Food Allergy In Atopic Dermatitis Research Articles

Is Food-Triggered Atopic Dermatitis a Form of Systemic Contact Dermatitis?

Food allergy in atopic dermatitis is mediated by complex immune interactions between genetics, diet, environment, and the microbiome. When contact between inflamed skin and food antigens occurs, contact hypersensitivity can develop. Consequently, systemic contact dermatitis (SCD) can occur after ingestion of allergenic foods or food additives in the setting of a Th2 response with CLA-positive T cells, triggering dermatitis where skin resident memory lymphocytes reside. This phenomenon explains food-triggered dermatitis. Atopy patch tests (APTs) detect sensitization to food proteins responsible for SCD, which in turn can be confirmed by oral food challenge with delayed interpretation. We summarize the literature on using APTs to identify foods for oral challenge with dermatitis as an outcome. In dermatitis patients at risk for Th2 skewing based on a history of childhood-onset flexural dermatitis, shared decision-making should include a discussion of identifying and avoiding food and food additive triggers, as well as identifying and avoiding all contact allergens, prior to initiation of systemic therapy for dermatitis.

Significance of food allergy in atopic dermatitis in children

Background. Atopic dermatitis is the most common inflammatory skin disease in childhood, affecting almost 20 % of children. Food allergies affect one of three children with atopic dermatitis, and allergies to peanuts, eggs and milk are the predominant food allergies in the world. The purpose was to assess the prevalence of food allergies in the group of patients with atopic dermatitis, to determine the association of food allergies with anamnestic and clinical parameters of atopic dermatitis. Materials and methods. Children with atopic dermatitis (n = 116) were included in the study from September 2020 to August 2021 in Kyiv, Ukraine. Food sensitization was established by determining specific immunoglobulin E (sIgE) to food allergens using immunochemiluminescent method on the ImmunoCAP 100 system (Thermo Fisher Scientific Inc., Phadia, Sweden). Results. The average age of children in the main group (59 boys and 57 girls) was 6.8 years. All 116 patients at the time of examination had manifestations of atopic dermatitis in the form of erythematous itchy rash. The number of children with food allergy was 23 (19.8 %). Among food allergens, positive sIgE were found: in 14 patients (12 %) — to milk, in 13 (11.2 %) — to eggs, in 5 (4.3 %) — to fish, and in 4 people (3.4 %) — to hazelnuts. Food sensitization was significantly more common in children with moderate-to-severe atopic dermatitis than in the group of patients with mild atopic dermatitis (χ2 = 7.555, p < 0.05). Children with food sensitization had an earlier onset of atopic dermatitis — the average age of manifestations onset was 8 months, and in the group of children without food allergy, it was 18 months. Children with a parental history of atopic diseases were significantly more likely to have concomitant food allergy (χ2 = 12.831, p < 0.05). Conclusions. Given the significant association between early onset as well as moderate-to-severe atopic dermatitis and food sensitization, it is likely that food sensitization occurs primarily through an inflamed skin barrier in eczematous skin, which could potentially lead to clinical food allergy.

Atopy patch test in the diagnosis of food-aggravated atopic dermatitis in adults in tertiary care

Food allergy and atopic dermatitis often co-exist. Symptoms can include IgE mediated reactions with immediate flushing, urticaria and angioedema to delayed T-cell mediated flares of eczema or a combination of both. Existing workup for food allergy in atopic dermatitis is currently based on clinical history, skin prick tests (SPT), or specific Ig E, followed by an elimination diet and/or standardized oral food challenge. The aim of this study is to evaluate the type of food allergy and the value of food atopy patch tests (APT) in the diagnosis of food allergy in adult patients with atopic dermatitis. We recruited 11 adult patients (3 Male, 8 Female) aged 26-47 years with atopic dermatitis (as per Hannifin and Rajka criteria). All patients kept detailed food diaries and symptoms correlation with questionnaires. They also had blood test specific Ig E, SPT and food APT. If positive, they were advised on a food elimination diet. They were followed up with at least 3 clinic visits over a course of 8-16 months. The results of these investigations were then correlated with their symptoms. Seafood including shrimp (n=8/11, 73%), lobster (n=8/11, 73%), crab (n=7/11, 64%), clam (n=6/11, 55%), and oyster (n=5/11, 46%) were the most perceived culpable food allergens based on the food diaries. The type of symptoms reported ranged from pruritus (n=10/11, 91%), wheals (n=5/11, 46%), flushing (n=5/11, 46%) and eczema flares (n=6/11, 55%). The most commonly observed reaction was that of pruritus, typically experienced within 1 hour of ingestion. Positive symptom correlation with elevated food-specific IgE levels were seen with shrimp (n=3/8, 38%), lobster (n= 2/7, 29%) and crab (n=1/7, 15%). Clinical correlation with positive SPTs were seen with oyster (n=1/6, 17%) and crab (n=1/6, 17%). Positive results across all 3 modalities of specific IgE, SPT and APT was noted with shrimp (n=1/8, 13%). Food APTs were negative for the other allergens. All patients reported improvement in their symptoms after trial of food elimination diet. 1 patient sustained an adverse reaction, he developed an angry back after APT. Seafood, in particular crustacean seafood is a common food allergy seen in adult patients in Singapore. In our small pilot study, food atopy patch test is not useful as a tool for diagnosing food allergy in adult patients with atopic dermatitis. We still need to rely on correlation with clinical history, specific Ig E, SPT, elimination diet +/- oral food challenge.

The PATHOGENesis of Food Allergy.

The current paper suggests that egg allergy may arise due to microbial proteins that are homologous to egg allergens. These microbial proteins elicit an allergic response and lead to the development of specific microbial IgE molecules. These molecules cross-react with egg allergens and result in egg allergy. Some examples of microbial proteins that share similar sequences as egg allergens are presented in this paper. Food allergy has a negative impact on the quality of life and nutrition. In addition, it can lead to life-threatening reactions. The pathogenesis of food allergy is still not fully understood. Many young children develop food allergy with no known prior ingestion of the food allergen in question. The strong connection between food allergy and atopic dermatitis has been well-documented. While the prevalence of food allergy in the general pediatric population is 4–5%, the prevalence of food allergy in atopic dermatitis is at least 20% (1). This connection between food allergy and atopic dermatitis has led to the suggestion that the skin may be the site of food IgE sensitization, leading to food allergy. The dual-allergen-exposure hypothesis suggests that food allergens are sensitized via eczema, whereas early gastro-intestinal exposure leads to tolerance (2). This hypothesis is supported by multiple basic studies that provide evidence for IgE sensitization via the skin [reviewed in (3)]. In addition, it has been shown that environmental level of peanut allergens is increased in children who developed peanut allergy (4). The early introduction of peanut has led to the prevention of peanut allergy (5). Likewise, early introduction of egg has also met with some success, although the results were not as consistent (3). It has been suggested that improvement in eczema, in addition to early introduction of egg, is needed for successful prevention of egg allergy (6). This suggestion further highlights the importance of skin in the pathogenesis of food allergy. A hypothesis is proposed here that the interaction between the neonatal skin and microbial proteins is important for the development of IgE sensitization and egg allergy. The current hypothesis predicts the presence of microbial proteins that are homologous to egg allergens. Table 1 shows the microbial proteins that share homology with the IgE-binding domains of Gal d 1 (ovomucoid) (7). Four out of the 6 microbial proteins share > 60 % identity with a clinically-relevant IgE-binding region of Gal d 1 (FNPVCGTDGVTYDN) (8). Significant homology was also found between microbial proteins and Gal d 2 (ovalbumin), but no homology was found in the IgE-binding domains of Gal d 2 (9) (data not shown). To further confirm the correlation between microbial proteins and Gal d 1, prospective studies may be carried out to look for these microbial pathogens in atopy-prone neonates and correlate with neonates who eventually develop allergy to Gal d 1. These microbial pathogens can also be inoculated in animal models to show the development of specific IgE that cross-react with Gal d 1. Atopy-prone neonates who are born to parent with atopic dermatitis, asthma or allergic rhinitis have inherent skin barrier defects that predispose them to develop atopic dermatitis. Microbial pathogens are capable of evading these barrier defects to interact with the cutaneous immune system in these children. The processing of microbial proteins by antigen-presenting cells and subsequent presentation of antigenic peptides to T helper type 2 cells leads to the production of IL-4 and IL-13, which induce B cells to express specific IgE molecules. Bacterial allergy has been described more than half a century ago (10). It is also known that specific IgE to staphylococcal toxins can develop in young children with atopic dermatitis (11). Bacteria such as bacteroides can be acquired during birth or they can be part of neonates' microbiome (12). The skin also contains a wide array of microbial pathogens that can participate in the development of allergy (13). More recent data suggests that many microbial organisms (e.g., proteobacteria and archaea) previously thought to exist only in the environment such as soil, fresh or marine waters are now found to be part of the human skin microbiome (14, 15). Proteobacteria and bacteroides are also known to be present in atopic dermatitis lesions (16). The current proposal is conceptual that microbial proteins can be a sensitizing source in the development of food allergy in predisposed children. Preliminary data also suggests the presence of homologous proteins between microbes and other food allergens including peanut and cow's milk (unpublished data). Whether these microbial pathogens have a direct interaction with neonates, leading to the development of specific IgE, remains to be proven. It is possible that the prevention of egg allergy requires a different approach by targeting microbial pathogens. Table 1 Microbial proteins that share similar sequences as the IgE-binding domains of Gal d 1.

In-vitro diagnostic in atopic dermatitis: Optionsand limitations.

Atopic dermatitis is a chronic inflammatory skin disease with a complex pathogenesis and different exogenous and endogenous trigger factors. One important factor is the sensitization to inhalant and/or food allergens. The detection of total IgE and specific IgE antibodies to inhalant and/or food allergens is one central aspect in diagnosing atopic dermatitis, especially if skin prick tests are not feasible. Many patients are polysensitized, but not all sensitizations are of clinical relevance. The challenge is to identify the sensitizations with clinical relevance and to initiate suitable therapeutic options. In this article we go into detail for the allergens house dust mite, pollen, food, and Malassezia sympodialis. Furthermore, the authors comment on the impact of the detection of specific IgG/IgG4 antibodies in the diagnosis of food allergy in atopic dermatitis. Moreover, new options in the in-vitro diagnostic will be explained briefly and their actual diagnostic significance in patients with atopic dermatitis will be highlighted. These options are the detection of specific IgE antibodies to recombinant allergens and the allergen chip.

Food Allergy in Atopic Dermatitis.

Food allergy in atopic dermatitis (AD) is debatable from decades. Role of diet in the cause and treatment of AD is controversial and is not well-defined. Allergists and pediatricians are convinced about the food allergy in AD whereas many dermatologists are contrary for this. However, there are studies in the Indian and western literature supporting the evidence that elimination diet may improve the severe type of AD. There is increasing awareness and lot of misconception among caregivers about food allergy and hence careful understanding about this concept is necessary to counsel parents. Recent evidence-based literature suggests avoidance of proven food allergens in AD could be beneficial in moderate to severe type of AD.

Food Allergy in Atopic Dermatitis

Food Allergy in Atopic Dermatitis

Prevalence and Impact of Past History of Food Allergy in Atopic Dermatitis

Increases in allergic diseases have been reported from various epidemiological surveys. However, a few reports demonstrate the comorbidity of food allergy (FA) and allergic march. The aim of this study was to assess the prevalence and comorbidity of allergic diseases in Japanese students. First-year students (n = 3,321; 2,209 male and 1,112 female) at Osaka University were asked about allergic diseases using postal interview sheets. Personal and family histories of doctor-diagnosed allergic diseases, clinical courses, and aggravating factors were included in the questionnaires. The lifetime prevalence of allergic rhinitis (AR), atopic dermatitis (AD), bronchial asthma (BA), and FA was 35.7%, 16.5%, 9.9%, and 7.0%, respectively. Disease-specific family histories existed for AR, AD, and BA. There was a positive correlation between the number of family histories of allergic disease and comorbidity (R = 0.370, P <0.001). Comorbidity with AD significantly lowered the onset age of both BA (P = 0.010) and AR (P <0.001). In addition, the onset age of AD was remarkably lowered by comorbidity with FA (P <0.001). Comorbidity with FA was the highest risk factor for the progression of allergic march. Although most students showed improvement in AD, BA, and AR over time, the peak recurrence period was observed in adolescence. These findings indicate that AD associated with FA accelerates the subsequent progression of allergic march. Early appropriate management for genetically high-risk groups is important for the prevention of allergic march.

Evaluation of Food Allergy in Patients with Atopic Dermatitis

Atopic dermatitis (AD) is a common skin disease characterized by inflammatory, chronically relapsing and pruritic eczematous flares. Its estimated incidence is 10% to 30% in children. Food allergy has been well documented in approximately one-third of children with a moderate-to-severe AD. Cow's milk, hen's egg, peanut, wheat, soy, nuts, and fish are responsible for >90% of food allergy in children with AD. The incidence and type of food can vary with age. In infants, cow's milk, hen's egg, peanut, and soy and, in older children, wheat, fish, tree nuts, and shellfish are the most common food allergens. Birch-associated foods have also been described as potential triggers of AD in children as well as in adults. The diagnosis of food allergy in AD is currently based on the clinical history, skin prick tests, or blood test screening, followed by an elimination diet and/or standardized oral food challenge. Once an underlying food allergy is confirmed, the avoidance of the incriminated food is generally recommended and usually leads to an improvement of the AD. Follow-up clinical evaluation with a detailed history and tracking of the level of specific IgE to implicated foods are typically used to evaluate the development of clinical tolerance, further confirmed by an oral food challenge.

Allergen-Specific Responses of CD19high and CD19low B Cells in Non-IgEMediated Food Allergy of Late Eczematous Reactions in Atopic Dermatitis: Presence of IL-17- and IL-32-Producing Regulatory B Cells (Br17 &amp; Br32)

Food allergies are important etiologic factors in atopic dermatitis. CD19 is a B-cell-specific cell-surface molecule, with a critical role in B-cell activation. Recently, B cells showed independent two subpopulations as CD19(high) and CD19(low). The allergen-specific responses of the CD19(high) and CD19(low) B-cell subpopulations were investigated in patients with non-IgE-mediated food allergy. Five milk-allergic subjects and eight milk-tolerant subjects were selected by a double-blind placebo-controlled food challenge. Peripheral blood mononuclear cells (PBMCs) were stimulated in vitro with casein or ovalbumin and stained with monoclonal antibodies to distinguish the B-cell subsets. After allergen stimulation, CD19(high) B cells increased in the number and the fraction in PBMCs in the milk-tolerant group, whereas those remained unchanged in the milk-allergic group. These responses were constant, regardless of the kind of food allergen (milk or egg). The resulting CD19(high)/CD19(low) B-cell ratio increased markedly in the milk-tolerant group after allergen stimulation, but was unchanged in the milk-allergic group. IL-10, IL-17, IL-32 and TGF-β- producing regulatory B cells and Foxp3-expressing regulatory B cells were identified predominantly on CD19 low and CD5(+) B cells. The response of the CD19(high) B-cell subpopulation to allergen stimulation is decisive for immune tolerance of non-IgE-mediated food allergy in atopic dermatitis. CD19 high and CD5(+) B cells dominantly produce cytokines and express Foxp3. Especially, IL-17 and IL-32 expressing B cells (Br17 & Br32) are present. The exact immunological role of CD19 and cytokines including IL-17 and IL-32 around B cells in immune tolerance requires further investigation.

Revision of Immunopathogenesis and Laboratory Interpretation for Food Allergy in Atopic Dermatitis

Atopic dermatitis is an allergic inflammatory skin disease that is characterized by late eczematous skin lesions which result from non-IgE-mediated immune responses. It is well known that food allergy is an important cause of atopic dermatitis. Moreover, with recent advances in the diagnosis and treatment of food allergy, it becomes possible to elucidate the role of IgE- and non-IgE-mediated food allergies. Interprerations for blood eosinophil counts and total serum IgE levels are updated based on the immunopathogenesis of AD relating with these IgE- and non-IgE-mediated food allergies. The clinical significances of skin prick test and allergen-specific IgE are re-evaluated according to the out-to in and in-to out sensitization. Atopic march is reconsturcted by the sequential sensitization of foods and aeroallergens. In this review, the revized immunopathogenesis and relevant interpretations of food allergy in atopic dermatitis are described for the evaluation of precise clinical status of AD.

The role of food allergy in atopic dermatitis

Atopic dermatitis (AD) affects ∼10% of children. Food allergy is a known provoking cause of AD in a subset of affected children. A literature search of PubMed and Medline was conducted to review the epidemiology and pathophysiology of AD, with special focus on the role of food allergy in the development of AD, its management, and its long-term preventive strategies. A literature search of PubMed and Medline was conducted. Food allergens readily provoke AD in ∼35% of patients, as proven through double-blind placebo-controlled food challenge studies. Milk, egg, wheat, soy, and peanut account for 75% of the cases of food-induced AD. However, the positive predictive values of the parental history, skin-prick tests, or serum tests for detecting food-specific IgE are low, making these unsuitable for use as single diagnostic modalities. Therefore, the use of a food challenge test is very helpful in objectively confirming the history or positive tests. Elimination diets are often helpful in challenge-proven cases, but care must be taken to evaluate the nutritional status of the child. There are few effective long-term strategies to prevent the development of food allergen-induced AD. Early onset of AD has been shown to be a risk factor for the development of other allergic diseases, including other food allergy/sensitization, as part of the atopic march. Treatment of other causes of AD, such as barrier dysfunction and cutaneous infection, are of equal importance to food allergen avoidance. Food allergy is an important provoking cause of AD, but it is only relevant in ∼35% of affected individuals.

Eosinophilia as a predictor of food allergy in atopic dermatitis

Food allergy plays an important role in atopic dermatitis (AD). Adequate predictors and guidelines for when dietary manipulation is indicated for AD are needed. The clinical significance of eosinophilia as a predictor for food allergy of late eczematous reactions in AD was investigated. Three hundred three patients with AD were studied, using elimination diets and food challenge tests. Food allergy prevalence was compared in groups of eczematoid AD patients with high or normal eosinophil levels. The effects on the blood eosinophil fraction of an elimination diet and milk allergy provocation of late eczematous reactions were evaluated. The prevalence of food allergy was 51.1% (135/264) in patients with eczematoid AD. The major type of food allergy in AD was late eczematous, rather than IgE mediated. Among eczematoid AD patients, 44.9% had high eosinophil levels. In patients with eczematoid AD, the food allergy prevalence was 70.8% (85/120) in the high eosinophil group and 34.7% (50/144) in the normal blood eosinophil group. An elimination diet improved clinical severity and decreased blood eosinophil levels. In milk allergy patients, a milk challenge significantly increased the blood eosinophil level. Skin-prick tests and food-specific IgE tests were useful for diagnosing IgE-mediated food allergy. Eosinophilia appeared to be a significant predictor of food allergy in AD and an indicating factor for diet manipulation, including an elimination diet. Food allergy may be responsible for eosinophilia in AD. Food allergy patterns for AD in Korea were different from those in western countries.

Approach to suspected food allergy in atopic dermatitis

The following guideline of the "Arbeitsgruppe Nahrungsmittelallergie der DGAKI" (Task Force on Food Allergy of the German Society of Allergology and Clinical Immunology) and the ADA ("Arzteverband Deutscher Allergologen", Medical Association of German Allergologists) and the GPA (German Society of Pediatric Allergology) summarizes the approach to be taken when food allergy is suspected in patients with atopic dermatitis (neurodermatitis, atopic eczema). The problem is clinically relevant because many patients assume that allergic reactions against foods are responsible for triggering or worsening their eczema. It is important to identify those patients who will benefit from an elimination diet but also to avoid unnecessary diets. Elimination diets (especially in early childhood) are associated with the risk of malnutrition and additional emotional stress for the patients. The gold standard for the diagnosis of food-dependent reactions is to perform placebo-controlled, double-blind oral food challenges because specific IgE, prick tests and history often do not correlate with clinical reactivity. This is particularly true in the case of delayed eczematous skin reactions. Diagnostic elimination diets should be used before an oral provocation test. If multiple sensitizations against foods are discovered in a patient, an oligoallergenic diet and a subsequent stepwise supplementation of the nutrition should be performed. If a specific food is suspected of triggering food allergy, oral provocation should be performed after a diagnostic elimination diet. As eczema-tous skin reactions may develop slowly (i. e. within one or two day), the skin be inspected the day after the provocation test and that a repetitive test be performed if the patient has not reacted to a given food on the first day of oral provocation. The guideline discusses various clinical situations for patients with atopic dermatitis to facilitate differentiated diagnostic procedures.

IgE Food Sensitization in Infants With Eczema Attending a Dermatology Clinic

Hill DJ, Heine RG, Hosking CS, et al. J Pediatr. 2007;151(4):359–363 PURPOSE OF THE STUDY. Because community-based studies, which report immunoglobulin E food sensitization (IgE-FS) in &amp;gt;80% of infants with moderate atopic eczema, may be influenced by referral bias, the researchers assessed the prevalence of IgE-FS in a cohort of infants with moderate atopic eczema who were attending a dermatology department clinic. STUDY POPULATION. Consecutive infants (n = 51 [39 boys]; median age: 34 weeks [range: 20–51 weeks]) with moderate atopic eczema severity were studied prospectively. METHODS. Clinical history and eczema severity were documented. IgE-FS was assessed by the skin-prick test (SPT) (n = 51) and food-specific serum IgE antibody levels (CAP-FEIA test; n = 41). IgE-FS was diagnosed if the SPT or CAP-FEIA level exceeded the &amp;gt;95% predictive reference cutoff for positive food-challenge results. RESULTS. On the basis of the SPT, 44 (86% [95% confidence interval (CI): 74%–95%]) of 51 infants had IgE-FS (cow's milk, 16%; egg, 73%; peanut, 51%). Using age-specific 95% predicted cutoff values, CAP-FEIA identified 34 (83% [95% CI: 68% to 93%]) of 41 infants with IgE-FS (cow's milk, 23%; egg, 90%). Forty-six (90%) infants had IgE-FS to at least 1 food item according to either the SPT or CAP-FEIA test. CONCLUSIONS. Atopic eczema was found to be closely associated with IgE-FS in infants attending a dermatology department. REVIEWER COMMENTS. These data should continue to fuel the ongoing debate, especially between allergists and dermatologists, regarding the role of food allergy in infants with atopic dermatitis (AD). This study addressed IgE-FS in infants who already had moderate-to-severe AD and who presented to a dermatology clinic for evaluation and management. These patients had test results (ie, skin testing or in vitro–specific IgE measurements) demonstrating likely clinical allergy to eggs, cow's milk, and/or peanuts on the basis of previous studies correlating test results with oral food-challenge outcomes. The vast majority (90%) of these infants with AD were sensitive to at least 1 of these foods, demonstrating a very strong association between infants with AD and IgE sensitization to common food allergens. Despite extensive data from this study and previous investigations demonstrating a relationship, the specific role of food allergy in AD remains a “hotly contested” area of clinical research and debate. At this point in time, the balance of clinical evidence favors a specific role of IgE-FS in the pathogenesis of AD.

LEDGF/DFS70, a Major Autoantigen of Atopic Dermatitis, Is a Component of Keratohyalin Granules

MEETING ABSTRACTS: Abstracts from the Fifth Georg Rajka International Symposium of Atopic Dermatitis, Kyoto, Japan, May 11-13, 2008: Part 1: 6. Role of Allergens and Food Allergy in Atopic Dermatitis

Sensitization to Turnip Rape: a Comparison between Finnish and French Children with Atopic Dermatitis

MEETING ABSTRACTS: Abstracts from the Fifth Georg Rajka International Symposium of Atopic Dermatitis, Kyoto, Japan, May 11-13, 2008: Part 1: 6. Role of Allergens and Food Allergy in Atopic Dermatitis

Pet Exposure and Risk of Eczema: A Systematic Review

MEETING ABSTRACTS: Abstracts from the Fifth Georg Rajka International Symposium of Atopic Dermatitis, Kyoto, Japan, May 11-13, 2008: Part 1: 6. Role of Allergens and Food Allergy in Atopic Dermatitis

Identification of Allergens in Wheat Allergy

MEETING ABSTRACTS: Abstracts from the Fifth Georg Rajka International Symposium of Atopic Dermatitis, Kyoto, Japan, May 11-13, 2008: Part 1: 6. Role of Allergens and Food Allergy in Atopic Dermatitis

Breastfeeding and Atopic Dermatitis: New Insights beyond the Controversy

MEETING ABSTRACTS: Abstracts from the Fifth Georg Rajka International Symposium of Atopic Dermatitis, Kyoto, Japan, May 11-13, 2008: Part 1: 6. Role of Allergens and Food Allergy in Atopic Dermatitis