Transcript Allergies – A Functional Medicine Model for Healing

Allergies:
Review, Relief, Prevention,
Patient Education
Kara Parker, MD
Oct 15, 2009
Objectives
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To present a larger picture of the factors that
create and prevent allergies.
To review the components of allergic disease –
genetics, immune reaction, environmental
triggers, and physical response.
To present the pharmaceutical, vaccination, and
nutraceutical therapies for allergies
To offer resources for environmental control and
prevention of allergy development and triggers
Goals
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To help prepare you for boards – all
material taken from AAFP reviews, and
residency guidelines are followed.
To help you be a clinician with a broader
understanding of development and
triggers of allergies and ways to prevent
and control symptoms.
Overview
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Review the epidemiology of allergic disease, and pre and
post-natal contributors
Review allergic rhinitis and conjunctivitis
Review anaphylaxis and drug allergy
Review allergy testing
Review immunotherapy (antigen vaccination)
Review food allergy, both IgE, and IgG
Review pharma and nutraceuticals for prevention/ relief
Review environmental control and patient education
Breathe!
Toxins vs allergens
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Toxins: Potentially injurious to any one,
depending on dose.
Allergens: Only injurious to predisposed
individuals.
Burden of disease
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Allergies are increasing in the Industrialized
world.
In America over 50 million people report allergic
symptoms, 20% have atopic disease
Allergies are the 6th most common chronic
disease in the US
14 million visits yearly for hay fever symptoms
Peanut allergy has doubled in the past 5 years
The Hygiene Hypothesis
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The decreasing incidence of early
infections due to sanitization, vaccination,
and antibiotics lead to underdevelopment
of TH1
And thus disproportionate TH2 activity
T cells are programmed in infancy, and
perpetuate what they have learned.
Th1/Th2 Imbalance and
Inflammatory Disease
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Th1: Intracellular defense
T cell-mediated activation of
macrophages and neutrophils
Th2 : Humoral defense.
B cell-mediated activation of mast
cells, eos, basos, ↑ IgE, IgG4
TH1/TH2 Imbalance
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TH1 predominance leads to organ specific
autoimmune disease (Rheumatoid arthritis, Multiple
sclerosis,Thyroiditis, Lyme arthritis, Crohn’s disease, IDDM )
TH2 predominance leads to atopic and
allergic disease.(Allergic diseases, asthma, contact
dermatitis, Scleroderma, Ulcerative colitis, Systemic lupus
erythematosus
)
Allergies are more common in:
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Nonwhite populations
People who live in high pollution areas
Higher socioeconomic classes
People with a FH of allergy
People born during peak allergy season
Firstborn children
Children exposed to cigarettes
Children given formula and food before 4 mo.
Allergies are less common
In people who:
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Come from a large family
Attended a daycare center at an early age
Were exposed to common early infections
Did NOT get antibiotics for treatment of
early childhood illnesses
Have high intakes of vitamin D, vitamin C,
bioflavonoids and, probiotics, omega-3 FA.
Genetic links
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Allergies run in families and have genetic
predisposition
One major allergy gene has a 24%
incidence, but a low penetrance.
Genetic links alone do not account for the
sharp rise in allergies in the past 30 years.
Gene Links to Allergies
Mold
Early Exposures - Mold
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Early exposure of infants to certain airborn
molds increases the risk of allergies to
molds, pets, pollen, dust mites, and foods.
Penicillum, aspergillis, and alternaria were
worst.
Other mold exposures seem to be
protective and beneficial.
Early Exposures - Tobacco.
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Early Exposure to tobacco smoke is linked
to development of allergic rhinitis
Infants exposed to 20 or more cigs/ day
had a 3 –fold increase in incidence of AR
43% of American infants are exposed to
tobacco smoke daily.
In Utero Exposures
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At 22 weeks gestation the fetus can make
IgE Ab to egg, milk, and dust mites.
23% of homes have beds with levels of
dust mites high enough to trigger atopy.
What is Mom exposed to that triggers a
fetal allergic response?
The Allergic Process:
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Initial exposure: Sensitization stage where
IL-4 is produced from antigen
presentation,
developing TH2,
Signaling IgE production to the antigen
Recruiting eosinophils, growing mast cells,
differentiating B cells to secrete IgE
antibodies
Second exposure
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Antigen is identified and bound by the IgE
antibodies on the surface of sensitized mast cells
and basophils.
Allergen/Antibody complex activates and
degranulates the cells.
Histamine, protease, chemotaxins, leukotrienes,
prostaglandins enter blood.
Localized inflammation is induced in diverse
areas of the body leading to allergic symptoms.
Allergic Inflammation:
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Acute: Rejection of a stressor (allergen)
Chronic: Persistence of the acute phase
response.
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Maladaptive – more detrimental than beneficial
Self perpetuating
Disrupts homeostasis
Alters cellular physiology
Destroys tissue
Systemic response
Allergic symptoms
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Recurrent Sneezing
Nasal pruritis
Nasal congestion
Eye, throat, and ear tingling and pruritis
Headache
Sleep disturbance
Concentration difficulties
Allergic Rhinitis
Allergic Rhinitis
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Can be seasonal, perennial, or
occupational
Is a systemic illness with constitutional
symptoms
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Fatigue
Malaise
HA
Associated Symptoms
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Excessive mucus production
Congestion
Sneezing paroxysm
Watery eyes
Nasal and ocular pruritis
Allergic Rhinitis
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Shares a co-morbidity with asthma,
eczema, and chronic sinusitis
Determining allergic rhinitis (IgE
mediated) from other types is important
as therapies are different
Allergic vs. non-allergic rhinitis
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Non- allergic includes:
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Vasomotor
Hormonal
Drug induced
Structural
Occupational (irritant)
Eosinophilia syndrome
Emotional rhinitis
New Classification of AR
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Instead of seasonal (pollens molds) and
perennial (indoor exposures)
Use intermittent, persistent, mild,
moderate, severe for allergic rhinitis
PE suggestive of AR
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Gen: fatigue, lack of concentration
Eyes: Allergic shiners, conjunctivitis
Ears: Air fluid levels – chronic congestion
Nose: Deviated septum, pale boggy
mucosa, and polyps
Mouth: Enlarged tonsils, clear postnasal dc
Chest: wheezing, Skin: atopic dermatitis
Medical History
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FH: allergies, asthma, eczema
PMH: any of the above
Age: 80% of illness starts before age 20
Success of past and current TX
Environmental factors: Got a cat, new job
with exposure, basement flooding, etc.
Stress – often mind body plays a part
Diagnosing AR
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If nasal and constitutional symptoms are
chronic, or last longer than 1 week after a
viral cold and PE and story likely for AR:
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Check for sinusitis
If negative, do a trial of antihistamines
If a positive response, Dx allergic rhinitis
Allergy Testing
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No clear guidelines for when to do allergy
testing.
If Diagnosis is unclear
If case is severe
If patient is a potential candidate for
immunotherapy
If testing will change treatment outcomes
Allergy Testing
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Not routinely recommended
Usually done by allergists or specialized
dermatologists
Will be covered in detail later.
Conventional treatment
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1) Allergen avoidance
2) Pharmacologic treatment
3) Allergen Immunotherapy
Allergen Avoidance
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Stay indoors during peak allergy season
Keep windows closed and air cond. on
HEPA filter for purifying airborne allergies
Wash hair before bed
Keep home dusted
Dust mite covers if needed
Removal of mold
Special precaution with pets
Rx: Antihistamines
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Antagonization of H1 receptor sites can reduce
histamine symptoms: sneezing, rhinorrhea,
nasal itching, lacrimation.
First generation OTC remedies produce sedation
(diphenhydramine, promethazine most;
chlorpheniramine, brompheniramine least
SE’s are dry mucous membranes, urinary
retention, blurred vision are common.
Second Generation Antihistamines
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Have minimal or no anti-cholinergic SE’s
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Do not readily cross the BBB
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Cardiotoxity from astimizole and
terfenidine – both removed from market
Nasal Decongestants
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Activate alpha adrenergic receptors in the
vascular smooth muscle of the resp. mucosa
Oral formulations (sudafed) cause insomnia,
restlessness, tachycardia, BP elevation
Topical decongestants can only be used for a 3-5
day period, as they cause rebound SX’s
Intranasal Corticosteroids
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Inhibit intranasal allergic inflammation,
relieve sneezing, nasal itching, rhinorrhea,
and congestion
Recent studies show them to be superior
to 2nd generation antihistamines
Should be administered daily not PRN
All appear to be equivalent in studies
SE’s local irritation and rarely erosion
Inhaled Cromolyn
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Relieves most histaminic symptoms, but
not nasal congestion
Therapeutic dosing is 3-4 times daily
Can be used before allergy season as a
preventive medication to lessen SX’s
Intranasal ipratroprium bromide reduces
hypersecretion, but not other SX’s.
References
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Quillen, Feller. Diagnosing Rhinitis: Allergic vs nonAllergic. American Family Physician Vol 73, no.9, (May 1,
2006).
American family Physician. Overview of methods for
treating allergic rhinitis. Tips from other journals. Vol 61,
no.1 (Jan 1, 2000).
ANAPHYLAXIS
Anaphylaxis
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Incidence is 1% of the world’s population
500 – 1000 deaths/ year from anaphylaxis
Symptoms mimic other diagnosis, so
under-diagnosed and reported.
“Anaphylaxis is a serious allergic reaction
that is rapid in onset and may cause
death.” 2006 National Inst All and Inf Dis/Food Allergy Network definition
Signs and Symptoms
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Dyspnea
Uriticaria
Angioedema
Flushing
Pruritis
GI symptoms (nausea, vomiting, diarrhea)
Syncope
Hypotension
Signs/SX cont
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Cutaneous manifestations present in 90%
Diagnoses are most often missed in cases
that angioedema /urticaria is missing
SX’s occur in seconds to minutes after
allergic contact
SX’s may last a short time or for hours
Often a second phase happens hours later
Observation
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Observation needs to be 4-6 hours for
mild symptoms
Hospitalization and overnight course for
moderate to severe symptoms
Differential Diagnosis
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Gastrointestinal symptoms or cardiopulmonary collapse
cause confusion
Anyone presenting with unexplained syncope or shock
needs consideration for anaphylaxis
Other differential Diagnosis:
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Acute anxiety, panic attack
MI
PE, or airway foreign body
Acute poisoning
Hypoglycemia
Seizure d/o
Septic shock
Clinical Criteria for Diagnosing
Anaphylaxis
Acute onset of illness with skin involvement
+/ respiratory compromise +/reduced BP
after known exposure for a patient
(See CME Bulletin for complete details)
Common Causes
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Food: 33% Peanuts, Eggs, Shellfish
Drugs – 27 million Americans – PCN,
NSAIDS
Latex rubber- 17% healthcare workers
Radiographic contrast media – 12%
Hymenoptera (bee, wasp, etc) stings -5%
Idiopathic
Aspirin
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Produces a range of reactions including
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asthma, urticaria, angioedema, anaphylactoid
reactions.
ASA sensitivity in 10% of people with
asthma.
Accounts for 3% of anaphylaxis
Penicillin
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Most common cause of anaphylaxis
5/10,000 courses of PCN result in allergic
reactions
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1/50,000 result in a fatal outcome
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75% of anaphylactic deaths result from PCN
Hymenoptera stings
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40-100 deaths per year
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3% of the US population is sensitized
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Systemic reaction to insect sting and
positive skin test = 50% risk of future
stings.
Latex
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Widespread since “universal precautions”
17% of healthcare workers have some
form of latex allergy, not all anaphylactic
Recognition is crucial as many products
contain latex- catheters, gloves, supplies
Fruit sensitivity – kiwi, pear, pineapple,
grape, papaya cross react with latex
Radiographic Contrast Media
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0.2% reactions in contrast media
.04% reactions for lower osmolality,
nonionic agents
Can pretreat with benadryl and steroids.
Risk of death is 1 in 100,000 for either
type.
Initial Management
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Focused examination – A,B,C’s
Procure a stable airway, intubate if needed
O2 as needed
Get IV access
Administer epinepherine 1:1,000
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Give 0.2 to 0.5 ml (mg) to adults
0.01 mg/kg in children
SQ into upper arm, massage to facilitate absorption
AdditionalTreatment
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Antihistamines - benadryl
Pressors
Steroids – if protracted anaphylaxis is predicted
Beta agonists
Nebulized beta agonists if wheezing
IVF
Tx pneomonic
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Epinephrine IM
Antihistamines PO, IM
Steroids PO, IM, IV
Inhaled b2-agonists, if wheezing; IV
fluids, if hypotensive
Anaphylaxis Labs
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When a diagnosis is unclear, laboratory
evaluation may help
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Plasma histamine rises 10 min after onset and
remain for 60 minutes
Urinary histamine levels remain longer
Serum tryptase levels rise in 60 min and
remain elevated for up to 5 hours.
Future Management
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Prescribe pre-loaded epinepherine
syringes (epipen).
Train patients how and when to use, and
to keep in purse, home, and car.
Teach people to keep antihistamines and
take at the same time.
Advise a medical alert bracelet be worn
Prevention of Recurrence
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Send the patient to an allergist to do
testing.
Take a detailed history of recent exposure
to foods, medications latex use, insect
stings.
Previous tolerance does not rule out a
trigger.
Anaphylaxis References
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AAFP CME Bulletin Recognition and Management of Anaphylaxis.
Vol.6/ No.7 (Oct 2007)
Muller. Urticaria and Angioedema: A Practical Approach. American
Family Physician. Vol. 69/ No.5 (Mar 1, 2004).
Tang. A Practical Guide to Anaphylaxis. American Family Physician.
Vol. 68/ No.7. (Oct 1, 2003).
Hosey, Carek, Goo. Exercise- Induced Anaphylaxis and Uritcaria.
American Family Physician. Vol. 64/ No.8 (Oct 15, 2001).
Allergic Conjunctivitis
Allergic Conjunctivitis
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Allergic inflammation of the membrane that lines
the eyelids and covers the sclera
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Characterized by eye itching and burning and
allergen exposure, usually cyclical.
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Absence of itching is likely not allergic
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Presence of personal of FH of allergies/atopy
often present
Other Symptoms
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Bilateral Distribution of:
Mucoid stringy discharge
Tearing
Redness
Mild eyelid swelling
Mild to intense itching
Allergic Conjunctivitis
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Differential diagnosis:
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Viral and bacterial conjunctivitis
Fungal conjunctivitis
Dry eyes
Non-allergic irritation (dust, etc)
Foreign body
Allergic Conjunctivitis Causes
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Pollens – grasses, ragweed, trees
Molds
Animal dander and saliva
Perfumes and cosmetics, lotions
Air pollution
Cigarette smoke
Allergic conjunctivitis TX
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Allergen avoidance
Cold, clean compress to eyes
Drugs:
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Vasoconstrictors
Antihistamine drops
Topical NSAIDS
Ocular mast cell stabilizers
Oral antihistamines – faster than MCS
Treatment, continued
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Each category of eye drops takes 6-8
weeks for full effect
(Topical steroids should not be chosen as
they can cause glaucoma and ulceration)
Side effects:
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Stinging,
eye pain, and
photophobia are common
References
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Morrow, and Abbott. Conjunctivitis. American Family
Physician. Vol 57/ no. 4. (Feb 15, 1998).
American Family Physician. Selecting a Topical treatment
for Seasonal Allergic Conjunctivitis. POEMs and Tips from
Other Journals. Vol. 71/ no. 7 (April 1, 2005).
Opthalmic Drugs for Patients with Allergic Conjuncivitis.
American Family Physician. Vol. 62/ no.9 (Nov 1, 2000).
Adverse Drug Reaction
Drug allergy versus reaction
Adverse Drug Reaction
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Drug reaction – term that encompasses all
adverse drug events
Drug hypersensitivity – Immune mediated
response resulting from interactions between a
pharmacologic agent and the immune system.
Drug allergy – IgE mediated event
Identifiable risk factors
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Age
Female gender
Concurrent illness
Previous hypersensitivity to related drugs
(or to drugs in other classes)
Drug reaction
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The majority (75-80%) of adverse drug
reactions are characterized by predictable,
non-immunological effects.
The remaining 25% are caused by nonpredictable effects that may or may not be
immune related.
Immune Mediated Drug
Hypersensitivity
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Constitute for 5- 10% of all drug reactions
and may or may not be IgE mediated.
Gell and Coombs classification describes
the predominant immune mechanisms
(type I – IV) leading to clinical symptoms
of drug hypersensitivity.
Drug Hypersensitivity
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Type
Type
Type
Type
I – immune mediated
II- cytotoxic
III- immune complex
IV- delayed, cell mediated
Type I Hypersensitivity
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IgE mediated, anaphylactic
Manifests as uritcaria, angioedema,
bronchospasm, pruritis, vomiting, diarrhea,
anaphylaxis
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Starts minutes to hours after exposure
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Ex: Anaphylaxis from B-lactam antibiotics
Type II Hypersensitivity
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Cytotoxic mediated
IgG or IgM Ab directed at drug hapten coated cells
Arises 1-3 weeks after exposure
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Manifests in:
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hemolytic uremia,
neutropenia,
thrombocytopenia
Ex: Hemolytic anemia from PCN, cephalosporins.
Type III Hypersensitivity
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Immune complex mediated:
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Tissue deposition of drug- antibody complexes with
complement activation, and
inflammation
Manifests as serum sickness, fever, rash,
arthralgias, urticaria, vasculitis,
glomerulonephritis, LAD.
Ex: Serum sickness from anti-thymocyte globulin
Type IV Hypersensitivity
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Delayed, cell mediated (cutaneous)
MHC presentation of drug molecules to T cells
with cytokine and inflammatory mediator release
Manifests as:
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allergic contact dermatitis,
maculopapular drug rash
Begins 2-7 days after cutaneous drug exposure
Ex: contact dermatitis from topical antihistamine
exposure
Laboratory evaluation
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Type I (IgE mediated): Use skin testing,
RAST testing, or serum tryptase
Type II (cytotoxic): Direct or indirect
Coombs
Type III (Immune complex): ESR, crp,
ANA, complement studies, tissue biopsy
Type IV (delayed): patch testing
Non-immunologic: Predictable
Reactions
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Drug SE – Dry mouth from antihistamines
Secondary Drug SE: Thrush from antibiotic
Drug toxicity: Hepatotoxicity from methotrexate
Drug-drug interactions: seizure from
theophylline while taking EES
Drug overdose: seizure from excessive lidocaine
Intolerance: tinnitus after a small dose of ASA
Difficult to classify
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Certain drug reactions are hard to classify
due to a lack of definite immune reaction
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Cutaneous drug reactions: maculopapular
rash, erythroderma, exfoliative dermatitis,
fixed drug reactions
Specific drug hypersensitivity syndromes.
Non- Immune reactions
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Pseudo-allergic reactions – direct mast cell
degranulation by drugs like opiates, vanco, and
radio-contrast. Look like allergies, but no IgE
involved.
Idiosyncratic reactions – Aberrant reactions in a
small percentage (hemolysis from G6PD
deficiency)
Drug Intolerance – a lower threshold to the
normal pharmacologic action of a drug (tinnitus,
ASA)
Patient Risk factors for adverse
drug reaction
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General drug reactions:
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Female gender
Serious illness
Renal insuffiency
Liver disease
Polypharmacy
HIV infection
Herpes infection
Alcoholism
SLE
Hypersensitivity Risk Factors
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Female gender
Adult
HIV infection
Concomitant viral infection
Previous hypersensitivity to related drug
Genetic polymorphisms
SLE
Clinical Evaluation
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History: All prescription and nonprescription Rx and supplements taken in
the last month
Temporal relationships between onset of
taking and SX (Usually between 1 week
and 1 month unless previously sensitized)
History of previous drug exposures and
reactions
Physical Exam
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Look for signs and symptoms of
immediate and generalized reaction
Urticaria, laryngeal or upper airway
edema, wheezing, hypotension
Fever, mucous membrane lesions, LAD,
joint tenderness and swelling
Detailed skin examination
Cutaneous Symptoms of Drug
Hypersensitivity RXN
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Exanthematous or mobilliform eruption originating on
trunk- classic drug rash
Urticaria - IgE mediated
Purpura- vasculitis or drug induced thrombocytopenia
Maculopapular lesions on fingers, toes, or soles- serum
sickness
Blistering lesions – Stevens Johnson, TEN
Eczematous rash in sun exposed areas – photoallergic
Solitary, circumcised, raised lesion – fixed drug eruption
Papulovesicular, scaly lesion – contact dermatitis
Documentation
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Once diagnosis established by you or pt history,
D/C any drugs in the offending class
DOCUMENT allergy/hypersensitivity
Use alternate medicine in unrelated classes
Monitor clinical reaction to discontinuation and
switching
Use supportive therapy based on symptoms
References Drug Allergies
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Riedl. Adverse Drug Reactions: Types and
treatment Options. American Family Physician.
Vol. 68/ no.9 (Nov 1, 2003).
Allergy Testing
Types of allergy testing
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Patch (band aid impregnated with
antigen)
Prick: Percutaneous (Place a drop of
antigen and scratch it in)
Poke: Intra Dermal (Injection of antigen)
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Poke: IgE blood testing (RAST and ELISA)
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Why Test?
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In a patient whom avoidance and
antihistamine/ drug therapy has failed
Patients with life threatening anaphylaxis
without clear cause
If the answer will change your therapy.
Prick: Percutaneous testing
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For immediate type hypersensitivity to airborne
allergy, foods, insect stings, PCN:
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A drop of antigen is placed, and scratched into the
skin
15 min later wheal and flare are recorded.
Histamine and negative controls are also used to test
reactivity
3 mm greater than control is considered positive.
Can be done in an FP office setting
Percutaneous testing
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Antihistamines interfere with the skin reaction:
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1st generation stop 3 days before
Newer generation (allegra, etc) need to be stopped
10 days before
Anticholinergic agents, phenothiazines, tricyclic
agents all have antihistamine properties
H2 receptor agents (tagamet, Zantac) may be
stopped the day of testing.
Oral and inhaled steroids do not affect skin rxn
Airborne allergens

Percutaneous testing is used for a panel of
40 standard airborne allergens:



94% sensitivity and 84% specificity for clinical
upper respiratory symptoms
97% sensitivity and 81% specificity for lower
respiratory tract symptoms
Thus, a negative dermal test make
airborne allergy unlikely, but positive test
is not always clinically significant
Percutaneous - Food Allergy


Sensitivity is 76-98%
Specificity is 29-57% depending on the
food tested


(Positive test may not be clinically relevant).
Negative reactions make a IgE mediated
food allergy unlikely.
Poke: Intra-dermal testing


Used by allergy specialists, not FP’s.
More sensitive than percutaneous, but less
specific

Re-test hymenoptera venom and PCN allergy
testing if negative by percutaneous testing
Patch: Patch testing




For delayed type testing of skin irritants
Available at HCMC from Dr. Glesne in
dermatology
Good for testing contact irritants such as
latex, medications, fragrances,
preservatives, hair dyes, metals, resins
Can use to confirm anaphylactic milk
allergy without re-challenging.
Patch testing



Antigen is placed on a pad that is kept in
place for 24-72 hours
Used to detect Contact dermatitis
Patch testing has a small risk of systemic
reaction. (6 fatal reactions in 40 years)
Poke: RAST blood testing



Serum IgE measured by
radioallergosorbant testing (RAST)
Useful in kids <3 years, people with skin
conditions, or on medications that skin
testing is not possible
Tests are equally specific, but less
sensitive than skin testing
RAST

Useful for identifying common allergens





Pet dander
Dust mites
Pollens
molds
Food, venom, and drug allergy testing not
helpful through RAST
References Allergy Testing


Li. Allergy Testing. American Family
Physician. Vol. 66/ No.4 (April 15, 2002).
Kurowski. Food Allergies: Detection and
Management. AAFP. Vol 77, No 12, June
15, 2008.
Allergen
Immunotherapy
Allergen vaccine therapy
Allergen Immunotherapy



Also called vaccine therapy, as the purpose is to
modify the immune system
The goal is to reduce immunologic response to
triggers in the short term to decrease symptoms
Gradually increasing amounts of allergens are
injected to raise the patient’s tolerance
Allergen Immunotherapy



Is effective for stinging insect
hypersensitivity, allergic rhinitis, allergic
conjunctivitis, and allergic asthma
Not effect for atopic dermatitis, uritcaria,
allergic headaches
Is potentially dangerous for food or
antibiotic allergies.
Who should be referred?


Patients who have clinically relevant, well
defined allergic triggers that negatively
impact their quality of life or daily function
And, they do not attain relief with
avoidance and pharmacotherapy
Indications for Immunotherapy




Allergic rhinitis, conjunctivitis, or allergic
asthma
Patient wishes to avoid long term use of
antihistamines, or avoid SE’s
Cost of immunotherapy is cheaper than
the cost of long-term meds
History of allergy to hymenoptera, and IgE
antibodies
Benefits of Immunotherapy

In RCT’s of 3-4 years of immunotherapy:


marked reduction in allergy symptoms, medication
usage, and development of future allergies is found.
Immunotherapy for rhinitis in kids:



Can prevent later development of asthma
Earlier use in the course of allergies is thus
recommended
It can also prevent development of multiple allergies
later in life.
Scheduling



Allergen immunotherapy is typically based
on 18-27 dose increments weekly in a
build-up schedule
Maintenance is then made for about 6
months
Long term benefit is related to the
cumulative dose over time
Safety




Has been shown to be safe, but precautions are
necessary
Immediate availability of a physician to diagnose
and TX anaphylaxis should it occur
Observation period of 20-30 min is mandatory
after administration
1% of people have systemic reactions, and 35
deaths in over 50 million injections recorded
References: Allergen
Immunotherapy

Huggins. Allergen immunotherapy. American
Family Physician. Vol. 70/ No.4 9Aug 15, 2004).
Food Allergies
Delayed Hypersensitivity
Food allergy and intolerance


Food allergies + environmental allergens=
respiratory distress
The total burden on a body determines
the total histamine release and allergic SX
Food Allergy Incidence



20% of the population alters the diet from
a perceived adverse reaction to food.
Double-blind, placebo-controlled, oral
food challenge shows less people affected.
6% of infants and young children and 4%
of adults have true food allergy.
Incidence, cont.



12 million Americans have food allergies
30,000 visits to the ER are made for food
allergy each year.
The number of children with food allergies
doubled in the last 5 years.
IgE Food Allergies


90% of food allergies in kids are caused
by eggs, milk, soy, wheat, peanuts
90% in adults are from peanuts, shellfish
wheat, tree nuts, and fish
Food allergies

One study placed children with asthma on
a restricted food diet and found:


43% had significant reduction in their SX’s
c.w. 6% in the control group.
Atopic dermatitis and seasonal allergies
have similar results when common food
allergens are eliminated.
Food Allergen Cross-reactivity









A legume/ Other legume 5–10%
A tree nut/ Other tree nut 40%
A fish Other/ fish 50%
A shellfish/ Other shellfish 50–75%
A grain/ Other grains 20%
Egg/ Chicken 5%
Cow’s milk/ Beef 10%
Cow’s milk/ Goat’s milk > 90%
Cow’s milk/ Mare’s milk 4%
Fireman P. Atlas of Allergies and clinical immunology.
3rd ed. P.223. Scurlock AM, AW Burks. Food Hypersensitivity.
Pollen/Food Relationships




Ragweed: Melons, bananas,
cucumber, apples.
Birch: Apples, stone fruit,
apricot,cherry, plum, hazelnut, carrot
Mugwort: Celery, carrot, some spices
Grass: Potato, tomato, peach
Food Allergies


Few food allergies are IgE mediated –
nuts, shellfish, and fish can cause
anaphylaxis and need lifelong abstinence.
Milk, wheat, and other IgE allergies
generally disappear by age 3-8.
IgE Food Allergies

Can be life threatening

Diagnosing and eliminating them is essential –
use an allergist for assistance

IgE Food allergy reactions, anaphylaxis can even
occur from handling or breathing the food.

Epipens and instruction need to be given to a
patient with an IgE food allergy
Historical Factors in Food Allergy






History of a reaction within minutes of ingestion
Inadvertent ingestions produce the same
reaction
Lack of other possible explanations for the
reaction besides food allergy
Suspected food is known to be a higher risk for
food allergies
Symptoms onset in a young child
Personal or FH of atopy
Future Therapies



Researchers are working on oral tolerance – to give
small amounts of food antigen and increase it over time
to induce tolerance.
This is done homeopathically by an allergist in Lacrosse,
WI, Dr. Kroker at Allergy Associates of LaCrosse.
Alternative Allergy therapies with acupuncture points on
the spine are also available through a DC in Wayzata, Dr.
Claussen.
Prevention of Food Allergy

If a history atopy and food allergy:



Breastfeed until 1 year and delay solid food until after
6 months of age.
50% of women secrete what they eat into their
breast milk, thus fish, nuts, wheat, dairy, eggs, milk,
crustaceans should be avoided in families with high
likelihood of allergy.
The child’s diet should avoid fish, nuts, shellfish until
3-4 years.

Guidelines from the American College of Allergy, Asthma, and
Immunology
References Food Allergy


Food Introduction and Allergy Development in Infants.
American Family Physician. Vol. 74/ No.8 (Oct 15, 2006)
Myths and Facts about Food Allergies. American Family
Physician. Vol 74/ No. 11(Dec. 1, 2006)
Resources for patients



www.foodallergy.org
www.aafp.org/afp/20080615/1687ph.html
www.childfoodallergy.com
IgG Food Allergy
IgG Food Allergy




By far the most common cause of immune reactions to
food.
Average human eats 25 tons of food in a lifetime.
Intestinal lumen sorts “friend” from “foe” and it is a
wonder so few allergic reactions to food
Enterocytes are protected by tight junctions to allow only
small, non-antigenic peptides through.
Food Allergy cause

Food allergies arise from conditions that
make the intestinal tract permeable such
that large, antigenic peptides from food
get into the bloodstream that normally do
not have access.
Intestinal permeability – Common
Causes








NSAIDS
Steroids
PPI and antacid use
Infection (enteritis)
Antibiotic use wiping out healthy bacteria
Yeast and parasites in gut
Stress, alcohol, over-exercise
Food allergies perpetuate with inflammation
Symptoms of Delayed Food
Allergies




Symptoms are delayed: occur 1 hour-3 days
after consumption.
Can range from mild fatigue and joint aches,
nasal congestion, brain fog, to chronic
debilitating fatigue and disability.
Long-term intestinal permeability leads to malabsorption and vitamin and mineral deficiencies.
See handout on food allergies
Systems affected by Food Allergies













Mouth: Itching, swelling, choking
Gastrointestinal: Nausea, heartburn, regurgitation, pain
(sharp and dull), vomiting, diarrhea, bleeding
Skin: Hives, edema, eczema, acne, bullous and exfoliative
reactions
Lungs: Bronchitis, cough, asthma, pneumonia
Kidneys: Bleeding, loss of protein, hypertension, failure
Muscles: Fatigue, wasting, soreness
Joints: Swelling, pain, limitation of motion
CNS: Migraine, epilepsy, cognitive and developmental
Heart: Arterial spasm, palpitations, arrhythmia
Blood Vessels: Atherosclerosis, spasms (Raynaud's
phenomena), dilatation (anaphylaxis).
Complications










Recurrent infections: ears, sinuses,
Respiratory Infections
Asthma
Mouth breathing, malocclusion, snoring
Migraine headaches
Arthritis
Chronic fatigue
Hearing loss
Under-performance at school, work, athletics
Weight gain
Testing for food allergies




IgG blood testing is minimally available
Several labs exist – Metametrix, Genova
Diagnostics, Meridian Valley
Patients can get from the web
www.vrp.com
IgG reactivity in serum does not mean
clinical symptoms – must be tested
Food Allergy Elimination Diet




The gold standard to see if a patient has clinical
reactivity to a food and benefit from elimination
Generally a 3 week process of going down to a low
antigenic diet and systematically adding foods every 2-3
days to see if a reaction occurs.
The reaction may be IgE, IgG, or non-immune
“intolerance.” The important part is to know which foods
a person reacts to and eliminate them.
See h.o. on elimination diet
Natural Medicines for Allergy
Reduction



There are several natural products with research
and proven safety that can be suggested to be
used along with or in place of medications.
Patients may ask for natural alternatives, or may
find their symptoms are not helped by
elimination/ avoidance/ and pharmaceuticals.
It is a Family Physician’s responsibility to know
some evidence-based natural alternatives.
Quercetin





Yellow plant bioflavonoid found in onions,
apples, wine, black tea, broccoli, squash
One of the most bioactive flavonoids forming the
backbone for many others.
Acts as a mast cell stabilizer and leukotriene and
prostaglandin inhibitor
Has a wider spectrum of activity that Cromolyn
Placed in products with bromelain to increase
absorption
Bromelain




A proteolytic enzyme derived from pineapple
stems
Stimulates the release of anti-inflammatory
prostaglandins, and inhibits pro-inflammatory
PGs
Active in a broad range of pH, thus digests
protein in stomach and small intestine
People allergic to pineapple or bee stings should
avoid bromelain
Vitamin C



A natural anti-histamine – prevents
release and aids in detoxification of hist
2 grams daily lowered histamine levels by
38% in just 1 week in 1 study
Population studies show people with the
highest vit C levels have the lowest
incidence of allergies
Butterbur

Butterbur – Petasites hybridus is a shrub that decreases
histamine and leukotrienes.
Has been standardized in tablets as Petadolex,
Petaforce, and Tesalin.
Butterbur has been found in studies to be as effective as
Allegra and Zyrtec.
Use a PA free (pyrrolizidine alkaloid) as it is toxic to liver
and kidneys.
People with ragweed allergy may react to butterbur.

2004 Clinical & Exp Allergy, 2005 Phytotherapy Research




Other Possibly helpful nutrients



Nettles – antihistamine herb used in many
traditions. Good safety profile, little
evidence
Zinc, Vitamin A, Vitamin D all help with
mucosal barrier integrity and immune
system function
Netti Pot – Nasal rinse.
Diet





An anti-allergy, histamine reducing diet is
one that is made of:
unrefined, whole foods,
high in colorful fruits and vegetables,
high in plant protein,
low in dairy and meats.
Home

An anti-allergy home is one that has
continually filtered air (HEPA), regular
dusting, no carpeting and pets, natural,
non-toxic, scent-free household and
personal care products, no perfumes,
smoking, or lingering cooking odors,
moderate humidity and no mold.
Stress


Prolonged stress leading to adrenal dysfunction
and burn out, thus less output of cortisol can
also be a contributor in increase in allergy
symptoms in the adult.
Stress reduction and often herbs and nutrients
are necessary to increase cortisol and thus
reduce inflammation and symtpoms.
Environmental Control –for dust
mites






Cover pillows and mattresses with semipermeable covers
Wash sheets, pillowcases, comforters every 1-2
weeks in hot water (130 F)
Remove carpet in bedroom or on concrete
Avoid sleeping on upholstered furniture
Clean floors with a wet mop every week
The above measures reduce dust mite exposure
100-1000 fold within 1 month.
Indoor Humidity – for Mold and
Dust Mite




Reduce indoor humidity to 50% or less
Humidity at 35% or less prevents dust
mites from being able to thrive
Low humidity also prevents growth of
molds and spores
Use of a humidifier is necessary in most
climates seasonally
Other environmental Control






Wash hair before going to bed.
Fix roof, plumbing, basement leaks from mold
Limit outdoors w/high pollution and pollen
counts
Do not use dryer sheets, deoderizers, sprays,
plug-ins that emit a perfumed scent
Do not keep or burn scented candles
Change laundry detergent, body and hair wash
to an “allergy –free” brand
References

German. Environmental Control of Allergic
Diseases. American Family Physician. Vol. 66/
No. 3 (Aug 1, 2002).
Work-up of the allergic patient







Thorough history
Thorough FH for atopic disease
Dietary history - counsel
Home/ Environmental history - counsel
Rx pharmaceutical or nutraceutical
Consider referral to an allergist
EDUCATE!
Why allergies?

For an individual patient in order to help
them eliminate/prevent allergies we need
to investigate and modify key factors…




What new stressors have they had?
How are they eating? Any changes needed?
How are they sleeping?
How is their adrenal function/ cortisol output?
In Summary:

Allergies in all forms are systemic diseases
with genetic origin, and modifiable
mediators including early exposures,
environmental control , nutrition/ diet,
pharmaceutical and nutriceutical.
Patient Education Sources






Internet – allergy resources
EPIC patient teaching sheets
Allergist – Dr. Blumenthal at the U of MN
AAFP: Myths and facts about food allergies
Environmental Control of Food Allergies
Local clinic: Allergy relief Center of MN.
Objectives, In review




Presented a larger picture of the factors that
create and prevent allergies.
Reviewed the components of allergic disease –
genetics, immune reaction, environmental
triggers, and physical response.
Presented the pharmaceutical, vaccination, and
nutraceutical therapies for allergies
Offered resources for environmental control and
prevention of allergy development and triggers