Food allergy diagnosis and oral food challenge — branching viva

Examiner: Opening question

Examiner: A 9-month-old boy with severe atopic dermatitis is referred to you for "food allergy testing" before introducing solids. His mother wants a comprehensive allergy panel. Take me through your approach. [1]

Model answer: [1]

My first step is to take a structured clinical history rather than order a panel. I need to know whether this child has had any acute reactions to foods already introduced — the six key elements are: what food, how much, when (timing from ingestion), what happened (specific symptoms by organ system), reproducibility, and cofactors such as exercise or illness. [1]

A broad food allergy panel without a supporting clinical history will generate false positives in approximately 30 to 50% of atopic children, because sensitisation without clinical allergy is common. Each false positive becomes a dietary restriction, a nutritional risk, and a psychological burden. So I would not order a panel — I would direct testing only to foods identified by the clinical history. [5][2]

Examiner: Branching — What if the history is negative?

Examiner: The history is negative — no acute reactions. He has eczema but has tolerated breast milk and rice cereal. What is your recommendation for allergenic food introduction? [6]

Model answer: [2]

This child is at high risk for food allergy because severe atopic dermatitis is the strongest single predictor. But the approach is not to test and avoid — it is to introduce early and maintain regular exposure. The dual-allergen-exposure hypothesis explains why: cutaneous exposure to food allergens through disrupted skin barrier drives Th2 skewing and IgE sensitisation, while early oral exposure promotes tolerance. [2]

The LEAP trial provided the definitive evidence: high-risk infants randomised to early peanut consumption from 4 to 11 months had an 80% reduction in peanut allergy at age 5 compared to avoidance. [3]

My recommendation, consistent with the 2017 NIAID addendum and ASCIA guidelines, is: introduce allergenic foods — including peanut, egg, and cow's milk products — from around 6 months, not later. Do not delay introduction; there is no evidence that delayed introduction prevents allergy and substantial evidence that it increases risk. Once introduced, maintain regular inclusion in the diet (2-3 times per week). For peanut specifically in high-risk infants, the addendum suggests either direct home introduction or evaluation by SPT followed by supervised introduction or OFC depending on the result. [6][3]

Examiner: Probe — Interpretation of SPT

Examiner: The mother insists on an SPT before introducing peanut. The SPT wheal to peanut is 4 mm. What does this mean? [1]

Model answer: [1]

A 4 mm wheal is positive — it is above the 3 mm positive cutoff — but it is well below the 95% positive predictive value threshold of 8 mm for peanut in young children. This means the child is sensitised (he has peanut-specific IgE) but I cannot conclude from this result alone that he has clinical peanut allergy. Approximately 50% of sensitised children tolerate the food on challenge. [1][4][5]

My next step would be component-resolved diagnostics — specifically IgE to Ara h 2, the 2S albumin storage protein that is the most predictive single component for clinical peanut allergy. If Ara h 2 is negative, the sensitisation is likely to a cross-reactive component (such as Ara h 8, which cross-reacts with birch pollen and typically produces only oral allergy syndrome), and the child is likely to tolerate peanut. If Ara h 2 is positive, the probability of clinical allergy is substantially higher. [5][2]

If Ara h 2 is also ambiguous, I would proceed to an oral food challenge — an open challenge in this low-risk setting, with a supervised escalating-dose protocol under medical observation. [4][1]

Examiner: Branching — Oral food challenge protocol

Examiner: Describe the oral food challenge protocol you would use. [4]

Model answer: [4]

First, the pre-challenge assessment: confirm no contraindication (uncontrolled asthma, acute illness, recent antihistamine use), establish informed consent, record baseline vital signs, and ensure the environment has IV access capability, IM adrenaline, oxygen, nebulised bronchodilators, and trained staff. [4][1]

The protocol follows the AAAAI-EAACI PRACTALL consensus: the total challenge dose is a serving-equivalent — for peanut, approximately 4 to 8 grams of protein (roughly 2 teaspoons of peanut butter). Start with a small initial dose, approximately 1 to 5% of the total. Administer escalating doses at 15 to 20 minute intervals, typically in 5 to 10 steps. After each dose, assess for objective signs of reaction: urticaria, angioedema, vomiting, wheeze, cough, hypotension. Stop the challenge if any objective reaction occurs (treat per anaphylaxis protocol), if the total dose is reached without reaction (negative result), or if safety concerns arise. After the final dose, observe the child for 1 to 2 hours. [4][1]

For a DBPCFC, neither the family nor the supervising clinician knows whether the active or placebo is being given — this eliminates reporting bias and is the gold standard for research and ambiguous cases. For routine clinical use in a low-risk child like this, an open challenge is appropriate. [4]

Examiner: Corner — FPIES

Examiner: The mother mentions that at 6 months, the child had profuse vomiting and became floppy and pale 2 hours after his first taste of yogurt. She was told it was a "stomach bug." What else are you thinking? [2]

Model answer: [2]

That is a classic presentation of food protein-induced enterocolitis syndrome (FPIES) — a non-IgE-mediated food allergy. The key features are: delayed onset (1 to 4 hours after ingestion), profuse projectile vomiting, lethargy and pallor, and reproducibility on re-exposure. Cow's milk is one of the most common FPIES triggers, along with soy, rice, and oats. FPIES frequently mimics sepsis or acute gastroenteritis and is often initially misdiagnosed. [2]

The diagnostic approach for FPIES is fundamentally different from IgE-mediated allergy: the SPT and serum specific IgE are characteristically negative. The diagnosis is made by a consistent clinical history plus elimination and supervised oral re-challenge — typically after a period of strict avoidance, a medically supervised re-challenge reproduces the delayed vomiting and confirms the diagnosis. [2]

This child should avoid cow's milk protein in all forms (including yogurt) until FPIES has been formally assessed and a supervised re-challenge is planned, typically at 12 to 18 months of age when many children have outgrown the condition. [2]

Examiner: Closing — Counselling

Examiner: How would you counsel this mother about the difference between the FPIES reaction and the IgE-mediated pathway? [1]

Model answer: [1]

I would explain that her child has two different types of immune response to food, and they require different management. The delayed reaction to yogurt was likely FPIES — a cell-mediated, non-IgE response. The SPT will be negative for this. He needs to avoid cow's milk protein (and possibly soy) and will be re-challenged under medical supervision at 12 to 18 months, when many children have outgrown it. [2]

For peanut and other allergens, he is at risk of IgE-mediated allergy because of his severe eczema, but he has not had a reaction. The SPT to peanut shows sensitisation without confirmed clinical allergy. The right approach is early introduction and regular exposure, guided by Ara h 2 component testing and, if needed, a supervised oral food challenge. [5][6]

I would reassure her that food allergy is common in children with severe eczema, that most allergies resolve, and that the diagnostic process is systematic — each test is interpreted in the context of his clinical history, and unnecessary dietary restriction is itself a harm we actively avoid. [1][5]