Peanut allergy L27.- L50.0 K52.1

The peanut (Arachis hypogaea) belongs to the legumes (pulses) and is the most common trigger of food-induced anaphylaxis.

So far identified and recognized allergens in Arachis hypogaea (peanut)

• Ara h 1 Cupin (Vicilin) marker allergen, indicator of risk sensitisation
• Ara h 2 Conglutin (marker allergen, indicator of risk sensitisation)
• Ara h 3 Cupin (marker allergen, indicator of risk sensitisation)
• Ara h 5 Profilin
• Ara h 6 Conglutin (marker allergen, indicator of risk sensitisation)
• Macaw h 7 Conglutin
• Ara h 8 Pathogenesis-related protein, PR-10 protein, Bet v 1 family member (cross-allergen, cross-reactivity mostly caused by Bet v 1 sensitization)
• Ara h 9 Nonspecific lipid-transfer protein (cross-allergen, cross-reactivity mostly caused by sensitization of members of the nsLTPs)
• Ara h 10 16 kDa Oleosin
• Ara h 11 14 kDa Oleosin
• Ara h 12 Defensin
• Ara h 13 Defensin
• Ara h 14 Oleosin
• Ara h 15 Oleosin
• Ara h 16 non-specific lipid transfer protein
• Ara h 17 non-specific lipid transfer protein

The prevalence of peanut allergies in the USA and England is 1-2% of the population. In a larger study (Burney 2104), European extract-related sensitization rates were between 0.5% and 5% depending on the country. In tests with marker allergens the sensitization rate was significantly lower. The high sensitization rates with the extracts can be explained in patients with primary sensitization to birch pollen or grass pollen by cross-reactions with highly conserved lipid transfer proteins (Ara h 9), profilins (Ara h 5) or cross-reactive carbohydrate determinants(CCD), among others.

The prognosis for peanut allergy is worse than for other food allergies in childhood (e.g. milk or egg allergy). Only about 25% of children with peanut allergy develop tolerance over the years.

Peanuts are hidden in many foods, including chocolate, pastries, sauces and oils. Even bath oils can contain peanut ingredients. For an allergic reaction, 100 µg of the allergenic proteins or the dust produced when opening a peanut package is sufficient.

The peanut allergens Ara h1 and h2 are heat-stable and are accentuated by the roasting of peanuts (e.g. in the case of peanut flips), but refined peanut oil no longer causes allergic reactions. There is the possibility of a cross-reaction with lupins, peas, chickpeas and soya. The responsible allergens were found among the storage proteins and protease inhibitors.

Further cross allergies have been observed with apples, birch pollen(PR-10 proteins), grass pollen(profilins, CCDs), liquorice, almonds, peach (Pru p 3), plane pollen, rice, walnuts and wheat flour.

The storage proteins Ara h 1, 2, 3,6,7 are the main allergens in primary peanut allergy. Specific IgE against Ara h2 and Ara h 6 are found in peanut-sensitized children and adolescents in the USA and Central Europe between 70% and 90%. It is remarkable that sensitization to these storage proteins only occurs if the allergy had already developed in childhood (Ballmer-Weber 2015).

Primary minor allergens include allergens from the oleosin family (Ara h 10/11), although the sensitization rate is not known.

Secondary allergens in peanut allergy sufferers include Ara h 9 (lipid transfer protein), especially in the Mediterranean countries, whereby the primary sensitization probably occurs via Pru p 3(peach allergen) or Pla a 1(plane tree allergen).

Secondary sensitization to Ara h 8 (PR-10 protein) and Ara h 5 (profilin) is based on previous pollen sensitizations. Ara h 8 for example is homologous with Bet-v 1, the major allergen of birch. This also explains a clear north-south gradient in Ara h 8 sensitizations (Lange 2015).

More recent evaluations of peanut allergies can be drawn from the LEAP (learn early about peanuts) study of 640 children: not the avoidance of allergens (the peanut sensitization rate in the avoidance group was 35.7%), but early and continuous peanut consumption (the peanut sensitization rate in the peanut consumption group was 10.6%) protects against peanut allergy (du Toit 2015).

In a larger study (Pitt et al. 2018), the consumption of peanuts by the mother during lactation had a protective effect (sensitization rate 1.7%). The incidence was significantly higher if mothers consumed peanuts during lactation but denied the children peanuts in the first year of life (sensitisation rate 151%), or if mothers themselves avoided peanuts but gave the child peanuts for consumption in the first year of life (17.6%).

The following terms in the list of ingredients may indicate the use of peanuts: peanut, peanut protein, peanut butter, peanut cream, peanut oil, vegetable protein, lecithin (E 322), vegetable fat. Lecithin and vegetable fat may also be of different origin.

The following should be noted for people allergic to nuts:

• Always check the list of ingredients when shopping and avoid products that contain or may contain peanut ingredients.
• In the case of chocolate, additives below 5% do not have to be indicated.
• Bread, rolls and baked goods may contain peanut ingredients or be contaminated with them.
• In the case of loose goods such as sausage or bread, no list of ingredients need be included.
• Peanuts are frequently used in Asian/Mexican and African cuisine (e.g. peanut sauce).
• Spice preparations such as curry powder may contain up to 10% legume flour (see also cross-reaction to lupine).
• Peanut contamination can occur wherever peanuts are used, i.e. in restaurants, bakeries, butcher shops, ice cream parlours, fast food chains.
• Infant foods may contain peanut ingredients under the terms "vegetable protein" or "vegetable fat".
• Cold-pressed oils from other plants (sunflower oil, etc.) may be contaminated with peanut ingredients.
• Peanut constituents may be found in encapsulated drugs, such as the capsule material of isotretinoin.

1. Ballmer-Weber BK et al.(2015) IgE recognition patterns in peanut allergy are age dependent: perspectives of the EuroPrevall study. Allergy 70: 391- 407
2. Blümchen K et al. (2010) Oral peanut immunotherapy in children with peanut anaphylaxis. J Allergy Clin Immunol 126: 83-91
3. Burney PG et al (2014) The prevalence and distribution of food sensitization in European adults. Allergy 69:365-371.
4. Du Toit G et al.(2015) Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med 372:803-813.
5. Du Toit G et al.(2016) Effect of Avoidance on Peanut Allergy after Early Peanut Consumption.
6. N Engl J Med 374:1435-1443.
7. Lange L et al. (2015) Molecular diagnostics in peanut allergy: lipid transfer proteins. In: Kleine-Tebbe J et al. eds Molecular allergy diagnostics. Springer Verlag Berlin-Heidelberg pp 205-216.
8. Pitt TJ et al. (2018) Reduced risk of peanut sensitization following exposure through breast-feeding
9. and early peanut introduction. J Allergy Clin Immunol 141:620-625.e1.
10. https://www.ema.europa.eu/en/documents/overview/palforzia-epar-medicine-overview_de-0.pdf
11. Ayazpoor U. (2022) Peanut allergy: first oral immunotherapy approved in Germany. Allergo Journal 31: 72