Among all persons with food allergies, those who are allergic to peanuts are at greatest risk for anaphylactic symptoms.1 About 30,000 cases of food allergy–related anaphylaxis are seen in the nation’s emergency departments (EDs) each year, and the food most commonly responsible is peanuts.2 What can primary care providers do to reduce the number of peanut allergy–associated anaphylactic reactions and fatalities, both in the ED and in the larger community?
According to a guideline from the National Institute of Allergy and Infectious Diseases (NIAID),3 prevalence of peanut allergy is about 0.6% of the US population, although in an 11-year survey involving more than 13,000 respondents, Sicherer et al4 reported allergy to peanuts, tree nuts, or both in 1.4%, possibly translating to some three million Americans; British researchers have reported peanut allergy in 1.8% of an 1,100-member children’s cohort.5 The risk of exposure to peanuts and the associated risk for severe and possibly fatal anaphylaxis present a lifelong struggle for both patient and family.
ETIOLOGY OF PEANUT ALLERGIES
Food allergy prevalence has reportedly doubled in recent decades, with a significant increase also seen in allergy severity.6 Allergies involving eggs, nuts, fish, milk, and other foods represent the leading cause of hospital-treated anaphylaxis throughout the world.1 Unlike other allergenic foods that affect only one age-group, peanuts are among the foods that trigger the “vast majority” of allergic reactions in young children, teenagers, and adults alike.3
Increases in reported episodes of peanut allergy reactions may be occurring for several reasons:
• Many people have adopted vegetarian diets, and nuts are considered a good protein source6
• Environmental exposures are increasingly common
• More people are genetically vulnerable, as the role of family history becomes clearer
• Food preparation methods (eg, shared processing equipment, contaminated raw materials, formulation errors) and inaccurate labeling lead to accidental exposures7,8
• Exposure to nuts in utero or during breastfeeding is more common.9 Nowak-Wegrzyn and Sampson6 point to the promotion of peanut butter as an economical, nutritious food source for children and for women during pregnancy and lactation; mothers’ consumption of peanuts more than once a week during pregnancy and lactation have been linked to overexposure for their children.9
Other trends that may contribute to peanut allergy prevalence are the early introduction of solid foods in the infant diet and the use of skin products that contain peanut oil.6
Environment and Genetics
The body of knowledge regarding the specific causes of peanut allergy is increasing constantly. Several known peanut proteins (Ara h1, Ara h2, Ara h3, Ara h6, Ara h7, and Ara h9; Ara h8 is a homologous allergen that may account for peanut/birch cross-reactivity) are thought to be responsible for the initial sensitization to peanuts in vulnerable persons, triggering the associated immunoglobulin E (IgE)–mediated response.10-12 Approximately 75% of known peanut-allergic patients will react to these proteins on their first ingestion after being sensitized.9
Since IgE antibodies do not cross the placenta, it is believed that sensitization to peanut proteins must occur in utero or through breast milk. This form of sensitization predisposes these patients to the initial life-threatening anaphylactic reaction.9
There is strong evidence that genetic factors may play a role in peanut allergies.2 In a study of 58 pairs of twins by Sicherer et al,13 heritability of peanut allergy was estimated at 82%, with 64% of monozygotic pairs, versus 7% of dizygotic pairs, showing concordance for peanut allergy. However, the genetic loci that may be responsible for specific food allergies have not yet been identified.2
It is believed that manifestations of food allergy are very similar to those of asthma and atopic dermatitis. According to Green and colleagues,14 82% of peanut-allergic children who visited a referral clinic also had atopic dermatitis. These conditions appear to be triggered by similar mechanisms, mediated by both environmental and genetic factors.2,14-16 Hong et al2 are optimistic about the advances being made in food allergy genetics. Increased understanding, they feel, may lead to new treatment options for potentially fatal food allergies.2
PATIENT PRESENTATION AND HISTORY
As with any IgE-mediated immune response, the patient must have been exposed to the allergen in question. Most patients present with a history of having ingested raw or boiled peanuts and/or foods produced in a facility that also processes nuts.1,18 Clinical symptoms of peanut allergy may develop within seconds of ingestion. For some patients, consumption of as little as 5 to 50 mg of peanut protein can trigger symptoms.19 (A single peanut from a jar of commercially processed peanuts contains approximately 300 mg of potentially allergenic protein.1)
Typically, the most dramatically affected patients have a medical history of asthma or other IgE-mediated immune reactions.1 In one study, young adults with IgE-mediated peanut allergy were found at especially high risk for severe anaphylaxis.6 Seventy-five percent of patients who have a reaction to peanuts do so following their first ingestion (after the initial exposure).