Paeds SAQs · allergy-and-immunology
Oral allergy syndrome and pollen-food syndrome — formative SAQs
Two formative short-answer questions on recognising and risk-stratifying pollen-food allergy syndrome, and on the lipid-transfer-protein systemic-risk phenotype.
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SAQ 1 — Recognise and risk-stratify (10 marks)
A ten-year-old with spring birch-pollen rhinitis gets lip tingling, palate itch and throat tightness within a minute of eating a raw apple at school. She eats baked apple every week with no symptoms. Her mother asks whether this is dangerous and what she should do. [1] [2]
Questions
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What is the most likely diagnosis, and which mechanism explains why the cooked apple is tolerated? (3 marks) [1] [2]
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Outline the immediate advice and the definitive management plan for this low-risk phenotype. (4 marks) [12]
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State three features in the history that would escalate this child out of the low-risk pathway, and what each implies. (3 marks) [10] [13]
Model answer
Diagnosis and mechanism (3). This is pollen-food allergy syndrome (oral allergy syndrome), driven by cross-reactivity between the major birch allergen Bet v 1 and the apple PR-10 protein Mal d 1. The protein is heat-labile and digestion-labile, so cooking denatures it and the cooked apple is tolerated — the defining 'raw but not cooked' history. [1] [2]
Immediate and definitive plan (4). Stop the raw apple, rinse the mouth, and give a non-sedating oral antihistamine for breakthrough oral symptoms. Confirm pollen sensitisation and the phenotype with a fresh-food prick-prick test (more sensitive than commercial extracts for labile proteins) and component-resolved diagnostics (rBet v 1, rMal d 1). Dietary advice: avoid the raw apple, keep cooked and peeled forms, and do not over-restrict tolerated foods. Provide a safety-net plan to return if any systemic symptom appears. [12]
Escalating features (3). Urticaria beyond the mouth, wheeze or collapse — these are systemic, so treat as anaphylaxis with IM adrenaline. Reaction to the cooked apple or to small amounts — suggests a primary food allergy or a heat-stable lipid transfer protein phenotype rather than classic PFAS. Cofactors such as exercise or NSAIDs preceding a systemic reaction — flag a cofactor-dependent or LTP phenotype and lower the threshold for adrenaline. [10] [13]
References6ShowHide
- [1]Mastrorilli C Pollen-Food Allergy Syndrome: A not so Rare Disease in Childhood. Medicina (Kaunas), 2019.PMID 31561411
- [2]Poncet P Update on pollen-food allergy syndrome. Expert Rev Clin Immunol, 2020.PMID 32691654
- [4]Dramburg S EAACI Molecular Allergology User's Guide 2.0. Pediatr Allergy Immunol, 2023.PMID 37186333
- [10]Asero R Why lipid transfer protein allergy is not a pollen-food syndrome: novel data and literature review. Eur Ann Allergy Clin Immunol, 2022.PMID 34092069
- [12]Sicherer SH Food allergy: A review and update on epidemiology, pathogenesis, diagnosis, prevention, and management. J Allergy Clin Immunol, 2018.PMID 29157945
- [13]Simons FE World Allergy Organization Anaphylaxis Guidelines: 2013 update of the evidence base. Int Arch Allergy Immunol, 2013.PMID 24008815