Documents
Resources
Learning Center
Upload
Plans & pricing Sign in
Sign Out

Allergies Allergies Review Relief Prevention Patient Education

VIEWS: 96 PAGES: 200

									        Allergies:
Review, Relief, Prevention,
    Patient Education
      Kara Parker, MD
       Oct 15, 2009
                   Objectives
   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
   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
   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

   Toxins: Potentially injurious to any one,
    depending on dose.

   Allergens: Only injurious to predisposed
    individuals.
             Burden of disease
   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

   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
   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

   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:
   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:
   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
   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

   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.
   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
   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:
   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
   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:
   Acute: Rejection of a stressor (allergen)
   Chronic: Persistence of the acute phase
    response.
       Maladaptive – more detrimental than beneficial
       Self perpetuating
       Disrupts homeostasis
       Alters cellular physiology
       Destroys tissue
       Systemic response
            Allergic symptoms

   Recurrent Sneezing
   Nasal pruritis
   Nasal congestion
   Eye, throat, and ear tingling and pruritis
   Headache
   Sleep disturbance
   Concentration difficulties
Allergic Rhinitis
                  Allergic Rhinitis

   Can be seasonal, perennial, or
    occupational
   Is a systemic illness with constitutional
    symptoms
       Fatigue
       Malaise
       HA
         Associated Symptoms

   Excessive mucus production
   Congestion
   Sneezing paroxysm
   Watery eyes
   Nasal and ocular pruritis
             Allergic Rhinitis

   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
   Non- allergic includes:
       Vasomotor
       Hormonal
       Drug induced
       Structural
       Occupational (irritant)
       Eosinophilia syndrome
       Emotional rhinitis
        New Classification of AR

   Instead of seasonal (pollens molds) and
    perennial (indoor exposures)

   Use intermittent, persistent, mild,
    moderate, severe for allergic rhinitis
          PE suggestive of AR

   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

   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

   If nasal and constitutional symptoms are
    chronic, or last longer than 1 week after a
    viral cold and PE and story likely for AR:

       Check for sinusitis
       If negative, do a trial of antihistamines
       If a positive response, Dx allergic rhinitis
              Allergy Testing

   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

   Not routinely recommended

   Usually done by allergists or specialized
    dermatologists

   Will be covered in detail later.
        Conventional treatment

   1) Allergen avoidance
   2) Pharmacologic treatment
   3) Allergen Immunotherapy
             Allergen Avoidance
   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
   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

   Have minimal or no anti-cholinergic SE’s

   Do not readily cross the BBB

   Cardiotoxity from astimizole and
    terfenidine – both removed from market
          Nasal Decongestants
   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
   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

   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
   Quillen, Feller. Diagnosing Rhinitis: Allergic vs non-
    Allergic. 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

   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
   Dyspnea
   Uriticaria
   Angioedema
   Flushing
   Pruritis
   GI symptoms (nausea, vomiting, diarrhea)
   Syncope
   Hypotension
              Signs/SX cont

   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

   Observation needs to be 4-6 hours for
    mild symptoms

   Hospitalization and overnight course for
    moderate to severe symptoms
             Differential Diagnosis
   Gastrointestinal symptoms or cardiopulmonary collapse
    cause confusion
   Anyone presenting with unexplained syncope or shock
    needs consideration for anaphylaxis
   Other differential Diagnosis:
       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

   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
   Produces a range of reactions including
        asthma, urticaria, angioedema, anaphylactoid
        reactions.

   ASA sensitivity in 10% of people with
    asthma.

   Accounts for 3% of anaphylaxis
                     Penicillin
   Most common cause of anaphylaxis

   5/10,000 courses of PCN result in allergic
    reactions

   1/50,000 result in a fatal outcome

   75% of anaphylactic deaths result from PCN
          Hymenoptera stings

   40-100 deaths per year

   3% of the US population is sensitized

   Systemic reaction to insect sting and
    positive skin test = 50% risk of future
    stings.
                     Latex

   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

   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
   Focused examination – A,B,C’s
   Procure a stable airway, intubate if needed
   O2 as needed
   Get IV access
   Administer epinepherine 1:1,000
       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

   Antihistamines - benadryl
   Pressors
   Steroids – if protracted anaphylaxis is predicted
   Beta agonists
   Nebulized beta agonists if wheezing
   IVF
              Tx pneomonic

   Epinephrine IM
    Antihistamines PO, IM
    Steroids PO, IM, IV
    Inhaled b2-agonists, if wheezing; IV
    fluids, if hypotensive
               Anaphylaxis Labs

   When a diagnosis is unclear, laboratory
    evaluation may help

       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

   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

   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
   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
   Allergic inflammation of the membrane that lines
    the eyelids and covers the sclera

   Characterized by eye itching and burning and
    allergen exposure, usually cyclical.

   Absence of itching is likely not allergic

   Presence of personal of FH of allergies/atopy
    often present
             Other Symptoms

   Bilateral Distribution of:
   Mucoid stringy discharge
   Tearing
   Redness
   Mild eyelid swelling
   Mild to intense itching
            Allergic Conjunctivitis

   Differential diagnosis:
       Viral and bacterial conjunctivitis
       Fungal conjunctivitis
       Dry eyes
       Non-allergic irritation (dust, etc)
       Foreign body
    Allergic Conjunctivitis Causes

   Pollens – grasses, ragweed, trees
   Molds
   Animal dander and saliva
   Perfumes and cosmetics, lotions
   Air pollution
   Cigarette smoke
         Allergic conjunctivitis TX
   Allergen avoidance
   Cold, clean compress to eyes
   Drugs:
       Vasoconstrictors
       Antihistamine drops
       Topical NSAIDS
       Ocular mast cell stabilizers
       Oral antihistamines – faster than MCS
           Treatment, continued
   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:
       Stinging,
       eye pain, and
       photophobia are common
                     References
   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
   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

   Age
   Female gender
   Concurrent illness
   Previous hypersensitivity to related drugs
   (or to drugs in other classes)
               Drug reaction

   The majority (75-80%) of adverse drug
    reactions are characterized by predictable,
    non-immunological effects.

   The remaining 25% are caused by non-
    predictable effects that may or may not be
    immune related.
         Immune Mediated Drug
            Hypersensitivity
   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

   Type   I – immune mediated
   Type   II- cytotoxic
   Type   III- immune complex
   Type   IV- delayed, cell mediated
         Type I Hypersensitivity
   IgE mediated, anaphylactic

   Manifests as uritcaria, angioedema,
    bronchospasm, pruritis, vomiting, diarrhea,
    anaphylaxis

   Starts minutes to hours after exposure

   Ex: Anaphylaxis from B-lactam antibiotics
          Type II Hypersensitivity
   Cytotoxic mediated
   IgG or IgM Ab directed at drug hapten coated cells
   Arises 1-3 weeks after exposure

   Manifests in:
       hemolytic uremia,
       neutropenia,
       thrombocytopenia


   Ex: Hemolytic anemia from PCN, cephalosporins.
         Type III Hypersensitivity
   Immune complex mediated:
       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
   Delayed, cell mediated (cutaneous)
   MHC presentation of drug molecules to T cells
    with cytokine and inflammatory mediator release
   Manifests as:
       allergic contact dermatitis,
       maculopapular drug rash
   Begins 2-7 days after cutaneous drug exposure
   Ex: contact dermatitis from topical antihistamine
    exposure
         Laboratory evaluation

   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
   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

   Certain drug reactions are hard to classify
    due to a lack of definite immune reaction

       Cutaneous drug reactions: maculopapular
        rash, erythroderma, exfoliative dermatitis,
        fixed drug reactions
       Specific drug hypersensitivity syndromes.
        Non- Immune reactions
   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
   General drug reactions:
       Female gender
       Serious illness
       Renal insuffiency
       Liver disease
       Polypharmacy
       HIV infection
       Herpes infection
       Alcoholism
       SLE
     Hypersensitivity Risk Factors

   Female gender
   Adult
   HIV infection
   Concomitant viral infection
   Previous hypersensitivity to related drug
   Genetic polymorphisms
   SLE
            Clinical Evaluation
   History: All prescription and non-
    prescription 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

   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
   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
   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


   Riedl. Adverse Drug Reactions: Types and
    treatment Options. American Family Physician.
    Vol. 68/ no.9 (Nov 1, 2003).
Allergy Testing
        Types of allergy testing

   Patch (band aid impregnated with
    antigen)
   Prick: Percutaneous (Place a drop of
    antigen and scratch it in)
   Poke: Intra Dermal (Injection of antigen)

   Poke: IgE blood testing (RAST and ELISA)
                 Why Test?

   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
   For immediate type hypersensitivity to airborne
    allergy, foods, insect stings, PCN:
       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
   Antihistamines interfere with the skin reaction:
       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 mal-
    absorption 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 semi-
    permeable 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

								
To top