Peanut allergy

Author: Bethany Frances Ferris, Foundation Year 2 Doctor, Isle of Man, United Kingdom. DermNet NZ Editor in Chief: A/Prof Amanda Oakley, Dermatologist, Hamilton, New Zealand. Copy edited by Gus Mitchell. February 2019.

What is peanut allergy?

Peanut allergy is an adverse immune response to a peanut allergen. Reactions include:

  • Systemic IgE-mediated type 1 immediate hypersensitivity reaction (anaphylaxis) [1]
  • Oral allergy syndrome — a localised IgE-mediated allergy caused by fresh fruits, vegetables and nuts with symptoms confined to the lips, mouth and throat [2]
  • Non-IgE mediated allergy — response can take hours to days and results in gastrointestinal symptoms (vomiting, diarrhoea and abdominal pain) [1].

Peanut allergy is the most common cause of food-related anaphylaxis [5].


What are the peanut allergens?

The peanut (Arachis hypogaea) belongs to the legume family and is distinct from the tree nut family.

There are 11 peanut allergens (Ara h 1 to Ara h 11) which are seed storage proteins; these are biological reserves that enable the seed to grow into a plant.

Who gets peanut allergy?

The prevalence of peanut allergy in the United Kingdom is reported to be in 0.2–2.5% of children and in 0.3–0.5% of adults [4,5]. A rise in the prevalence was reported in the USA, with 1.4% of children with peanut allergy in 2008 compared to 0.4% in 1997 [6].

There is a greater risk of peanut allergy in children who have:

  • Egg allergy
  • Severe atopic dermatitis
  • Used topical preparations containing peanut oil.

Having a peanut allergy does not increase the risk of allergy to another legume (eg, peas, beans, lentils, soybeans) with the exception of lupin. Yet, one-third of those with a peanut allergy will have a concurrent reaction to a tree nut (eg, walnut, almond, brazil nut, coconut) [7].

Peanut allergy is more prevalent in the Western world than in China, possibly due to the greater consumption of roasted peanuts rather than raw peanuts [8].

The Learning Early About Peanut Allergy (LEAP) study found that high-risk infants with eczema or egg allergy were less likely to develop a peanut allergy if they had early and sustained consumption of peanuts [9].

Non-allergic mothers are now encouraged to eat potentially allergenic foods such as peanuts regularly during pregnancy and not to delay introducing their babies to them [10].

What causes peanut allergy?

The cause of peanut allergy is not fully understood.

  • Peanuts are highly allergenic due to the abundance of allergen in seed storage proteins.
  • Peanuts are highly resistant to enzymatic digestion in the gastrointestinal tract and the allergens maintain their conformational epitope (a 3-dimensional folded polypeptide structure). Most IgE binds to Ara h 2 conformational epitopes.
  • Peanuts have carbohydrate residues on their surface. Dendritic cells have specific receptors for identifying carbohydrate residues.
  • When peanuts are roasted, they undergo a non-enzymatic glycosylation reaction called the Maillard reaction, which makes the peanut more allergenic [11].

To develop a peanut allergy, the individual must be exposed to one of the peanut allergens via a gastrointestinal, cutaneous, or respiratory route.

  • The peanut allergen is detected by a dendritic cell, which moves to a lymph node to interact with a specific T-cell receptor. In an abundance of interleukin-4 (IL-4), IL-5 and IL-13, a T-helper 2 (TH2) cell response is initiated.
  • The TH2 response signals B cells to produce allergen-specific clonal IgE. The IgE binds to the high-affinity FC receptor for IgE (FCεRI) on the surface of mast cells. The expression of FCεRI on mast cells is upregulated (increased) so that more IgE can bind to the mast cell (allergic priming or sensitisation).
  • When the individual is subsequently exposed to the peanut allergen, the allergen can immediately bind to IgE on the surface of the mast cell (elicitation). The mast cell degranulates and releases several chemicals including histamine, which causes vasodilation, increased vascular permeability and the clinical signs and symptoms of an allergic reaction.
  • In non-allergic individuals, T regulatory cells lead to tolerance to the peanut allergen [11].

What are the clinical features of peanut allergy?

Peanut allergy results in urticaria, angioedema and anaphylaxis within 30 minutes of exposure to a peanut allergen [1]. It may also cause a late phase allergic reaction.

Anaphylaxis causes dyspnoea and wheeze (due to bronchospasm and laryngeal oedema), tachycardia, hypotension, dizziness and loss of consciousness. Anaphylaxis is a life-threatening clinical emergency [1].

A late phase allergic reaction can develop 2–6 hours after the initial exposure to the allergen and peaks at around 6–9 hours. This is due to the recruitment of leukocytes and antigen-specific T cells. The late phase reaction results in erythema and oedema, sneezing, itching, and coughing. It usually fully resolves in 1–2 days [12,13].

What are the complications of peanut allergy?

Anaphylaxis can be fatal if not promptly recognised and treated with adrenaline, bronchodilator and antihistamines.

Children with asthma have higher mortality from peanut-induced anaphylaxis than non-asthmatic children [14].

How is peanut allergy diagnosed?

Peanut allergy is principally a clinical diagnosis based on the rapid development of allergic symptoms and signs after eating a peanut.

Skin prick testing and serum specific IgE tests are used to identify sensitisation and to confirm the diagnosis [4].

Skin prick testing involves placing a drop of peanut allergen on the skin, then pricking to see if a weal is produced within 15 minutes. The British Society of Allergy and Clinical Immunology (BSACI) states that a weal ≥ 8 mm is highly predictive of peanut allergy. Skin prick testing must be performed in a specialist centre with emergency equipment available in case of anaphylaxis [4].

Serum specific IgE testing, also known as radioallergosorbent testing (RAST), is performed to detect allergen-specific IgE in the blood. Specific IgE ≥15 kU/L is highly predictive of peanut allergy [4].

The tests do not predict the severity of clinical allergy [4].

What is the differential diagnosis for peanut allergy?

An IgE-mediated type 1 hypersensitivity reaction and ensuing anaphylaxis can be due to another cause. For example:

The sudden development of a rash might be due to the non-allergic release of histamine, as in scombroid fish poisoning.

What is the treatment of peanut allergy?

The treatment of anaphylaxis is a medical emergency with stabilisation of airway, breathing, and circulation.

  • Intramuscular adrenaline (epinephrine) must be given immediately to patients with signs of shock, airway swelling, or definite difficulty in breathing.
  • This may followed by treatment with an antihistamine, corticosteroid and other drugs.

Confirmed peanut allergy needs a comprehensive management plan, which should be shared with the wider family and school [4,15,16].

Treatment of anaphylaxis

Nut avoidance

Ingesting or touching peanuts, peanut butter, peanut flour, arachis oil and other peanut-containing products must be completely avoided. Read ingredient lists and warnings on manufactured food (in New Zealand, the USA, and many other countries, the possibility of an item containing peanuts must be declared on the packet). Be particularly careful when eating away from home, where unintended contamination of other foods with peanuts may occur.

It is unclear whether patients with peanut allergy should also avoid all legumes and tree-nuts.

  • If a specific type of legume or nut has previously been tolerated, it should be safe to continue eating it.
  • If the legume or nut has not been tried before, it is safer to assume allergy to it [4].

Be prepared for an attack

Antihistamines should be carried at all times and taken if an allergic reaction occurs. The patient and their carers should be regularly trained in how to use an adrenaline auto-injector or adrenaline in a prepared syringe, and if the device has to be used, they must seek immediate medical attention [4].

Test family members for peanut allergy

Between 5 and 9% of siblings of children with a peanut allergy will also have a peanut allergy. In high-risk individuals (with asthma, eczema or other food allergies) or in cases of parental anxiety, it is advisable to perform skin prick testing or specific IgE before the child introduces peanut into their diet. In low-risk individuals, peanuts can be carefully introduced to test for an allergic reaction [4].


Clinical trials of oral, sublingual and epicutaneous peanut immunotherapy have shown some promising results, but at present, are not routinely offered as a treatment for peanut allergy [4].

Humanised anti-IgE monoclonal antibody therapy using omalizumab has been shown to speed up desensitisation in peanut immunotherapy [17].

What is the outcome for peanut allergy?

About 20% of children with peanut allergy will grow out of peanut allergy [18]. The allergy persists into adult life in the majority of affected individuals.

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Related information



  1. National Institute for Health and Clinical Excellence (2011). Food allergy in under 19s: assessment and diagnosis [CG116]. Available from: (accessed 16 January 2019)
  2. Boyce JA, Assa'ad A, Burks AW, et al. Guidelines for the diagnosis and management of food allergy in the United States report of the NIAID-sponsored expert panel. J Allergy Clin Immunol 2010; 126: S1–58. DOI: 10.1016/j.jaci.2010.10.007. PubMed
  3. Pumphrey RS, Gowland MH. Further fatal allergic reactions to food in the United Kingdom, 1999–2006. J Allergy Clin Immunol 2007; 119: 1018–9. DOI: 10.1016/j.jaci.2007.01.021. Journal
  4. Stiefel G, Anagnostou K, Boyle RJ, et al. BSACI guideline for the diagnosis and management of peanut and tree nut allergy. Clin Exp Allergy 2017; 47: 719–39. DOI: 10.1111/cea.12957. PubMed
  5. Venter C, Hasan Arshad C, Grundy J, et al. Time trends in the prevalence of peanut allergy: three cohorts of children from the same geographical location in the UK. Allergy 2010; 65(1): 103–8. DOI: 10.1111/j.1398-9995.2009.02176.x. PubMed
  6. Sicherer SH, Muñoz-Furlong A, Godbold JH, Sampson HA. US prevalence of self-reported peanut, tree nut, and sesame allergy: 11-year follow-up. J Allergy Clin Immunol 2010; 125: 1322–6. DOI: 10.1016/j.jaci.2010.03.029. PubMed
  7. Sicherer SH, Burks AW, Sampson HA. Clinical features of acute allergic reactions to peanut and tree nuts in children. Paediatrics 1998; 102: e6. DOI: 10.1542/peds.102.1.e6. PubMed
  8. Finkelman FD. Peanut allergy and anaphylaxis. Curr Opin Immunol 2010; 22: 783–88. DOI: 10.1016/j.coi.2010.10.005. PubMed
  9. Du Toit GD, Roberts G, Sayre PH, et al. Randomised trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med 2015; 372: 803–13. DOI: 10.1056/NEJMoa1414850. Journal
  10. Update on infant feeding and food allergy prevention. Paediatric Society of New Zealand. Available at: (accessed 2 January 2019)
  11. Vickery BP, Chin S, Burks AW. Pathophysiology of food allergy. Pediatr Clin North Am. 2011; 58(2): 363–76. DOI: 10.1016/j.pcl.2011.02.012. Journal
  12. Al-Muhsen S, Clarke AE, Kagan RS. Peanut allergy: an overview. CMAJ 2003; 168: 1279–85. PubMed Central
  13. Galli SJ, Tsai M, Pilponsky AM. The development of allergic inflammation. Nature 2008; 454: 445–54. DOI: 10.1038/nature07204. PubMed Central
  14. Simpson AB, Yousef E, Hossain J. Association between peanut allergy and asthma morbidity. J Pediatr 2010; 156: 777–81. DOI: 10.1016/j.jpeds.2009.11.080. Journal
  15. Royal College of Paediatrics and Child Health (2011) Allergy care pathway for children with food allergy. Available at:
  16. Royal College of Paediatrics and Child Health (2011) Care Pathway for Children with Anaphylaxis. Available at:
  17. MacGinnitie AJ, Rachid R, Gragg H, et al. Omalizumab facilitates rapid oral desensitisation for peanut allergy. J Allergy Clin Immunol 2017; 139: 873–81. DOI: 10.1016/j.jaci.2016.08.010. Journal
  18. Update on Infant feeding and food allergy prevention. Paediatric Society of New Zealand. Available at: (accessed 2 January 2019)

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