Peanut, tree-nut and seed allergy

Overview & Definition

Peanut, tree-nut and seed allergy together form the group of food allergies most likely to persist for life and to cause severe or fatal reactions in children. A child who reacts to a trace of peanut within minutes of eating it, with urticaria spreading across the face and a tightening throat, sits at the severe end of a spectrum that also includes the toddler with only lip swelling from cashew paste and the school-age child whose only problem is itchy mouth after a hazelnut cross-reacting with birch pollen. The clinician's job is to separate the dangerous, persistent, storage-protein-driven allergies from the milder cross-reactive and the non-IgE-mediated forms, and to do so without over-labelling children who are only sensitised. [8]

Peanut is a legume, not a nut, and its cross-reactivity with tree nuts is driven less by botanical kinship than by shared stable storage proteins that resist digestion and cooking. Tree nuts include walnut, cashew, hazelnut, almond, pecan, pistachio, Brazil nut and macadamia, while the major seed allergens are sesame, sunflower, poppy and mustard. Each carries distinctive allergen components — Ara h 2 in peanut, Ana o 3 in cashew, Ses i 1 in sesame — and knowing which components matter transforms a vague positive test into a meaningful clinical prediction. [9]

The single most important advance in this field is preventive. The LEAP trial showed that early, sustained consumption of peanut in high-risk infants reduced the later development of peanut allergy by roughly 80 per cent compared with avoidance, overturning decades of advice to delay allergenic foods. Alongside prevention, modern management pairs strict avoidance and adrenaline autoinjectors with the emerging option of oral immunotherapy, which desensitises rather than cures and must be weighed against its real risk of allergic reactions during treatment. [1]

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