food allergy Flashcards
Food Allergy:
an abnormal immunologic response to a food protein
Food Intolerance:
result of nonimmunological mechanisms
Food Sensi/vity:
generic term referring to a troublesome reac-on aCer the inges-on of a food
Categories Adverse Food Reac-ons • Immune Mediated:
Food Allergy and Celiac Disease IgE Mediated - anaphylaxis, oral allergy syndrome Non-IgE Mediated – enterocoli-s, food protein-induced proctocoli-s Mixed IgE and non IgE Mediated –, eosinophilic esophagi-s, eosinophilic gastroenteri-s
• Non-Immune Mediated:
Food Intolerance Metabolic – Lactose Intolerance Pharmacologic – Caffeine Toxic – fish toxin Idiopathic - sulfites
IgE
key immunoglobin in allergy
Immunological process in an allergic reac-on involves ac-va-on of the immune system in response to a ‘foreign’ an-gen (protein) and the produc-on and release of adverse reac-ve chemicals that act on body -ssues to produce symptoms of allergy
Immunological Process
When a foreign an-gen enters the body, lymphocytes are ac-vated. • 2 types lymphocytes à T cells: controllers of the immune system -trigger a series of immunological reac-ons, mediated by cytokines. • There are two subclasses of T-helper cells • Type 1: Th1 • Type 2: Th2 • Th1 triggers the protec’ve response to a pathogen such as a virus or bacterium -IgM, IgG, IgA an-bodies are produced • Th2 is responsible for the IgE-mediated hypersensi’vity reac’on (allergy) -IgE an-bodies are produced
Immunological Process • Cytokines (the “control chemicals” of the immune system) are released • Each subclass produces a different set of cytokines • The types of cytokines generated determine the resul-ng immune response ie: Th2(IL-4, IL-13) à B cells: an-body secre-ng cells memory cells
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Allergic Response
-Mast cell or ‘allergic cell’ -IgE molecules are bound to surface of the mast cell -uniqueness of the mast cell is __________________ -When an allergen specific with IgE molecules is in contact: -‘degranula-on’ occurs: a series of reac-ons–releasing wide array of molecules ie: histamine, serotonin, (platelet ac-va-ng factor) PAF, leukotrienes, prostaglandins -
Pathogenesis
Ingestion of food à “initiatial sensitization” stimulates produc-on of IgE an-bodies à binds to -ssue basophils and mast cells. • Upon “subsequent ingestion -> binds to specific IgE an-bodies -triggers release of mediators (ie: histamine, or prostaglandins and leukotrienes causing “clinical responseà allergic symptoms)
complex interplay of environmental influence and gene-cs underlying the immunopathogenesis • microbiome “internal” environmental exposure
Risk Factors
Hygiene Hypothesis • Increased pollu-on -cofactor (not specific) • Family History • Time of food introduc-on
Prevalenc
Food allergy common in N.A and western countries • Children (<3yrs. of age) assessed by food challenge: affects 2-10% of popula-on • 5% children: - ⇪ prevalence between 1 ½ - 3 yr. olds 3-4% adults - self repor-ng ⇪ • 18% increase of food allergy prevalence b/w: 1997-2007. • Israeli children less likely to have peanut allergy vs. Jewish children in UK
Symptoms
- skin and mucous membranes :eczema, hives, itching, swelling of the mouth, face
2. diges-ve tract
:abdominal pain/bloating nausea, vomiting diarrhea constipation
3. respiratory tract
itchy watery eyes, hay fever, throat tightening
4. nervous system
- headache, irritability dizziness, dark circles under eyes
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Food Allergens
à almost any food can potentially licit an allergic reaction
• Rela-vely small # of allergens cause a high propor-on of food allergy (Evidence B)
• Most Common: cow’s milk, soy, wheat, egg, peanut, tree nuts, finned fish, shellfish, sesame Children: < 3 yrs. of age: Cow’s milk, egg, wheat, soy, peanut/treenuts Adults: peanut/treenut, shellfish
• Popula-on of ‘standard risk’ infants or infants with a family history of a 1st degree rela-ve with atopy con-nue to breasqeed while they are introduced to complementary foods, including commonly allergenic foods, at about 6 months of age. • Importance for food introduc-on to infants in their 6th month -iron content
developementally
immature gi
- - • “High risk” –infants with severe eczema or egg allergy – rec. to consult a physician/allergist for tes-ng/diagnosis of allergy including food introduc-on
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diagnosis
Diagnosis • Comprehensive medical history / Physical exam -rule out other medical condi-ons -include symptom diary of adverse reac-ons to foods
• Skin tests • Serum specific IgE tes-ng • Test results alone à not diagnos-c -focus on foods provoking reac-on Evidence B) • Oral Food Challenge for IgE mediated ( Evidence: A) • Elimina-on diet; food/symptom diary (Evidence D)
Skin Tests
Serum specific IgE skin tests > inflammatory mediators • Measures of ‘wheal and flare’ • size of “wheal and flare” reac-on in the skin. • size measured posi-ve 1 to 3+ • diameter > 3mm’s + • Foods with higher predic-ve accuracy: egg, fish, tree nuts, milk wheat and peanuts
False Posi-ve Tests
-difference is the form which food is applied to the skin compared to immune cells in diges-ve tract • -skin mast cells by s-muli don’t degranulate the mast cells in the diges-ve tract Ie: raw form in extracted may be degraded during cooking
gastric acid and digestion enzymes can degrade antigens
Serum Specific Tests
blood tests indicators of probable sensi-za-on to an allergen Ie: Radioallergosorbent test (RAST) Enzyme-linked Immunosorbent Assay • sensi-vity broader range than skin tests • classified in mul-ple classes to increase predic-ve values of test -varied correla-on b/w severity of allergic response and an-bodies in blood • Clinical hx., level of posi-ve result also influence relevance of test
Unproven Tests
IE: Allergen specific IgG measurement
Inaccurate tes-ng, creates false diagnosis, inappropriate guidelines and unbalanced diet plans suggested (Evidence C)
Anaphylaxis
Acute, systemic, severe, poten-ally fatal reac-on • occurs à minutes à up to 2 hrs. • Any food can trigger anaphylaxis • Pathophysiology: Mediated by immunoglobulin (IgE) à leads to mast cell and basophil ac-va-on - subsequent quick release of inflammatory mediators ie: histamine, leukotrienes, prostaglandins
Pathophysiology of Anaphylaxis
Systemis vasodialation of blood vessels - sudden severe decrease of blood pressure
In the lungs edema of the mucosa and constriction of bronchiiole - obstructing air flow
Second Phase: Biphasic
Treatment of Anaphylaxis
Self-Injectable Epinephrine (adrenalin) immediately- 1st line management (Evidence C) • An-histamines (Benadryl)-block the response of -ssues to histamine • Transport to hospital • Hospital: O2 and IV fluids to stabilize • Other: Steroids (Prednisone), inhaled beta 2 agonists, an-histamines
Exercise-Induced Anaphylaxis
Defini/on: • When a specific food allergen triggers anaphylaxis aCer or during exercise • Occurs up to 2 hrs. aCer ea-ng • exerciseà hives, itching, SOB, low blood pressure
Proposed mechanism histamine and other mediators from mast cells • Exercise triggers the poten-al for release of à • Factors involved? Ie: Exercise, NSAID’s, weather, stress, menstrual cycle • Which foods affect? Ie: wheat, celery, shellfish, chicken, peaches, nuts,
