosis and the Allergic Patient

Allergies & Past Medical History

Allergies & Family History

20 10 0 None One Two

Chance of having atopy based on family history

Number of parents allergic

Physical Examination of Allergy Patient

R = turbinate congestion & hypertrophy from allergies; L = allergic conjunctivitis

Physical Examination of Allergy Patient

Testing for Allergic Rhinitis

In Vivo or In Vitro Allergy Screens

Nasal Cytogram - mucous, epithelial cells and some

Clinical Approach to the Allergic Patient

Diagnosis and Treatment of Inhalant Allergy

Perennial dust, mold, danders

Education, Environmental Control, Pharmacotherapy If Failure

Allergy Testing : Consider screen, then if positive, full battery of tests

Air Filtration: Personal, Room, House, Car

Indoor Environmental Allergen Control: Example for Allergic (Extrinsic) Asthma

Treatment Considerations in Allergic Rhinitis

Immunotherapy Factors (Allergy shots) :

Treatment of Allergic Rhinitis

Effects of Various Pharmacotherapies

H1-antihistamines Oral Intranasal Intraocular Corticosteroids Intranasal Cromolyn sodium

Management of Allergic Rhinitis

Immunotherapy, if other therapies fail

Traditional Drug Therapies

Topical & Oral Decongestants

Topical Nasal Steroids

Minimal systemic absorption for most (in younger

Effectiveness depends on regular use & adequate