allergy n food allergy (dr siti hajar sp.kk)

7/29/2019 ALLERGY n Food Allergy (Dr Siti Hajar Sp.kk)

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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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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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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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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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T I


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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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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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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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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
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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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allergy n food allergy (dr siti hajar sp.kk)

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