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FOOD ALLERGYAND HYPERSENSITIVITY
Sitti Hajar , dermatologistMedical Faculty
Syiah Kuala University
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FOOD ALLERGYAND HYPERSENSITIVITY
INTRODUCTION
HISTORY OF FOOD ALLERGY
REVIEW OF BASIC IMMUNOLOGY OF ALLERGY
TYPES OF ADVERSE REACTIONS TO FOOD
DIAGNOSTIC FOR FOOD ALLERGY
TREATMENT OF FOOD ALLERGY
CONCLUSION
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INTRODUCTION
Alergy : antigens immune responses tissueinflammation and organ dysfunction.
Food allergy :
food immune mediated symptoms.
US: 25-30%, in children (cow milk 2.5%, eggs 2%,
peanuts 0.5-0.7%).
Internationally:2.5% of infants, 1.4-1.8% of adults.
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HISTORY OF FOOD ALLERGY
China (3000 B.c) :
cutaneous reactions caused by food
Hippocrates :
milk gastric distress and urticaria
Von Pirquet (1906) :introduced the concept of allergy
skin tests detect food allergies
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HISTORY OF FOOD ALLERGY
Rinkel (1934) :
developed the oral food challenge
Schloss, Rowe, and Coca :delayed food sensitivity
Dr. Carleton Lee (1958) :
serial endpoint skin testing responses tosinglefood antigens
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HISTORY OF FOOD ALLERGY
1963 :
provocation techniques
neutralization techniques
dietary management
treatment of food allergies
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BASIC IMMUNOLOGY OF
ALLERGY
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Immune System
Made up : cells (in the circulation & the bodytissues) chemical substances interacting andaffecting foreign molecules.
An antigen
The nonspecific immune response :reacts to broad categories of antigens
The specific immune response :develops differently in every individual
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Immune System
The specific immune response :
antigen activates specific lymphocytes
lymphocytes coordinate an immune response
eliminates the antigen
The immune response : humoral & cellular.
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Lymphocytes
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Lymphocytes
20% of total leukocytes
T cells :
cell mediated immunity and cytotoxicity regulate the immune system
B cells : differentiates and secrete immunoglobulin
presence of specific surface ab receptors antigen
Natural killer cells : large granular lymphocytes
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Lymphocytes
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Lymphocyt B NK Cell
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NK Cell
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Lymphocytes
T helper cells :
interacts and stimulates B cells
T suppressor cells :
antigen specific suppressor role
inhibit B-cell functions
T cytotoxic cells :
the destruction of infected or malignant cells
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Immunoglobulins
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Immunoglobulins
the primary effectors of the humoral immuneresponse
basic structure : the heavy chain : determines the ability of an antibody to bind
to cells confers immunoglobulin class
the light chains : determine the specific antigen binding site
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Immunoglobulins
Immunoglobulin E :
responsible for hypersensitivity reactions
bind to basophils and mast cells
Immunoglobulin M (10%) : activates the classic complement pathway assists IgA in defending external surfaces
Immunoglobulin A :
major immune barrier to antigen penetration
Immunoglobulin G (70-75 %) : Protective, and forms blocking antibodies
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Antigen Processing Cells
Antigens enters the body phagocytes engulf and destroy smaller fragments presenting these antigen fragments tolymphocytes lymphocyte T or B cell is activated
B cells produces and secretes antibody specific to theantigen, producing the sensitization.
T cell become a helper, suppressor, or cytotoxic cell.
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Antigen-Processing Cells
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Mediator Cells
Antigen antibody complexes mediator cells releasemolecules :
histamine
chemotactic factors :attract other leukocytes affect local tissues
leukotrienes :
control the development and duration of immunereactions
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Mediator Cells
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Mediator Cells
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Complement
The complement system :
classic and alternative pathways.
Complement :
Amplification and regulation of immuneinflammation.
Enhances uptake and removal of immunecomplexes by phagocytosis.
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Complement
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Hypersensitivity Reaction
Allergy is a malfunction of the immune system thatinvolve any immune effector cells.
Hypersensitivity reactions immune responses acting
inappropriately cause inflammatory reactions andtissue damage.
Hypersensitivity usually appears on subsequent contact.
Gell and Coombs classified into four classes of immunereactions.
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Type IImmediate Hypersensitivity
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Type IImmediate Hypersensitivity
T I
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Type IImmediate Hypersensitivity
Prevalence approximately a 5%.
Each exposure to the offending food produces
an immediate symptom response.
Often severe and can be life threatening.
Can result : urticaria, rhinitis, angioedema, andasthma, and anaphylaxis
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Type llCytotoxic Reactions
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Type llCytotoxic Reactions
Antibody binds antigen leads to :
phagocytosis
killer cell activity complement mediated lysis
Clinical :
hemolytic anemia, transfusion reactions, andrare cases of food reactions.
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Type IIIImmune Complex Reactions
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Type IIIImmune Complex Reactions
Formation of antigen antibody complexes withsubsequent tissue damage.
IgG + circulating antigens
macromolecularcomplexes precipitate in capillary beds,
binding and activating complement to producetissue inflammation.
Delayed in onset and prolonged in symptomproduction.
Most common causing food hypersensitivity.
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Type IVDelayed Type Hypersensitivity
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Type IVDelayed Type Hypersensitivity
T-cell mediated .
Response occurring 24-48 hours after contact.
Sensitization the cell activated by a newcontact with the antigen T cells release avariety of cytokines mobilize other
inflammatory cells produce a direct effect onthe target organ.
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Mixed Type Reactions
Mixtures of Gel and Coombs reaction types :
Circulating complexes.
Immunoglobulin (particularly IgE and IgG).
Complement activation.
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THEORY OF ACTION OFNEUTRALIZATION TREATMENT
Jerne :immune system negative feedback regulation.
This network turns on or turns off :antibody formation and the activities of Tcells.
Low doses of antigen regulatory system isshifted toward shutting off Ab 1 to theoriginal immunogen.
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THEORY OF ACTION OF NEUTRALIZATIONTREATMENT
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THEORY OF ACTION OFNEUTRALIZATION TREATMENT
Direct effect of antigen on T cells :Low dose antigen T-cell regulatorymechanism favors the suppression of antibody
production.
The nonimmunologic mechanism involvesprostaglandin production : cytoprotectiveeffects of prostaglandin (Robert et al).
Low dose antigen desensitization ofbasophils for histamine release.
O O C O O
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THEORY OF ACTION OFNEUTRALIZATION TREATMENT
Low dose antigen therapy :
Downregulating both B cell antibodyproduction and T-cell function.
Increasing intracellular cyclic adenosine
monophosphate levels.
Decreasing cell metabolism.
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TYPES OF ADVERSE
REACTIONS TO FOODS
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Food Intolerance
Nonimmunologic Reactions.
Anaphylactoid reactions :
Due to the nonimmune release of chemical mediatorscontained in foods .
Idiosyncraticreactions : Due to abnormal responses genetically predisposed
patients. Asthmatic patient reacting to salicylates.
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Food Intolerance
Digestive enzyme deficiencies :Lactase deficiency gastrointestinal symptoms.
Toxic reactions :Food components or additives and toxins released bymicrobes in food.
Pharmacologic reactions :Chemicals in foods produce drug like effects.
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Food Hypersensitivity
Penetration of antigen crossing the gut triggering the formation of specific antibodies .
Factors influencing food allergies : The permeability of the gut mucosa. Crossreactivity between a food and an
inhalant allergen.
Clinically : fixed food allergy and cyclic types.
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ADVERSE REACTIONS TO FOODS
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Fixed Food Allergy
IgE mediated responses.
Immediate reaction after contact with theallergen.
Sensitivity to the food usually persists foryears.
Symptom doesnt depend on the quantity offood eaten.
Present in various ways.
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Atopic Dermatitis
37% of children with moderate to severe atopicdermatitis have type I food allergy.
Most common : cow's milk, fish, and eggs .
Mechanism unrelated to IgE mediatedhistamine release also can trigger mast celldegranulation after the ingestion : alcohol,spicy foods, or additives.
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Asthma
Inhalation of airborne food antigens, steamfrom cooking food or also can be triggered byingestion of the offending food
Symptoms may include rhinoconjunctivitis,urticaria, laryngeal edema, and shock.
Foods : eggs, flour, cocoa, peanut, soy, garlic,tea, fish.
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Urticaria
Urticaria is a wheal and flare cutaneous reaction.
Contact urticaria :
cutaneous contact with prolonged handling of raw food,and occur around the mouth in children.
Angioedema (45% of the cases ):
nonpruritic swelling, sometimes painful, developingsuddenly and no more than 3 days.
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Oral Allergy Syndrome
Local IgE mediated mast cell activation swelling of the lips, tingling of the tongue andthroat, and blistering of the oral mucosa.
Associated with the ingestion of food crossreactwith their specific allergic inhalant (40% ).
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The Gastrointestinal Syndrome
Accompanied allergic manifestations in othertarget organs.
Symptoms :
abdominal cramps, nausea, vomiting, andwatery diarrhea, hypotension.
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Anaphylaxis
Death : respiratory or cardiac failure.
Clinicaly :
Early stages : urticaria, angioedema, bronchospasm,laryngeal edema.
Gastrointestinal tract : nausea, vomiting, diarrhea.
Cardiovascular : hypotension, dysrhythmia, collapse.
Factors associated severe reaction : Asthma. History of previous severe reactions. Failure to initiate therapy expeditiously.
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Cyclic Food Allergy
IgG mediated, type III immune complex disease (6O%to 80% of food sensitivity).
Dose and frequency related.
antigens immune complexes
frequency sensitivity
More often IgG forms immune complexformation.
Omission of the food antibody levels andimmune complexes symptoms.
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Stage of Cyclic Food Allergy
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DIAGNOSTIC
FOR FOOD ALLERGY
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HISTORY
Diagnosis depends on a patient's history.
Actual diet habits, time of ingestion.
Time of any symptoms observed.
Record any improvement of symptoms.
Analyzes : frequently eaten foods and symptomproduction.
Most people tend to be habit eaters, the hidden foodsare an universal problem.
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HISTORY
Problem : hidden food, allergic crossreactions
between closely related foods .
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Signs and Symptoms
Depend on : fixed or cyclic.
Fixed allergy :
Obvious signs and symptoms.
Symptoms are secondary to release of histamine,preformed mediators, and the late phase reaction.
Patients can not identify what food is causing :
mixture of foods
chronic allergy conditions
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Signs and Symptoms
Cyclic food allergy :
More complex and difficult to recognize.
Secondary to the slow accumulation ofimmune complexes in the capillary beds oftarget organs.
Symptoms depends on frequency and theamount of antigen consumed.
There are many common symptoms andsigns .
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Neurologic Symptoms
Neurologic symptoms :
headaches
learning disabilities
forgetfulness
short attention
insomnia
even seizures can be food triggered
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Ophthalmologic Symptoms
Mild symptoms :pruritus, stinging, (conjunctival, eyelid,periorbital, lid) edema with itching, scaling,and erythema.
Severe symptoms :tearing, burning, discharge, photophobia,rough tarsal mucosa, blurred vision, the
cornea should not be inflamed, or eroded.
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Otologic Symptoms
External : chronic otitis externa, narrowed earcanals, red auricles, scaling.
Middle ear : pressure sensation, lancinatingpains, otitis media with effusion, persistentotorrhea.
Inner ear : dizziness, disequilibrium, tinnitus,
and dull ear pain.
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Nasal Symptoms
Nasal obstruction
Voice change, Snoring
Sleep disturbance
Edema of the turbinates Rhinorrhea
Thick postnasal discharge
Crusting
Pruritus, Sneezing Decreased olfaction
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Oral Symptoms
Pruritus oral, perioral, and palatal.
Dry mouth.
Halitosis.
Geographic tongue.
Angioedema of the lips and oral mucosa.
Pharyngeal and Laryngeal
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Pharyngeal and LaryngealSymptoms
chronic sore throat
pharyngitis
chronic throat clearing
perception of a lump in throat enlarged lateral pharyngeal bands and
posterior pharyngeal lymphoid islands (due topostnasal drip)
laryngeal edema with intermittent hoarseness
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Pulmonary Symptoms
chronic cough
shortness of breath
chest tightness
chest pain with breathing
Wheezing
thick-tenacious-colorless sputum
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Gastrointestinal Symptoms
intermittent abdominal pain
vomiting
diarrhea
abdominal distention
constipation
pruritus ani
perirectal inflammation ("burned butt") acute cramps
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Genitourinary Symptoms
Enuresis
Pruritic
Vaginitis
Food or inhalant induced allergic nephroticsyndrome
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Musculoskeletal Symptoms
Arthralgias
Myalgias
Stiffness
Erythema or edema over joints
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The Skin Symptoms
Atopic dermatitis and eczema.
Urticaria.
Angioedema.
The Id reaction.
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DIAGNOSTIC TECHNIQUES
FIXED FOOD ALLERGY
S ifi I l b li E T ti
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Specific Immunoglobulin E Testing
History : serious reaction, significant asthma.
Low sensitivity results :
Commonly are seen without history foodallergic.
High sensitivity results :
Significant symptoms will be produced ifthat food is ingested. Those foods should be permanently avoided.
P i k T t
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Prick Tests
Lewis and Grant (1926), and Pepys (1970s).
Specific, easily, and infrequently cause systemic allergicreactions.
Variations : precisely reproducing the depth ofpenetration, amount of force used, and the amount ofskin lifting.
Correlations : 85% to 90% (in vivo tests), 81% to 89%(intradermal skin endpoint titration tests).
Patch Tests
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Patch Tests
Detect delayed allergic reactions.
Allergens are applied to the intact skin occlusive dressing allowed to react.
Variations of patch testing : skin preparation technique antigen dose
method of antigen solubilization the type of occlusion
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DIAGNOSTIC TECHNIQUES
CYCLIC FOOD ALLERGY
In Vit o Food Tests
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In Vitro Food Tests
Cytotoxic test .
IgG and IgG4 in vitro assays.
The antigen leukocyte antibody test.
The ELISA activated cell test.
Basophil histamine release tests.
Positive results should be corroborated by oralfood challenge.
Oral Challenge Test
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Oral Challenge Test
The oral challenge test :
Dietary analysis.
Elimination of a specific food for 4 to 5 days.
Ingestion of that food in large amounts.
Difficulty : only one food can be tested at a time.
Easier to perform and more closely mimics normal food
the open, unblinded oral challenge.
Rechallenge
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Rechallenge
Initial avoidance period of 2 or more months rechallenge produce no symptoms rotatedfood.
Positive food should be avoided for severalmonths another challenge no reaction, oruntil 2 years of avoidance.
Positif after 2 years fixed food allergen
lifelong avoidance.
d k f d l
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Food Skin Testing Safety Guidelines
Never test : food fixed allergy.
Test only for foods on a regular basis.
Carefully for a history of any past seriousallergic reaction.
All foods to be tested must have been eaten
within 24hours of testing.
Consider IgE in vitro testing.
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TREATMENT OF FOOD ALLERGY
TREATMENT OF FOOD ALLERGY
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TREATMENT OF FOOD ALLERGY
Medical Care.
Education.
Consultations.
Elimination of food allergen.
Neutralization.
Avoid high-risk situations.
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Education
Education is of paramount importance.
Resource information by contacting the
Food Allergy and Anaphylaxis Network (toll-free
phone number is 800-929-4040) International Food Information Council (phone
number is 202-296-6540 and email address [email protected]).
Remember that appropriate restriction of the relevantfood allergen(s) is the only current effective therapy.
Medication
http://www.foodallergy.org/http://www.ific.org/http://www.ific.org/http://www.ific.org/http://www.ific.org/http://www.ific.org/http://www.ific.org/http://www.ific.org/http://www.ific.org/http://www.foodallergy.org/http://www.foodallergy.org/http://www.foodallergy.org/http://www.foodallergy.org/http://www.foodallergy.org/http://www.foodallergy.org/http://www.foodallergy.org/http://www.foodallergy.org/http://www.foodallergy.org/7/29/2019 ALLERGY n Food Allergy (Dr Siti Hajar Sp.kk)
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Medication
Medication : accidental may occur.
For patients with mild reaction :
treatment may be limited to an oral antihistamine.
For patient with significant systemic symptoms :
the treatment of choice is epinephrine injection.
Medical therapy of food allergen induced allergicreactions :
the use of antianaphylactic agents, antihistamines,bronchodilators, and corticosteroids is suggested.
COMBINING
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DIETS AND NEUTRALIZATION
The best treatment is elimination of the food :
Fixed food allergy : eliminated indefinitely.
Cyclic food allergy : eliminated for several months reintroduction (a rotary, diversified diet).
Neutralization immunotherapy + the best possible diet :
Allergies to ubiquitous foods.
Cannot eliminate those foods from the diet.
Difficult to rotate in the diet or to eliminate.
CONCLUSION
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CONCLUSION
True food allergies are those reactions that occurbecause of the activity of the immune system whenexposed to sensitizing foods.
Clinically, true food allergies occur in two very differenttypes: immediate, fixed reactions, and delayed, cyclicreactions.
Fixed food allergies develop rapidly after food exposure,and therefore usually are easy to diagnose.
CONCLUSION
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CONCLUSION
Conversely, cyclic food allergies often develop slowly andvary with both the quantity and frequency with whichallergenic foods' are eaten.
It is important to learn about cyclic food allergiesbecause they represent most of the clinically observedfood allergies, and are a very important cause oftreatable chronic allergy symptoms.
Understanding the clinical behavior of cyclic food
allergies allows the physician and patient to cooperatefor both diagnosis and successful intervention..
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THANK YOU