Lec14Food Allergy Flashcards

1
Q

What are some things often confused with allergies?

A

toxic/pharmacologic causes

  • bacterial food poisoning
  • scromboid fish poisoning
  • caffeine
    intolerance: lactase deficiency
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2
Q

What is the pathogenesis of food allergy

A

Ingest food into gut, instead of getting Treg stimulation to produce regulatory cytokines [TGF-B, IL-10] —> either IgE or non IgE mediated response

    • TH2 cells generated and direct IgE antibodies
  • —- IgE antibodies specific to epitope on food protein bind mast cells [that have high affinity IgE receptors] and mast cells
  • —- Re-expsorue causes IgE cross linking –> mediators [ie histamine] released
  • —- IgE mediated response
    • OR T cells produce cytokines that cause allergic [eosinophilic] inflammation [IL-5]
  • —- non-IgE mediated response
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3
Q

What is IgG response in gut?

A
  • when soluble proteins pass through barriers [glycocalyx, epithelial cells, etc] they are processed in lamina propria
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4
Q

What is IgA response in gut?

A

When viruses or bacteria processed by M cells overlying Peyer’s patches

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5
Q

What allergy reactions traditionally IgE mediated?

A
  • urticaria angioedema
  • ashtma
  • rhinitis
  • GI anaphylaxis
  • oral allergy
  • system anaphylaxis or food associated/exercise induced anaphylaxis
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6
Q

What allergy rxns traditionally non-IgE mediated

A
  • enterocolitis
  • enteropathy
  • celiac
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7
Q

What allergies mixed?

A
  • eosinophilic esophagus

- atopic dermatitis

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8
Q

Symptoms of allergy

A
  • hives, sweeling itchy
  • vomit, diarrhea, pain, mouth symptoms
  • altered consciousness, poor pulse, low BP
  • throat closing, coughing, hoarse wheeze
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9
Q

Are IgE or non IgE faster rxn

A

IgE

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10
Q

Prick skin test

A
  • rapid, sensitive test to detect specific IgE
  • get wheal [bump] and flare [surrounding red]
  • histamine = positive control [makes blood vessels leaky]
  • salt water = negative control
  • must be off antihistamines
  • positive test does not prove symptomatic sensitivity just suggests likelihood
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11
Q

Serum Food-Specific IgE “RAST” Test

A
  • blood test to measure specific IgE
  • put protein of interest on matrix
  • add patient serum
  • wash
  • used secondary anti-IgE labeled antibody with marker
  • Measure fluoresence to see amount of IgE specific to protein [ex. almond]
  • less sensitive than prick skin test
  • not affected by antihistamine use
  • report level, class, percent of antibodies
  • if nevative means there is no IgE mediated allergy
  • if positive still not proof of symptomatic allergy
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12
Q

Why do some people with IgE positive RAST or skin test have no allergic symptoms? What factors involved

A
  • if cell mediated: may get positive skin but negative IgE test
  • Different amount of Ig: more Ig = more likely to have symptoms to allergy
  • Different affinity: if lower affinity Ig may not stick well to almond, don’t get symptoms
  • Different binding pattern: Ig that binds one part of protein may have bigger effect than Ig that binds another part
  • binds to protein that breaks down easily: then antibody might not really have time to see and interact with the antigen
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13
Q

How does digestion of protein antigen [ex peanut] affect allergic response?

A
  • antibody might bind to an epitope in its normal conformation
  • when antigen digested –> if epitope destroyed then antibody may no longer be able to bind properly
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14
Q

oral food challenge

A
  • food eaten gradually in increasing amount with physician supervising and emergency treatment on hand
  • open, single-blind, or double-blind/placebo controlled challenge
  • allows you to verify allergy/tolerance AND diagnose non-IgE mediated food allergy
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15
Q

Oral allergy syndrome [pollen-food syndrome]

A
  • oral syndrome of mouth itch
  • related to pollen allergy
  • usually no symptoms beyond mouth
  • cooking destroys protein
  • – do commercial skin test [cooked] vs fresh skin test
  • may be concentrated in peel
  • birch allergy: apple, plum, cherry, apricot
  • ragweed allergy: watermelon, melon
  • type of IgE mediated
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16
Q

3 Food Protein-Induced Enteric syndromes

A

non-IgE mediated

  • food induced enterocolitis syndrome
  • food induced enteropathy/malabsorption
  • benign eosinophilic proctitis
17
Q

food induced enterocolitis syndrome

A
  • age onset: 1 day - 9 months
  • duration: 9-18 months
  • features: diarrhea, bloody stool, injury to villi, edema, vomiting, failure to thrive
  • get high WBC count
  • cause: milk, soy, rice, oat
  • mech: reduced TGF beta receptor expression, increased TNF-alpha
18
Q

food induced enteropathy/malabsorption

A
  • onset: 2-18 months
  • duration: 18-36 months
  • failure to thrive emesis [vommitting], edema, diarrhea, blood stool, injury to villi
  • cause: milk, soy
19
Q

Benign eosinophilic proctitis

A
  • onset: 4 day - 4 months
  • duration: 6-9 months
  • features: maybe edema, diarrhea, blood stool
    no villous injury, no emesis/vommitting, resolves in a few months on its own
  • cause: breast feeding [milk]
20
Q

Atopic dermatitis

A
  • chronic, itchy skin rash
  • classic distribution on body
  • waxes and wanes
  • triggers: allergies, temp, emotion, irritants, infection
  • about 1/3 of kids have food allergy: egg, milk, wheat soy
  • mix of IgE and non-IgE mediated
21
Q

Allergic eosinophilic esophagitis [EOE]

A
  • mix of IgE and non-IgE mediated
  • onset: infancy to adulthood
  • symptoms: reflux esophagitis, vomiting, food refusal, abdominal pain, chest pain, sleep disturbance
  • foods implicated: milk, wheat, soy, egg, beef
  • diagnosis
  • – fails to respond to reflux meds
  • – endoscopy and biopsy of esophagus
  • – response to food elimination or steroids
  • furrows in esophagus, rings, white plaques that represent dead cells and eosinophils
22
Q

Hygiene hypothesis

A
  • we make the environment super clean
  • this tips the balance because the immune system doesn’t have enough to react to thus get immune attacking non-pathogens
23
Q

6 theories of food allergies

A
  • hygiene
  • delaying ingestion of allergens
  • exposures by non-ingestion routes
  • not enough vitamin D
  • obesity, unhealthy fats in diet, etc
  • how food is processed [ex oil in peanut butter at adjuvant for peanut allergy]
24
Q

Anti-IgE

A
  • engineered protein
  • attaches to IgE Fc region [if it was the variable region would induce anaphylaxis, thus can only bind free floating IgE because receptor IgE Fc is not available for binding]
  • inactivates IgE as long as it is being taken [need to keep administering it]
  • has shown to raise threshold of peanut allergy maybe
  • mech: anti IgE binds IgE and blocks it from reaching and binding mast cell to initiate inflammation
25
Q

Traditional chinese medicine methods

A
  • herbal remedies used for centuries

- FAHF2: stops peanut-induced anaphylaxis in sensitized mice

26
Q

What is FAHF-2

A

herbal chinese medicine remedy that stops peanut-induced anaphylaxis in sensitized mice

27
Q

2 main goals of food immunotherapy

A
  • provide protection from anaphylaxis

- restore permanent oral tolerance

28
Q

What is desensitization

A
  • temporarily increased threshold for food allergic reaction
  • protection from life-threatening anaphylaxis
  • affected by illness, exercise, menstruation, pollen season
  • dependent on regular intake of food [if you stop giving treatment will stop being desensitized]
29
Q

What is tolerance

A
  • permanent or long-term
  • independent of regular food intake or therapeutic agent
  • unaffected by illness, exercise, menstruation, pollen season
30
Q

Typical food challenge study routine

A
  • initial food challenge and escalation until desensitization
  • after 12 months stop treatment for 4-6 wks then challenge again and see if tolerance has developed
31
Q

Mechanistic studies during exposure therapy

A
  • skin tests get smaller
  • specific IgG increases
  • specific IgE increases then decreases
  • basophil activation decreases
  • T regulatory cells more active
32
Q

Epicutaneous Immunotherapy [EPIT]

A
  • skin exposure not likely to result in serious side effects

- epithelial langerhands cells may cause some regulatory or TH1 like response with chronic exposure

33
Q

Milk oral immunotherapy + Xolair [anti -IgE]

A
  • evaluatemilk OIT alone and together with xolair