No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Resolution of childhood peanut allergy
Abstract
Background: Peanut allergy creates great fear in many families because it is one of the leading causes of fatal and near-fatal food-induced allergies.' Earlier reports suggested that peanut allergy was life-long, but a recent study described resolution of peanut allergy in some children. Objective: Tolerance to peanut allergy in childhood was studied. Examination of the natural history of childhood peanut allergy was explored. Methods: A retrospective review of all children with peanut allergy seen at the Children's Hospital of Philadelphia in a 3-year period (n = 293). Children with histories of peanut allergy were challenged at the mean age [3.8 years; range 1.5 to 8 year] which was 1.8 years [range: 0.5 to 6.8 years], following their last known clinical reaction. Food allergy or tolerance was confirmed by open challenges. Results: Thirty-three patients with histories of peanut allergy and a positive skin test to peanut underwent oral challenges. Not one patient (n = 5) with a history of peanut anaphylaxis developed tolerance to peanuts. In comparison, 9 of 17 patients with history of urticaria upon ingestion to peanuts developed tolerance. Also, 4 of 10 patients with flaring of their atopic dermatitis upon ingestion to peanuts developed tolerance. The 14 patients with a negative challenge to peanut had a significantly smaller wheal and flare reaction than the 19 patients with positive challenges. Tolerance to peanut was documented by a positive challenge reverting to a negative challenge in one patient. Oral challenge of 13 additional patients with positive skin tests and histories of only refusing to eat peanut resulted in 5 (39%) positive challenges. Conclusion: A selected group of peanut-allergic children, who do not have a history anaphylaxis to peanut, may develop tolerance to peanuts.
... [19] Peanut allergy is persistent in the majority of cases, and only outgrown in ~20% of patients. [20][21][22][23] A low peanut-specific IgE (sIgE) at initial diagnosis may predict tolerance acquisition. A North American study of 84 patients with peanut allergy showed that those with a peanut IgE level <5 kU/L at diagnosis had a 50% chance of outgrowing their allergy. ...
... [24] Those who had an anaphylactic reaction to peanut were less likely to outgrow their allergy. [22] A further North American study that followed up 223 patients with peanut allergy showed that 21.5% outgrew their allergy. [25] Peanut sIgE was not different at diagnosis, but significantly lower in the tolerance group at the time of rechallenge (median 0.69 kU/L in those who developed tolerance v. 2.06 kU/L in those with persistent allergy). ...
... RESEARCH accidental peanut exposure after 5 years, and half of those had experienced potentially life-threatening reactions, regardless of the nature of their initial reaction. [22] Data on food allergy in low-and middle-income countries are sparse. In a South African (SA) study of food allergy prevalence in children with moderate to severe AD, 25% had egg allergy and 24% pea nut allergy. ...
Background:
There are no previous data on tolerance development in children with atopic dermatitis (AD) and concomitant food allergy in low- and middle-income settings.
Objectives:
To determine the rate of tolerance acquisition to egg and peanut 5 years after diagnosing food allergies in South African (SA) children with AD, and to explore factors influencing tolerance acquisition.
Methods:
Five years after first diagnosing food allergy in 37 SA children with egg and/or peanut allergy, they were reassessed for their allergies by questionnaire, skin-prick tests (SPTs) and ImmunoCAP-specific IgE (sIgE) tests (Thermo Fisher Scientific/Phadia, Sweden) to egg white, ovomucoid, peanut and Arachis hypogaea allergen 2 (Ara h 2), and incremental food challenges.
Results:
Eighteen of 25 originally egg-allergic patients and 19 of 24 originally peanut-allergic children were followed up at a median age of 8 years and 3 months and 9 years and 6 months, respectively. A high percentage of children (72.2%) outgrew their egg allergy, and 15.8% outgrew their peanut allergy. Allergic comorbidity remained high, with asthma increasing over time, and AD remaining moderate in severity in the cohort overall. At diagnosis, sIgE egg white ≤9.0 kU/L and sIgE ovomucoid ≤2.0 kU/L were associated with tolerance development to egg 5 years later. At follow-up, sIgE egg white ≤0.70 kU/L, sIgE ovomucoid ≤0.16 kU/L, SPT egg-white extract ≤1 mm and SPT fresh egg ≤5 mm were associated with tolerance. At diagnosis, sIgE Ara h 2 ≤1.7 kU/L and SPT peanut ≤10 mm were associated with tolerance development to peanut 5 years later. At follow-up, sIgE peanut ≤0.22 kU/L, sIgE Ara h 2 ≤0.18 kU/L and SPT peanut ≤5.5 mm were associated with tolerance.
Conclusions:
Egg allergy was outgrown in 72.2% and peanut allergy in 15.8% of SA children 5 years after diagnosis of AD. This is in keeping with findings derived from studies in higher socioeconomic settings, and can help to guide the counselling of patients with allergies to these foods of high nutritional value.
... There are several factors that can help predict the likelihood of resolution of a food allergy (Table 1). Having more severe symptoms on ingestion or having a lower eliciting dose required to bring on an allergic reaction has been associated with allergy persistence [2,[19][20][21]. The presence of other comorbid allergic diseases has been associated with more persistent food allergy [4,5,21]. ...
... The presence of other comorbid allergic diseases has been associated with more persistent food allergy [4,5,21]. Larger SPT wheal size and higher food-specific IgE levels are also associated with a more persistent food allergy phenotype (15)(16)(17)(18)(19)(20) [2,3,5,14,19,22,23]. As will be discussed in more detail later in this paper, the likelihood of outgrowing a food allergy also relates to the particular food allergen, with children allergic to certain foods such as milk, egg, and wheat being more likely to outgrow their allergies than children with allergy to peanut or tree nuts [2][3][4][5][6][7][8]24]. ...
... Similar to children with milk allergy, the majority of children with egg allergy can tolerate extensively heated Table 1 Factors helping to predict food allergy resolution Factors indicating someone is less likely to outgrow a food allergy -More severe symptoms with a past ingestion of the allergen [2,19,20] -A lower eliciting dose to bring on a previous allergic reaction [21] -The presence of other comorbid allergic diseases [2,3] -Larger skin prick test wheal size [2,3,22] -Higher food-specific IgE levels [2,3,5,14,19,23] Factors indicating someone is more likely to outgrow a food allergy -Tolerance of extensively heated milk (for developing tolerance to uncooked milk) [13] -Tolerance of extensively heated egg (for developing tolerance to lightly cooked forms of egg) [14] A calculator to help predict the age of resolution of milk or egg allergy can be found at http://cofargroup.org [3] egg [14,39]. Extensively heated egg does not include lightly cooked forms of egg such as scrambled egg or French toast but does include egg baked more thoroughly, such as in the form of a muffin. ...
Numerous studies have demonstrated that the prevalence of food allergy is increasing. Not only are more children being diagnosed with food allergies, but studies suggest that when people outgrow their food allergies, it is taking longer than was previously thought. Studies in recent years have noted factors that may lead to a lower likelihood of developing a food allergy, including the early introduction of common food allergens, having a sufficient vitamin D level, or having a higher maternal intake of peanut early in pregnancy. Given a recent report that sensitization to common food allergens did not increase from the late 1980s/early 1990s to the mid-2000s, further studies will need to examine if the rise in food allergy prevalence is due to a change in the relationship between sensitization and clinical allergy or changes in the recognition and diagnosis of food allergy.
... Além da prevalência de alergia alimentar estar aumentando, o tempo para o desenvolvimento de tolerância tem sido maior do que previamente descrito 172,173 . A evolução da alergia alimentar depende de algumas variáveis, principalmente do tipo de alimento envolvido, das características do paciente, e do mecanismo imunológico responsável pelas manifestações clínicas [174][175][176][177][178][179][180] . ...
... As causas mais comuns de alergia alimentar na infância como o leite, a soja, o ovo e o trigo, com frequência se associam à remissão da alergia ao longo do tempo, enquanto que para amendoim, nozes e castanhas, a alergia é considerada persistente [173][174][175][176][177][178][179][180][181][182][183] . Embora alguns casos possam desenvolver tolerância clínica para peixe e camarão, existem poucos estudos que avaliaram a história natural de alergia a frutos do mar, as quais também são consideradas persistentes 186 . ...
Over the last decade, knowledge about the etiopathogenesis of food allergy (FA) has advanced a great deal. The identification of new clinical presentations, associated with the acquisition of new laboratory methods, have made the diagnostic process more accurate, especially with regard to cross-reactivity between foods and the identification of biomarkers suggestive of transitory, persistent clinical forms and/or more severe manifestations. The standardization of oral provocation tests has made their perfor- mance safer and has allowed their inclusion among the tools available for use in the etiological confirmation of FA. Despite this, exclusion of the food involved in the clinical manifestations remains as the main therapeutic strategy. Among patients allergic to cow’s milk proteins, the availability of special formulas, e.g., partiallyhydrolyzed and extensively hydrolyzed cow’s milk protein-based formulas, in addition to amino acid formulas, has facilitated the introduction of substitute formulas for these patients. The current approach to anaphylaxis is reviewed, since food is the major etio- logical agent in children. Advances in the management of some gastrointestinal manifestations are also addressed. Currently, oral immunotherapy has been increasingly used. The acquisition of new agents, namely, immunobiological agents, is also described in light of current scientific and clinical evidence. Considerations on the natural history of FA, as well as on ways how to prevent FA, are addressed. In conclusion, the 2018 Brazilian Consensus on Food Allergy aimed to review the diagnostic methods and treatment schemes available and used in the follow-up of patients with FA, with a view to adopting the best possible therapeutic approach to these patients.
... Une estimation de 10 % est plus vraisemblable... [38]. La guérison parait être plus fréquente chez des enfants ayant moins de 5 KU/l d'IgE-spécifiques ou n'ayant présenté que des réactions modérées (rash sur dermatite atopique ou urticaire isolée) et sans réactions accidentelles à des expositions intempestives [39,40]. Le pronostic serait également plus favorable si les prick-tests sont faiblement positifs (< 6 mm) et si l'AA à l'arachide reste isolée [41]. ...
... Le pronostic serait également plus favorable si les prick-tests sont faiblement positifs (< 6 mm) et si l'AA à l'arachide reste isolée [41]. Les réactions systémiques ne paraissent pas accéder à la guérison [39]. ...
Peanut allergy is one of the commonest food allergies in children and has a low natural recovery rate. It is severe and possibly causes fatal anaphylaxis. Current treatment is limited to strict eviction which, although it prevents accidents, does not abate sensitization and the risk of recurrence remains. A risk of increased sensitization has been demonstrated for milk and egg allergy in a randomized study comparing eviction with an oral tolerance induction protocol. Trials evaluating injectable immunotherapy could only be conducted when recombinant allergens, mutated to remove decisive B cell epitopes, would become available. Induction of specific oral tolerance is possible in experimental models. Studies in allergic children whose allergy resolved spontaneously have showed immunological modifications involving Th1–Th2 balance and indicating the role of regulatory T-lymphocytes. However, the slow natural evolution of food allergy in children justifies a therapeutical intervention consisting in daily administration of increasing doses of the food to reach the amount normally eaten. This aims to trigger, or accelerate, immunological tolerance. Studies on egg, milk and wheat flour allergies have produced satisfactory results, indicating a possible application to peanut allergy. This paper summarizes the main facts concerning natural oral tolerance mechanisms, the development of food allergy and spontaneous recovery, before considering specific oral tolerance induction protocols. Criteria of selection of patients are discussed. Protocol implementation modalities are presented, including the increment of doses, the duration of the treatment, parameters for the specific monitoring and later prescription concerning maintenance doses.
... Although it is believed that approximately 80% of egg and milk allergy and 20% of peanut and tree nut allergy resolve by adulthood, previous estimates are potentially biased, as findings were based largely on retrospective data in patients presenting to specialist allergy clinics. [1][2][3][4][5][6][7][8] In these scenarios, children may not have repeat food challenges for tolerance until sensitization test results are negative, or conversely, children who develop tolerance may not return to a tertiary setting for follow-up. 9,10 Furthermore, food allergy was often defined by using sensitization data rather than oral food challenges (OFCs), and food allergy in tertiary allergy clinics is rarely confirmed at both baseline and end point with the criterion standard OFC. 10 Little is known about prognostic biomarkers and risk factors for persistence of food allergy, and clinicians are currently unable to accurately predict whether food allergy presenting in infancy will resolve naturally or persist into adolescence and beyond. ...
Background
Prospectively collected data on the natural history of food allergy are lacking.
Objective
We examined the natural history of egg and peanut allergy in children from age 1 to 6 years and assessed whether a skin prick test (SPT) result or other clinical factors at diagnosis are associated with the persistence or resolution of food allergy in early childhood.
Methods
The HealthNuts cohort consists of 5276 children who were recruited at age 1 year and have been followed prospectively. Children with food allergy at age 1 year (peanut [n = 156] or raw egg [n = 471] allergy ) and children who developed new sensitizations or food reactions after age 1 year were assessed for food sensitization and allergy (confirmed by oral food challenge when indicated) at the 6-year follow-up.
Results
New-onset food allergy developed by age 6 years was more common for peanut (0.7% [95% CI = 0.5%-1.1%]) than egg (0.09% [95% CI = 0.03%-0.3%]). Egg allergy resolved more commonly (89% [95% CI = 85%-92%]) than peanut allergy (29% [95% CI = 22%-38%]) by age 6 years. The overall weighted prevalence of peanut allergy at age 6 years was 3.1% (95% CI = 2.6-3.7%) and that of egg allergy was 1.2% (95% = CI 0.9%-1.6%). The factors at age 1 year associated with persistence of peanut allergy were peanut SPT result of 8 mm or larger (odds ratio [OR] = 2.35 [95% CI 1.08-5.12]), sensitization to tree nuts (adjusted OR [aOR] = 2.51 [95% CI = 1.00-6.35]), and early-onset severe eczema (aOR = 3.23, [95% CI 1.17-8.88]). Factors at age 1 associated with persistence of egg allergy at age 6 were egg SPT result of 4 mm or larger (OR = 2.98 [95% CI 1.35-6.36]), other (peanut and/or sesame) food sensitizations (aOR = 2.80 [95% CI = 1.11-7.03]), baked egg allergy (aOR = 7.41 [95% CI = 2.16-25.3]), and early-onset severe eczema (aOR = 3.77 [95% CI = 1.35-10.52]).
Conclusion
Most egg allergy and nearly one-third of peanut allergy resolves naturally by age 6 years. The prevalence of peanut allergy at age 6 years was similar to that observed at age 1 year, largely owing to new-onset food peanut allergy after age 1 year. Infants with early-onset eczema, larger SPT wheals, or multiple food sensitizations and/or allergies were less likely to acquire tolerance to either peanut or egg.
... Der natürliche Verlauf ist stark von der Nahrungsmittelquelle abhängig: Kuhmilch- [113,114], Hühnerei [115,116,117], Wei zen [118] und Sojaallergien [119] tendieren zu einer Spontanremission über die ersten Lebensjahre. Erdnuss [120,121,122,123,124,125], Baumnuss [126], Fisch und Krebstierallergien [127] Sofortwirkung zur Abwendung der patho physiologischen Effekte der Anaphylaxie eingesetzt. Hierzu gehören Adrenalin, Bron chodilatatoren, Antihistaminika und Gluko kortikosteroide [130]. ...
... In meerdere onderzoeken echter wordt het verdwijnen van allergie voor pinda beschreven. Een negatief sIgE sluit niet uit dat de patiënt allergisch zal reageren, wel is het risico op anafylaxie dan heel klein [Ho 2008;Hourihane 1998;Savage 2007a;Spergel 2000;Vander Leek 2000]. ...
... e natural course depends on the food source: cow's milk [55], hen's egg [56,57], wheat [58], and soy allergies [59] tend to develop into spontaneous remission during the rst years of life. Peanut [60,61,62,63,64], tree nut [65], but also sh and crab allergies [66], o en persist. High speci c IgE titers frequently correlate with clinical relevance and are less likely to develop into clinical tolerance. ...
... 21 En nuestro estudio no observamos reacciones adversas, lo que coincide con trabajos realizados por otros autores en los que la incidencia de reacciones adversas fue muy baja. [26][27][28][29][30][31] La tendencia central de los valores de IgE fue superior, de manera general, en los enfermos con respecto a los sanos. La discreta proporcionalidad de la desviación estándar entre ambos grupos y el mismo valor máximo obtenido en sanos y enfermos puede obedecer a que no se consideró el hábito de fumar y parasitosis intestinal, factores comunes en nuestro medio y que pueden incrementar la concentración de IgE. ...
Antecedentes: la alergia a la soya tiende a incrementarse por ser fuente básica de alimentación en países subdesarrollados y
de amplio uso industrial, lo que demanda la disponibilidad de extractos alergénicos con adecuada exactitud diagnóstica, seguros
y económicos para pruebas cutáneas.
Objetivo: evaluar la exactitud y seguridad diagnóstica de un extracto cubano de soja para diagnóstico por punción de alergia
alimentaria.
Método: estudio prospectivo y observacional efectuado en una muestra de 60 individuos; 30 con diagnóstico clínico de alergia
a la soya que acudieron, de enero a julio de 2007, a la consulta externa de Alergia del Hospital CQ Hermanos Ameijeiras y 30
controles del Banco de Sangre del mismo hospital. A los dos grupos se les hicieron pruebas cutáneas por punción (prick) con
extractos de cáscara y grano de soya (a concentraciones de 0.1 mg/mL y 1 mg/mL) elaborados por la Planta de Alergenos del
Centro Nacional de Biopreparados de la Habana, Cuba.
Resultados: en las pruebas cutáneas los extractos de grano y cáscara de soya con la mayor concentración tuvieron mayor
sensibilidad (60 y 40%, respectivamente) que a menor concentración (20 y 3%). La especificidad fue de 100% para todos los
extractos. La eficacia fue mayor con la concentración más alta del extracto (80 y 70%, respectivamente) que con la menor (60 y
50%). A mayor concentración los valores predictivos positivos fueron: 1.67 y 2.31%, respectivamente, y a menor concentración
de 6 y 30%. El valor predictivo negativo para todos los extractos fue de 1.
Conclusión: el extracto del grano de soya a la mayor concentración tiene exactitud diagnóstica y es seguro en las pruebas
cutáneas de pacientes con alergia alimentaria.
Palabras clave: pruebas cutáneas, alergia alimentaria, extracto alergénico, soya
... e natural course depends on the food source: cow's milk [55], hen's egg [56,57], wheat [58], and soy allergies [59] tend to develop into spontaneous remission during the rst years of life. Peanut [60,61,62,63,64], tree nut [65], but also sh and crab allergies [66], o en persist. High speci c IgE titers frequently correlate with clinical relevance and are less likely to develop into clinical tolerance. ...
S2k-Guidelines of the German Society for Allergology and Clinical Immunology (DGAKI) in collaboration with the German Medical Association of Allergologists (AeDA), the German Professional Association of Pediatricians (BVKJ), the German Allergy and Asthma Association (DAAB), German Dermatological Society (DDG), the German Society for Nutrition (DGE), the German Society for Gastroenterology, Digestive and Metabolic Diseases (DGVS), the German Society for Oto-Rhino-Laryngology, Head and Neck Surgery, the German Society for Pediatric and Adolescent Medicine (DGKJ), the German Society for Pediatric Allergology and Environmental Medicine (GPA), the German Society for Pneumology (DGP), the German Society for Pediatric Gastroenterology and Nutrition (GPGE), German Contact Allergy Group (DKG), the Austrian Society for Allergology and Immunology (OGAI), German Professional Association of Nutritional Sciences (VDOE) and the Association of the Scienti‰c Medical Societies Germany (AWMF)
... This paper describes repeated PN and TN OFC outcomes in a cohort of children unselected on the basis of SPT size and with initial 'mild/moderate' reactions and high threshold doses. A number of previous studies describe the severity of initial and subsequent reactions to peanut and in some cases TN but either did not use controlled OFCs at both time points or participants were selected based on SPT or specific-IgE results [7,[11][12][13][14][15][16][17]. In addition the current study included both peanut and TN allergic children and there are few studies describing the progression of TN allergy [17]. ...
In peanut and tree nut allergic children a history of anaphylaxis is associated with subsequent severe reactions.
We aimed to prospectively rechallenge peanut and tree nut allergic children with a history of mild/moderate reactions to assess their allergy over time.
In this cohort study peanut and tree nut allergic children with a history of mild/moderate reactions during a controlled oral challenge were invited to have a follow-up oral challenge to the same food at least 1 year later.
Twenty-six children participated in the study. The mean time interval between the first and second challenge for all participants was 35.5 months. Peanut or tree nut allergy resolved in 38.5% of participants. Those with persistent peanut or tree nut allergy showed a decrease in their reaction threshold and/or increased severity in 81% of cases. There were no demographic features or skin test results that were predictive of changes in severity over time.
Peanut and tree nut allergic children with a history of mild/moderate reactions who remained allergic demonstrated a high rate of more severe reactions and/or reduced thresholds upon rechallenge over a year later, however, the rate of resolution of allergy in this group may be higher than previously reported.
... 6 Studies of mixed age groups have reported similar findings. 7,25,32 Two smaller previous studies have reported SPT thresholds with 95% PPVs for persistent peanut allergy, and despite methodological differences, the results are consistent with ours. Nolan et al 10 6.3 years) that SPT responses of 7 mm or greater at follow-up have a 93% PPV to persistent peanut allergy; however, this study excluded children with sIgE levels of greater than 10 kU A /L at diagnosis and might not have been representative of the more severe end of the spectrum of peanut allergy. ...
Background:
There are no prospectively collected data available on the natural history of peanut allergy in early childhood. Previous studies of predictors of tolerance development have been biased by failure to challenge high-risk children when IgE antibody levels are high, therefore potentially introducing bias to persistent allergy.
Objectives:
We sought to describe the natural history of peanut allergy between 1 and 4 years of age and develop thresholds for skin prick test (SPT) results and specific IgE (sIgE) levels measured at age 1 and 4 years that have 95% positive predictive value (PPV) or negative predictive value for the persistence or resolution of peanut allergy.
Methods:
One-year-old infants with challenge-confirmed peanut allergy (n = 156) from the population-based, longitudinal HealthNuts Study (n = 5276) were followed up at 4 years of age with repeat oral food challenges, SPTs, and sIgE measurements (n = 103). Challenges were undertaken in all peanut-sensitized children at 1 and 4 years of age, irrespective of risk profile.
Results:
Peanut allergy resolved in 22% (95% CI, 14% to 31%) of children by age 4 years. Decreasing wheal size predicted tolerance, and increasing wheal size was associated with persistence. Thresholds for SPT responses and sIgE levels at age 1 year with a 95% PPV for persistent peanut allergy are an SPT-induced response of 13 mm or greater and an sIgE level of 5.0 kU/L or greater. Thresholds for SPT and sIgE results at age 4 years with a 95% PPV for persistent peanut allergy are an SPT response of 8 mm or greater and an sIgE level of 2.1 kU/L or greater. Ara h 2, tree nut, and house dust mite sensitization; coexisting food allergies; eczema; and asthma were not predictive of persistent peanut allergy.
Conclusion:
These thresholds are the first to be generated from a unique data set in which all participants underwent oral food challenges at both diagnosis and follow-up, irrespective of SPT and sIgE results.
... More than 50% of school-aged children with specific IgE to peanut less than 5 kIU/L had negative oral food challenges. 279,280 Long-term follow-up on individuals who outgrew their peanut allergy has not been published. It appears that patients may rarely redevelop this allergy. ...
... 21 En nuestro estudio no observamos reacciones adversas, lo que coincide con trabajos realizados por otros autores en los que la incidencia de reacciones adversas fue muy baja. [26][27][28][29][30][31] La tendencia central de los valores de IgE fue superior, de manera general, en los enfermos con respecto a los sanos. La discreta proporcionalidad de la desviación estándar entre ambos grupos y el mismo valor máximo obtenido en sanos y enfermos puede obedecer a que no se consideró el hábito de fumar y parasitosis intestinal, factores comunes en nuestro medio y que pueden incrementar la concentración de IgE. ...
Allergy to soybean has an increasing tendency due to the high consumption of soybean as a basic food resource available in poor countries, and also for being so widely used for commercial purposes. This fact demands the development of safer and cheaper allergenic extracts for skin prick tests, with better diagnostic accuracy.
To evaluate the safety and diagnostic accuracy of a soybean¥s extract for skin prick test to diagnose food allergy.
In this observational and prospective research 60 individuals were studied, 30 of them with the clinical diagnosis of soybean¥s allergy and 30 controls. Skin prick tests were performed with both, shell and soybean grain extracts (0,1mg/mL and 1mg/mL), and specificity, sensitivity and accuracy were calculated.
Sixty percent of all patients with soybean allergy showed a positive result to soybean grain extract. On the other hand, the patients in the control group had all negative results for both allergen extract concentrations (p < 0.05). All extracts¥ dilutions have 100% specificity. We observed that the soybean grain extract at 1 mg/mL was sensitive in 60%, specific in 100% and effective in 80% for soybean allergy diagnosis.
The soybean grain extract has both safety and diagnostic accuracy for the diagnosis of food allergy to soybean at the higher concentration.
... In meerdere onderzoeken echter wordt het verdwijnen van allergie voor pinda beschreven. Een negatief sIgE sluit niet uit dat de patiënt allergisch zal reageren, wel is het risico op anafylaxie dan heel klein [Ho 2008;Hourihane 1998;Savage 2007a;Spergel 2000;Vander Leek 2000]. Een derdelijns onderzoek in Amerika evalueerde bij 223 kinderen (4 tot 20 jaar) een eerder vastgestelde pinda-allergie. ...
Samenvatting De NHG-Standaarden geven richtlijnen voor het handelen van de huisarts; de rol van de huisarts staat dan ook centraal. Daarbij
geldt echter altijd dat factoren van de kant van de patiënt het beleid mede bepalen. Om praktische redenen komt dit uitgangspunt
niet telkens opnieuw in de richtlijn aan de orde, maar wordt het hier expliciet vermeld. De huisarts stelt waar mogelijk zijn
beleid vast in samenspraak met de patiënt, met inachtneming van diens specifieke omstandigheden en met erkenning van diens
eigen verantwoordelijkheid, waarbij adequate voorlichting een voorwaarde is.
... Allergien gegenüber Kuhmilch und Ei verlieren sich übli− cherweise früh im Leben bis zum 3. bzw. 5. Le− bensjahr [2]. Bei Kindern und Erwachsenen wird die Ausbildung einer Toleranz nach vorausgegan− gener Allergie durch einen doppel−blinden, Plaze− bo−kontrollierten oralen Nahrungsmittelprovo− kationstest bewiesen (DBPCFC [6]. Offensichtlich sind einschnei− dende immunologische Ereignisse notwendig, um eine Toleranz zu induzieren. ...
Einige Allergologen argumentieren, dass sich eine Nahrungsmittelallergie nach Jahren der Allergenkarenz verliert. Patienten mit schwerer Nahrungsmittelallergie sind zurückhaltend gegenüber einem Plazebo kontrollierten oralen Provokationstest. Dieser Test wäre aber notwendig, um die Entwicklung einer Toleranz zu bestätigen oder zu widerlegen. Wir haben das Fortbestehen positiver Hauttestungen auf Nahrungsmittel nach 3 Jahren der Allergenkarenz untersucht. 45 von 157 Patienten mit systemischen anaphylaktischen Reaktionen Grad III und IV stimmten einer erneuten Testung im Prick/Scratch-Test zu. 20 (44,4 %) der erneut Getesteten waren weiterhin positiv auf das bekannte Nahrungsmittelallergen, 14 (29,9 %) waren noch auf einige, aber nicht auf alle der ehemaligen Allergene positiv und 11 (31,1 %) zeigten negative Testergebnisse auf das bekannte Nahrungsmittelallergen. Bei den Wiederholungstestungen fanden wir einen Verlust der Hauttestpositivität vor allem gegenüber Fischen, Krustentieren und exotischen Früchten, während die Testungen weiterhin positiv waren bei Gewürzen, Nüssen, Gemüse und regionalen Früchten. Das konsequente Meiden des Allergens bei Nahrungsmittelallergikern führt bei einem Drittel der Patienten zu negativen Hauttestergebnissen. Wir empfehlen danach die doppelt-blinde, Plazebo-kontrollierte orale Nahrungsmittelprovokationstestung durchzuführen, um mit letzter Sicherheit nachzuweisen, dass die Allergie sich zurückgebildet hat.
... For patients with peanut allergy, we have found that the more severe the presenting allergic reaction, the less likely the patient is to outgrow food allergy, which raises the question of whether this is true for cow's milk allergy. 12 Combining the previous studies with the current data allows the creation of a survival curve for the development of tolerance to cow's milk (Fig 1). These combined data (Table I and Fig 1) suggest that 50% of the children have tolerance to cow's milk by 5 years and 75% by the early teenage years, which is consistent with the recent data from Wood et al. 3 A concern in the article by Wood et al 3 is that some of the children might not have food allergy to cow's milk because they were included in the study based on specific IgE levels (>5 kU A /L) to cow's milk in children with atopic dermatitis. ...
... Allergic reactions to food items, such as cow's milk, hen's egg, peanut, tree nuts, wheat, soy and fish often develop within the first few years of life. Whereas cow's milk and hen's egg allergy can resolve by school age (18,19), peanut and fish allergy tend to persist throughout childhood and adulthood (20,21). To detect factors associated with the persistence or resolution of food allergies over time, prospective longitudinal studies are necessary. ...
The true prevalence and risk factors of food allergies in children are not known because estimates were based predominantly on subjective assessments and skin or serum tests of allergic sensitization to food. The diagnostic gold standard, a double-blind placebo-controlled food provocation test, was not performed consistently to confirm suspected allergic reactions in previous population studies in children. This protocol describes the specific aims and diagnostic protocol of a birth cohort study examining prevalence patterns and influential factors of confirmed food allergies in European children from different regions.
Within the collaborative translational research project EuroPrevall, we started a multi-center birth cohort study, recruiting a total of over 12 000 newborns in nine countries across Europe in 2005-2009. In addition to three telephone interviews during the first 30 months, parents were asked to immediately inform the centers about possible allergic reactions to food at any time during the follow-up period.
All children with suspected food allergy symptoms were clinically evaluated including double-blind placebo-controlled food challenge tests. We assessed sensitization to different food allergens by measurements of specific serum immunoglobulin E and skin prick tests, collect blood, saliva or buccal swabs for genetic tests, breast milk for measurement of food proteins/cytokines, and evaluate quality-of-life and economic burden of families with food allergic children.
This birth cohort provides unique data on prevalence, risk factors, quality-of-life, and costs of food allergies in Europe, leading to the development of more informed and integrated preventative and treatment strategies for children with food allergies.
... After diagnosis and despite avoidance measures, most peanut-allergic children have accidental exposures to peanut resulting in allergic symptoms, and > 40% of subsequent allergic reactions may be more severe than the initial reaction (Bock and Atkins 1989;Vander Leek et al. 2000). However, in a subset of peanut-allergic children, up to 20% will become tolerant to peanut and will be able to reintroduce peanut into their diets (Hourihane et al. 1998;Skolnick et al. 2001;Spergel et al. 2000). Factors that appear to predict resolution of peanut allergy include mild cutaneous allergic features at onset, fewer associated atopic features, loss or diminution of skin prick test reactions to peanut, and low levels of peanut-specific IgE. ...
Food allergy affects between 5% and 7.5% of children and between 1% and 2% of adults. The greater prevalence of food allergy in children reflects both the increased predisposition of children to develop food allergies and the development of immunologic tolerance to certain foods over time. Immunoglobulin (Ig) E-mediated food allergies can be classified as those that persist indefinitely and those that are predominantly transient. Although there is overlap between the two groups, certain foods are more likely than others to be tolerated in late childhood and adulthood. The diagnosis of food allergy rests with the detection of food-specific IgE in the context of a convincing history of type I hypersensitivity-mediated symptoms after ingestion of the suspected food or by eliciting IgE-mediated symptoms after controlled administration of the suspected food. Presently, the only available treatment of food allergies is dietary vigilance and administration of self-injectable epinephrine.
... The oral challenge test is the ''gold standard'' to confirm or refute histories of adverse reactions to foods when conducted in a double-blind, placebo-controlled manner (17). On the other hand, open challenge testing might be acceptable in young children or for screening the least suspected foods (18,19), especially when the physician picked specific endpoints that were not subjective. Also, OFC is easy to perform, inexpensive, and not a time-intensive procedure when compared with doubleblind, placebo-controlled food challenge. ...
Although beef allergy has long been considered a rare condition, the number of studies regarding the nature, epidemiology, and symptoms of beef allergy has been increasing. We aimed to describe the results of allergy work-up of 12 patients who have a convincing history of acute allergic symptoms following beef ingestion.
Detailed histories of 10 children and two adult relatives were obtained and patients underwent skin prick tests with commercial beef extract, raw beef and cooked beef. Serum total and beef-specific IgE were measured. Labial, and in selected cases, open food challenges were undertaken.
Interestingly, the rate of family history of beef allergy was 67% (8/12). Three patients (two with commercial extract, and one with cooked beef) had positive skin test responses to beef. Ten (83%) patients had elevated serum IgE concentrations (median 316.5 kU/l, range 9-1321 kU/l) and the beef-specific IgE was positive in all patients (median 6.23 kUA/l, range 0.83-36.6 kUA/l). Labial food challenge was positive in four (30%) patients. Of the five patients who underwent open food challenges, three were positive and two tolerated the beef administered.
We conclude that skin prick tests do not accurately diagnose IgE-mediated sensitization to beef. Thus, patients with suspected beef allergy should be screened additionally for beef-specific IgE antibodies, and in selected cases oral food challenge should be carried out to verify the diagnosis.
... Other groups have similarly concluded that peanut allergy can resolve in some people. 24,61 Skolnick and coauthors 24 reported on the frequency and characteristics of peanut allergy resolution in 223 people who were selected for an oral challenge because they had not had an allergic reaction to peanuts during the preceding year, they had low peanut-specific IgE levels or they met both criteria. Fortyeight (21%) of the children had no reaction from the challenge, which suggests that the peanut allergy had resolved. ...
Peanut allergy accounts for the majority of severe food-related allergic reactions. It tends to present early in life, and affected individuals generally do not outgrow it. In highly sensitized people, trace quantities can induce an allergic reaction. In this review, we will discuss the prevalence, clinical characteristics, diagnosis, natural history and management of peanut allergy.
... In practice, however, this argument does not appear to be valid, since only a small proportion of the food proteins to which individuals are regularly exposed in their diet is associated with allergic disease (Sampson, 1988;Young et al. 1994;Bush & Hefle, 1996;Hefle et al. 1996). Furthermore, some protein allergens, such as those associated with allergy to peanuts, often cause persistent and severe sensitisation reactions, whereas others (including, for instance, some milk proteins) are characterised by less profound and more transient sensitisation (Pumphrey, 2000;Spergel et al. 2000;Bock et al. 2001). ...
There is considerable interest in the development and evaluation of approaches for the safety assessment of novel foods, and in particular in methods for characterisation of allergenic potential. One strategy that has found favour is a tiered approach in which the potential of novel proteins to induce allergic sensitisation is assessed based on considerations of stability of the protein in a simulated gastric juice and homology with, or structural similarity to, known allergens. Linked to such an approach may be evaluation of serological identity with proteins known to cause allergic disease. With the aim of supplementing such approaches with a more direct measurement of potential allergenic activity, attempts have been made to characterise the quality of immune responses elicited in BALB/c strain mice. Such evaluations comprise measurement of IgG and IgE antibody production and (to a lesser extent) of induced cytokine expression patterns. Investigations to date suggest that in mice proteins provoke variable immune responses, those with the potential to cause allergic sensitisation stimulating IgE (and IgG) antibody production. In contrast, non-allergenic, but nevertheless immunogenic, proteins are associated with IgG antibody responses in the absence of marked IgE production. Consistent with the selective activation of selective type 2 T lymphocyte responses, exposure of mice to allergenic protein is associated with preferential expression of IL-4, -5, -10 and -13. Collectively these data suggest that characterisation of the nature of immune response induced in mice by proteins may provide a useful adjunct or alternative to current strategies for the assessment of allergenic potential.
... Whereas some food allergies are largely outgrown during childhood (e.g. milk allergy), the resolution of peanut allergy in children is rare (Spergel et al. 2000;Skolnick et al. 2001;Rangaraj et al. 2004). All these factors stress the importance of providing information on the allergenic ingredients of food products to the consumer, enabling him or her to adhere to a strict elimination diet. ...
Accidental exposure to hazelnut or peanut constitutes a real threat to the health of allergic consumers. Correct information regarding food product ingredients is of paramount importance for the consumer, thereby reducing exposure to food allergens. In this study, 569 cookies and chocolates on the European market were purchased. All products were analysed to determine peanut and hazelnut content, allowing a comparison of the analytical results with information provided on the product label. Compared to cookies, chocolates are more likely to contain undeclared allergens, while, in both food categories, hazelnut traces were detected at higher frequencies than peanut. The presence of a precautionary label was found to be related to a higher frequency of positive test results. The majority of chocolates carrying a precautionary label tested positive for hazelnut, whereas peanut traces were not be detected in 75% of the cookies carrying a precautionary label.
Cette thèse actualise les connaissances de l'évaluation de l'allergénicité des aliments et son application au diagnostic de l'allergie alimentaire. Après la définition, les caractéristiques et la classification des allergènes alimentaires, les phénomènes physico-chimiques modifiant l'allergénicité des aliments ainsi que les réactivités croisées sont décrites. Ainsi sont introduits les outils cliniques et biologiques utiles au diagnostic de l'allergie alimentaire et à la détection des traces d'allergènes alimentaires. Une collaboration étroite entre cliniciens et chercheurs biologistes, permet d'optimiser la prise en charge diagnostique et thérapeutique de l'allergie alimentaire. Cette démarche se concrétise par la mise à disposition et l'utilisation de divers outils (développement d'allergènes recombinants, dosage de contaminants alimentaires dans des médicaments ou aliments, ...) et est illustrée par diverses mises en situation clinique réelles.
Éric a sept ans et bien que n’ayant aucun antécédent personnel d’allergies alimentaires, le test de réintroduction à l’arachide que sa maman nous presse instamment de réaliser (du fait des antécédents de réaction à la noix de Cajou de son jumeau homozygote) est très fortement positif. Cette observation est intéressante à plus d’un titre, permettant de réviser les données les plus récentes concernant les facteurs de risque, les réactions croisées, la démarche diagnostique et la conduite à tenir devant une suspicion d’allergie à l’arachide.
Food allergy is an important public health problem affecting 5% of infants and children in Korea. Food allergy is defined as an immune response triggered by food proteins. Food allergy is highly associated with atopic dermatitis and is one of the most common triggers of potentially fatal anaphylaxis in the community. Sensitization to food allergens can occur in the gastrointestinal tract (class 1 food allergy) or as a consequence of cross reactivity to structurally homologous inhalant allergens (class 2 food allergy). Allergenicity of food is largely determined by structural aspects, including cross-reactivity and reduced or enhanced allergenicity with cooking that convey allergenic characteristics to food. Management of food allergy currently focuses on dietary avoidance of the offending foods, prompt recognition and treatment of allergic reactions, and nutritional support. This review includes definitions and examines the prevalence and management of food allergies and the characteristics of food allergens.
Peanut allergy affects 1% of children, and for those with persistent disease, few data have been published on trends in peanut-specific immunoglobulin E (P-IgE) levels or the value of P-IgE in predicting reaction severity.
The primary outcome was the frequency of inadvertent peanut exposure. Secondary outcomes included clinical characteristics, trends in P-IgE, characteristics of accidental exposures, and predictors of reaction severity in patients with persistent peanut allergy.
Records of patients with persistent peanut allergy were reviewed. Other allergic conditions, P-IgE levels, and peanut exposures were documented.
Seven hundred eighty-two patients were studied, 524 of them male. The median age at initial observation was 1.4 years; the median duration of follow-up was 5.3 years. Of the 782 patients, 93.1% were avoiding other foods, 70.8% had atopic dermatitis, 57.3% allergic rhinitis, and 55.8% asthma. The median initial P-IgE was 28.0 kU/L, and the median peak P-IgE was 68.1. Six hundred eighty-five exposures were seen among 455 patients: 75.9% ingestion, 13.6% contact, 4.5% airborne. 73.7% resulted in urticaria/angioedema, 22.2% lower respiratory symptoms, 21.2% gastrointestinal symptoms, and 7.7% oral erythema/pruritus. Treatment included antihistamines (33.4%), emergency department visits (16.5%), epinephrine (13.1%), corticosteroids (7.7%), albuterol (3.2%), no treatment (26.3%), and not recorded (29.6%). The rate of postdiagnosis ingestion was 4.7%/year; exposures with severe reactions, 1.6%/year; reactions treated with epinephrine, 1.1%/year. Reaction severity did not change with repeated exposure. Severe reactions were associated with higher P-IgE, but not with age, sex, or asthma.
In this referral population, the rates of accidental peanut exposures and severe reactions were low. There was a strong association between higher P-IgE levels and reaction severity.
IgE-mediated allergic reactions to foods represent the earliest and most important manifestation of allergic diseases in childhood. Sensitization to foods may happen very early in life. Basic options for alimentary allergy prevention are breast-feeding of at least 4 months and in case nursing is impossible, use of an alternative hypoallergenic formula. The most common food allergens in childhood are cow's milk, hen's egg, peanuts, tree nuts and wheat. The prevalence of food allergies in childhood is 2 to 6%. In up to 50% of infants and children with atopic eczema, food allergies play a role; vice versa 95% of children with an IgE-mediated food allergy have atopic eczema as an underlying disease. Diagnostic reliability in suspected allergic reactions to food is only achieved in most cases by performing controlled oral food challenges. The long-term prognosis is good for cow's milk and hen's egg allergy, while peanut and tree nut allergies often last life-long. The most important therapeutic option is a specific elimination diet; especially in infancy, a nutritionally adequate substitution diet has to be considered. Children who might inadvertently get into contact with their potentially life threatening food allergen, should be provided with an epinephrine autoinjector.
Data from many studies have suggested a rise in the prevalence of food allergies during the past 10 to 20 years. Currently, no curative treatments for food allergy exist, and there are no effective means of preventing the disease. Management of food allergy involves strict avoidance of the allergen in the patient's diet and treatment of symptoms as they arise. Because diagnosis and management of the disease can vary between clinical practice settings, the National Institute of Allergy and Infectious Diseases (NIAID) sponsored development of clinical guidelines for the diagnosis and management of food allergy. The guidelines establish consensus and consistency in definitions, diagnostic criteria, and management practices. They also provide concise recommendations on how to diagnose and manage food allergy and treat acute food allergy reactions. The original guidelines encompass practices relevant to patients of all ages, but food allergy presents unique and specific concerns for infants, children, and teenagers. To focus on those concerns, we describe here the guidelines most pertinent to the pediatric population.
Article Outline Contents 1. Introduction 1.1. Overview 1.2. Relationship of the US Guidelines to other guidelines 1.3. How the Guidelines were developed 1.3.1. The Coordinating Committee 1.3.2. The Expert Panel 1.3.3. The independent, systematic literature review and report 1.3.4. Assessing the quality of the body of evidence 1.3.5. Preparation of the draft Guidelines and Expert Panel deliberations 1.3.6. Public comment period and draft Guidelines revision 1.4. Defining the strength of each clinical guideline 1.5. Summary 2. Definitions, prevalence, and epidemiology of food allergy 2.1. Definitions 2.1.1. Definitions of food allergy, food, and food allergens 2.1.2. Definitions of related terms 2.1.3. Definitions of specific food-induced allergic conditions 2.2. Prevalence and epidemiology of food allergy 2.2.1. Systematic reviews of the prevalence of food allergy 2.2.2. Prevalence of allergy to specific foods, foodinduced anaphylaxis, and food allergy with comorbid conditions 3. Natural history of food allergy and associated disorders 3.1. Natural history of food allergy in children 3.2. Natural history of levels of allergen-specific IgE to foods in children 3.3. Natural history of food allergy in adults 3.4. Natural history of conditions that coexist with food allergy 3.4.1. Asthma 3.4.2. Atopic dermatitis 3.4.3. Eosinophilic esophagitis 3.4.4. Exercise-induced anaphylaxis 3.5. Risk factors for the development of food allergy 3.6. Risk factors for severity of allergic reactions to foods 3.7. Incidence, prevalence, and consequences of unintentional exposure to food allergens 4. Diagnosis of food allergy 4.1. When should food allergy be suspected? 4.2. Diagnosis of IgE-mediated food allergy 4.2.1. Medical history and physical examination 4.2.2. Methods to identify the causative food 4.2.2.1. Skin prick test 4.2.2.2. Intradermal tests 4.2.2.3. Total serum IgE 4.2.2.4. Allergen-specific serum IgE 4.2.2.5. Atopy patch test 4.2.2.6. Use of skin prick tests, sIgE tests, and atopy patch tests in combination 4.2.2.7. Food elimination diets 4.2.2.8. Oral food challenges 4.2.2.9. Nonstandardized and unproven procedures 4.3. Diagnosis of non-IgE-mediated immunologic adverse reactions to food 4.3.1. Eosinophilic gastrointestinal diseases 4.3.2. Food protein-induced enterocolitis syndrome 4.3.3. Food protein-induced allergic proctocolitis 4.3.4. Food protein-induced enteropathy syndrome 4.3.5. Allergic contact dermatitis 4.3.6. Systemic contact dermatitis 4.4. Diagnosis of IgE-mediated contact urticaria 5. Management of nonacute allergic reactions and prevention of food allergy 5.1. Management of individuals with food allergy 5.1.1. Dietary avoidance of specific allergens in IgEmediated food allergy 5.1.2. Dietary avoidance of specific allergens in non-IgE-mediated food allergy 5.1.3. Effects of dietary avoidance on associated and comorbid conditions, such as atopic dermatitis, asthma, and eosinophilic esophagitis 5.1.4. Food avoidance and nutritional status 5.1.5. Food labeling in food allergy management 5.1.6. When to re-evaluate patients with food allergy 5.1.7. Pharmacologic intervention for the prevention of food-induced allergic reactions 5.1.7.1. IgE-mediated reactions 5.1.7.2. Non-IgE-mediated reactions 5.1.8. Pharmacologic intervention for the treatment of food-induced allergic reactions 5.1.9. Immunotherapy for food allergy management 5.1.9.1. Allergen-specific immunotherapy 5.1.9.2. Immunotherapy with cross-reactive allergens 5.1.10. Quality-of-life issues associated with food allergy 5.1.11. Vaccinations in patients with egg allergy 5.1.11.1. Measles, mumps, rubella, and varicella vaccine 5.1.11.2. Influenza vaccine 5.1.11.3. Yellow fever vaccine 5.1.11.4. Rabies vaccines 5.2. Management of individuals at risk for food allergy 5.2.1. Nonfood allergen avoidance in at-risk patients 5.2.2. Dietary avoidance of foods with crossreactivities in at-risk patients 5.2.3. Testing of allergenic foods in patients at high risk prior to introduction 5.2.4. Testing in infants and children with persistent atopic dermatitis 5.3. Prevention of food allergy 5.3.1. Maternal diet during pregnancy and lactation 5.3.2. Breast-feeding 5.3.3. Special diets in infants and young children 5.3.3.1. Soy infant formula versus cow’s milk formula 5.3.3.2. Hydrolyzed infant formulas versus cow’s milk formula or breast-feeding 5.3.4. Timing of introduction of allergenic foods to infants 6. Diagnosis and management of food-induced anaphylaxis and other acute allergic reactions to foods 6.1. Definition of anaphylaxis 6.2. Diagnosis of acute, life-threatening, foodinduced allergic reactions 6.3. Treatment of acute, life-threatening, foodinduced allergic reactions 6.3.1. First-line and adjuvant treatment for foodinduced anaphylaxis 6.3.2. Treatment of refractory anaphylaxis 6.3.3. Possible risks of acute therapy for anaphylaxis 6.3.4. Treatment to prevent biphasic or protracted foodinduced allergic reactions 6.3.5. Management of milder, acute food-induced allergic reactions in health care settings 6.4. Management of food-induced anaphylaxis Appendix A. Primary author affiliations and acknowledgments Acknowledgments Appendix B. List of abbreviations Reference
Data on the frequency of resolution of anaphylaxis to foods are not available, but such resolution is generally assumed to be rare.
To determine whether the frequency of negative challenge tests in children with a history of anaphylaxis to foods is frequent enough to warrant challenge testing to re-evaluate the diagnosis of anaphylaxis, and to document the safety of this procedure.
All children (n=441) who underwent a double-blind, placebo-controlled food challenge (DBPCFC) between January 2003 and March 2007 were screened for symptoms of anaphylaxis to food by history. Anaphylaxis was defined as symptoms and signs of cardiovascular instability, occurring within 2 h after ingestion of the suspected food.
Twenty-one children were enrolled (median age 6.1 years, range 0.8-14.4). The median time interval between the most recent anaphylactic reaction and the DBPCFC was 4.25 years, range 0.3-12.8. Twenty-one DBPCFCs were performed in 21 children. Eighteen of 21 children were sensitized to the food in question. Six DBPCFCs were negative (29%): three for cows milk, one for egg, one for peanut, and one for wheat. In the positive DBPCFCs, no severe reactions occurred, and epinephrine administration was not required.
This is the first study using DBPCFCs in a consecutive series of children with a history of anaphylaxis to foods, and no indications in dietary history that the food allergy had been resolved. Our study shows that in such children having specific IgE levels below established cut-off levels reported in other studies predicting positive challenge outcomes, re-evaluation of clinical reactivity to food by DBPCFC should be considered, even when there are no indications in history that anaphylaxis has resolved. DBPCFCs can be performed safely in these children, although there is a potential risk for severe reactions.
A voluntary registry of individuals with peanut and/or tree nut allergy was established in 1997 to learn more about these food allergies.
The purpose of this study was to elucidate a variety of features of peanut and tree nut allergy among the first 5149 registry participants.
The registry was established through use of a structured questionnaire distributed to all members of the Food Allergy and Anaphylaxis Network and to patients by allergists. Parental surrogates completed the forms for children under the age of 18 years.
Registrants were primarily children (89% of registrants were younger than 18 years of age; the median age was 5 years), reflecting the membership of the Network. Isolated peanut allergy was reported by 3482 registrants (68%), isolated tree nut allergy by 464 (9%), and allergy to both foods by 1203 (23%). Registrants were more likely to have been born in October, November, or December (odds ratio, 1.2; 95% CI, 1.18-1.23; P <.0001). The median age of reaction to peanut was 14 months, and the median age of reaction to tree nuts was 36 months; these represented the first known exposure for 74% and 68% of registrants, respectively. One half of the reactions involved more than 1 organ system, and more than 75% required treatment, frequently from medical personnel. Registrants with asthma were more likely than those without asthma to have severe reactions (33% vs 21%; P <.0001). In comparison with initial reactions, subsequent reactions due to accidental ingestion were more severe, more common outside the home, and more likely to be treated with epinephrine.
Allergic reactions to peanut and tree nut are frequently severe, often occur on the first known exposure, and can become more severe over time.
We eat approximately two to three tons of food in our lifetime, but most people do not have an adverse reaction to foods. Many people believe that they have an allergic reaction to foods; however, the actual incidence confirmed by history and challenges suggests a prevalence rate closer to 2% to 8% in young infants and less than 2% in adults.
Hidden peanut in consumer products can endanger patients with peanut allergy. Individual threshold doses for eliciting allergic reactions need to be elucidated to assess the risks for development of allergic reactions after accidental ingestion of peanut in a population with peanut allergy.
We sought to determine the distribution of individual threshold doses in a population with peanut allergy and to correlate these thresholds to the severity of peanut-induced symptoms.
Twenty-six adult patients with a convincing history of peanut-related symptoms, a specific IgE level of 0.7 kU/L or greater, or a positive skin prick test response of 2+ or greater to peanut were included. These patients underwent double-blind, placebo-controlled food challenges with increasing doses of peanut. A threshold dose could be established when objective or repetitive subjective reactions occurred after active doses.
All patients had subjective oral symptoms (n = 26), prior subjective gastrointestinal symptoms (n = 14), or objective symptoms (n = 5). Reactions started within 30 minutes after ingestion of peanut, but in 2 patients additional symptoms were delayed by 1 to 2 hours. Threshold doses for allergic reactions ranged from a dose as low as 100 microg up to 1 g of peanut protein. Fifty percent of the study population (95% CI, 30%-70%) already had an allergic reaction after ingestion of 3 mg of peanut protein. Patients with severe symptoms had lower threshold doses compared with those of patients with mild symptoms (P =.027).
A substantial part of a population with peanut allergy will react to very low amounts of peanut, requiring accurate declaration of peanut content in consumer products. This is even more important because patients with severe reactions react to lower doses than patients with mild symptoms.
It was once thought that peanut allergy is a lifelong problem. We previously reported that about 20% of children outgrow their peanut allergy and that more than 60% of patients with a peanut-IgE level of 5 or less passed an oral challenge.
The goal of this study was to further describe the natural progression of peanut allergy by reviewing patients who have undergone oral peanut challenges since the previous study.
Patients with peanut-IgE levels of 5 or less were offered a peanut challenge. Those who passed were further evaluated by questionnaire to assess reintroduction of peanut into their diet and whether any recurrence has occurred.
Eighty-four patients were evaluated, and 80 underwent complete analysis. Fifty-five percent with peanut-IgE levels of 5 or less and 63% with peanut-IgE levels of 2 or less passed challenges, compared to 61% and 67%, respectively, in our previous study. The 4 additional patients passed peanut challenges in this study after previously failing. Three patients with initial anaphylactic reactions and 2 patients with initial peanut-IgE levels greater than 70 passed their challenge. Follow-up of those who passed in both studies showed that the majority of patients reintroduced peanut into their diet, but that continued label reading, infrequent/limited ingestion, and aversion to peanut were all common in this population. Two patients had suspected subsequent reactions to peanut after passing their challenge.
Patients with a history of peanut allergy and peanut-IgE levels of 5 or less have at least a 50% chance of outgrowing their allergy. Recurrence of peanut allergy may occur but appears to be uncommon.
There are few studies on the incidence or recurrence of anaphylaxis.
To examine the incidence of anaphylaxis and risk factors for recurrence.
A prospective study of 432 patients referred to a community-based specialist practice in the Australian Capital Territory with anaphylaxis, followed by a survey to obtain information on recurrence.
Of 432 patients (48% male, 73% atopic, mean 27.4 years, SD 19.5, median 26) with anaphylaxis, 260 patients were seen after their first episode; 172 experienced 584 previous reactions. fifty-four percent of index episodes were treated in hospital. Aetiology was identified in 91.6% patients: food (61%), stinging insects (20.4%) or medication (8.3%). The minimum occurrence and incidence of new cases of anaphylaxis was estimated at 12.6 and 9.9 episodes/100,000 patient-years, respectively. Follow-up data were obtained from 304 patients (674 patient-years). One hundred and thirty experienced further symptoms (45 serious), 35 required hospitalization and 19 administered adrenaline. Accidental ingestion of peanut/tree nut caused the largest number of relapses, but the highest risk of recurrence was associated with sensitivity to wheat and/or exercise. Rates of overall and serious recurrence were 57 and 10 episodes/100 patient-years, respectively. Of those prescribed adrenaline, 3/4 carried it, 2/3 were in date, and only 1/2 patients faced with serious symptoms administered adrenaline. Five patients each developed new triggers for anaphylaxis, or re-presented with significant psychiatric symptoms.
In any 1 year, 1/12 patients who have suffered anaphylaxis will experience recurrence, and 1/50 will require hospital treatment or use adrenaline. Compliance with carrying and using adrenaline is poor. Occasional patients develop new triggers or suffer psychiatric morbidity.
With the increasing interest in novel foods derived from transgenic crop plants, there is a growing need for the development of approaches for the characterization of the allergenic potential of proteins. Whereas immunogenicity is a common property of foreign proteins, including food proteins, relatively few are significant dietary allergens with the inherent capacity to provoke IgE antibody production and immediate-type hypersensitivity responses.
In order to evaluate an approach for the measurement of the allergenic potential of proteins, detailed dose-response analyses of humoral immune responses induced following systemic exposure of BALB/c strain mice to proteins known to differ in terms of sensitizing activity have been conducted.
Mice were exposed to a range of concentrations of ovalbumin, a major allergenic constituent of hen's egg, a purified peanut allergen, Arachis hypogea agglutinin, or to the milk allergen bovine serum albumin, and to materials considered to lack significant allergenicity: a crude potato protein extract and a purified potato protein, potato agglutinin. The specific IgE antibody was measured by homologous passive cutaneous anaphylaxis assay, and the specific IgG antibody was measured by enzyme-linked immunosorbent assay. Each of the five proteins was immunogenic in mice, inducing IgG antibody responses at all doses tested, although there was some variation with respect to the vigour of IgG responses. Marked differences in the capacity of these proteins to induce IgE responses were observed, however, with relatively high-titre IgE antibody provoked by all three allergens over the dose ranges examined, whereas the potato proteins stimulated low-titre IgE antibody at the highest dose (10%) only. Importantly, differences in IgE antibody production have been observed against a background of equivalent immunogenicity (IgG antibody responses).
The data presented here suggest that the measurement of antibody (IgE) responses in BALB/c mice appears to identify allergens accurately and to distinguish them from those materials that apparently lack allergenicity.
The use of double-blind, placebo-controlled food challenges (DBPCFCs) is considered the gold standard for the diagnosis of food allergy. Despite this, materials and methods used in DBPCFCs have not been standardized.
The purpose of this study was to develop and validate recipes for use in DBPCFCs in children by using allergenic foods, preferably in their usual edible form.
Recipes containing milk, soy, cooked egg, raw whole egg, peanut, hazelnut, and wheat were developed. For each food, placebo and active test food recipes were developed that met the requirements of acceptable taste, allowance of a challenge dose high enough to elicit reactions in an acceptable volume, optimal matrix ingredients, and good matching of sensory properties of placebo and active test food recipes. Validation was conducted on the basis of sensory tests for difference by using the triangle test and the paired comparison test. Recipes were first tested by volunteers from the hospital staff and subsequently by a professional panel of food tasters in a food laboratory designed for sensory testing. Recipes were considered to be validated if no statistically significant differences were found.
Twenty-seven recipes were developed and found to be valid by the volunteer panel. Of these 27 recipes, 17 could be validated by the professional panel.
Sensory testing with appropriate statistical analysis allows for objective validation of challenge materials. We recommend the use of professional tasters in the setting of a food laboratory for best results.
The purpose of this investigation was to verify if avoidance of allergenic foods in children adhering to a food allergen avoidance diet from birth was complete and feasible, and whether dietary assessment can be used as a tool in predicting the outcome of double-blind, placebo-controlled food challenges (DBPCFCs).
Children adhering to an allergen avoidance diet from birth underwent DBPCFCs. The investigator-dietician verified whether the elimination was complete, using food frequency questionnaires for common allergenic foods.
University Medical Centre Groningen, the Netherlands.
Thiry-eight children aged 1-13 years, who were consecutively referred to the University Medical Centre Groningen for DBPCFC between January 2002 and February 2004.
Among the 38 children undergoing DBPCFCs, there were 15 challenges with egg, 15 with peanut, five with hazelnut and three with soy. Fifteen food challenges (39%) were positive. Small quantities of allergenic foods were inadvertently present in the diets of 13 patients (34%), were possibly present in the diets of 14 patients (37%) and could not be identified in the diets of 11 patients (29%). Seven patients (54%) who had inadvertently ingested small quantities of allergenic foods without sequelae had a positive DBPCFC.
Dietary avoidance was incomplete and not feasible in most cases. Tolerance of small amounts of allergenic foods does not preclude positive challenge reactions. Dietary assessment does not seem a useful tool in predicting the outcome of DBPCFC in children adhering to an elimination diet.
The Stichting Astma Bestrijding (Foundation for the Prevention of Asthma), The Netherlands.
Objective: To make recommendations based on a critical review of the evidence for the timing of the introduction of solid foods and its possible role in the development of food allergy. Data Sources: MEDLINE searches using the following search algorithm: [weaning AND infant AND allergy]/[food allergy AND sensitization]/[dietary prevention AND food allergy OR allergens]/[Jan 1980-Feb 2006]. Study Selection: Using the authors' clinical experience and research expertise, 52 studies were retrieved that satisfied the following conditions: English language, journal impact factor above 1 or scientific society, expert, or institutional publication, and appraisable using the World Health Organization categories of evidence.
Lipids, particularly bacterial lipopolysaccharide, can impact on immune responses to proteins, with low doses enhancing type 2 responses.
We have examined the influence of natural plant lipid extracts on antibody responses provoked in mice by recombinant Ber e 1, the major allergen in Brazil nuts.
BALB/c strain mice were immunized (by intraperitoneal injection) with natural or recombinant Ber e l produced in Pichia pastoris and admixed with various lipid fractions isolated from Brazil nuts. Serum samples were analysed for specific IgE antibody by homologous passive cutaneous anaphylaxis assay and for IgG by enzyme-linked immunosorbant assay.
Exposure to recombinant (lipid-free) Ber e 1 alone failed to induce detectable IgG or IgE antibody. Co-administration of the total lipid fraction (with reduced triglyceride levels), sterol-rich, or polar lipid fractions, resulted in marked adjuvant effects on IgG and IgE. However, the beta-sitosterol and glycolipid-rich fractions were associated with only low-level IgG antibody, and had little impact on IgE antibody production. Natural Ber e 1 containing endogenous lipids also provoked IgG and IgE antibody responses. Identical IgE and IgG antibody responses were detected regardless of whether natural or recombinant Ber e 1 was used as substrates for analyses.
Endogenous Brazil nut lipids are required for the induction of optimal antibody responses to Ber e 1 in the BALB/c strain mouse. Appropriate antibody binding sites are present on both natural and recombinant forms of Ber e 1, suggesting that the impact of lipid is at the induction phase, rather than antibody recognition, and is possibly required for efficient antigen presentation.
A cardinal feature of the double-blind, placebo-controlled food challenge (DBPCFC) is that placebo administration is included as a control. To date, the occurrence and diagnostic significance of placebo events have not extensively been documented.
To analyse the occurrence and features of placebo events in DBPCFCs and to assess their contribution to the diagnostic accuracy of the DBPCFC in children.
The study population consisted of 132 challenges in 105 sensitized children (age range 0.7-16.6 years, median 5.3 years), who underwent DBPCFCs with cow's milk, egg, peanut, hazelnut and soy. Placebo and active food challenges were performed on different days.
A total number of 17 (12.9%) positive placebo events occurred, which could be classified as immediate (9/17), late-onset (8/17), objective (11/17) or subjective (6/17). Four of 74 (5.4%) positive active food challenges were revealed to be false positive by administration of a placebo challenge. This is 3% (4/132) of all challenges. When computed by a statistical model, the false positive rate was 0.129 (12.9% of all challenges).
Placebo events with diverse clinical characteristics occur in DBPCFCs in a significant number of children. The diagnostic significance of the administration of a placebo challenge is first, to identify false positive diagnoses in DBPCFCs by refuting false positive tests in individual patients. Secondly, to allow for blinding of the active food challenge. Thirdly, applying a statistical model demonstrates that some positive challenges may be false positive and that the test may need to be repeated in selected cases.
Peanut allergy is receiving increasing attention. Only one study has estimated the prevalence in North America, but it did not corroborate history with diagnostic testing.
We estimated the prevalence of peanut allergy in Montreal by administering questionnaires regarding peanut ingestion to children in kindergarten through grade 3 in randomly selected schools.
Respondents were stratified as follows: (1). peanut tolerant, (2). never-rarely ingest peanut, (3). convincing history of peanut allergy, and (4). uncertain history of peanut allergy. Groups 2, 3, and 4 underwent peanut skin prick tests (SPTs), and if the responses were positive in groups 2 or 4, measurement of peanut-specific IgE were undertaken. Children in group 3 with a positive SPT response were considered allergic to peanut without further testing. Children in groups 2 and 4 with peanut-specific IgE levels of less than 15 kU/L underwent oral peanut challenges.
Of the 7768 children surveyed, 4339 responded, 94.6% in group 1. The prevalence of peanut allergy was 1.50% (95% CI, 1.16%-1.92%). When multiple imputation was used to incorporate data on those responding to the questionnaire but withdrawing before testing, the estimated prevalence increased to 1.76% (95% CI, 1.38%-2.21%). When data regarding the peanut allergy status of nonresponders (as declared to the school before the study) were also incorporated, the estimated prevalence was 1.34% (95% CI, 1.08%-1.64%).
Our prevalence study is the first in North America to corroborate history with confirmatory testing and the largest worldwide to incorporate these techniques. We have shown that, even with conservative assumptions, prevalence exceeds 1.0%.
The vast majority of children will undergo their first exposure to common allergenic foods at home. However, the first exposure may lead to clinical reactions. It has been proposed to introduce allergenic foods gradually into the diets of children at risk for food allergy, but no practical dietary advice has been devised.
The aim of this study was to devise safe introduction schedules for common allergenic foods for use at home, based on the challenge doses as administered in double-blind, placebo-controlled food challenge (DBPCFCs) in children who were never exposed previously to these foods.
Seventy-two DBPCFCs were performed in 63 children as a first known exposure. The incrementing challenge doses were converted into equivalent portions of these foods in their usual household form and incorporated in introduction schedules. The feasibility of the introduction scales was tested in parents of the children attending our clinic.
Based on the results of the positive challenges (37) in which severe reactions did not occur, detailed introduction schedules and a reference photograph of the required increasing amounts of food were devised for use at home. Feasibility testing showed that, when using these introduction schedules, parents portioned the initial doses significantly lower than without detailed instructions.
The introduction schedules and reference photograph provide information for parents to introduce the required amounts of allergenic foods in initial low doses at home. This is expected to improve the safety of this procedure.
To determine rates of other atopic manifestations in people with peanut allergy and the prevalence of such allergy in their families.
A survey of people with self reported peanut allergy and people referred by their general practitioner for suspected peanut allergy; survey and skin testing of 50 children with reported peanut allergy and their available first degree relatives.
622 adults and children with reported, suspected, or known peanut allergy.
Prevalence of peanut allergy and other allergies in the families of people with peanut allergy.
622 valid completed questionnaires were returned out of the 833 questionnaires dispatched (74.7%). All forms of atopy were both more common in successive generations (P < 0.0001) and more common in maternal than paternal relatives (P < 0.0001). Peanut allergy was reported by 0.1% (3/2409) of grandparents, 0.6% (7/1213) of aunts and uncles, 1.6% (19/1218) of parents, and 6.9% (42/610) of siblings. Consumption of peanuts while pregnant or breast feeding was more common among mothers of probands aged < or = 5 years than mothers of probands aged > 5 years (P < 0.001). Age of onset correlated inversely with year of birth (r = -0.6, P < 0.001). Skin prick testing of 50 children with reported peanut allergy and their families: 7 probands (14%) had a negative result for peanut. Peanut allergy was refuted by food challenge in all those tested (5/7). No parent and 13% (5/39) of siblings had a positive result on skin prick testing for peanut. Two of these siblings had negative challenge with peanuts. The prevalence of peanut allergy in siblings is therefore 3/39 (7%).
Peanut allergy is more common in siblings of people with peanut allergy than in the parents or the general population. Its apparently increasing prevalence may reflect a general increase of atopy, which is inherited more commonly from the mother. Peanut allergy is presenting earlier in life, possibly reflecting increased consumption of peanut by pregnant and nursing mothers.
To determine the prevalence of sensitisation to peanuts and tree nuts in all children born during one year in one geographical area.
Birth cohort study with structured review at ages 1, 2, and 4 years.
All children born on the Isle of Wight between January 1989 and February 1990.
Of 1456 children originally included, 1218 were reviewed at age 4 years. Of these, 1981 had skin prick tests.
Positive skin test results, clinical atopic disease, and risk factors for the development of atopy.
15 of 1218 (1.2%) children were sensitised to peanuts or tree nuts (13 to peanuts). Six had had allergic reactions to peanuts (0.5% of the population), one to hazelnuts, and one to cashew nuts; three had had anaphylactic reactions. Seven children had positive skin test results or detectable IgE to peanuts without clinical symptoms. Two children who reacted to peanut in infancy had lost their sensitivity by 4 years. Family history of atopy, allergy to egg (odds ratio 9.9, 95% confidence interval 2.1 to 47.9, and eczema (7.3, 2.1 to 26.1) were important predictors for peanut allergy.
IgE mediated allergy to peanuts is common in early childhood. In many the allergy persists but a minority may develop tolerance.
To determine whether there are any differences between children who remain mildly or moderately allergic to peanut and children with similar histories but a negative reaction on challenge with peanut.
Case-controls matched for age and sex.
Children's day wards in two teaching hospitals.
Open food challenge with peanut.
15 children with resolved peanut allergy (resolvers) and 15 with persistent allergy (persisters).
Reaction on challenge with peanut, serum total and peanut specific IgE concentrations.
The groups had a similar median age at first reaction to peanut (11 months, range 5-38) and similar symptoms. Allergy to other foods was less common in resolvers (2/15) than persisters (9/15) (P=0.02). On skin prick testing with peanut all 13 resolvers tested but only 3/14 persisters had a weal of <6 mm (P<0.0001). Total and peanut specific IgE concentrations did not differ much between the groups.
Appropriately trained clinicians must be prepared to challenge preschool children with peanut as some will be tolerant despite a history of reactions to peanut and a positive skin prick test with peanut. Preschool children whose apparent peanut allergy is refuted by food challenge show allergy to other foods less often than those in whom peanut allergy persists. The size of weal on skin prick testing to peanut predicts reactivity but not severity on peanut challenge.
A cohort of 1749 newborns from the municipality of Odense born during 1985 at the University Hospital were followed prospectively for the development of IgE-mediated and non-igE-mediated cow milk allergy (CMA) during their first year. The diagnosis of CMA was based on the results of strict elimination/milk challenge procedures in a hospital setting, and continued clinical sensitivity to cow milk (CM) was assessed by rechallenging every 6–12 months until the age of3 years. Further, in infants with CMA, the Clinical course of adverse reactions to other foods and the development of allergy to inhalant allergens In 3 years were investigated. Of 117 (6.7 %) with symptoms suggestive of CMA, the diagnosis of CMA was proven m 39 infants (2.2%), 64% showed cutaneous symptoms. 59% gastrointestinal symptoms, and 33% had respiratory symptoms. 92% had two or more symptoms and 72 % symptoms from 2 organ systems. Based on a positive skin prick test ( 2 +) and/or AL-RAST class 2 to CM 16 infants at the time of diagnosis, and at reinvestigation at 1 year, a further five infants giving a total of 21, were classified as having IgE-mediated CMA, 19 infants showed “immediate reactions to CM (within 1 h after intake of 2.3 g milk protein) and 20 infants were “late reactors”, No significant correlation between IgE-mediated CMA and “immediate reactions” to CM was demonstrated, The overall prognosis of CMA was good with a total recovery of 22/39 (56%) at 1 year. 30/39 (77%) at 2 years, and 34/39 (87%) at 3 years. Adverse reactions to other foods, particularly egg, citrus, tomato, developed in a total of 21/39 (54%) with the maximum point prevalence of 15/39 (38%) at 18 months, and 9/39 (23%) were still intolerant to other foods at 36 months. Inhalant allergy before 3 years developed in 11/39 (28%), particularly against dog and cat to which the infants had been exposed. Infants with CMA and early IgE, sensitization to CM had an increased risk of persisting CMA (24%) development of persistent adverse reactions to other foods (38%), particularly egg white (29%), and finally, inhalant allergy (48%) before 3 years of age.
A cohort of 1749 newborns from the municipality of Odense born during 1985 at the University Hospital were followed prospectively for the development of IgE-mediated and non-IgE-mediated cow milk allergy (CMA) during their first year. The diagnosis of CMA was based on the results of strict elimination/milk challenge procedures in a hospital setting, and continued clinical sensitivity to cow milk (CM) was assessed by rechallenging every 6-12 months until the age of 3 years. Further, in infants with CMA, the clinical course of adverse reactions to other foods and the development of allergy to inhalant allergens by 3 years were investigated. Of 117 (6.7%) with symptoms suggestive of CMA, the diagnosis of CMA was proven in 39 infants (2.2%). 64% showed cutaneous symptoms, 59% gastrointestinal symptoms, and 33% had respiratory symptoms. 92% had two or more symptoms and 72% symptoms from greater than or equal to 2 organ systems. Based on a positive skin prick test (greater than or equal to 2+) and/or AL-RAST class greater than or equal to 2 to CM 16 infants at the time of diagnosis, and at reinvestigation at 1 year, a further five infants giving a total of 21, were classified as having IgE-mediated CMA, 19 infants showed "immediate reactions" to CM (within 1 h after intake of 2.3 g milk protein) and 20 infants were "late reactors". No significant correlation between IgE-mediated CMA and "immediate reactions" to CM was demonstrated. The overall prognosis of CMA was good with a total recovery of 22/39 (56%) at 1 year, 30/39 (77%) at 2 years, and 34/39 (87%) at 3 years. Adverse reactions to other foods, particularly egg, citrus, tomato, developed in a total of 21/39 (54%) with the maximum point prevalence of 15/39 (38%) at 18 months, and 9/39 (23%) were still intolerant to other foods at 36 months. Inhalant allergy before 3 years developed in 11/39 (28%), particularly against dog and cat to which the infants had been exposed. Infants with CMA and early IgE sensitization to CM had an increased risk of persisting CMA (24%), development of persistent adverse reactions to other foods (38%), particularly egg white (29%), and finally, inhalant allergy (48%) before 3 years of age.
Between 1973 and 1985, 114 children, aged 2 to 14 years, underwent double-blind, placebo-controlled, food challenge (DBPCFC) to peanut. Thirty-two of 46 children with symptoms produced by DBPCFC to peanut were included in this longitudinal evaluation. Contact was made with the 32 subjects 2 to 14 years after their positive DBPCFC to peanut. All 32 subjects had exhibited a positive puncture skin test to peanut at the time of the original evaluation. Sixteen subjects had experienced symptoms caused by accidental peanut ingestion in the year before contact. Eight subjects had reacted to accidental ingestion in more than 1 year but less than 5 years before contact. Eight subjects had completely avoided peanut since the original evaluation and positive DBPCFC. No subjects could be demonstrated to have "outgrown" their peanut reactivity. All subjects tested continued to have skin reactivity to a puncture skin test with peanut extract. It appears uncommon for peanut-sensitive patients to lose their clinical reactivity, even after many years have elapsed. In addition, data were collected concerning reactions to other legumes and other (nonlegume) nuts. Only two patients with DBPCFC to peanut reacted on DBPCFC to soy or pea (one each). None of the subjects with a positive DBPCFC to peanut reacted to nonlegume nuts.
One hundred thirteen patients with severe atopic dermatitis were evaluated for food hypersensitivity with double-blind placebo-controlled oral food challenges. Sixty-three (56%) children experienced 101 positive food challenges; skin symptoms developed in 85 (84%) challenges, gastrointestinal symptoms in 53 (52%), and respiratory symptoms in 32 (32%). Egg, peanut, and milk accounted for 72% of the hypersensitivity reactions induced. History and laboratory data were of marginal value in predicting which patients were likely to have food allergy. When patients were given appropriate restrictive diets based on oral food challenge results, approximately 40% of the 40 patients re-evaluated lost their hypersensitivity after 1 or 2 years, and most showed significant improvement in their clinical course compared with patients in whom no food allergy was documented. These studies demonstrate that food hypersensitivity plays a pathogenic role in some children with atopic dermatitis and that appropriate diagnosis and exclusionary diets can lead to significant improvement in their skin symptoms.
A quality-control retrospective review of medical records was conducted for cases of anaphylaxis encountered at Mayo Clinic Rochester during a 3 1/2-year period.
For inclusion in the study, all patients had to manifest general symptoms of mediator release such as generalized pruritus, urticaria, angioedema, and flushing. Of the 179 patients with anaphylaxis (mean age, 36 years), 66% were female, 49% had atopy, and 37% had a previous history of immediate reactions to allergens. Of these study patients, 11 were receiving medications capable of exacerbating anaphylaxis (beta-blockers in 7 of them).
Consultation with an allergist was obtained in 142 cases, and a probable diagnosis was made after review of the medical records. Causes of anaphylaxis included foods in 59 patients, idiopathic in 34, Hymenoptera in 25, medications in 23, and exercise in 12; false-positive diagnoses were recorded in 18. Allergy prick tests were done in 104 patients, 71 of whom had positive results; allergen-specific IgE tests were done in 44 patients, 23 of whom had positive results. In 19 patients, only allergen-specific IgE testing was done, and results were positive in 12. Normal test results included C1 esterase inhibitor in 33 patients, metabisulfite challenge in 15, and dye or preservative challenge in 10. Food skin tests were graded on a relative value scale and revealed 15 highly allergic, 24 moderately allergic, and 39 weakly allergic food groups.
A standard protocol should be used for assessment of patients with anaphylaxis, and fresh food extracts should be used for prick skin testing. A national incidence study of anaphylaxis is needed. The public and school personnel should be educated about food anaphylaxis, and emergency treatment for anaphylaxis should be readily available for patients.
Current clinical advice regarding peanut allergy is based on small series of patients.
To determine, in a large group of peanut allergic subjects, the patterns of clinical severity, symptom progression and availability and use of rescue medications.
Questionnaire study of 622 self-reported allergic subjects.
A total of 406 patients (66%) reported symptoms on contact with peanut. Only 121 (19%) had been knowingly exposed to peanut before the first documented reaction, implying a high frequency of occult sensitization. Severe symptoms were more common in adults. Abdominal symptoms were significantly associated with collapse. Fifty per cent reported reactions in the previous year. Only 82 (13%) had been admitted to hospital because of a reaction. Adrenaline was carried in some form by 65% though only 78 subjects (12.5%) had ever received injected adrenaline. Only 18/43 subjects (41%) who collapsed were given adrenaline. Skin-prick test weal size correlated weakly with severity but there were large overlaps between the groups. Peanut-specific IgE peaked in the teenage group, but did not correlate with severity.
Peanut allergy is characterized by more severe symptoms than other food allergies and by high rates of symptoms on minimal contact. Skin-prick testing and peanut-specific IgE levels do not predict clinical severity. Avoidance of peanut is difficult. Many people suffering severe relations are inadequately treated. Sufferers need education and training in the use of rescue medication.
Peanut is the major allergen in the United States. It is increasing in importance in Europe and has become the principal food allergen affecting children over the age of three years, once hypersensitivity to eggs has resolved. We report 132 pediatric cases of peanut hypersensitivity, confirmed by food challenge. The study group included 86 boys and 46 girls aged between 6 months and 15 years. More than half the children with peanut hypersensitivity were diagnosed before the age of three. The most common symptom was atopic dermatitis (43.1% of cases). The other symptoms observed were hoarseness (34.8%), asthma attacks (13.6%), anaphylaxis (6%), gastrointestinal symptoms (1.5%) and oral syndrome (0.7%). All patients had positive skin prick tests, with a mean wheal diameter of 8 mm (range: 2 to 25 mm). Wheal diameter was significantly smaller in the youngest children (mean 4.5 mm for children under the age of 1 year, p < 0.01). Specific IgE concentration was below 0.75 IU/ml in 16 cases (14.3%), the mean for the entire group being 30.9 IU/ml (range: 0.75 to 100 IU/ml). Food challenges were not performed in three of the eight children with a history of anaphylaxis. Labial food challenge (LFC) was positive in 85 cases (64.8%). An oral food challenge (OFC) was carried out for 45 children (34.3%) and the mean reactive dose was 850 mg (range: 1 mg to 7g). LFC with peanut oil was positive in 2 cases of 50 tested (4%) and 17 of 63 children (29.9%) tested by OFC were also found to be sensitized to peanut oil. Half the children were also hypersensitive to other foods, as demonstrated by oral challenge (53.7%) or sensitized to airborne allergens (62.8%). Hypersensitivity in the very youngest children raises questions about how sensitization occurs. Diagnosis was confirmed by food challenge. Peanut products are very difficult to eliminate from the diet because of inadequate labeling of food products. An ELISA test, available in a number of countries, can be used to detect the allergen.
Allergy to peanuts and tree nuts (TNs) is one of the leading causes of fatal and near-fatal food-induced allergic reactions. These allergies can be lifelong and appear to be increasing in prevalence. Despite the seriousness of these allergies, the prevalence of peanut and TN allergy in the general population is unknown.
We sought to determine the prevalence of peanut and TN allergy among the general population of the United States.
We used a nationwide, cross-sectional, random digit dial telephone survey with a standardized questionnaire.
A total of 4374 households contacted by telephone participated (participation rate, 67%), representing 12,032 individuals. Peanut or TN allergy was self-reported in 164 individuals (1.4%; 95% confidence interval [CI], 1.2%-1.6%) in 151 households (3.5%; 95% CI, 2.9%-4.0%). The prevalence of reported allergy in adults (1.6%) was higher than that found in children under 18 years of age (0.6%). In 131 individuals, details of the reactions were obtained. When applying criteria requiring reactions to be typical of IgE-mediated reactions (hives, angioedema, wheezing, throat tightness, vomiting, and diarrhea) within an hour of ingestion, 10% of these subjects were excluded. Among the remaining 118 subjects, allergic reactions involved 1 organ system (skin, respiratory, or gastrointestinal systems) in 50 subjects, 2 in 45 subjects, and all 3 in 23 subjects. Forty-five percent of these 118 respondents reported more than 5 lifetime reactions. Only 53% of these 118 subjects ever saw a physician for the allergic reaction, and only 7% had self-injectable epinephrine available at the time of the interview. The prevalence of peanut and TN allergy was adjusted by assuming that 10% of the remaining 33 subjects without a description of their reactions would also be excluded and correcting for a 7% false-positive rate for the survey instrument. A final "corrected" prevalence estimate of 1.1% (95% CI, 1.0%-1.4%) was obtained.
Peanut and/or TN allergy affects approximately 1.1% of the general population, or about 3 million Americans, representing a significant health concern. Despite the severity of reactions, about half of the subjects never sought an evaluation by a physician, and only a few had epinephrine available for emergency use.
Patients with food-induced allergic disorders may be first seen with a variety of symptoms affecting the skin, respiratory tract, gastrointestinal tract, and/or cardiovascular system. The skin and respiratory tract are most often affected by IgE-mediated food-induced allergic reactions, whereas isolated gastrointestinal disorders are most often caused by non-IgE-mediated reactions. When evaluating possible food-induced allergic disorders, it is often useful to categorize disorders into IgE- and non-IgE-mediated syndromes. The initial history and physical examination are essentially identical for IgE- and non-IgE-mediated disorders, but the subsequent evaluation differs substantially. Proper diagnoses often require screening tests for evidence of food-specific IgE and proof of reactivity through elimination diets and oral food challenges. Once properly diagnosed, strict avoidance of the implicated food or foods is the only proven form of treatment. Clinical tolerance to food allergens will develop in many patients over time, and therefore follow-up food challenges are often indicated. However, a number of novel immunomodulatory strategies are in the developmental stage and should provide more definitive treatment for some of these food-induced allergic disorders in the next several years.
This study attempted to determine the underlying factors that may influence the development of peanut sensitization in young children in South Africa. One of our objectives was to ascertain whether the consumption of peanuts or peanut-containing foods during pregnancy and lactation by mothers from atopic families impacted upon the development of an allergic response to peanuts in the child. Forty-three children between the ages of 0 and 3 yr participated in this study. There were 25 peanut-sensitized subjects and 18 control subjects (children sensitized to milk and/or egg, but not to peanuts). A significant association was found between peanut sensitization and sensitivity to soya (p=0.0002), wheat (p=0.03), and cod fish. We found that mothers who consumed peanuts more than once a week during pregnancy were more likely to have a peanut-allergic child than mothers who consumed peanuts less than once a week (odds ratio=3.97, 98% confidence interval 0.73-24). Peanuts or peanut butter was introduced into the child's diet from a significantly younger age in the peanut-allergic subjects (p<0.03). There was a positive correlation in the peanut-allergic subjects between age of introduction of peanuts and age at the onset of symptoms (r=0.63). Exclusive breast feeding did not protect against the development of peanut sensitization. Peanut allergy is associated with an increased risk of sensitization to other foods. It is more likely to occur if mothers eat peanuts more frequently during pregnancy and introduce it early to the infant's diet. These features highlight potentially avoidable factors that might prevent sensitization.