Peanut Reactions Research Articles

Saliva antibody profiles are associated with reaction threshold and severity of peanut allergic reactions

BackgroundReaction threshold and severity in food allergy are difficult to predict, and there is a lack of non-invasive predictors. ObjectivesWe sought to determine the relationships between pre-challenge levels of peanut (PN)-specific antibodies in saliva and reaction threshold, severity, and organ-specific symptoms during peanut allergic reactions. MethodsWe measured PN-specific antibody levels in saliva collected from 127 children with suspected peanut allergy prior to double-blind, placebo-controlled peanut challenges where reaction threshold, severity, and symptoms were rigorously characterized. Low-threshold peanut allergy was defined as reaction to <300mg of peanut protein cumulatively consumed. A consensus severity grading system was used to grade severity. We analyzed associations between antibody levels and reaction threshold, severity, and organ-specific symptoms. ResultsAmong the 127 children, those with high pre-challenge saliva PN IgE had higher odds of low-threshold peanut allergy (OR 3.9, 95%CI 1.6-9.5), while those with high saliva PN IgA: PN IgE or PN IgG4:PN IgE had lower odds of low-threshold peanut allergy (OR 0.3, 95%CI 0.1-0.8, and OR 0.4, 95%CI 0.2-0.9, respectively). Children with high pre-challenge saliva PN IgG4 had lower odds of severe peanut reactions (OR 0.4, 95%CI 0.2-0.9). Those with high saliva PN IgE had higher odds of respiratory symptoms (OR 8.0, 95%CI 2.2-26.8). Saliva PN IgE modestly correlated with serum PN IgE levels (Pearson r=0.31, P=0.0004). High and low saliva PN IgE levels further distinguished reaction threshold and severity in participants stratified by serum PN IgE, suggesting endotypes. ConclusionSaliva PN antibodies could aid in non-invasive risk stratification of peanut allergy threshold, severity, and organ-specific symptoms.

Joint transcriptomic and cytometric study of children with peanut allergy reveals molecular and cellular cross talk in reaction thresholds

BackgroundReaction thresholds in peanut allergy are highly variable. Elucidating causal relationships between molecular and cellular processes associated with variable thresholds could point to therapeutic pathways for raising thresholds. ObjectiveTo characterize molecular and cellular systemic processes associated with reaction threshold in peanut allergy and causal relationships between them. Methods105 children ages 4 to 14 years with suspected peanut allergy underwent double-blind, placebo-controlled food challenges to peanut. The cumulative peanut protein quantity eliciting allergic symptoms was considered the reaction threshold for each child. Peripheral blood samples collected at 0, 2, and 4 hours after challenge start were used for RNA sequencing, whole blood staining, and cytometry. Statistical and network analyses were performed to identify associations and causal mediation between the molecular and cellular profiles and peanut reaction threshold. ResultsWithin the cohort (n=105), 81 (77%) experienced allergic reactions after ingesting varying quantities of peanut, ranging from 43 to 9043 mg cumulative peanut protein. Peripheral blood expression of transcripts (e.g., IGF1R, FDR=5.4e-5 and PADI4, FDR=5.4e-5) and neutrophil abundance (FDR=9.5e-4) were associated with peanut threshold. Co-expression network analyses revealed that the threshold-associated transcripts were enriched in modules for FcγR-mediated phagocytosis (FDR=3.2e-3) and TLR (FDR=1.4e-3) signaling. Bayesian network, key driver, and causal mediation analyses identified key drivers (AP5B1, KLHL21, VASP, TPD52L2 and IGF2R) within these modules involved in bi-directional causal mediation relationships with neutrophil abundance. ConclusionKey driver transcripts in FcγR-mediated phagocytosis and TLR signaling bi-directionally interact with neutrophils in peripheral blood and are associated with reaction threshold in peanut allergy.

User-Centered Design and Evaluation of Clinical Decision Support to Improve Early Peanut Introduction: Formative Study.

Peanut allergy has recently become more prevalent. Peanut introduction recommendations have evolved from suggesting peanut avoidance until the age of 3 years to more recent guidelines encouraging early peanut introduction after the Learning Early about Peanut Allergy (LEAP) study in 2015. Guideline adherence is poor, leading to missed care opportunities. In this study, we aimed to develop a user-centered clinical decision support (CDS) tool to improve implementation of the most recent early peanut introduction guidelines in the primary care clinic setting. We edited the note template of the well-child check (WCC) visits at ages 4 and 6 months with CDS prompts and point-of-care education. Formative and summative usability testing were completed with pediatric residents in a simulated electronic health record (EHR). We estimated task completion rates and perceived usefulness of the CDS in summative testing, comparing a test EHR with and without the CDS. Formative usability testing with the residents provided qualitative data that led to improvements in the build for both the 4-month and 6-month WCC note templates. During summative usability testing, the CDS tool significantly improved discussion of early peanut introduction at the 4-month WCC visit compared to scenarios without the CDS tool (9/15, 60% with CDS and 0/15, 0% without CDS). All providers except one at the 4-month WCC scenario gave at least an adequate score for the ease of use of the CDS tool for the history of present illness and assessment and plan sections. During the summative usability testing with the 6-month WCC new build note template, providers more commonly provided comprehensive care once obtaining a patient history concerning for an immunoglobulin E-mediated peanut reaction by placing a referral to allergy/immunology (P=.48), prescribing an epinephrine auto-injector (P=.07), instructing on how to avoid peanut products (P<.001), and providing an emergency treatment plan (P=.003) with CDS guidance. All providers gave at least an adequate score for ease of use of the CDS tool in the after-visit summary. User-centered CDS improved application of early peanut introduction recommendations and comprehensive care for patients who have symptoms concerning for peanut allergy in a simulation.

Health-care resource utilization associated with peanut allergy management under allergen avoidance among commercially insured individuals.

Background: Until recently, the standard approach to care for individuals with peanut allergy (PA) was limited to allergen avoidance and treatment of reactions with emergency medicines. Objectives: To assess health-care resource utilization (HRU) and costs associated with PA management under allergen avoidance and to identify risk factors associated with peanut reactions that resulted in inpatient (IP) and/or emergency department (ED) visits. Methods: Privately insured individuals with PA diagnosis codes were identified from a large U.S. administrative claims data base (January 1, 1999, to March 31, 2017). PA-related HRU, indicated by a PA diagnosis and/or diagnostic procedure codes and by epinephrine autoinjectors (EAI) prescription fills in medical and pharmacy claims, respectively, and all-cause costs were described per patient-year (PPY). Risk factors associated with peanut reactions in an IP and/or ED setting were identified by using a multivariable logistic regression model. Results: A total of 86,483 patient-years from 14,136 individuals with PA were included. At the patient-year level, 28.1% were ages 0-3 years, 43.6% were ages 4-11 years, 13.7% were ages 12-17 years, and 14.5% were ages ≥ 18 years; 35.6% had PA-related outpatient visits; 50.6% had EAI fills; and 2.4% had PA-related IP and/or ED visits PPY. Younger individuals had more PA-related outpatient visits and EAI fills, with peak intensive use at ages 4-11 years. The proportion of individuals with PA-related IP and/or ED visits was highest among those aged ≥ 18 years. Mean all-cause costs were $3084 PPY; individuals with PA-related IP and/or ED visits incurred $8902 PPY ($17,451 for those with one or more IP visits). Risk factors associated with peanut reactions that resulted in IP and/or ED visits included young adults (odds ratio [OR] 3.19 [95% confidence interval {CI}, 2.66-3.83]), previous peanut reaction(s) (OR 1.66 [95% CI, 1.23-2.24]), asthma (OR 1.33 [95% CI, 1.18-1.51]), and male sex (OR 1.14 [95% CI, 1.01-1.28]). Conclusion: Individuals with PA and under allergen avoidance had significant HRU that varied across all age groups, with more PA-related outpatient visits during preschool and/or school age and PA-related urgent care among adults. Individuals with previous peanut reaction(s), asthma, and males had a higher risk of peanut reactions that resulted in IP and/or ED visits.

A Review Of Peanut Oral Food Challenges In Patients With No Or Minimal Sensitization To Ara H2

Ara h2 is considered the best predictor of systemic peanut reactions with some studies showing a negative predictive value of 100% using a cutoff value of <0.1 kU/L. However, the data are varied. We retrospectively examined the outcomes of 82 peanut oral food challenges (P-OFCs) conducted on patients with minimal or no Ara h2 sensitization. Patients had either no (Ara h2 ≤0.1 kU/L) sensitization (NS) or minimal (Ara h2 >0.1 but <0.35 kU/L) sensitization (MS) to Ara h2. Of 82 patients, 91% (75/82) had NS and 9% (7/82) had MS. The mean age of patients was 6.3 years (7 months to 29 years). Of all P-OFCs, 84% (69/82) had a pass outcome and 16% (13/82) had failed outcomes. Epinephrine use in failed challenges was 31% (4/13). Pass rate was 87% (65/75) in the subgroup with NS and 57% (4/7) with MS. Patients with NS were 5.7 times more likely to pass a P-OFC than those with MS (p=0.008). The odds of failing P-OFC was 4.9 times greater in patients with MS versus NS (p =0.058). In the NS group, mean skin prick test wheal of those failing P-OFCs was 4.1 mm (0-14 mm) and 3.2 mm (0-14 mm) for those passing P-OFCs. The majority of patients with no or minimal sensitization to Ara h2 pass P-OFCs (84%). Of those who fail challenges in this group, a substantial proportion require epinephrine (31%). The trend towards increased risk of P-OFC failure with minimal sensitization to Ara h2 warrants further exploration.

AR101 Oral Immunotherapy for Peanut Allergy

To determine if AR101 is a safe and effective treatment to prevent peanut reactions due to accidental exposure.Participants (496, 4–17 years old) were randomly assigned 3:1 to receive AR101 (peanut-derived investigational drug) or placebo (oat flour). The majority of the participants had a history of peanut anaphylaxis (72%), asthma (53%), and multiple food allergies (66%). All participants had dose-limiting symptoms at a dose of 100 mg of peanut protein in a double-blind placebo-controlled food challenge at baseline.Participants began a 1-day supervised dose escalation phase from 0.5 to 6 mg. The dose was then increased gradually every 2 weeks from 3 to 300 mg. A maintenance dose of 300 mg was continued for 24 weeks.A double-blind placebo-controlled food challenge was done at the end of the trial. Among the participants, 250 of the 372 (67.2%) in the active drug group and 5 of 124 (4%) in the placebo group were able to tolerate a dose of 600 mg or more of peanut protein without dose-limiting symptoms. The key secondary endpoints were tolerating 300 mg (76.6%) or 1000 mg (50.3%) compared with those in the placebo group (8.1% and 2.4%, respectively). Severe reactions occurred in 4.3% of the active drug group and 0.8% of the placebo group. Participants in the active treatment group compared with placebo had a higher incidence of gastrointestinal events (85.8% vs 69.4%), respiratory tract events (81.2% vs 71.8%), skin reactions (66.9% vs 55.6%), and immune system concerns (68.9% vs 8.9%). Overall, 43 (11.6%) in the active treatment group and 3 (2.4%) in the placebo group withdrew because of adverse events. Gastrointestinal symptoms causing study withdrawal occurred in 6.5% of the active treatment group and 1.2% of the placebo group. During the course of the trial, 52 participants (14%) in the active drug group and 8 participants (6.5%) in the placebo group were given epinephrine for grade 1 or 2 reactions; of these, the majority (92.7%) was treated with a single dose of epinephrine.Overall, 67% of the participants 4 to 17 years old were able to tolerate 600 mg of peanut protein (2 kernels) during the exit food challenge.These data are important, and AR101 will give health care providers a standardized way forward to treat this potentially life-threatening condition. It is hopeful that the product will be US Food and Drug Administration approved by the time this synopsis is published.

Earlier ingestion of peanut after changes to infant feeding guidelines: The EarlyNuts study

Randomized controlled trials demonstrate that timely introduction of peanut to infants reduces the risk of peanut allergy. However, much debate remains regarding how to best achieve earlier peanut introduction at the population level. Our previous study in 2007-2011 (HealthNuts, n=5300) indicated that few infants were consuming peanut in the first year. Australian infant feeding guidelines were updated in 2016 to recommend introducing peanut before 12months for all infants. There were no data available on the subsequent effect on peanut introduction or peanut reactions. We sought to assess the consequences of a nonscreening approach to allergenic food introduction in a population-based sample of infants in their first year of life. EarlyNuts is a population-based, cross-sectional study of 12-month-old infants in Melbourne, Australia, recruited by using an identical sampling frame and methods to HealthNuts (72% response rate vs 73% response rate in HealthNuts). We report here on the first 860 participants recruited between November 2016 and October 2018. Most infants (88.6%; 95% CI, 86.1% to 90.7%) had introduced peanut by 12months (median age, 6months), an increase from 28.4% (95% CI, 27.2% to 29.7%) in the HealthNuts study. By 12months, the majority of these (76.4%) had consumed peanut more than 4 times, and 28% were eating peanut more than once per week. Preliminary results on parent-reported reactions show that 4.0% of those consuming peanut by 12months had possible IgE-mediated reactions. There has been a striking shift toward earlier peanut introduction, with a 3-fold increase in peanut introduction by age 1year in 2018 compared with 2007-2011.

CONTINUOUS LIKELIHOOD RATIOS TO PREDICT THE PROBABILITY OF A PEANUT REACTION

Introduction Peanut-specific IgE (PsIgE) is used to predict the probability of a reaction using likelihood ratios (LR) which convert pretest to posttest probabilities. While dichotomous (positive or negative) LRs are defined using a cutoff of 0.35, it is better to use a continuous LR which corresponds to each value of PsIgE. This is particularly important when there is only a PsIgE and no history of prior ingestion to rely on. Methods PsIgEs were measured and oral peanut challenges performed on 58 children ages 9 months to 18 years. An ROC curve was determined using SPSS. The slope of the ROC curve, which is the likelihood ratio for each value of PsIgE, was determined by differentiated the ROC curve and used to convert sIgEs to likelood ratios. Results PsIgE ranged from 0 to 23. There were 33 negative and 25 positive oral challenges. The area under the ROC curve was 0.71 (p Conclusions Continuous LRs can provide a more accurate assessment of the probability of a peanut reaction for a given sIgE when the history of peanut ingestion is not known. Additional data points will refine these estimates.

Prevalence and factors associated to peanut allergy in Mexican school children

BackgroundIn our country, the prevalence and the factors associated to peanut allergy are unknown, a health problem that has been emerging worldwide. ObjectiveTo establish the prevalence and the factors that are associated to peanut allergy amongst school children. MethodsThis is a population-based cross-sectional study. We included 756 children aged 6–7 years. The children's parents were questioned about their peanut intake habits. A structured questionnaire was applied, it included questions regarding peanut intake; family and personal history of asthma; rhinitis; and atopic dermatitis. Allergic reactions to peanuts were registered as: probable, convincing and systematic. The statistical analyses included logistical regression models to look for associated factors. ResultsMales were 356/756 (47.1%). Peanut allergy prevalence: probable reaction: 14/756 (1.8%), convincing reaction: 8/756 (1.1%) and systemic reaction: 3/756 (0.4%). Through multivariate analysis, the presence of symptoms of allergic rhinitis (OR=4.2 95% CI 1.3–13.2) and atopic dermatitis (OR=5.2; 95% CI 1.4–19.5) during the previous year, showed significant association to probable peanut reaction. The former year, the presence of atopic dermatitis was the only variable that was substantially associated to a convincing reaction (OR=7.5; 95% CI 1.4–38.4) and to a systematic reaction (OR=45.1; 95% CI 4.0–510.0), respectively. ConclusionsThe reported prevalence of peanut allergy was consistent with that found in previous studies; symptoms of allergic rhinitis and atopic dermatitis were identified as associated factors to peanut allergy.

Prevalence of Peanut Allergy in Offspring of Peanut Farmers

Introduction: While exposure to environmental peanut during infancy appears to promote sensitization by the epicutaneous route, early and frequent peanut ingestion during infancy may prevent peanut allergy through oral tolerance. Due to parental occupation, the offspring of peanut farmers are likely exposed to peanut protein in their environment, but they may also have early introduction into their diet due to ready access. The purpose of this study was to determine the prevalence of peanut allergy in offspring of peanut farmers. Methods: A survey was mailed by the National Peanut Board to peanut farmers in the United States collecting information on peanut consumption, peanut reactions, physician-confirmed peanut allergy (PA), epinephrine auto-injector prescription and history of other allergies in offspring. Egg allergy (EA) served as a comparator to peanut allergy. Results: Of 10,349 households surveyed, 1050 responses were received (2493 offspring, participation rate 10%). The self-reported prevalence of peanut allergy in the general population in the USA is 0.9%, 1.3%, and 0.7% for children 0 - 5 years, 6 - 10 years, and 11 - 17 years, respectively. In offspring of peanut farmers, PA vs EA was reported in 3.69% (10/271) vs 2.6% (7/271), 2.8% (14/493) vs 2.0% (10/493), and 1.48% (37/2493) vs 1.4% (35/2493) of offspring ≤10 years, offspring ≤15 years and all offspring, respectively. Physician-confirmed PA was reported in 3.3% (9/271), 2.6% (13/493), and 1.24% (31/2493) in the three groups, respectively. Physician-confirmed PA with epinephrine auto-injector prescription was reported in1.8% (5/271), 1.8% (9/493), and 0.68% (17/2493) in the three groups, respectively. Conclusions: We found that the self-reported prevalence of peanut allergy in offspring of peanut farmers was similar to that reported in the general population. This is a unique population that may provide insight into factors that influence development of peanut allergy.

Component‐resolved diagnostics for the evaluation of peanut allergy in a low‐prevalence area

Major allergenic components of peanut from distinct geographical regions are widely dispersed. Most of the diagnostic studies are from countries with a high prevalence. There have been only few reports of allergen component sensitizations from countries with a low prevalence of peanut allergy. We aimed to investigate roles of component-resolved diagnostic (CRD) to differentiate peanut allergy and peanut tolerance in the Asian population from a country with low prevalence of peanut allergy. Participants with peanut sensitization were enrolled. Clinical reactions were determined. Skin prick test (SPT) and specific IgE (sIgE) to peanut and related allergen components were performed. Forty subjects with peanut sensitization were included. The mean wheal sizes of SPT and peanut sIgE were not good predictors for differentiating peanut reactions. SIgE to rAra h 2 was more often found in patients with peanut allergy and anaphylaxis. sIgE to rAra h 9 was also more frequent in the peanut-allergic group but not related to severe reactions. In the peanut-tolerant group, despite positive SPT and/or sIgE to peanut, 90% had negative sIgE to rAha h 2 and rAra h 9. Combining rAra h 2 and rAra h 9 resulted in high performance of the test with sensitivity, specificity, positive predictive value, and negative predictive value of 84%, 90%, 0.89, and 0.86, respectively. The ratio between rAra h 2 sIgE to peanut sIgE of 0.6 can be helpful in predicting patients who will develop severe reaction. SIgE to cross-reactive carbohydrate determinants (CCD) was exclusively found in the peanut-tolerant group (33.3% vs. 0%, p=0.012). Our study identifies three allergen components: rAra h 2, rAra h 9, and CCD as important components in the diagnosis of peanut allergy in an Asian country with low prevalence. The ratio between rArah h 2 sIgE to peanut sIgE can be used for predicting patients who will develop anaphylaxis.

Evaluation of Ara h2 IgE thresholds in the diagnosis of peanut allergy in a clinical population

Evaluation of Ara h2 IgE thresholds in the diagnosis of peanut allergy in a clinical population

Serological and clinical characteristics of children with peanut sensitization in an Asian community

In the past two decades, peanut allergy prevalence has increased in the West but has been perceived as having remained low in Asia. To review the clinical presentation of Asian children with peanut hypersensitivity and measure their IgE responses to major peanut allergens. We enrolled 31 children presenting with various allergies and a positive skin prick test to peanut from the Children's hospital outpatient allergy clinic in Singapore. A detailed questionnaire was completed by parents. The children's serum IgE specific to native Ara h 1, native Ara h 2, and recombinant Ara h 3 were detected using ELISA. Of the 31 patients, 19 had previously documented reactions to peanuts, while 12 had no previous clinical reaction. Most, 89.5% (17/19) of first reactions featured skin changes (urticaria, erythema, angioedema), but only 36.8% (7/19) involved skin symptoms alone. Respiratory symptoms and GI symptoms occurred in 42.1% and 26.3% of patients respectively and did not occur as the sole manifestation of reaction. The most common GI manifestation was emesis, present in 26.3% (5/19) of subjects. Two children experienced impaired consciousness with systemic, anaphylactic events. Although most sought treatment for their first peanut reaction only one patient received epinephrine. Half of our patients reported a subsequent accidental ingestion after the diagnosis of peanut allergy, with a median time from diagnosis to first accidental ingestion of 4 months and a reported increased severity of reaction in approximately half of the repeat exposures. Eighty-seven percent of children had specific IgE directed against at least one of the major peanut allergens. Among all patients, 87.1% had IgE specific to both Ara h 1 and Ara h 2 and 54.8% to rAra h 3. Asian children with peanut sensitization have clinically similar presentations and respond to the same major allergenic proteins as their Western counterparts. The perceived differences between the populations in this context do not stem from divergent clinical or immunological responses.

Maternal peanut exposure during pregnancy and lactation reduces peanut allergy risk in offspring

Maternal allergy is believed to be a risk factor for peanut allergy (PNA) in children. However, there is no direct evidence of maternal transmission of PNA susceptibility, and it is unknown whether maternal peanut exposure affects the development of PNA in offspring. To investigate the influence of maternal PNA on offspring reactions to the first peanut exposure, and whether maternal low-dose peanut exposure during pregnancy and lactation influences these reactions and peanut sensitization in a murine model. Five-week-old offspring of PNA C3H/HeJ mothers (PNA-Ms) were challenged intragastrically with peanut (first exposure), and reactions were determined. In a subset of the experiment, PNA-Ms were fed a low dose of peanut (PNA-M/PN) or not fed peanut (PNA-M/none) during pregnancy and lactation. Their 5-week-old offspring were challenged intragastrically with peanut, and reactions were determined. In another subset of the experiment, offspring of PNA-M/PN or PNA-M/none were sensitized with peanut intragastrically for 6 weeks, and serum peanut-specific antibodies were determined. PNA-M offspring exhibited anaphylactic reactions at first exposure to peanut that were associated with peanut-specific IgG(1) levels and prevented by a platelet activation factor antagonist. In a subset experiment, PNA-M/PN offspring showed significantly reduced first-exposure peanut reactions, increased IgG(2a), and reduced mitogen-stimulated splenocyte cytokine production compared with PNA-M/none offspring. In an additional experiment, PNA-M/PN offspring showed reduction of peanut-specific IgE to active peanut sensitization. We show for the first time maternal transmission of susceptibility to first-exposure peanut reactions and active peanut sensitization. Low-dose peanut exposure during pregnancy and lactation reduced this risk.

Clinical Characteristics of Peanut-Allergic Children: Recent Changes

Green TD, LaBelle VS, Steele PH, et al. Pediatrics. 2007;120(6):1304–1310 PURPOSE OF THE STUDY. To determine if patients seen in a referral clinic are experiencing initial allergic reactions to peanuts earlier, compared with a similar population profiled at a different medical center 10 years earlier. STUDY POPULATION. The primary study group comprised children evaluated and diagnosed as having peanut allergy in the Duke University pediatric allergy and immunology clinic in North Carolina between July 2000 and April 2006. METHODS. This was a retrospective chart review with some follow-up telephone calls to determine missing data. Food-allergy diagnoses were based on clinical and laboratory data or oral food-challenge results. Results were compared with those previously published from a referral practice at Johns Hopkins Hospital in Baltimore, Maryland, from a decade earlier. RESULTS. One hundred forty patients (70 born between 1988 and 1999 and 70 born between 2000 and 2005) were included in the study. Eighty-three percent reacted on their first known exposure to peanut. The median age of first peanut exposure was 14 months, and median age at first reaction was 18 months. This contrasts to the study at Johns Hopkins Hospital between 1995 and 1997, in which the median age at first exposure was 22 months and median age at first reaction was at 24 months. Within the Duke University patient group, those born before 2000 were first exposed to peanuts at a median age of 19 months and reacted at a median age of 21 months, compared with first exposure at 12 months and first reaction at 14 months for those born in or after 2000. Most (68%) patients demonstrated sensitization or clinical allergy to other foods (53% to eggs, 26% to cow's milk, 20% to tree nuts, 11% to fish, 9% to shellfish, 7% to soy, 6% to wheat, and 6% to sesame seeds). CONCLUSIONS. The ages of first peanut exposure and reaction have declined among peanut-allergic children seen in a referral clinic. The decline in the age of first peanut reaction seems to be attributable to earlier exposure. REVIEWER COMMENTS. Assuming there is not a referral bias driving these results between the 2 sites or within the Duke University site over time, there are 2 ways to interpret these data: either peanut-allergic reactions are occurring earlier because we are feeding peanut earlier, or peanut reactions will occur in those disposed to it whenever they are fed it, whether at age 1 or 2 years. I am going to argue for the latter explanation on the basis of there being no difference in the percentage who reacted at first exposure or in the time between first exposure and first reaction. We have much more to learn regarding the influence of timing of feeding an allergenic food such as peanut; studies on this unresolved issue are underway. Many factors may play a role, but it is intriguing that, counter to what is implied in this study (that early exposure may be bad and related to an apparent rise in peanut allergy), peanut allergy is uncommon in countries that feed peanut earlier (eg, Israel). Other important messages in this study are that (1) sesame allergy is prominent, and (2) if you see egg or milk allergy, consider the possibility that peanut allergy is lurking.

Clinical Characteristics of Peanut-Allergic Children: Recent Changes

The goal was to determine whether patients seen in a referral clinic are experiencing initial allergic reactions to peanuts earlier, compared with a similar population profiled at a different medical center 10 years ago, and to investigate other changes in clinical characteristics of the patients between the 2 groups. We reviewed the medical charts of peanut-allergic patients seen in the Duke University pediatric allergy and immunology clinic between July 2000 and April 2006. The median ages of first peanut exposure and reaction were 14 and 18 months, respectively; the respective ages in a similar population profiled between 1995 and 1997 were 22 and 24 months. Within our patient group, those born before 2000 were first exposed to peanuts at a median age of 19 months and reacted at a median age of 21 months, compared with first exposure at 12 months and first reaction at 14 months for those born in or after 2000. Most patients (68%) demonstrated sensitization or clinical allergy to other foods (53% to eggs, 26% to cow's milk, 20% to tree nuts, 11% to fish, 9% to shellfish, 7% to soy, 6% to wheat, and 6% to sesame seeds). In the past decade, the ages of first peanut exposure and reaction have declined among peanut-allergic children seen in a referral clinic. Egg allergy is very common in peanut-allergic patients, and sesame seeds should perhaps be considered one of the major food allergens. The decline in the age of first peanut reaction seems to be attributable to earlier exposure.

Tough nut is cracked: Antibody treatment stifles peanut reactions

Tough nut is cracked: Antibody treatment stifles peanut reactions

The natural history of peanut allergy in young children and its association with serum peanut-specific IgE

Objectives: To observe the nature and frequency of adverse reactions caused by accidental peanut exposure in young children with clinical peanut hypersensitivity and to determine the value of serum peanut-specific IgE levels during follow-up. Study design: Eighty-three children with clinical peanut hypersensitivity diagnosed before their fourth birthdays were contacted yearly to track adverse peanut reactions. Serum peanut-specific IgE levels were determined in 51 of 83 subjects. Results: Fifty-eight percent (31/53) of subjects followed up for 5 years experienced adverse reactions from accidental peanut exposure. Regardless of the nature of their initial reaction, the majority with subsequent reactions (52%, 31/60) experienced potentially life-threatening symptoms. The group with isolated skin symptoms (11/51, 22%) had lower serum peanut-specific IgE levels than the group with respiratory and/or gastrointestinal symptoms (40/51, 78%) (median: 1.25 kUA/L vs 11.65 kUA/L, P =.004, Wilcoxon rank sums test). Despite this, there was no threshold level below which only skin symptoms appeared to occur. Four selected subjects had negative double-blind placebo-controlled food challenge responses to peanuts during follow-up. Conclusions: The majority of children with clinical peanut hypersensitivity followed up for 5 years will have adverse reactions from accidental peanut exposure. Symptoms experienced during subsequent adverse peanut reactions may not be consistent with symptoms reported during initial reactions. Therefore proper education regarding peanut avoidance and treatment of adverse reactions is necessary in all cases of clinical peanut hypersensitivity. Young children who are allergic to peanuts can lose clinical hypersensitivity. (J Pediatr 2000;137:749-55)

Clinical features of acute allergic reactions to peanut and tree nuts in children.

Peanut (PN) and tree nut (TN) allergies are potentially life-threatening, rarely outgrown, and appear to be increasing in prevalence. However, there is relatively little reported about the clinical features of acute reactions to these foods and their potential association. To describe the clinical features of acute reactions during initial and subsequent accidental ingestions of PN and TN among children with a history of at least one acute allergic reaction to these foods. Questionnaire survey, examination, and serologic testing for specific IgE antibody of patients with convincing histories of acute reactions (at least one organ system involved within 60 minutes of ingestion) to PN or TN. A total of 122 patients (63% males; median age, 8 years at time of study) had acute reactions; 68 had reactions only to PN, 20 only to TN, and 34 to both PN and TN. Of those reacting to TN, 34 had reactions to one, 12 to two, and 8 to three or more different TN, the most common being walnut, almond, and pecan. Initial reactions usually occurred at home (median age, 24 months for PN and 62 months for TN) and were considered to result from a first exposure in 72% of cases. Eighty-nine percent of the reactions involved the skin (urticaria, angioedema), 52% the respiratory tract (wheezing, throat tightness, repetitive coughing, dyspnea), and 32% the gastrointestinal tract (vomiting, diarrhea). Two organ systems were affected in 31% of initial reactions, and all three in 21% of reactions. Thirty-eight of 190 first reactions to PN or TN were treated with epinephrine. Accidental ingestions occurred in 55% of PN-allergic children (average of two accidents per patient with an accidental ingestion) and in 30% of TN-allergic children over a median period of 5.5 years. On average, symptoms after accidental exposure were generally similar to those at initial exposure. Accidents occurred commonly in school but also at home and in restaurants. Modes of accidental ingestion included sharing food, hidden ingredients, cross-contamination, and school craft projects using peanut butter. Eighty-three percent of the children were breastfed, with >90% of the mothers ingesting PN and at least one TN during lactation. Among patients reporting no history of exposure (>60% of patients for each TN), IgE antibodies were found to a particular TN in 50% to 82% of patients and to PN in 100% of patients. Acute allergic reactions to PN occur early in life. PN and TN allergic reactions coexist in one third of PN-allergic patients, frequently occur on first known exposure, and may be life-threatening, requiring emergency treatment. Accidental ingestions are common, occur frequently outside of the home, and often require emergency treatment. Consequently, early diagnosis followed by education on avoidance and treatment measures (including self-administered epinephrine) is imperative.

Anaphylactic deaths in asthmatic patients.

We reviewed seven documented deaths to peanuts and two near deaths. We excluded hearsay undocumented deaths to peanuts. Peanut allergy is one of the most common food allergies and probably the most common cause of death by food anaphylaxis in the United States. About one-third of peanut-sensitive patients have severe reactions to peanuts. Asthmatics with peanut sensitivity appear more likely to develop fatal reactions probably because of the exquisite sensitivity that asthamatics have to chemical mediators of anaphylaxis. Severe reactions occur within a few minutes of ingestion and these patients must carry preloaded epinephrine syringes, antihistamines, and medic-alert bracelets. Treatment should include repeated doses of epinephrine, antihistamines and corticosteroids as well as availability of oxygen, mechanical methods to open airways, vasopressors, and intravenous fluids. Hidden sources of peanuts such as chili, egg rolls, cookies, candy, and pastry should be recognized and identified. Scratch/prick test to peanuts are highly diagnostic. Peanut is one of the most sensitive food allergens known requiring only a few milligrams to cause a reaction. In some individuals, even contact of peanut with unbroken skin can cause an immediate local reaction. Unfortunately, peanut reaction is not outgrown and remains a life-long threat.