Despite efforts to prevent food allergy (FA) in children, IgE-mediated FAs are increasing in westernized countries. Previous preventive strategies, such as prolonged exclusive breast-feeding and ...delayed weaning onto solid foods, have recently been called into question. The present review considers possible risk factors and theories for the development of FA. An alternative hypothesis is proposed, suggesting that early cutaneous exposure to food protein through a disrupted skin barrier leads to allergic sensitization and that early oral exposure to food allergen induces tolerance. Novel interventional strategies to prevent the development of FA are also discussed.
Epidemiologic risks for food allergy Lack, Gideon, MD
Journal of allergy and clinical immunology,
06/2008, Letnik:
121, Številka:
6
Journal Article
Recenzirano
This article reviews possible risk factors and theories for the development of food allergy. It is noted that previous strategies to prevent food allergy through allergen avoidance during pregnancy, ...breast-feeding, and infancy have more recently been called into question. Alternative hypotheses are examined with respect to food allergy, namely the hygiene hypothesis, the dietary fat hypothesis, the antioxidant hypothesis, and the vitamin D hypotheses. An alternative hypothesis is proposed, suggesting that sensitization to allergen occurs through environmental exposure to allergen through the skin and that consumption of food allergen induces oral tolerance. This hypothesis provides a possible explanation for the close link between eczema and the development of food allergies. It also suggests novel interventional strategies to prevent the development of food allergies.
Six foods commonly associated with food allergy were introduced in the diets of children at 3 months or 6 months of age. Intention-to-treat analysis showed no benefit of early introduction with ...respect to the prevalence of food allergy; a per-protocol analysis showed a difference.
The World Health Organization recommends exclusive breast-feeding of infants for their first 6 months of life.
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Two national guidelines that had previously recommended the delayed introduction of allergenic foods have been withdrawn (see the Introduction section in the Supplementary Appendix, available with the full text of this article at NEJM.org). In the 2010 United Kingdom Infant Feeding Survey, 45% of the mothers of infants 8 to 10 months of age reported avoiding giving their infant a particular food: 48% avoided nuts, 14% eggs, 10% dairy, and 6% fish.
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Fear of allergy was the most common reason for avoiding foods, followed by . . .
Children 4 to 11 months of age who were at high risk for development of peanut allergy were assigned to consumption or avoidance of peanuts until 60 months of age. Peanut allergy was more than five ...times as likely to develop in children assigned to peanut avoidance.
The prevalence of peanut allergy among children in Western countries has doubled in the past 10 years, reaching rates of 1.4 to 3.0%,
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and peanut allergy is becoming apparent in Africa and Asia.
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This allergy is the leading cause of anaphylaxis and death due to food allergy and imposes substantial psychosocial and economic burdens on patients and their families.
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Peanut allergy develops early in life and is rarely outgrown.
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Clinical practice guidelines from the United Kingdom in 1998
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and from the United States in 2000
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recommended the exclusion of allergenic foods from the diets of infants at . . .
A previous trial showed that early consumption of peanuts resulted in fewer cases of allergy than did avoidance. In a follow-up study, all participants avoided peanuts from 5 to 6 years of age; those ...who had eaten peanuts in early life retained the ability to do so.
Peanut allergy is a common and potentially life-threatening food allergy for which prevention and treatment strategies are required.
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The Learning Early about Peanut Allergy (LEAP) trial showed that among infants at high risk for allergy, the sustained consumption of peanut, beginning in the first 11 months of life, resulted in an 81% lower rate of peanut allergy at 60 months of age than the rate among children who avoided peanuts.
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In a study of oral immunotherapy to hen’s egg white, although children achieved unresponsiveness to an oral food challenge with egg, the majority had a reversion to egg . . .
Prevention of food allergy du Toit, George, MD; Tsakok, Teresa, MRCP; Lack, Simon, BA ...
Journal of allergy and clinical immunology,
04/2016, Letnik:
137, Številka:
4
Journal Article
Recenzirano
Odprti dostop
The past few decades have witnessed an increase in the prevalence of IgE-mediated food allergy (FA). For prevention strategies to be effective, we need to understand the causative factors ...underpinning this rise. Genetic factors are clearly important in the development of FA, but given the dramatic increase in prevalence over a short period of human evolution, it is unlikely that FA arises through germline genetic changes alone. A plausible hypothesis is that 1 or more environmental exposures, or lack thereof, induce epigenetic changes that result in interruption of the default immunologic state of tolerance. Strategies for the prevention of FA might include primary prevention , which seeks to prevent the onset of IgE sensitization; secondary prevention , which seeks to interrupt the development of FA in IgE-sensitized children; and tertiary prevention , which seeks to reduce the expression of end-organ allergic disease in children with established FA. This review emphasizes the prevention of IgE-mediated FA through dietary manipulation, among other strategies; in particular, we focus on recent interventional studies in this field.
Background The management of peanut allergy relies on allergen avoidance and epinephrine autoinjector for rescue treatment in patients at risk of anaphylaxis. Biomarkers of severity and threshold of ...allergic reactions to peanut could significantly improve the care for patients with peanut allergy. Objective We sought to assess the utility of the basophil activation test (BAT) to predict the severity and threshold of reactivity to peanut during oral food challenges (OFCs). Methods The severity of the allergic reaction and the threshold dose during OFCs to peanut were determined. Skin prick tests, measurements of specific IgE to peanut and its components, and BATs to peanut were performed on the day of the challenge. Results Of the 124 children submitted to OFCs to peanut, 52 (median age, 5 years) reacted with clinical symptoms that ranged from mild oral symptoms to anaphylaxis. Severe reactions occurred in 41% of cases, and 57% reacted to 0.1 g or less of peanut protein. The ratio of the percentage of CD63+ basophils after stimulation with peanut and after stimulation with anti-IgE (CD63 peanut/anti-IgE) was independently associated with severity ( P = .001), whereas the basophil allergen threshold sensitivity CD-sens (1/EC50 × 100, where EC50 is half maximal effective concentration) value was independently associated with the threshold ( P = .020) of allergic reactions to peanut during OFCs. Patients with CD63 peanut/anti-IgE levels of 1.3 or greater had an increased risk of severe reactions (relative risk, 3.4; 95% CI, 1.8-6.2). Patients with a CD-sens value of 84 or greater had an increased risk of reacting to 0.1 g or less of peanut protein (relative risk, 1.9; 95% CI, 1.3-2.8). Conclusions Basophil reactivity is associated with severity and basophil sensitivity is associated with the threshold of allergic reactions to peanut. CD63 peanut/anti-IgE and CD-sens values can be used to estimate the severity and threshold of allergic reactions during OFCs.
Background Most children with detectable peanut-specific IgE (P-sIgE) are not allergic to peanut. We addressed 2 non–mutually exclusive hypotheses for the discrepancy between allergy and ...sensitization: (1) differences in P-sIgE levels between children with peanut allergy (PA) and peanut-sensitized but tolerant (PS) children and (2) the presence of an IgE inhibitor, such as peanut-specific IgG4 (P-sIgG4 ), in PS patients. Methods Two hundred twenty-eight children (108 patients with PA, 77 PS patients, and 43 nonsensitized nonallergic subjects) were studied. Levels of specific IgE and IgG4 to peanut and its components were determined. IgE-stripped basophils or a mast cell line were used in passive sensitization activation and inhibition assays. Plasma of PS subjects and patients submitted to peanut oral immunotherapy (POIT) were depleted of IgG4 and retested in inhibition assays. Results Basophils and mast cells sensitized with plasma from patients with PA but not PS patients showed dose-dependent activation in response to peanut. Levels of sIgE to peanut and its components could only partially explain differences in clinical reactivity between patients with PA and PS patients. P-sIgG4 levels ( P = .023) and P-sIgG4 /P-sIgE ( P < .001), Ara h 1–sIgG4 /Ara h 1–sIgE ( P = .050), Ara h 2–sIgG4 /Ara h 2–sIgE ( P = .004), and Ara h 3–sIgG4 /Ara h 3–sIgE ( P = .016) ratios were greater in PS children compared with those in children with PA. Peanut-induced activation was inhibited in the presence of plasma from PS children with detectable P-sIgG4 levels and POIT but not from nonsensitized nonallergic children. Depletion of IgG4 from plasma of children with PS (and POIT) sensitized to Ara h 1 to Ara h 3 partially restored peanut-induced mast cell activation ( P = .007). Conclusions Differences in sIgE levels and allergen specificity could not justify the clinical phenotype in all children with PA and PS children. Blocking IgG4 antibodies provide an additional explanation for the absence of clinical reactivity in PS patients sensitized to major peanut allergens.
Background The influence of early exposure to allergenic foods on the subsequent development of food allergy remains uncertain. Objective We sought to determine the feasibility of the early ...introduction of multiple allergenic foods to exclusively breast-fed infants from 3 months of age and the effect on breastfeeding performance. Methods We performed a randomized controlled trial. The early introduction group (EIG) continued breastfeeding with sequential introduction of 6 allergenic foods: cow's milk, peanut, hard-boiled hen's egg, sesame, whitefish (cod), and wheat; the standard introduction group followed the UK infant feeding recommendations of exclusive breastfeeding for around 6 months with no introduction of allergenic foods before 6 months of age. Results One thousand three hundred three infants were enrolled. By 5 months of age, the median frequency of consumption of all 6 foods was 2 to 3 times per week for every food in the EIG and no consumption for every food in the standard introduction group ( P < .001 for every comparison). By 6 months of age, nonintroduction of the allergenic foods in the EIG was less than 5% for each of the 6 foods. Achievement of the stringent per-protocol consumption target for the EIG proved more difficult (42% of evaluable EIG participants). Breastfeeding rates in both groups significantly exceeded UK government data for equivalent mothers ( P < .001 at 6 and at 9 months of age). Conclusion Early introduction, before 6 months of age, of at least some amount of multiple allergenic foods appears achievable and did not affect breastfeeding. This has important implications for the evaluation of food allergy prevention strategies.
Background History and severity of atopic dermatitis (AD) are risk factors for peanut allergy. Recent evidence suggests that children can become sensitized to food allergens through an impaired skin ...barrier. Household peanut consumption, which correlates strongly with peanut protein levels in household dust, is a risk factor for peanut allergy. Objective We sought to assess whether environmental peanut exposure (EPE) is a risk for peanut sensitization and allergy and whether markers of an impaired skin barrier modify this risk. Methods Peanut protein in household dust (in micrograms per gram) was assessed in highly atopic children (age, 3-15 months) recruited to the Consortium of Food Allergy Research Observational Study. History and severity of AD, peanut sensitization, and likely allergy (peanut-specific IgE, ≥5 kUA /mL) were assessed at recruitment into the Consortium of Food Allergy Research study. Results There was an exposure-response relationship between peanut protein levels in household dust and peanut skin prick test (SPT) sensitization and likely allergy. In the final multivariate model an increase in 4 log2 EPE units increased the odds of peanut SPT sensitization (1.71-fold; 95% CI, 1.13- to 2.59-fold; P = .01) and likely peanut allergy (PA; 2.10-fold; 95% CI, 1.20- to 3.67-fold; P < .01). The effect of EPE on peanut SPT sensitization was augmented in children with a history of AD (OR, 1.97; 95% CI, 1.26-3.09; P < .01) and augmented even further in children with a history of severe AD (OR, 2.41; 95% CI, 1.30-4.47; P < .01); the effect of EPE on PA was also augmented in children with a history of AD (OR, 2.34; 95% CI, 1.31-4.18; P < .01). Conclusion Exposure to peanut antigen in dust through an impaired skin barrier in atopically inflamed skin is a plausible route for peanut SPT sensitization and PA.
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