Food allergy is a potentially severe immune response to a food or food additive. Although a majority of children will outgrow their food allergies, some may have lifelong issues. Food allergies and other atopic conditions, such as asthma, are increasing in prevalence in Western countries. As such, it is not uncommon to note the co-existence of food allergy and asthma in the same patient. As part of the atopic march, many food allergic patients may develop asthma later in life. Each can adversely affect the other. Food allergic patients with asthma have a higher risk of developing life-threatening food-induced reactions. Although food allergy is not typically an etiology of asthma, an asthmatic patient with food allergy may have higher rates of morbidity and mortality associated with the asthma. Asthma is rarely a manifestation of food allergy alone, but the symptoms can be seen with allergic reactions to foods. There may be evidence to suggest that early childhood environmental factors, such as the mother’s and child’s diets, factor in the development of asthma; however, the evidence continues to be conflicting. All food allergic patients and their families should be counseled on the management of food allergy and the risk of developing co-morbid asthma.
food allergy; diagnosis; treatment; asthma
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.
Food allergy; Allergens; Cross reactions; Disease management
Gut flora are important immunomodulators that may be disrupted in individuals with atopic conditions. Probiotic bacteria have been suggested as therapeutic modalities to mitigate or prevent food allergic manifestations. We wished to investigate whether perinatal factors known to disrupt gut flora increase the risk of IgE-mediated food allergies.
Birth records obtained from 192 healthy children and 99 children diagnosed with food allergies were reviewed retrospectively. Data pertaining to delivery method, perinatal antibiotic exposure, neonatal nursery environment, and maternal variables were recorded. Logistic regression analysis was used to assess the association between variables of interest and subsequent food allergy diagnosis.
Retrospective investigation did not find perinatal antibiotics, NICU admission, or cesarean section to be associated with increased risk of food allergy diagnosis. However, associations between food allergy diagnosis and male gender (66 vs. 33; p=0.02) were apparent in this cohort. Additionally, increasing maternal age at delivery was significantly associated with food allergy diagnosis during childhood (OR, 1.05; 95% CI, 1.017 to 1.105; p=0.005).
Gut flora are potent immunomodulators, but their overall contribution to immune maturation remains to be elucidated. Additional understanding of the interplay between immunologic, genetic, and environmental factors underlying food allergy development need to be clarified before probiotic therapeutic interventions can routinely be recommended for prevention or mitigation of food allergies. Such interventions may be well-suited in male infants and in infants born to older mothers.
Antibiotics; Atopic dermatitis; Bifidobacteria; Cesarean section; Food allergy; Group B Streptococcus; Gut flora; Lactobacillus; PBMC peripheral blood mononuclear cell
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.
food allergy; food hypersensitivity; infants; children; guidelines; anaphylaxis
Food-induced allergic reactions are responsible for a variety of symptoms and disorders involving the skin, gastrointestinal and respiratory tracts and can be attributed to IgE-mediated and non–IgE-mediated (cellular) mechanisms.
Food allergy frequency varies according to age, local diet, and many other factors. The diagnosis of food allergy is based on clinical history, skin prick test (SPT), food specific IgE and more recently atopy patch tests (APT). If needed the use of an oral food challenge to confirm allergy or tolerance.
Describes the case of a patient with multiple manifestations of food allergy after eating habit change.
Man 20 years with a history of food allergy to egg in childhood (at date in remission) asthma and rhinitis and urticaria in contact to cats. He presents an atopic dermatitis, recurrent abdominal pain and diarrhea 18 months after change in eating habits (he became vegetarian). He also presents oral syndrome with cow's milk. The patient had 4 episodes of anaphylaxis post prandial grade 3. In 3 of them the patient ate goat cheese and the other cow cheese. Also 2 of the episodes were associated with exercise. Skin prick tests with goat`s cheese: 13 mm, cow´s milk: 8 mm wheat: 3 mm, corn 3 mm, chicken 3.5 mm, egg yolk: 3.5 mm, avocado and rice 3 mm. Atopy patch test: (+ +) goat`s milk (+) peanuts and coffee. Total IgE 686 IU/mL.
Foods with positive results were excluded from the diet and a complete remission of atopic dermatitis, abdominal pain, diarrhea and anaphylaxis was observed. All foods were reintroduced successfully except milk of goats and cows milk. The patient is currently asymptomatic.
The literature describes different kinds of manifestations of food allergy: immediate hypersensitivity (IgE mediated), delayed hypersensitivity (T lymphocytes mediated) and mixed. Highlights in this case an adult patient with a history of atopy who makes changes in eating habits, developping a food allergy to goat´s and cow s milk, with immediate (anaphylaxis, oral syndrome) and delayed manifestations (atopic dermatitis and chronic diarrhea).
Cohort studies are of great importance in defining the mechanism responsible for the development of allergy-associated diseases, such as atopic dermatitis, allergic asthma, and allergic rhinoconjunctivitis. Although these disorders share genetic and environmental risk factors, it is still under debate whether they are linked or develop sequentially along an atopic pathway. The current study was aimed to determine the pattern of allergy sensitization in the Lithuanian birth cohort “Alergemol” (n = 1558) established as a part of the multicenter European birth cohort “EuroPrevall”. Early sensitization to food allergens in the “Alergemol” birth cohort was analysed. The analysis revealed 1.3% and 2.8% of symptomatic-sensitized subjects at 6 and 12 months of age, respectively. The sensitization pattern in response to different allergens in the group of infants with food allergy symptoms was studied using allergological methods in vivo and in vitro. The impact of maternal and environmental risk factors on the early development of food allergy in at 6 and 12 months of age was evaluated. Our data showed that maternal diet, diseases, the use of antibiotics, and tobacco smoke during pregnancy had no significant impact on the early sensitization to food allergens. However, infants of atopic mothers were significantly more often sensitized to egg as compared to the infants of nonatopic mothers.
Food-allergy is a substantial and evolving health issue. We evaluate the frequency of food sensitization by prick-to-prick and atopy patch test (APT) in allergic children in a tertiary pediatric care center.
Cross-sectional retrospective study of prick-to-prick and APT tests made in atopic children attending to the Pediatric Allergy and Clinical Immunology outpatient clinic aged 6 months to 19 years. Patients were stratified in 4 groups according to age (<1, 1–5, 6–10 and >11 years), and by atopy-related diagnosis (asthma, rhinitis, food allergy, atopic dermatitis and eosinophilic gastroenteropathy).
Total of 170 prick-to-prick with fresh foods were made, 135 were positive with the next distribution: milk 28.8%, (95% CI, 21.3-36.3%), egg white 20.1% (95% CI, 13.5-26.8%), banana 19.4% (95% CI, 12.8-26%). Sensitization to milk was most common in children aged 1 to 5 years old with 26.9% (95% CI, 17.1-36.8%) compared with corn, nuts and peanuts P < 0.05. Sensitization to milk was the most frequent in the food allergy diagnosis group with 27.1% (95% CI,15.8-38.5%) compared with wheat, corn and peanuts P < 0.05.
A total of 140 APT tests were made, 105 were positive with the next distribution: soybeans 53.3% (95% CI,43.8-62.8%), peanut and chocolate both with 50.5% (95% CI,40.9-60,.0). This finding was sustained in patients with atopic dermatitis with soybean 55.6% (95% CI,36.8-74.3) compared to egg yolk. Sensitization to soybeans was most common in children aged 1 to 5 years old with 52.1% (95% CI,40.6-63.6) compared to rice and egg yolk P < 0.05. A different distribution was found for the 6 to 10 years old aged group: peanut 41.9% (95% CI,27.1-56.6) compared with egg yolk P < 0.05.
Milk is the most common food-allergen found by prick-to-prick in children independent of age or allergic diagnosis, with statistical significant difference, when compared to other food-allergens, in the group of food-allergy diagnosis and in the 1 to 5 years old age-group. Soybean is the most common food-allergen found in atopy patch test in the groups <1, 1 to 5 and >11 years old, independent of atopy related diagnosis, with statistical significant difference, when compared to other food-allergens in the group of atopic dermatitis and in the 1 to 5 years old age-group. For the 6 to 10 years old group peanut was the most common food-allergen found by APT, independent of atopy related diagnosis
Children with food allergies often have concurrent asthma.
The authors aimed to determine the prevalence of asthma in children with food allergies and the association of specific food allergies with asthma.
Parental questionnaire data regarding food allergy, corroborated by allergic sensitization were completed for a cohort of 799 children with food allergies. Multivariate regression analysis tested the association between food allergy and reported asthma.
In this cohort, the prevalence of asthma was 45.6%. After adjusting for each food allergy, environmental allergies, and family history of asthma, children with egg allergy (odds ratio [OR] = 2.0; 95% confidence interval [CI] = 1.3–3.2; P < .01) or tree nut allergy (OR = 2.0; 95% CI = 1.1–3.6; P = .02) had significantly greater odds of report of asthma.
There is a high prevalence of asthma in the food-allergic pediatric population. Egg and tree nut allergy are significantly associated with asthma, independent of other risk factors.
asthma; food allergy; food hypersensitivity; nut allergy; nut hypersensitivity; egg allergy; egg hypersensitivity; pediatrics; allergy; asthma epidemiology
It has been hypothesized that vitamin D deficiency (VDD) contributes to the development of food sensitization (FS) and then food allergy. However, the epidemiological evidence is conflicting. We aim to examine if cord blood VDD is associated with FS and if such association can be modified by genetic variants in a prospective birth cohort.
This study included 649 children who were enrolled at birth and followed from birth onward at the Boston Medical Center. We defined VDD as cord blood 25(OH)D < 11ng/ml, and FS as specific IgE ≥ 0.35kUA/L to any of eight common food allergens in early childhood. We genotyped potentially functional single nucleotide polymorphisms (SNPs) in 11 genes known to be involved in regulating IgE and 25(OH)D concentrations. Logistic regressions were used to test the effects of VDD on FS individually and jointly with SNPs.
Among the 649 children, 44% had VDD and 37% had FS. When examined alone, VDD was not associated with FS. When examined jointly with SNPs, a significant interaction between IL4 gene polymorphism (rs2243250) and VDD (pinteraction=0.003, pFDR=0.10) was found: VDD increased the risk of FS among children carrying CC/CT genotypes (OR=1.79, 95%CI: 1.15–2.77). Similar but weaker interactions were observed for SNPs in MS4A2 (rs512555), FCER1G (rs2070901), and CYP24A1 (rs2762934). When all four SNPs were simultaneously considered, a strong gene-VDD interaction was evident (pinteraction=9×10−6).
Our data demonstrate that VDD may increase the risk of FS among individuals with certain genotypes, providing evidence of gene-vitamin D interaction on FS.
cord blood plasma 25(OH)D; food sensitization; gene-vitamin D deficiency interaction; SNP
Allergic disorders, including asthma, allergic rhinitis, atopic dermatitis, eosinophilic esophagitis, and food allergy, are a major global health burden. The study and management of allergic disorders is complicated by the considerable heterogeneity in both the presentation and natural history of these disorders. Biorepositories serve as an excellent source of data and biospecimens for delineating subphenotypes of allergic disorders, but such resources are lacking.
In order to define subphenotypes of allergic disease accurately, we established an infrastructure to link and efficiently utilize clinical and epidemiologic data with biospecimens into a single biorepository called the Greater Cincinnati Pediatric Clinic Repository (GCPCR). Children with allergic disorders as well as healthy controls are followed longitudinally at hospital clinic, emergency department, and inpatient visits. Subjects' asthma, allergy, and skin symptoms; past medical, family, social, diet, and environmental histories; physical activity; medication adherence; perceived quality of life; and demographics are ascertained. DNA is collected from all participants, and other biospecimens such as blood, hair, and nasal epithelial cells are collected on a subset.
To date, the GCPCR has 6,317 predominantly Caucasian and African American participants, and 93% have banked DNA. This large sample size supports adequately powered genetic, epidemiologic, environmental, and health disparities studies of childhood allergic diseases.
The GCPCR is a unique biorepository that is continuously evaluated and refined to achieve and maintain rigorous clinical phenotype and biological data. Development of similar disease-specific repositories using common data elements is necessary to enable studies across multiple populations of comprehensively phenotyped patients.
Parents of children with food allergy, primary care physicians, and members of the general public play a critical role in the health and well-being of food-allergic children, though little is known about their knowledge and perceptions of food allergy. The purpose of this paper is to detail the development of the Chicago Food Allergy Research Surveys to assess food allergy knowledge, attitudes, and beliefs among these three populations.
From 2006–2008, parents of food-allergic children, pediatricians, family physicians, and adult members of the general public were recruited to assist in survey development. Preliminary analysis included literature review, creation of initial content domains, expert panel review, and focus groups. Survey validation included creation of initial survey items, expert panel ratings, cognitive interviews, reliability testing, item reduction, and final validation. National administration of the surveys is ongoing.
Nine experts were assembled to oversee survey development. Six focus groups were held: 2/survey population, 4–9 participants/group; transcripts were reviewed via constant comparative methods to identify emerging themes and inform item creation. At least 220 participants per population were recruited to assess the relevance, reliability, and utility of each survey item as follows: cognitive interviews, 10 participants; reliability testing ≥ 10; item reduction ≥ 50; and final validation, 150 respondents.
The Chicago Food Allergy Research surveys offer validated tools to assess food allergy knowledge and perceptions among three distinct populations: a 42 item parent tool, a 50 item physician tool, and a 35 item general public tool. No such tools were previously available.
Cow’s milk and hen’s egg are the most frequently encountered food allergens in the pediatric population. Skin prick testing (SPT) with commercial extracts followed by an oral food challenge (OFC) are routinely performed in the diagnostic investigation of these children. Recent evidence suggests that milk-allergic and/or egg-allergic individuals can often tolerate extensively heated (EH) forms of these foods. This study evaluated the predictive value of a negative SPT with EH milk or egg in determining whether a child would tolerate an OFC to the EH food product.
Charts from a single allergy clinic were reviewed for any patient with a negative SPT to EH milk or egg, prepared in the form of a muffin. Data collected included age, sex, symptoms of food allergy, co-morbidities and the success of the OFC to the muffin.
Fifty-eight patients had negative SPTs to the EH milk or egg in a muffin and underwent OFC to the appropriate EH food in the outpatient clinic. Fifty-five of these patients tolerated the OFC. The negative predictive value for the SPT with the EH food product was 94.8%.
SPT with EH milk or egg products was predictive of a successful OFC to the same food. Larger prospective studies are required to substantiate these findings.
The effect of food introduction timing on the development of food allergy remains controversial. We sought to examine whether the presence of childhood eczema changes the relationship between timing of food introduction and food allergy. The analysis includes 960 children recruited as part of a family-based food allergy cohort. Food allergy was determined by objective symptoms developing within 2 hours of ingestion, corroborated by skin prick testing/specific IgE. Physician diagnosis of eczema and timing of formula and solid food introduction were obtained by standardized interview. Cox Regression analysis provided hazard ratios for the development of food allergy for the same subgroups. Logistic regression models estimated the association of eczema and formula/food introduction with the risk of food allergy, individually and jointly. Of the 960 children, 411 (42.8%) were allergic to 1 or more foods and 391 (40.7%) had eczema. Children with eczema had a 8.4-fold higher risk of food allergy (OR, 95% CI: 8.4, 5.9–12.1). Among all children, later (>6 months) formula and rice/wheat cereal introduction lowered the risk of food allergy. In joint analysis, children without eczema who had later formula (OR, 95% CI: 0.5, 0.3–0.9) and later (>1 year) solid food (OR, 95% CI: 0.5, 0.3–0.95) introduction had a lower risk of food allergy. Among children with eczema, timing of food or formula introduction did not modify the risk of developing food allergy. Later food introduction was protective for food allergy in children without eczema but did not alter the risk of developing food allergy in children with eczema.
Cow's milk is one of the most common food allergens in children with atopic dermatitis (AD). This study was conducted to describe the natural course of cow's milk allergy in children with AD, and to identify factors predictive of outcome. To accomplish this, we reviewed the medical records of 115 children who were diagnosed with AD and cow's milk allergy before 24 months of age to evaluate their clinical characteristics and prognostic factors. During a follow-up period of 24 to114 months, the median age for tolerance to cow's milk was found to be 67 months. Multivariate analysis using the Cox proportional hazard model revealed that the peak cow's milk-specific IgE level within 24 months after birth was the most important factor for prediction of the outcome of cow's milk allergy. In conclusion, half of the children younger than 24 months of age with AD and cow's milk allergy could tolerate cow's milk at 67 months of age. The peak cow's milk-specific IgE level within the first 24 months of birth is useful to predict the prognosis of cow's milk allergy in children with AD.
Milk; Food Hypersensitivity; Immunoglobulin E; Prognosis
Allergic sensitization to food can occur through skin exposure. We investigated anaphylactic cases due to carmine, a food additive extracted from Dactylopius coccus.
Screening all patients, who visited our department from January 2000 to December 2009, we identified 2 new such cases. Both had history of rash induced by certain cosmetics containig carmine. We further investigated previous case reports of carmine allergy, whether skin sensitization antedated food allergy or not.
Case 1: A 26-year-old woman visited our hospital because of anaphylaxis occurred within 5 minutes after ingesting a Japanese YOKAN (sweetened and jellied bean paste). IgE antibodies against common food allergens including beans and wheat were all negative. As the paste contains carmine, we tested specific IgE antibody, which was positive. She had been avoiding using certain cheeks and lips for 2 years, since they cause erythema. These cosmetics emerged as containing carmine. Abstaining from the food additive made her free from anaphylaxis. Case 2: A 30-year-old woman came to our hospital for dyspnea, uriticaria, and bilateral blepharedema, immediately after drinking Campari soda. Her past history was prominent, as she had 4 episodes of anaphylaxis in 4 years, requiring emergency transport twice. All anaphylactic episodes occurred in Italian restaurants when she drank cocktails, which might contain carmine in Campari soda. She had been also sensitive to certain rouges since several years before the first onset of anaphylaxis. It became clear that the rouges contained carmine. In literatures, we found 22 cases with allergy to ingested carmine. It is surprising that all cases were women (aged 25 to 52), while occupationally sensitized patients are predominantly men. As far as we could know, 85.7 % of (6/7) mentioned cases had previous history of sensitization to cosmetics containing carmine.
In many cases with allergy against ingested carmine, the route of first sensitization was not via intestine but skin. This is similar to suspected peanut sensitization mechanism and might be a paradigm of food allergy. As allergic reaction to carmine mainly directed to impurities, using highly purified carmine is desired not only for foods but also for cosmetics.
IgE-mediated peanut allergy is a complex trait with strong heritability, but its genetic basis is currently unknown. Loss-of-function mutations within the filaggrin gene are associated with atopic dermatitis and other atopic diseases; therefore, filaggrin is a candidate gene in the etiology of peanut allergy.
To investigate the association between filaggrin loss-of-function mutations and peanut allergy.
Case-control study of 71 English, Dutch, and Irish oral food challenge–positive patients with peanut allergy and 1000 non peanut-sensitized English population controls. Replication was tested in 390 white Canadian patients with peanut allergy (defined by food challenge, or clinical history and skin prick test wheal to peanut ≥8 mm and/or peanut-specific IgE ≥15 kUL−1) and 891 white Canadian population controls. The most prevalent filaggrin loss-of-function mutations were assayed in each population: R501X and 2282del4 in the Europeans, and R501X, 2282del4, R2447X, and S3247X in the Canadians. The Fisher exact test and logistic regression were used to test for association; covariate analysis controlled for coexistent atopic dermatitis.
Filaggrin loss-of-function mutations showed a strong and significant association with peanut allergy in the food challenge–positive patients (P = 3.0 × 10−6; odds ratio, 5.3; 95% CI, 2.8-10.2), and this association was replicated in the Canadian study (P = 5.4 × 10−5; odds ratio, 1.9; 95% CI, 1.4-2.6). The association of filaggrin mutations with peanut allergy remains significant (P = .0008) after controlling for coexistent atopic dermatitis.
Filaggrin mutations represent a significant risk factor for IgE-mediated peanut allergy, indicating a role for epithelial barrier dysfunction in the pathogenesis of this disease.
Atopic dermatitis; filaggrin; IgE; peanut allergy; risk factor; AD, Atopic dermatitis; ALSPAC, Avon Longitudinal Study of Parents and Children; FLG, Filaggrin; OR, Odds ratio; SPT, Skin prick test; UK, United Kingdom
Exposure to endotoxin in early life has been proposed as a factor that may protect against the development of allergic diseases such as eczema. The objective of this study was to examine the relation between endotoxin exposure in early life and eczema in the first year of life in children with parental history of asthma or allergies.
This study used a prospective birth cohort study of 498 children who had a history of allergy or asthma in at least 1 parent and lived in metropolitan Boston. A subset of 401 living rooms had house dust samples adequate for analysis of endotoxin.
In multivariate analyses adjusting for gender, income, and season of birth, endotoxin levels in the living room at 2 to 3 months of age was inversely associated with physician- or nurse-diagnosed eczema in the first year of life (odds ratio [OR] for each quartile increment: 0.76; 95% confidence interval [CI]: 0.61–0.96). Exposure to a dog in the home at age 2 to 3 months was also inversely associated with eczema in the first year of life, but the CI widened when endotoxin was included in the multivariate model (OR: 0.54; 95% CI: 0.27–1.09). Other variables associated with eczema in the first year of life included paternal history of eczema (OR: 1.91; 95% CI: 1.03–3.55) and maternal specific immunoglobulin E positivity to ≥1 allergen (OR: 1.61; 95% CI: 1.01–2.56).
Among children with parental history of asthma or allergies, exposure to high levels of endotoxin in early life may be protective against eczema in the first year of life. In these children, paternal history of eczema and maternal sensitization to at least 1 allergen are associated with an increased risk of eczema in the first year of life.
Ig, immunoglobulin; OR, odds ratio; CI, confidence interval; Th2, T-helper cell type 2
The atopic march is well documented, but the inter-relationship of food allergy (FA) and asthma is not well understood.
To examine the strength of the association and temporal relationships between food allergy and asthma.
This analysis included 271 children ≥6 years (older group) and 296 children <6 years (younger group) from a family-based FA cohort in Chicago, IL. Asthma was determined by parental report of physician diagnosis. FA status was determined based on type and timing of clinical symptoms after ingestion of a specific food, and results of prick skin test (Multi-Test II) and allergen specific IgE (Phadia ImmunoCAP). Analyses were carried out using logistic regression accounting for important covariates and autocorrelations among siblings. Kaplan-Meier curves were used to compare the time to onset of asthma by FA status.
Symptomatic FA was associated with asthma in both older (OR=4.9, 95%CI:2.5–9.5) and younger children (OR=5.3, 95%CI:1.7–16.2). The association was stronger among children with multiple or severe food allergies, especially in older children. Children with FA developed asthma earlier and at higher prevalence than children without FA (Cox Proportional hazard ratio=3.7, 95%CI:2.2–6.3 for children ≥6 years and hazard ratio=3.3, 95%CI:1.1–10 for children <6 years of age). No associations were seen between asymptomatic food sensitization and asthma.
Independent of markers of atopy such as aeroallergen sensitization and family history of asthma, there was a significant association between FA and asthma. This association was even stronger in subjects with multiple food allergies or severe food allergy.
Food allergy; asthma; child
The relationships between a history of egg or cows' milk allergy, positive skin tests to these allergens, and atopic illness were examined in a sample of 126 children. Positive skin tests were found more often in children with a history of egg or cows' milk allergy than in children with no such history. 40 children suspected of being allergic to egg or milk, by history or by positive skin tests, were tested by double-blind food challenge. 54 challenges were given to these children, and 26 (49%) were positive. Children suspected of being allergic to egg had a greater incidence of positive challenges than children suspected of having milk allergy. Children with both a present history of food allergy and a positive skin test for that allergen were more likely to have positive challenges than children having only one of these indicators. Most children with positive challenges failed to satisfy Goldman's criterion of a minimum of three positive challenges because of the severity of their reactions. Less stringent criteria are needed for the diagnosis of food allergy in children who are particularly sensitive to food allergens.
Food allergies affect 6% of children and 3% to 4% of adults in the United States. Although several studies have examined the prevalence of food allergy, little information is available regarding the prevalence of multiple food allergies. Estimates of prevalence of people allergic to multiple foods is difficult to ascertain because those with allergy to one food may avoid additional foods for concerns related to cross-reactivity, positive tests, or prior reactions, or they may be reluctant to introduce foods known to be common allergens. Diagnosis relies on an accurate history and selective IgE testing. It is important to understand the limitations of the available tests and the role of cross-reactivity between allergens. Allergen avoidance and readily accessible emergency medications are the cornerstones of management. In addition, a multidisciplinary approach to management of individuals with multiple food allergies may be needed, as avoidance of several food groups can have nutritional, developmental, and psychosocial consequences.
Multiple food allergy; IgE; Sensitization; Cross-reactivity; Diagnosis; Allergy management
Food allergy (FA) is prevalent among children however natural history of FA is not fully clarified.
We sought to investigate the natural course of childhood FA. To follow up the transition of same patients, we collected clinical records of patients with 3 years’ interval from 2008 to 2010. Four hundred ninety-one patients (male 321 and female 170) were recruited to this study.
The onset of FA was at the age of 5 months ± 1 year 3 month (mean ± SD). The clinical type at the onset was with infantile atopic eczema (84.1%), and followed by immediate reactions without eczema (14.9%). The initial diagnosis age was 10 months ± 1 year 4 months, and the first visit to our department was 1 year 11 month ± 2 years 5 months. Current age of the patients was 7 years 5 months ± 2 years 11 months, and 444 patients (90.4%) had experienced immediate reactions. The number of eliminated foods decreased from 2.4 ± 1.5 items/patient (n = 1191) to 1.9 ± 1.6 items/patient (n = 926) in 3 years. The ratio of stopping elimination of major allergens was 35.9% (121/337 patients) for hen's egg, 25.6% (52/203 patients) for cow's milk and 47.8% (44/92 patients) for wheat. Fourteen patients (2.9%) had developed new food allergies, and 2 of them had experienced anaphylaxis by tree nuts. Newly diagnosed allergens were only 0.1 ± 0.3 items/patient (n = 32), and nuts (n = 6) and peanut (n = 5) were the most frequent. Seventy-nine patients (16.1%) had developed complete remission of FA in 3 years, and 21.5% of them (17 patients) had never developed immediate reactions.
Most of pediatric FA started during infancy with atopic eczema, and developing tolerance is expected with aging. In some patients, persistent FA is troublesome for school age children.
Cow's milk allergy is one of the most common food allergies among younger children. We investigated IgE antibodies to milk, and IgE and IgG4 antibodies to casein, α-lactalbumin and β-lactoglobulin in cow's milk allergic (CMA) and non-allergic (non-CMA) children in order to study their clinical usefulness.
Eighty-three children with suspected milk allergy (median age: 3.5 years, range: 0.8-15.8 years) were diagnosed as CMA (n = 61) or non-CMA (n = 22) based on an open milk challenge or convincing clinical history. Their serum concentrations of allergen-specific (s) IgE and IgG4 antibodies were measured using ImmunoCAP®. For the sIgG4 analysis, 28 atopic and 31 non-atopic control children were additionally included (all non-milk sensitized).
The CMA group had significantly higher levels of milk-, casein- and β-lactoglobulin-sIgE antibodies as compared to the non-CMA group. The casein test showed the best discriminating performance with a clinical decision point of 6.6 kUA/L corresponding to 100% specificity. All but one of the CMA children aged > 5 years had casein-sIgE levels > 6.6 kUA/L. The non-CMA group had significantly higher sIgG4 levels against all three milk allergens compared to the CMA group. This was most pronounced for casein-sIgG4 in non-CMA children without history of previous milk allergy. These children had significantly higher casein-sIgG4 levels compared to any other group, including the non-milk sensitized control children.
High levels of casein-sIgE antibodies are strongly associated with milk allergy in children and might be associated with prolonged allergy. Elevated casein-sIgG4 levels in milk-sensitized individuals on normal diet indicate a modified Th2 response. However, the protective role of IgG4 antibodies in milk allergy is unclear.
casein; cow's milk allergy; IgE; IgG4; ImmunoCAP
Food allergies are potentially fatal immune-mediated disorders that are growing globally. The relationship between sex and food allergy remains incompletely understood. Here we tested the hypothesis that, should sex influence the clinical response to food allergens, this would be reflected by a sex disparity in published studies of food allergy. We performed a systematic search of the PubMed literature for IgE-mediated allergy to 11 allergenic foods of international regulatory importance. No date restriction was used and only articles in English were considered. Of the 4744 articles retrieved, 591 met the inclusion criteria representing 17528 subjects with food allergies. Whereas among children with food allergies, 64.35% were males and 35.65% were females (male/female ratio, 1.80), among adults 34.82% were males and 65.18% were females (male/female ratio, 0.53). Consequently, these data argue that there is need for further investigation to define the role of sex in the pathogenesis of food allergy.
Little is known about the prevalence of atopic dermatitis and food allergy outside North America and Europe. We evaluated the prevalence of atopic dermatitis and food allergy with the comparison of prevalence between 1995 and 2000 in Korea and evaluated the correlation of prevalence between atopic dermatitis and food allergy. A cross-sectional questionnaire survey was conducted on random samples of schoolchildren 6 to 14 yr at two time points, 1995 and 2000 throughout Korea. The last twelve months prevalence of atopic dermatitis in Korean school-aged children was increased from 1995 to 2000. The twelve-month prevalence of atopic dermatitis and food allergy were higher in Seoul than in any other provincial cities in 1995, but the prevalence of both diseases in Seoul and Provincial Centers became to be similar in 2000. The rate responded to food allergy of children with atopic dermatitis (9.5%) was lower than that of the western countries (60%). And our data demonstrated paternal and maternal allergy history is very significantly correlated to developing atopic dermatitis in their offspring. The further objective evaluations are required to confirm these outcomes because the environmental and risk factors may be different among the countries according to their living cultures.
Dermatitis, Atopic; Food Hypersensitivity; Prevalence
Nine patients had attacks of joint pain and sometimes swelling precipitated by certain foods or associated with allergic manifestations. All were atopic subjects--three having strong evidence of Type I (immediate) allergy and three 'urticarial arthralgia', in which attacks of severe urticaria and joint pain occurred coincidentally. Food allergy appeared to be responsible for the joint symptoms in three patients and in one it was possible to precipitate swelling of a knee due to synovitis with effusion by drinking milk a few hours beforehand, the synovial fluid having mildly inflammatory features and a relatively high eosinophil count. It seems that allergy is an occasional cause of episodic rheumatic pain or synovitis in certain atopic patients, whether or not they have an underlying arthritis. These are usually Type I hypersensitivity reactions, though it is thought that some food-allergic reactions are immune complex-mediated.