Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Diagnose immediate food allergy from a reproducible clinical history, use targeted sensitisation testing correctly, distinguish allergy from tolerance and build safe avoidance, nutrition, emergency and school plans.
Take an allergy-focused history before testing. Record the exact ingredient and brand, raw or cooked form, amount, time to first symptom, skin, airway, breathing, circulation and gastrointestinal features, duration, treatment and reproducibility. Ask whether the food was previously tolerated and what has been eaten safely since. Review eczema, asthma, rhinitis, family atopy and exercise, infection or medicine cofactors.
Immediate hives or swelling alone suggests IgE-mediated allergy but does not predict the next reaction's severity. Anaphylaxis is defined by dangerous airway, breathing or circulation compromise, usually with rapid onset; skin signs can be absent. Isolated perioral redness from irritant contact and vomiting from texture aversion require different reasoning.
Skin-prick and serum specific-IgE tests measure sensitisation. Select the suspected food rather than a panel and use trained services with valid extracts and controls. Component-resolved testing can distinguish stable storage proteins from pollen-related cross-reactivity in selected peanut or tree-nut questions, but no result replaces clinical context.
Immune sensitisation to stable or labile food proteins permits allergen-specific IgE to bind mast cells and basophils before clinical exposure.
Cow's milk, hen's egg, peanut, tree nuts, wheat, sesame, fish and shellfish account for most clinically important childhood reactions.
Moderate or severe eczema, especially in infancy, permits cutaneous allergen exposure and is associated with later IgE-mediated food allergy.
Exercise, infection, NSAIDs, alcohol in older adolescents or menstruation can lower reaction threshold and explain inconsistent episodes.
Allergen binds adjacent mast-cell-bound IgE molecules, triggering rapid release of histamine, tryptase, leukotrienes and other mediators.
Vasodilation, capillary leak, bronchoconstriction, mucosal oedema, itch and gastrointestinal smooth-muscle activation create the acute reaction phenotype.
Dose, food processing, digestion and cofactor exposure change how much allergen reaches immune targets and whether symptoms occur.
Milk and egg allergy commonly resolves with age, particularly to baked forms, while peanut and tree-nut allergy more often persists.
Migratory urticaria, flushing and lip or eyelid angioedema within minutes of eating supports mast-cell mediator release.
Hoarse voice, stridor, persistent cough, wheeze or hypoxia after exposure indicates anaphylaxis requiring immediate adrenaline.
Rapid repetitive vomiting or severe abdominal pain can accompany IgE allergy, especially when combined with skin or respiratory signs.
Immediate mouth and throat itch to raw plant foods with tolerance when cooked suggests labile pollen-cross-reactive proteins.
A positive test in a child who eats a normal portion without symptoms demonstrates tolerance and should not trigger exclusion.
Delayed vomiting, diarrhoea, blood or faltering growth hours to days later lacks immediate mast-cell skin and respiratory features.
Lactose malabsorption, pharmacological food effects and fermentable carbohydrate symptoms are dose-related and do not involve allergen-specific IgE.
Urticaria and vomiting during infection can coincide with eating and create a false food association without reproducible exposure timing.
Near-daily migratory wheals for more than six weeks are usually spontaneous or autoimmune rather than caused by repeatedly eaten foods.
Chronic dysphagia, food sticking, reflux-like symptoms or feeding aversion reflects oesophageal eosinophilic inflammation requiring endoscopy and biopsy.
Rapid mediator release can obstruct the airway, impair ventilation and collapse circulation, sometimes without urticaria or angioedema.
Unsupervised exclusion of milk, egg, wheat or multiple foods can impair energy, protein, calcium, vitamin and growth requirements.
Hidden ingredients, cross-contact, unclear labels and inconsistent school procedures create avoidable reactions outside the home and during travel.
Fear of exposure can impair eating, school, travel and social development even when objective reaction risk is lower.
A child who regularly eats a normal portion without symptoms is not clinically allergic merely because sensitisation is detected.
Heat destroys some labile allergens but not stable storage proteins, explaining tolerance of baked milk or pollen-related cooked fruit.
Skin-test diameter estimates probability of reaction, not how dangerous the next accidental exposure will be.
Testing foods without a history identifies sensitisation and often converts a diverse safe diet into unnecessary avoidance.
Clear responsibilities, accessible medicine and rehearsal reduce delay more effectively than a form filed away unread.
Diagnosing allergy from a positive test alone.
Ordering broad food panels without a clinical hypothesis.
Using IgG or alternative commercial intolerance tests.
Removing multiple staple foods without dietetic replacement.
Letting antihistamine delay adrenaline in anaphylaxis.
Advising home challenge after a convincing immediate reaction.
Forgetting asthma and school emergency planning.
Your practice draft is saved in this browser.
A child eats a full serving of peanut weekly without symptoms but has a low positive peanut-specific IgE found on a broad panel. What is the best interpretation?
National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Management removes the allergen while protecting nutrition and ordinary childhood. Teach label reading, precautionary-allergen interpretation, cross-contact prevention, restaurant communication and age-appropriate self-advocacy. Supply school with a current written plan, named devices, expiry checks and trained staff. Children should not be isolated from activities solely because food allergy exists.
Follow-up reviews accidental reactions, asthma, growth, dietary diversity and changing test or challenge probability. Do not test repeatedly without a clinical question. For milk or egg, falling sensitisation and tolerated baked forms may support supervised progression. Persistent peanut, nut, fish or shellfish allergy requires transition planning and adolescent risk counselling.