Pearls and pitfalls of implementing LEAP strategy for peanut: A case report

Abstract

Early introduction of peanut in infants at high risk has been widely adopted and implemented in pediatric outpatient clinics since 2017. It is often overlooked that almost 2% of infants went on to develop peanut allergy despite regular consumption in a previous study. Here we described a case of anaphylaxis to peanut in a 6-month-old infant after a negative skin-prick test result, supervised introduction in the clinic, and successful home consumption, which, to our knowledge, has only previously been described once in the literature.

In February 2015, the Learning Early About Peanut Allergy (LEAP)¹ study demonstrated compelling evidence that early introduction of peanut significantly decreases the risk of developing peanut allergy in infants at high risk.¹ Subsequently, in 2017, the National Institute of Allergy and Infectious Diseases created guidelines and recommendations² on peanut introduction and testing. Those infants who are at high risk for peanut allergy (those with severe atopic dermatitis and/or egg allergy) should be screened before introduction of peanut. In the case of a negative skin-prick test (SPT) result (defined as 0–2 mm greater than the negative control), the guidelines offer two options: home peanut introduction or a supervised feeding in the office, given that the risk of allergy is low.² For those with an SPT result of 3–7 mm, an observed open feeding or graded oral food challenge (OFC) in the clinic or a specialized facility is recommended.² These options should be followed by continued, regular home consumption. Epinephrine autoinjectors are not recommended for home introduction or if in-office procedures were tolerated.

We present the case of a white male infant who was born full-term without complications. At two months of age, he developed atopic dermatitis (AD) on his face that progressed to involve his entire body. At 4 months of age, he presented to the pediatric allergy clinic with severe full-body AD despite 1 week of aggressive skin treatment with twice daily soaking baths, wet wraps, and application of desonide 0.05% ointment to areas of active AD. At this visit, he demonstrated a negative SPT result to a commercial peanut extract (but had a positive result to commercial egg extract) and underwent medically supervised initial feeding due to parental anxiety and provider preference. Because SPT is the preferred method for screening in the 2017 guidelines,² specific immunoglobulin E (sIgE) levels were not initially obtained. He tolerated a single dose of 2 teaspoons of peanut butter (2 g of peanut protein) that was thinned in rice cereal, without any reaction.

The family was instructed to feed the child 2 teaspoons of peanut butter 3 days a week; the family started this at home on the day after challenge. This was well tolerated for 5 weeks, until the family went on vacation, and he missed two doses of peanut over 1 week. In accordance with the guidelines,² no recommendations or precautions were given with regard to missed doses. The day after returning from vacation, the family attempted to resume his peanut regimen. After eating 1 teaspoon of peanut butter, he immediately developed lip swelling and was described by his parents as gasping for air. The mother administered epinephrine via autoinjector (prescribed for an egg allergy), which resulted almost immediately in complete resolution of his symptoms. He was taken to the emergency department, where he was given diphenhydramine for fussiness, monitored for 2 hours, and discharged home without any other interventions. On a repeated SPT 3 weeks after the reaction, his peanut SPT result rem`ained negative with appropriate positive and negative controls. He had blood drawn at this second visit, with a total IgE level of 93.1 kU/L and peanut sIgE level of 6.54 kU_A/L. His sIgE levels to peanut components were the following: Ara h1 1.66 kU_A/L, Ara h2 6.33 kU_A/L, Ara h3 0.32 kU_A/L, and Ara h8 and Ara h9 < 0.1 kU_A/L. A confirmatory OFC was declined by the family after he developed anaphylaxis during observed OFCs to tree nuts (hazelnut, cashew, and pistachio). Nevertheless, the convincing clinical history and sensitization to peanut confirmed by the sIgE level is highly suggestive of peanut-induced anaphylaxis.

This case challenges the false assumption that, if a child passes an initial home introduction, supervised feeding, or graded OFC to peanut as per the 2017 guideline,² then there is no risk of developing anaphylaxis if regular peanut consumption is continued. It should be noted that our case is not the first report of an infant with a negative SPT result to peanut who developed anaphylaxis after previous tolerance. A similar reaction is described in the supplemental appendix to the LEAP study.¹ In this case, a 6-month-old infant in the early introduction cohort who had initially tolerated peanut a few times had subsequent peanut-induced wheezing and angioedema that required intramuscular epinephrine. Thus, the subject was diagnosed with a peanut allergy and discontinued peanut consumption. The initial SPT result was 1 mm, and a repeated SPT result after the episode was 3 mm. A repeated OFC was not performed.¹ In addition to this infant with anaphylaxis in the LEAP study,¹ 6 of 272 children (2.2%) with a negative SPT result passed their initial OFC but subsequently developed a mild reaction (most commonly rash) to peanut during regular consumption.¹

There is limited data that addresses the rate of reactions after negative SPT results to peanut. However, Healthnuts³ and EarlyNuts,⁴ two consecutive birth cohort studies from Australia, reported reaction rates of 2% and 4%, respectively, after home introduction without a previous SPT. Reactions were typically mild, mostly limited to rash and vomiting, with only a few episodes of wheezing. Without a previous SPT, it is unknown how many of these infants would have been offered a graded OFC or been instructed to strictly avoid peanut based on the 2017 guidelines in the United States.² This report highlights an uncommon but non-negligible risk of experiencing an IgE-mediated reaction to peanut, which potentially involves anaphylaxis, in infants at high risk and with a negative peanut SPT result who have successfully initiated early peanut consumption.

Based on this report, we offer the following clinical pearls and pitfalls of early peanut consumption that may not be generally known. Although it is clear that the protective effect of LEAP study¹ strategy outweighs the small risk of peanut allergy in a child with a negative SPT result, there is a small but non-negligible risk of anaphylaxis, even after the safe initiation of early peanut consumption. This may reflect the limits of SPT specifically in infants 4 months to 11 months of age⁵ and/or the limits of protection against sensitization even after initiating early peanut consumption. As such, we suggest that clinicians consider offering the option of a prescription for an epinephrine autoinjector for patients at high risk for peanut allergy (moderate-to-severe eczema and older age)⁶ who are not sensitized to other allergens. This report also highlights the importance of continuous consumption in these infants because it seems that missing only two doses of peanut may increase the risk of a reaction. Therefore, families should be encouraged to continue frequent peanut consumption at home and minimize gaps in consumption. In some special situations, providing injectable epinephrine might be considered.