Immunology and AllergyTier 1Disease (DEADMAN)

Allergic disorders - food allergy

Description

Reproducible adverse immune response to a food protein
- Distinguish from food intolerance - non-immune, dose-dependent, no anaphylaxis risk (lactase deficiency, FODMAP, histamine)

Mechanistic types

	Mechanism	Onset	Features
IgE-mediated	Mast cell degranulation	Minutes to 2h	Urticaria, angioedema, vomiting, wheeze, anaphylaxis
Non-IgE (cell-mediated)	T-cell	Hours to days	FPIES (profuse vomiting 1-4h, pallor, shock), proctocolitis, enteropathy
Mixed	Both	Variable	Eosinophilic oesophagitis, atopic dermatitis

The big allergens

Children: milk, egg, peanut, tree nut, wheat, soy, sesame
Adults: peanut, tree nut, shellfish, fish
Pollen-food (oral allergy) syndrome - PR-10/profilin cross-reactivity
- Birch/grass pollen sensitised, itchy mouth with raw stone fruit, apple, carrot
- Destroyed by cooking; systemic reaction rare

~10% Australian infants at 12 months - highest documented prevalence worldwide
~5% older children, ~2-4% adults
Peanut ~3%, egg ~9% at 12 months
Rising incidence; later introduction of solids and low vitamin D latitude implicated
Food-related anaphylaxis admissions rising; fatalities rare (~1-3/yr in Australia)

Sensitisation -> allergen-specific IgE binds FcepsilonRI on mast cells and basophils
- Re-exposure -> cross-linking -> degranulation (histamine, tryptase) + newly synthesised leukotrienes/prostaglandins
Dual allergen exposure hypothesis
- Cutaneous exposure through an impaired barrier (filaggrin loss-of-function, eczema) -> sensitisation
- Early oral exposure -> tolerance
- -> eczema severity in infancy is the strongest risk factor
Oral tolerance depends on gut regulatory T cells and TGF-beta
Cofactors lower the reaction threshold: exercise, NSAIDs, alcohol, infection, menstruation
- Wheat-dependent exercise-induced anaphylaxis (omega-5 gliadin)
Alpha-gal syndrome - tick bite -> IgE to galactose-alpha-1,3-galactose -> delayed 3-6h anaphylaxis to mammalian meat

The history drives everything. Testing without a history generates false positives.

Clinical

A. Skin prick testing

B. Specific IgE (ImmunoCAP)

Use where SPT unavailable, skin disease, or antihistamines cannot be stopped
Magnitude correlates with likelihood of reaction, not severity
Component-resolved diagnostics
- Ara h 2 - peanut storage protein, predicts systemic reaction
- Ara h 8 (PR-10) - pollen cross-reactivity only, mild
- Omega-5 gliadin - WDEIA

C. Oral food challenge - the gold standard

What not to do

Total IgE, IgG/IgG4 food panels, hair analysis, kinesiology, VEGA - no diagnostic validity, cause harmful elimination diets
Do not screen asymptomatic children with panels - sensitisation is not allergy

A. Avoidance - the mainstay

Written allergen list, label reading (Australian PEAL labelling: the declared allergens must be in plain English)
Dietitian input to prevent nutritional deficiency, especially multiple exclusions
Avoidance does not accelerate resolution

B. Anaphylaxis preparedness

ASCIA Action Plan for every patient - personalised, given to school/childcare
Adrenaline autoinjector if: previous anaphylaxis, or food allergy plus asthma, or nut/seafood allergy with risk factors, or remote from care
- 150 mcg 7.5-20 kg; 300 mcg >20 kg; 500 mcg available for adults
- Train the patient and carers; check expiry
Manage asthma aggressively - poorly controlled asthma is the dominant risk factor for fatal food anaphylaxis

C. Prevention - primary

Introduce peanut and egg in the first year of life, ideally by 6-12 months, and continue regularly (LEAP, EAT)
- Deliberate delay increases risk. No need to delay for a family history
Treat infant eczema early and aggressively
Continue allergenic foods once introduced

D. Immunotherapy

Oral immunotherapy (peanut) desensitises but does not cure - protection lost if dosing stops
Palforzia licensed overseas; Australian access limited, largely specialist/trial-based
Not routine practice - avoidance plus adrenaline remains standard

E. Non-IgE

FPIES: acute episode needs IV fluid resuscitation and ondansetron, not adrenaline
EoE: PPI, swallowed topical steroid, elimination diet, dupilumab

Resolution rates - the key discriminator

Nut and seafood allergy persist into adulthood; egg and milk usually resolve in childhood
Baked (extensively heated) egg/milk tolerance predicts and may hasten resolution
Falling specific IgE and shrinking SPT wheal support re-challenge

Fatal anaphylaxis - risk factors

Adolescent/young adult, coexisting asthma, delayed adrenaline, peanut/tree nut, upright posture during the reaction
Deaths cluster where adrenaline was withheld or given late

Complications

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