Peanut Allergy

Etiology

Several studies have tested age-related peanut exposure in the development of peanut allergy. One study evaluated the prevalence of peanut allergy in Israeli Jewish children compared to Jewish children living in the United Kingdom (UK). Peanut introduction differs in these two populations whereby peanut-containing food is not restricted in Israel while it is typically delayed until the age of 2 in the UK. The results showed that Israeli children have a decreased frequency of developing a peanut allergy compared to the UK group, suggesting that the early introduction of peanuts may offer protection from developing a peanut allergy.[3] Another important study, the Learning Early About Peanut Allergy (LEAP) study, was a prospective randomized trial with one group avoiding peanuts until age 5 while the other group had repeated exposure to peanuts from 4 to 6 months until age 5. The purpose of the study was to compare the incidence of peanut allergy between the two groups after 5 years. The children in this study were at high risk of developing a peanut allergy. They defined high risk as either having severe eczema or egg allergy. The results of the LEAP study showed that early introduction of peanuts to high-risk infants early could prevent the development of a peanut allergy.[4][5] Current guidelines recommend peanut introduction as early as 4 to 6 months of age in high-risk infants.

Risk factors include:

• History of atopy
• Family history of peanut allergy
• Maternal consumption of peanuts during pregnancy
• Use of certain oils to fry/roast peanuts

Epidemiology

Food allergies affect approximately 4% to 8% of children and 1% to 2% of adults.[1] Peanut allergy typically manifests initially during childhood with symptom occurrence as early as 4 months of age and usually within the first 2 years of life. Approximately 20% of children will naturally outgrow their peanut allergy and tolerate them without events later on in life.  

In general, there appears to have been an increase in peanut allergy over the past 2 decades. The first evidence of peanut allergy may come to light between ages 12-24 months and unlike egg or milk allergies, peanut allergy does not always decrease with time. Some studies indicate that the severity of reactions to peanuts also increases with age.

Pathophysiology

Food allergy classifies as a type I IgE mediated hypersensitivity reaction. Initial sensitization to peanuts stimulates the production of peanut-specific IgE antibodies. The major peanut antigens identified by the specific antibodies response include AraH1, H2, H3. In a sensitized individual, peanut ingestion can trigger specific IgE antibody cross-linking to IgE receptors on effector cells such as basophils and mast cells, which triggers mediator release such as histamine and a variety of cytokines and chemokines. Inflammatory cell recruitment ensues to propagate the allergic response.[1]

The allergy to peanuts is due to low molecular weight proteins that are resistant to heat, proteases, and denaturants. Eleven peanut allergens have been described (Ara h 1-11).

History and Physical

Diagnosis of a peanut allergy relies on patient history and physical exam. The type/amount of food ingested, onset/duration of symptoms, and relieving factors are key in making an accurate diagnosis. A history of eczema is important as it is a significant risk factor for peanut sensitization. Common symptoms of peanut allergy include skin reactions, such as urticaria, erythema, or edema. More severe symptoms include tingling of the mouth and throat, edema of the lips, and dyspnea. These symptoms will often frequently progress to anaphylaxis.

Evaluation

Skin testing is the preferred testing method in those patients with a history compatible with food allergies. A skin-prick test is performed by applying a drop of a peanut extract to the skin, commonly on the arm or back. A wheal/flare response is measured approximately 20 minutes after pricking the skin where the drop of peanut extract was placed. Positive testing indicates sensitization to peanuts and can predict the probability of a future reaction. Measurement of peanut-specific IgE antibodies in serum is another useful method to estimate sensitization and the probability of future reaction. It is important to note that this type of testing does not predict the severity of the reaction and is limited by poor sensitivity; results are reassuring when negative. Ultimately a clinician-supervised oral food challenge is the best and most reliable method for diagnosing peanut allergy. Serum-specific IgE and skin-prick testing can aid in determining which patients should have an oral food challenge.[6][7] An oral food challenge can also assist in confirming reactivity in those patients without a clear history or never having ingested peanuts despite sensitization.

Treatment / Management

To date, the recommended management of peanut allergy relies on avoidance of peanut ingestion. Unfortunately, severe reactions such as anaphylaxis may occur despite best efforts in avoidance. Epinephrine is the first-line medication for the treatment of anaphylaxis. Intramuscular (IM) or intravenous (IV) epinephrine should be administered, although the IM route is preferred, with injection placement in the lateral thigh. IV administration ideally should be done in the inpatient setting with appropriate monitoring.[8] Antihistamines, corticosteroids, and bronchodilators, may also be used, but it is essential to realize these medications do not treat anaphylaxis, rather they are adjunctive therapies for anaphylaxis management. IV fluids should be provided to prevent and treat tissue hypoperfusion. In rare cases, the patient may require intubation for airway protection. Severe cases of anaphylaxis should be admitted and monitored at least overnight until stable. Biphasic anaphylaxis may occur in some cases where symptoms recur up to 8 hours after the initial reaction. The treating clinician should take this into account before discharge.[9] In less severe presentations the patient can be observed in the emergency department after standard treatment, and with sufficient improvement safely discharged home. 

Although avoidance is the mainstay of treatment, new strategies are being tested to prevent food allergies. Peanut immunotherapy clinical trials have been promising to date using incremental ingestion of small amounts of peanut over time with oral immunotherapy (OIT). The goal of OIT may be either to prevent a reaction if accidental peanut ingestion occurs or to induce tolerance where the patient can regularly ingest peanuts safely.[1][10] Epicutaneous immunotherapy is another desensitization method tested where peanut is transdermally introduced over time to build up a tolerance.  (B3)

Immunization with plasmid DNA encoding food allergens is a novel method to treat peanut allergy. However, this approach requires a large amount of plasmid DNA required for vaccination.

Mutated peanut protein substitutes are another way to manage peanut allergies.

Finally, sublingual immunotherapy involves placing emulsified purified peanut protein under the tongue for 120 seconds and then swallowing. Data show that this can help prevent peanut allergic reactions with time.

Differential Diagnosis

• Acute urticaria
• Food intolerance (e.g., lactose intolerance)
• Toxic reaction (e.g., scombroid poisoning)
• Oral allergy syndrome
• Eosinophilic esophagitis

Prognosis

Approximately 20% of patients with a peanut allergy will naturally acquire tolerance to peanuts over time. Unfortunately, peanut allergy is usually lifelong and remains potentially fatal.

Complications

Symptoms can occur within seconds of ingestion, with peak occurrence by 30 minutes but can delay up to 2 hours. Major target organs of an allergic reaction include the skin, gastrointestinal (GI), and respiratory tracts. Skin-related symptoms include urticaria, angioedema, and occasional worsening of existing eczema. GI symptoms include abdominal pain, vomiting, and/or diarrhea. Respiratory symptoms can manifest as repetitive coughing, stridor, and wheezing. Also, it can affect the cardiac and the central nervous systems in the setting of anaphylactic shock whereby diminished tissue perfusion leads to cardiac arrest and syncope.[10] Symptom presentation must be interpreted in the context of the patient's history, i.e., symptoms are relevant to a food allergy when ingestion occurs in the appropriate time frame expected for food-induced allergic reactions.