Immunoglobulin E-mediated Food Allergy Research Articles

Food allergy testing in infantile eczema: A clinical approach and algorithm

The complex relationship between food allergy and infantile eczema has prompted divergent approaches to investigating potential food triggers in eczematous patients. It is well recognised that a significant proportion of infants with eczema have immunoglobulin E-mediated food allergy, reported to range between 20-80%. Determining whether certain foods trigger an eczematous flare in individual infants with eczema is difficult. For all infants with eczema, good skin care is the mainstay of treatment but identifying and avoiding triggers (both allergic and non-allergic) is important in some infants. Given this, we have a developed an algorithm that can be used by dermatologists in the investigation and management of food allergies in infantile eczema. Issues such as patient selection, investigation and elimination diets are addressed, with reference to relevant evidence in the literature. Our aim is to provide dermatologists with a framework to manage food allergies in infantile eczema, allowing the problem to be addressed with confidence.

The predictive value of skin prick testing for challenge‐proven food allergy: A systematic review

Immunoglobulin E-mediated (IgE) food allergy affects 6-8% of children, and the prevalence is believed to be increasing. The gold standard of food allergy diagnosis is oral food challenges (OFCs); however, they are resource-consuming and potentially dangerous. Skin prick tests (SPTs) are able to detect the presence of allergen-specific IgE antibodies (sensitization), but they have low specificity for clinically significant food allergy. To reduce the need for OFCs, it has been suggested that children forgo an OFC if their SPT wheal size exceeds a cutoff that has a high predictability for food allergy. Although data for these studies are almost always gathered from high-risk populations, the 95% positive predictive values (PPVs) vary substantially between studies. SPT thresholds with a high probability of food allergy generated from these studies may not be generalizable to other populations, because of highly selective samples and variability in participant's age, test allergens, and food challenge protocol. Standardization of SPT devices and allergens, OFC protocols including standardized cessation criteria, and population-based samples would all help to improve generalizability of PPVs of SPTs.

Quercetin effectively quells peanut-induced anaphylactic reactions in the peanut sensitized rats.

Peanut allergy is the major leading cause of fatal or life-threatening anaphylactic reactions to foods. At present, there is no remedy for this condition. The applied pharmaceutical cares are merely palliative, while their deleterious side effects have already been established. Hence, many sufferers search for complementary and alternative medicines. A versatile-, "flavonol" subgroup-member of the flavonoid family, quercetin, is of paramount interest to investigators. In this study the effects of quercetin on peanut-induced anaphylactic reactions were investigated in a rat model of peanut allergy. Wistar rats were sensitized with crude peanut extract in the presence of Cholera toxin and Aluminium hydroxide. Sensitized rats were then allotted into three groups; Positive control, Quercetin-treatment and Sham, (n=7, each). Naive rats (n=7) served as negative controls. One week post-sensitization period, the rats in treatment group were treated with quercetin at a dose of 50 mg/kg(Body Weight)/mL Di-methyl-sulfoxide 5%/rat, over a period of four weeks. Subsequently, rats were challenged, and anaphylactic reaction parameters including variations in plasma histamine levels, vascular permeability, systemic anaphylaxis scores, and total serum Immunoglobulin E levels were measured. After daily-gavaging for four weeks, quercetin completely abrogated peanut-induced anaphylactic reactions following challenges, so that the mean of plasma histamine levels in the quercetin-treated rats, were lower significantly (p=0.004) as compared with positive control group. Our findings suggest that the flavonoid quercetin is potent enough to suppress the on-going Immunoglobulin E responses against peanut proteins, and can be propounded as an alternative medicine to protect against Immunoglobulin E-mediated food allergies.

Future Approaches to Food Allergy

Food allergy affects approximately 2% of the general US population, and its prevalence seems to be increasing. Despite the potential for a fatal outcome, no definitive therapies are available for food allergy. This article reviews novel approaches for the diagnosis and treatment of food allergy. Improved diagnostic methods include more precise in vitro and in vivo tests for immunoglobulin E-mediated food allergies, in vitro assays for predicting development of oral tolerance, and novel noninvasive tests for cell-mediated food allergies such as patch testing, cytokine assays, and detection of eosinophil activation markers. Several promising novel immunomodulatory approaches to food allergy are discussed, including monoclonal anti-immunoglobulin E; probiotics; traditional Chinese medicine; and immunotherapy with modified food proteins, peptides, bacterial adjuvants, and immunostimulatory sequences.

Food allergy: an overview.

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.

Bronchial challenges with aerosolized food in asthmatic, food-allergic children.

Allergic asthma is usually considered to be provoked by aeroallergens. However, we have recently recognized a group of children with food allergies who also develop asthma when exposed to the aerosolized form of the food. Between 1997 and 1999 we prospectively identified children with an immunoglobulin (Ig)E-mediated food allergy who develop asthma on inhalational exposure to the relevant food allergen while it is being cooked. Subjects were exposed for 20 min to the aerosolized form of the allergen and the symptoms and the lung function were monitored. Aerosolization was achieved by cooking the food in a small room. Where possible challenges were double-blinded. We identified 12 children with an IgE-mediated food allergy who developed asthma on inhalational exposure to food. The implicated foods were fish, chickpea, milk, egg or buckwheat. Nine out of the 12 children consented to undergo a bronchial food challenge. Five challenges were positive with objective clinical features of asthma. Additionally, two children developed late-phase symptoms with a decrease in lung function. Positive reactions were seen with fish, chickpea and buckwheat. There were no reactions to the seven placebo challenges. We have presented a prospective series of children with food allergy who developed symptoms of asthma with exposure to aerosolized food allergens. Our data demonstrates that, as in the case of other aeroallergens, inhaled food allergens can produce both early- and late-phase asthmatic responses. This highlights the importance of considering foods as aeroallergens in children with coexistent food allergy and allergic asthma. For these children, dietary avoidance alone may not be sufficient and further environmental measures may be required to limit exposure to aerosolized food.

Prevalence of food allergies in young adults and their relationship to asthma, nasal allergies, and eczema

The true prevalence of food allergy in adults is generally thought to be uncommon. It is unknown whether there are any relationships between food allergy and atopic diseases. To determine the prevalence of probable immunoglobulin (Ig)E-mediated food allergy to peanut, shrimp, cow's milk, wheat, and egg as defined by a positive skin prick test result and relevant clinical history to the same food, and to explore the relationship with atopic diseases. Cross-sectional epidemiologic study. One thousand one hundred forty-one randomly selected young adults (aged 20 to 45 years) underwent skin prick testing to five common food allergens (cow's milk, peanut, egg white, shrimp, and wheat), completed a detailed questionnaire, including validated items on respiratory symptoms, history of asthma and other allergic conditions, as well as undergoing lung function testing. Just over one percent (1.3%, n = 15) had probable IgE-mediated food allergy. The prevalence of probable IgE food allergy was: <0.27% for wheat, 0.09% (95% confidence interval = 0.0 to 0.49%) each for cow's milk and egg, 0.53% (0.21 to 1.09%) for shrimp, and 0.61% (0.25 to 1.26%) for peanut. Those with probable IgE peanut and shrimp allergy were significantly more likely to have current asthma and doctor-diagnosed asthma. Wheeze and history of eczema were also associated with peanut allergy, whereas nasal allergies were associated with shrimp allergy. The prevalence of probable IgE-mediated food reactions is rare in young adults. Some positive associations between probable IgE-mediated food allergy and allergic diseases were found, but larger study numbers are required to confirm these results.

Genotype of N-acetyltransferase 2 (NAT2) polymorphism in children with immunoglobulin E-mediated food allergy.

We investigated whether patients with immunoglobulin E-mediated food allergy differed from healthy individuals with regard to genotype of the polymorphic enzyme N -acetyltransferase 2 (NAT2). The genetic polymorphism of acetylation can alter the toxic and therapeutic response to certain xenobiotics and may be also a factor that influences the susceptibility toward certain partly chemically induced diseases. We compared 136 children with immunoglobulin E-mediated food allergy with 123 healthy children. The NAT2 alleles (*4, *5, *6, and *7 ) were determined by polymerase chain reaction-restriction fragment length polymorphism methods with DNA extracted from peripheral blood. A statistically significant increase in the proportion of homozygous slow acetylators (76.5%) was found among patients with food allergy compared with healthy subjects (53.7%; P < .001). There were no homozygous fast acetylators within this group of individuals with severe forms of food allergy. The risk of development of immunoglobulin E-mediated food allergy was almost 3-fold greater in slow acetylators than that in the healthy subjects (odds ratio, 2.8; 95% confidence interval, 1.6 to 4.9). We therefore concluded that the slow acetylation genotype may be an important factor of individual susceptibility to immunoglobulin E-mediated food allergy.

Immunology of delayed food allergy

Studies here and abroad are stockpiling evidence that immunoglobulin E explains only a small part of food allergy. Involvement of the entire immune system is evident if the more prevalent delayed-type food allergy is to be explained. To adequately diagnose food hypersensitivity a testing technique must be used that identifies delayed food allergy, such as the patch test here described, along with a test that diagnoses immediate immunoglobulin E-mediated food allergy. (OTOLARYNGOL HEAD NECK SURG 1995;113:702-4.)

Immunology of Delayed Food Allergy

Studies here and abroad are stockpiling evidence that immunoglobulin E explains only a small part of food allergy. Involvement of the entire immune system is evident if the more prevalent delayed-type food allergy is to be explained. To adequately diagnose food hypersensitivity a testing technique must be used that identifies delayed food allergy, such as the patch test here described, along with a test that diagnoses immediate immunoglobulin E-mediated food allergy.