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
Season of birth has been reported as a risk factor for food allergy, but the mechanisms by which it acts are unknown.
Two populations were studied; 5862 children from the National Health and Nutrition Examination Survey (NHANES) III, 1514 well-characterized food allergic children from the Johns Hopkins Pediatric Allergy Clinic (JHPAC). Food allergy was defined as self report of an acute reaction to a food (NHANES), or as milk, egg and peanut allergy. Logistic regression compared fall or non-fall birth between (1) food allergic and non-allergic subjects in NHANES, adjusted for ethnicity, age, income and sex, and (2) JHPAC subjects and the general Maryland population. For NHANES, stratification by ethnicity and for JHPAC, eczema, was examined.
Fall birth was more common among food allergic subjects in both NHANES (OR: 1.91, 95%CI: 1.31–2.77) and JHPAC/Maryland (OR: 1.31, 95%CI: 1.18–1.47). Ethnicity interacted with season (OR 2.34, 95%CI 1.43–3.82 for Caucasians, OR 1.19, 95%CI 0.77–1.86 for non-Caucasians, p=0.04 for interaction), as did eczema (OR 1.47, 95%CI 1.29–1.67 with eczema, OR 1.00, 95%CI 0.80–1.23 without eczema, p=0.002 for interaction).
Fall birth is associated with increased risk of food allergy, and this risk is greatest among those most likely to have seasonal variation in vitamin D during infancy (Caucasians) and those at risk for skin barrier dysfunction (subjects with a history of eczema), suggesting that vitamin D and the skin barrier may be implicated in seasonal associations with food allergy.
food allergy; season of birth; eczema; vitamin D
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.
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
Background: Despite scarce scientific evidence, current feeding guidelines recommend delayed introduction of solids for the prevention of asthma and allergy.
Aims: To explore whether late introduction of solids is protective against the development of asthma, eczema, and atopy.
Methods: A total of 642 children were recruited before birth and followed to the age of 5½ years. Main outcome measures were: doctor's diagnosis of eczema ever, atopy according to skin prick test results against inhalant allergens, preschool wheezing, transient wheezing, all defined at age 5–5½ years. Introduction of solids as main exposure measure was assessed retrospectively at age 1 year.
Results: There was no evidence for a protective effect of late introduction of solids for the development of preschool wheezing, transient wheezing, atopy, or eczema. On the contrary, there was a statistically significant increased risk of eczema in relation to late introduction of egg (aOR 1.6, 95% CI 1.1 to 2.4) and milk (aOR 1.7, 95% CI 1.1 to 2.5). Late introduction of egg was furthermore associated with a non-significant increased risk of preschool wheezing (aOR 1.5, 95% CI 0.92 to 2.4). There was no statistical evidence of feeding practices playing a different role in the development of asthma and eczema after stratification for parental asthma and atopy status.
Conclusions: Results do not support the recommendations given by present feeding guidelines stating that a delayed introduction of solids is protective against the development of asthma and allergy.
Eczema is very common and increasing in prevalence. Prospective studies investigating environmental and genetic risk factors for eczema in a birth cohort are lacking. We evaluated risk factors that may promote development of childhood eczema in the Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS) birth cohort (n = 762) of infants with at least one atopic parent. Objective environmental exposure data were available for each participant. At annual physical examinations, children underwent skin prick tests (SPTs), eczema was diagnosed by a clinician, and DNA was collected. Among Caucasian children, 39% developed eczema by age 3. Children with a pet dog were significantly less likely to have eczema at age one (odds ratio (OR) 0.62, 95% confidence interval (CI): 0.40–0.97) or at both ages 2 and 3 (OR = 0.54, 95% CI: 0.30–0.97). This finding was most significant among children carrying the CD14–159C/T CC genotype. Carriers of the CD14–159C/T and IL4Rα I75V single-nucleotide polymorphisms (SNPs) had an increased risk of eczema at ages 2 and 3 (OR 3.44, 95% CI: 1.56–7.57), especially among children who were SPT+. These results provide new insights into the pathogenesis of eczema in high-risk children and support a protective role for early exposure to dog, especially among those carrying the CD14–159C/T SNP. The results also demonstrate a susceptible effect of the combination of CD14 and IL4Rα SNPs with eczema.
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
Objective To investigate whether filaggrin gene defects, present in up to one in 10 western Europeans and North Americans, increase the risk of developing allergic sensitisation and allergic disorders.
Design Systematic review and meta-analysis.
Data sources Medline, Embase, ISI Science Citation Index, BIOSIS, ISI Web of Knowledge, UK National Research Register, clinical trials.gov, the Index to Theses and Digital dissertations, and grey literature using OpenSIGLE.
Study selection Genetic epidemiological studies (family, case-control) of the association between filaggrin gene defects and allergic sensitisation or allergic disorders.
Data extraction Atopic eczema or dermatitis, food allergy, asthma, allergic rhinitis, and anaphylaxis, along with relevant immunological variables relating to the risk of allergic sensitisation as assessed by either positive skin prick testing or increased levels of allergen specific IgE.
Data synthesis 24 studies were included. The odds of developing allergic sensitisation was 1.91 (95% confidence interval 1.44 to 2.54) in the family studies and 1.57 (1.20 to 2.07) in the case-control studies. The odds of developing atopic eczema was 1.99 (1.72 to 2.31) in the family studies and 4.78 (3.31 to 6.92) in the case-control studies. Three studies investigated the association between filaggrin gene mutations and allergic rhinitis in people without atopic eczema: overall odds ratio 1.78 (1.16 to 2.73). The four studies that investigated the association between filaggrin gene mutations and allergic rhinitis in people with atopic eczema reported a significant association: pooled odds ratio from case-control studies 2.84 (2.08 to 3.88). An overall odds ratio for the association between filaggrin gene mutations and asthma in people with atopic eczema was 2.79 (1.77 to 4.41) in case-control studies and 2.30 (1.66 to 3.18) in family studies. None of the studies that investigated filaggrin gene mutations and asthma in people without atopic eczema reported a significant association; overall odds ratio was 1.30 (0.7 to 2.30) in the case-control studies. The funnel plots suggested that publication bias was unlikely to be an explanation for these findings. No studies investigated the association between filaggrin gene mutations and food allergy or anaphylaxis.
Conclusions Filaggrin gene defects increase the risk of developing allergic sensitisation, atopic eczema, and allergic rhinitis. Evidence of the relation between filaggrin gene mutations and atopic eczema was strong, with people manifesting increased severity and persistence of disease. Filaggrin gene mutations also increased the risk of asthma in people with atopic eczema. Restoring skin barrier function in filaggrin deficient people in early life may help prevent the development of sensitisation and halt the development and progression of allergic disease.
The cumulative rate of childhood eczema during the first three years was studied in a birth cohort of 1265 New Zealand infants. A parental history of eczema was the strongest predictor of rates of childhood eczema but parental asthma was also related to childhood eczema. Children exposed to an early diverse solid-food diet also had increased risks of eczema, but there was no evidence to suggest that breast-feeding practices had any effect on rates of eczema. Analysis of the data suggested that the apparent association between exclusive breast-feeding and reduced rates of eczema reported in previous studies may be because exclusively breast-fed infants were not exposed to early solid feeding rather than to any beneficial effect of breast milk itself.
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
Several studies conducted during the past two decades suggested increasing trend of childhood allergic diseases in China. However, few studies have provided detailed description of geographic variation and explored risk factors of these diseases. This study investigated the pattern and risk factors of asthma, allergic rhinitis and eczema in eight metropolitan cities in China.
We conducted a cross-sectional survey during November-December 2005 in eight metropolitan cities in China. A total of 23791 children aged 6-13 years participated in this survey. Questions from the standard questionnaire of the International Study of Asthma and Allergies in Children (ISAAC) were used to examine the pattern of current asthma, allergic rhinitis and eczema. Logistic regression analyses were performed to assess the risk factors for childhood allergies.
The average prevalence of childhood asthma, allergic rhinitis and eczema across the eight cities was 3∙3% (95% Confidence interval (CI): 3∙1%, 3∙6%), 9∙8% (95% CI: 9∙4%, 10∙2%) and 5∙5% (95% CI: 5∙2%, 5∙8%), respectively. Factors related to lifestyle, mental health and socio-economic status were found to be associated with the prevalence of childhood allergies. These risk factors were unevenly distributed across cities and disproportionately affected the local prevalence.
There was apparent geographic variation of childhood allergies in China. Socio-environmental factors had strong impacts on the prevalence of childhood allergies; but these impacts differed across regions. Thus public health policies should specifically target at the local risk factors for each individual area.
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.
The purpose of this study was to estimate the national prevalence of childhood asthma and other allergic diseases in Korea, and to determine potential risk factors for the diseases. Stratified random samples of 42,886 were selected from 34 elementary (6-12 yr olds) and 34 middle schools (12-15 yr olds) nationwide, and 38,955 were in the final analysis. The Korean-translated modified version of the International Study of Asthma and Allergies in Childhood questionnaire was used in this cross-sectional survey. Twelve-month prevalences of the symptoms of asthma, rhinoconjunctivitis, and flexural eczema were 8.7%, 10.5%, 7.3% in 6-12 yr olds, and 8.2%, 10.0%, 3.9% in 12-15 yr olds, respectively. For allergic conjunctivitis, food allergy, and drug allergy, the prevalences in 6-12 yr olds were 11.2%, 6.5%, and 1.5%, respectively. Asthma and flexural eczema decreased significantly with age. Other significant risk factors were also noted. For 6-12 yr-old asthma, adjusted odds ratio (aOR) of body mass index was 1.21 with 95% confidence interval (CI) 1.0-1.48, aOR of passive smoking was 1.37 with 95%CI 1.24-1.51, aOR of carpet use was 1.28 with 95%CI 1.10-1.49. For 6-12 yr-old eczema, aOR of affluence was 1.22 with 95%CI 1.07-1.39. The control of obesity and passive smoking would be the most important preventive measures of allergic diseases.
Children with asthma have increased prevalence of food allergies. The relationship between food allergy and asthma morbidity is unclear.
We aimed to investigate the presence of food allergy as an independent risk factor for increased asthma morbidity using the School Inner-City Asthma (SICAS), a prospective study evaluating risk factors and asthma morbidity among urban children.
We prospectively surveyed 300 children from inner-city schools with physician-diagnosed asthma, followed by clinical evaluation. Food allergies were reported including symptoms experienced within one hour of food ingestion. Asthma morbidity, pulmonary function, and resource utilization were compared between children with food allergies and without.
Seventy-three (24%) of 300 asthmatic children surveyed had physician- diagnosed food allergy, and 36 (12%) had multiple food allergies. Those with any food allergy independently had increased risk of hospitalization (OR: 2.35, 95% CI: 1.30–4.24, p=0.005), and use of controller medication (OR: 1.99, 95% CI: 1.06–3.74, p=0.03). Those with multiple food allergies also had an independently higher risk of hospitalization in the past year (OR: 4.10 95% CI: 1.47–11.45, p=0.007), asthma-related hospitalization (OR: 3.52, 95% CI: 1.12–11.03, p=0.03), controller medication use (OR: 2.38 95% CI: 1.00–5.66, p=0.05), and more provider visits (median 4.5 versus 3.0, p=0.008). Furthermore, lung function was significantly lower (% predicted FEV1 and FEV1/FVC ratios) in both food allergy category groups.
Food allergy is highly prevalent in inner-city school-aged children with asthma. Children with food allergies have increased asthma morbidity and health resource utilization with decreased lung function, and this association is stronger in those with multiple food allergies.
asthma; food allergy; hospitalization; morbidity; prevalence; resource utilization; risk
Aims: To establish whether development of eczema is influenced by feeding practices in preterm infants, while taking account of confounding factors.
Methods: Data were assembled from 257 infants born prematurely and studied to 12 months post-term. Logistic regression analysis was performed to establish the association between feeding practices and eczema, allowing for potential confounding factors including the infants' gender, parental atopic status, social background, and parental smoking habits.
Results: For the development of eczema (with or without other symptoms) by 12 months post-term, the introduction of four or more solid foods by or before 17 weeks post-term was a significant risk (odds ratio 3.49). Male infants were at significantly higher risk (odds ratio 1.84). In addition, having non-atopic parents who introduced solid foods before 10 weeks post-term or having at least one atopic parent represented a significant risk scenario (odds ratio 2.94).
Conclusions: Early introduction of a diverse range of solid foods may predispose the preterm infant to eczema development by 12 months post-term. Furthermore, non-atopic parents who practice early as opposed to late introduction of solid foods may be exposing preterm infants to a greater risk of eczema by 12 months post-term.
The prevalence of food allergy is rising and etiologic factors remain uncertain. Evidence implicates a role of vitamin D in the development of atopic diseases. Based on seasonal patterns of UVB exposure (and consequent vitamin D status), we hypothesized that food allergy patients are more often born in fall or winter.
Investigate whether season of birth is associated with food allergy.
We performed a multicenter chart review of all patients presenting to three Boston emergency departments (EDs) for food-related acute allergic reactions between 1/1/01 and 12/31/06. Months of birth among food allergy patients were compared to those of patients visiting the ED for reasons other than food allergy.
We studied 1,002 food allergy patients. Among younger children with food allergy (age <5 years) – but not among older children or adults – 41% were born in spring/summer compared to 59% in fall/winter (P=0.002). This approximately 40/60 ratio differed from birth season of children treated in the ED for non-food allergy reasons (P=0.002). Children <5 years old born in fall/winter had a 53% higher odds of food allergy compared to controls. This finding was independent of the suspected triggering food and allergic comorbidities.
Food allergy is more common in Boston children who were born in the fall and winter seasons. We propose that these findings are mediated by seasonal differences in UVB exposure. These results add support to the hypothesis that seasonal fluctuations in sunlight and perhaps vitamin D may be involved in the pathogenesis of food allergy.
Food allergy; season of birth; epidemiology; UVB; vitamin D
Food allergy prevalence is increasing in US children. Presently, the primary means of preventing potentially fatal reactions are avoidance of allergens, prompt recognition of food allergy reactions, and knowledge about food allergy reaction treatments. Focus groups were held as a preliminary step in the development of validated survey instruments to assess food allergy knowledge, attitudes, and beliefs of parents, physicians, and the general public.
Eight focus groups were conducted between January and July of 2006 in the Chicago area with parents of children with food allergy (3 groups), physicians (3 groups), and the general public (2 groups). A constant comparative method was used to identify the emerging themes which were then grouped into key domains of food allergy knowledge, attitudes, and beliefs.
Parents of children with food allergy had solid fundamental knowledge but had concerns about primary care physicians' knowledge of food allergy, diagnostic approaches, and treatment practices. The considerable impact of children's food allergies on familial quality of life was articulated. Physicians had good basic knowledge of food allergy but differed in their approach to diagnosis and advice about starting solids and breastfeeding. The general public had wide variation in knowledge about food allergy with many misconceptions of key concepts related to prevalence, definition, and triggers of food allergy.
Appreciable food allergy knowledge gaps exist, especially among physicians and the general public. The quality of life for children with food allergy and their families is significantly affected.
To determine the patterns of food allergens in children presenting to pediatric gastroenterology clinic at the Aga Khan University Hospital, Nairobi.
This data includes children evaluated from March to November, 2010.All the children presenting for evaluation of various gastrointestinal symptoms and who had positive history of atopy in at least one first degree relative were included. History of reccurent cough was sought and the skin was examined for eczema. Skin Prick Test was perfomed by an expert in allergy and immunology. Prick to Prick Test was done for local foods where commercial antigens were not available. Positive tests were followed by an exclusion and rechallenge progamme but this was excluded from analysis due to poor compliance. Analysis was performed to determine frequencies and associations of the different gastrointestinal symptoms and food allergens. Both skin Prick and Prick to Prick results were analysed together.
The commonest food allergens in order of frequency were cow milk (65%), egg (35%), beef (26%), beans (14%), chicken, corn, wheat, soya and rice (9%), fish (8%) and peanut (5%).Common local infant complementary foods including potatoes, bananas and vegetables all tested positive in 4% of the children. Pumpkin tested positive in one infant who had presented with rectal bleeding. Majority of the children had positive tests to multiple foods. Only 14% of the children had negative tests. The commonest gastrointestinal (GI) symptoms were abdominal pain (38%), constipation (36%), vomiting (14%), diarrhoea (11%), failure to thrive (9%) and colics (3%). Majority of the children had multiple GI symptoms. Eczema and cough were associated symptoms in 9% and 3% of the children respectively.
The prevalence of food allergy as suggested by this study is high in Kenyan children and contributes signficantly towards gastrointestinal morbidity. While cow milk, egg and beef are the commonest allergens, the emerging allergy to local infant complementary foods is also significant. The high frequency of multiple allergens partly contributed to poor compliance in the exclusion rechallenge programme due to lack of options on alternative foods.
Prenatal factors may contribute to the development of peanut allergy. We evaluated the risk of childhood peanut allergy in association with pregnancy exposure to Rh immune globulin, folic acid and ingestion of peanut-containing foods.
We conducted a web-based case-control survey using the Anaphylaxis Canada Registry, a pre-existing database of persons with a history of anaphylaxis. A total of 1300 case children with reported peanut allergy were compared to 113 control children with shellfish allergy. All were evaluated for maternal exposure in pregnancy to Rh immune globulin and folic acid tablet supplements, as well as maternal avoidance of dietary peanut intake in pregnancy.
Receipt of Rh immune globulin in pregnancy was not associated with a higher risk of peanut allergy (odds ratio [OR] 0.86, 95% confidence interval [CI] 0.51 to 1.45), nor was initiation of folic acid tablet supplements before or after conception (OR 0.53, 95% CI 0.19 to 1.48). Complete avoidance of peanut-containing products in pregnancy was associated with a non-significantly lower risk of peanut allergy (OR 0.53, 95% CI 0.27 to 1.03).
The risk of childhood peanut allergy was not modified by the following common maternal exposures in pregnancy: Rh immune globulin, folic acid or peanut-containing foods.
Rh immune globulin, folic acid supplement use and peanut avoidance in pregnancy have yet to be proven to modulate the risk of childhood anaphylaxis to peanuts.
Identification of prenatal factors that contribute to peanut allergy might allow for prevention of this life-threatening condition. This article explores the role of three such factors.
Allergy; peanut; shellfish; prenatal; antenatal; pregnancy; folic acid; Rh immune globulin; survey
Rather than other drugs, propofol is more likely to be used for induction of anesthesia to cause an allergic reaction. Propofol is becoming the most common intravenous agent used for induction as well as maintenance of anaesthesia. Allergy to propofol is rarely reported. We present a case of 4–year-old boy presented for elective adenotonsillectomy with past medical history of eczema and multiple allergies to food. He developed what seems to be an allergic reaction to propofol. We concluded that anaesthetists should be alerted when using propofol in patients with history of atopy or several drug allergies. Current evidence suggests that egg allergic patients are not more likely to develop anaphylaxis when exposed to propofol. If reactions to drugs occurred, it is always advisable to ascertain the exact allergen in each individual case before deciding causality. Serum tryptase, skin prick, intradermal testing, or serologic testing should be done to confirm the diagnosis of an anaphylactic reaction.
Allergy; egg allergic patient; propofol
Purpose of review
This article reviews the AAP’s statement on early nutritional interventions on the development of atopic disease in infants and children.
Recent findings suggest that restriction of maternal diet during pregnancy and lactation does not play a major role in the development of allergic disease. In high risk infants exclusive breastfeeding for at least 4 months prevents or delays atopic dermatitis, cow milk allergy, and wheezing early in life. There is evidence that supplementing breastfeeding with a hydrolyzed formula protects against atopic disease, especially atopic dermatitis in at risk infants. Finally there is little evidence that delaying the introduction of complimentary foods beyond 4 to 6 months of age has any protective effect against allergy. There is insufficient data that any dietary intervention beyond 4 to 6 months of age has any protective effect against developing atopic disease.
In high risk infants there is evidence for exclusive breastfeeding for at least 4 months and delaying of complimentary foods until 4 to 6 months prevents the development of allergy. There is some evidence that supplementing hydrolyzed formulas in high risk infants may delay or prevent allergic disease. There is no convincing evidence that maternal manipulation of diet during pregnancy or lactation, use of soy products, or infant dietary restrictions beyond 4 to 6 months has any effect on the development of atopic disease.
Atopic disease; breastfeeding; nutritional interventions; diet restrictions; allergy
Australia's rate of children with food allergy is still on an upward trend. In infants the earliest manifestation is usually atopic eczema. Australian Bureau of Statistics National Health Survey (ABNHS, 2007–2008, p.305) reported hayfever, allergic rhinitis and asthma in the top 10 most commonly reported long-term conditions for children and young people. Early effective management of eczema is essential. Australia's medical model means long wait for allergy appointments with a specialist, limiting review appointment availability. Following diagnosis of atopic eczema and treatment recommendations by a clinical immunologist/allergist or dermatologist, parents report having many unanswered questions -contributing to anxiety and confusion. They feel overwhelmed that eczema is incurable and long-term management and constant vigilance is required. Many feel a lack of support and despair. Education, demonstration and support by a nurse specialist in eczema management at a Children's hospital in Adelaide has improved outcomes and reduced the psychosocial burden of the condition. Parents and children receive 30 minutes explanation, demonstration of required treatments and an individualised, written eczema action/care plan. The education sessions use a conceptual framework based on Social Cognitive Theory where active participation, goal setting and forward planning enhance understanding assisting the long-term behavioural changes needed to master eczema management effectively. The families are reviewed by the nurse several weeks later to review progress and answer questions that have arisen over the preceding weeks. The education sessions are tailored to the individual family needs, encourage self-management and aim for increased confidence to self-regulate the condition as it waxes and wanes.
Twenty-two families in a novel clinic at Children's Youth and Women's Health Service, Adelaide undertook a pre-post intervention questionnaire surveys.
All 22 families (2009) reported that the service had assisted their understanding, enhanced management and compliance and called for expansion as soon as possible. A research project is scheduled in the near future to expand the service within the recommendations of the South Australian Chronic Diseases Action Plan 2009-2018.
Specialist nurse's support assists parents to gain the required practical skills, understanding increased confidence and compliance with their recommended treatments.
Skin prick tests are the first investigation in allergy diagnostics and their use is described in all the guidelines on atopic eczema. However, the clinical usefulness of skin prick tests is the subject of great debate. On the one hand, skin prick tests allow the identification both of individuals at risk for food allergy and of the allergen inducing the eczematous flare. On the other hand, when performed by a non-specific specialist, positive skin prick tests to foods may wrongly lead to prolonged elimination diets, which may induce nutritional deficiencies and perhaps loss of tolerance to the avoided foods. Furthermore, skin prick tests increase health costs. A consensus on this topic has not yet been reached. Considering the diversity of clinical stages in which it occurs, atopic eczema presentation should be the starting point to determine whether or not skin prick tests should be carried out.
Atopic dermatitis; Atopic eczema; Skin prick test; Food allergy
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).
Eczema is a common chronic disease which has significant morbidity and costs for children and their families. Phase One (1993) of the International Study of Asthma and Allergies in Childhood (ISAAC) found a high prevalence of symptoms of eczema in New Zealand.
In Phase Three (2001-3) we aimed to answer these three questions: Is the prevalence of eczema changing over time?; Are there ethnic differences in prevalence?; and What are the risk factors for eczema?
Five New Zealand centres participated in ISAAC Phases One and Three using the same methodology. Questionnaires about ethnicity, symptoms of eczema and environmental factors were completed by parents of 6-7 year olds (children) and self-completed by 13-14 year olds (adolescents). Prevalence and change per year were calculated by centre, ethnicity and gender. Prevalence differences between centres and associations with environmental factors were examined using logistic regression.
There was little change in prevalence over time for the children, and a decrease in prevalence for the adolescents. Prevalence was higher among Māori and even higher among Pacific participants than among European children. Positive associations with current eczema symptoms were found for both age groups for truck traffic in the street of residence, and current paracetamol consumption, and for children only, antibiotics or paracetamol in the 1st year of life. Inverse associations were found with residence in New Zealand less than 5 years, consumption of milk, seafood, and eggs, and presence of a dog in the home.
Eczema remains a significant problem, particularly for young Māori and Pacific New Zealanders in whom less recognition of eczema and poorer access to effective, sustained eczema management may be contributing factors. Reverse causation may explain all the environmental findings apart from truck traffic which is increasing in New Zealand.
Eczema; Children; Adolescents; Ethnicity; New Zealand; Environment