Food Allergy-Associated Cutaneous Manifestations in Children: A Narrative Review

Abstract

The rising prevalence of pediatric food allergies represents a growing public health concern, with hospitalizations for food-induced anaphylaxis on the rise. Early cutaneous manifestations, particularly in the setting of atopic dermatitis (AD), may indicate sensitization via the skin—a critical route for allergen exposure in early life. Pediatric food allergies can be IgE-mediated, non-IgE-mediated, or mixed, with each type presenting distinct pathophysiological and clinical features. IgE-mediated reactions often involve acute urticaria and angioedema, while non-IgE forms, such as food protein-induced enterocolitis syndrome (FPIES), manifest with delayed gastrointestinal symptoms and limited skin involvement. AD is closely linked with food allergies, both in pathogenesis and symptom exacerbation, with a high prevalence of co-occurrence. Diagnosis primarily relies on clinical evaluation, supported by testing such as skin prick testing, serum IgE, and oral food challenges, though limitations exist in sensitivity and specificity. Management emphasizes allergen avoidance, symptom control, and multidisciplinary care. While many pediatric food allergies resolve with age, others persist or present chronically, necessitating long-term strategies. Coordinated management between allergy and dermatology is key to minimizing complications and supporting better long-term outcomes for affected children.

1. Introduction

The rising prevalence of pediatric food allergies (FAs) is an emerging public health concern, with increasing hospital admissions for food-induced anaphylaxis [1]. One study has found that food allergies affect 8% of children globally [2]. Given that the skin is often the first site of allergic expression, recognizing the skin as a primary target organ and the probable cutaneous manifestations is crucial to reduce preventable hospitalizations.

Proposed mechanisms for the development of FAs is allergen exposure through the skin before oral exposure around the time of weaning, exposure through disrupted skin barrier in atopic dermatitis, or through the airway [3,4,5]. Since the skin is the body’s largest organ and acts as a physical barrier, regulates temperature, and is home to a microbiome that maintains skin health, it is imperative to recognize that alterations in any of its properties can lead to food allergies and subsequent allergic reactions.

Allergy mechanisms are typically categorized as IgE-mediated, non-IgE-mediated, or mixed-IgE-mediated. An IgE-mediated reaction is a type I hypersensitivity reaction that results in the immediate release of histamine and inflammatory cytokines upon allergen crosslinking IgE on sensitized mast cells. Histamine release leads to the characteristic “allergic reaction” characterized by urticaria, bronchoconstriction, angioedema, and possibly anaphylaxis. In contrast, non-IgE-mediated and mixed responses often present with delayed or more chronic symptoms. It is noted that non-IgE reactions can lead to the presentation of anaphylaxis via alternative pathways such as IgG-mediated neutrophil activation [6]. In these reactions, a skin test will be negative with normal tryptase and histamine suggesting absence of an IgE-mediated reaction. As non-IgE allergies do not typically show positive results on standard allergy testing, diagnosis is clinically based on symptom onset and improvement.

Cutaneous manifestations are among the most visible signs of food allergies in children. While IgE-mediated presentations consist of wheals, urticaria, angioedema, erythema, and pruritus, non-IgE-mediated presentations are less well-defined and may overlap with chronic dermatological conditions. This work will explore the cutaneous manifestations of both IgE- and non-IgE-mediated pediatric food allergies, with an emphasis on clinical presentation, diagnostic testing, and long-term management.

2. Materials and Methods

This narrative literature review was conducted to identify and synthesize current evidence on cutaneous manifestations associated with food allergies in the pediatric population. A comprehensive search of the PubMed database was performed in June 2025 using combinations of the following search terms: food allergy, pediatric, children, cutaneous, urticaria, atopic dermatitis, eczema, and anaphylaxis. The search was limited to English-language articles published from January 2000 to June 2025.

The goal of the initial search was to identify all available literature describing or analyzing skin-related manifestations of food allergy in pediatric patients. Both original research articles and relevant review articles were considered. Titles and abstracts were screened for relevance, and full texts of eligible articles were reviewed. Articles focused solely on adult populations, non-allergic food intolerances, or non-cutaneous symptoms were excluded.

From this initial pool, data were reviewed to identify key patterns in the types of cutaneous manifestations described, underlying immunologic mechanisms, diagnostic considerations, and treatment approaches. These recurring themes informed the structure of the Results and Discussion sections of the manuscript. Once the thematic framework was established, targeted secondary searches were performed to ensure that each identified category was thoroughly addressed as its own subsection with current and representative evidence. Reference lists of included studies were also hand-searched to identify additional relevant articles.

Due to the heterogeneity of study designs, definitions, and outcome measures, this review is descriptive in nature and does not include quantitative synthesis—a recognized limitation of our methods. The aim is to provide a comprehensive and clinically relevant overview of food allergy-associated skin findings in the pediatric population, as well as to highlight areas for future investigation.

3. Results

3.1. IgE-Mediated Cutaneous Manifestations

The main symptoms seen in IgE-mediated cutaneous reactions are urticaria and angioedema. Urticaria, commonly referred to as hives, presents as transient, well-demarcated, erythematous and edematous plaques (wheals) that are raised, intensely pruritic, and typically range from a few millimeters to several centimeters in diameter. Lesions appear suddenly and resolve within 24 h without residual skin changes. Acute urticaria arises within minutes to hours after ingestion of the antigen due to cross-linking of IgE on sensitized mast cells, leading to release of preformed histamine and vasodilatory mediators. Histamine release primarily leads to pruritus and vasodilators cause edema in the superficial dermis [7]. Many of these food allergens causing acute urticaria include eggs, milk, peanuts, tree nuts, soy, wheat, crustacean shellfish, and fish [8].

Chronic urticaria is defined by the recurrent appearance of pruritic wheals lasting for more than six weeks, with each individual lesion typically resolving within 24 h. It is generally not associated with food triggers. The two types of chronic urticaria are spontaneous and inducible, with inciting factors being temperature, sunlight, water, or mechanical forces [9]. Urticaria can also be seen as an initial presenting symptom of anaphylaxis and is essential to be able to identify. Anaphylaxis is an acute life-threatening reaction to an allergen involving the skin or mucosal tissue and respiratory compromise or hypotension. End organ dysfunction and gastrointestinal symptoms may also be present.

Angioedema is another IgE-mediated reaction that can be seen in food allergies, consisting of nonpitting edema and swelling of subcutaneous and submucosal tissue. Angioedema is most notable around the lips, eyes, tongue, and occasionally the airway, necessitating airway stabilization. As food allergens pass through the gastrointestinal tract, angioedema may also occur throughout as it encounters sensitized mast cells. Allergen-induced angioedema should be differentiated from hereditary angioedema resulting from continual activation of the complement cascade and resulting in elevated levels of bradykinin, a potent vasodilator. Allergic angioedema can be differentiated from hereditary angioedema by the acute onset after exposure and commonly associated pruritus. Hereditary angioedema is typically triggered by stress and symptom onset is gradual (over hours) and may last for days [10].

Diagnosis is primarily clinical, driven by a thorough history (possible exposure, timing, symptoms) and physical exam. If anaphylactic angioedema is suspected, first-line treatment is intramuscular (IM) epinephrine, followed by H1 and H2 antihistamines, and corticosteroids. For angioedema alone, corticosteroids and antihistamines alone are to be used; epinephrine is an escalation for anaphylaxis [8]. Supplemental oxygen, bronchodilators, and intravenous (IV) fluids may be necessary depending on severity.

3.2. Atopic Dermatitis and Food Allergy

Atopic dermatitis is a chronic skin condition commonly affecting children and manifests as intensely dry, pruritic, eczematous skin. It can be triggered by irritants, allergens, or environmental factors and is often the first sign of a progression of allergic diseases named the atopic march. Subsequent reactions include IgE-mediated food allergies, asthma, and allergic rhinitis [11]. The severity of atopic dermatitis increases the probability of developing subsequent food allergies and a recent study found that children with AD were 6 times more likely to acquire FA compared to healthy counterparts [12]. Since IgE antibodies play a role in both AD and FA, the manifestation and exacerbation of one can trigger the other. One study found that children with FA were significantly more likely to have persistent and uncontrolled AD and this association was more pronounced in milk, egg, and peanut allergies [13]. A separate study found that 40% of children with AD have concurrent FA and 45% of children with FA have concurrent AD [14]. Some studies suggest that atopic dermatitis associated with food allergy may present with an earlier age of onset, more severe disease, and a higher likelihood of persistent eczema beyond early childhood, though cutaneous morphology itself may not differ significantly. In contrast, AD without food allergy is more likely to follow a transient or less severe course. This distinction may be influenced by underlying immune mechanisms such as enhanced Th2 skewing, elevated IgE levels, and impaired barrier function, which are often more pronounced in food-sensitized children [15,16,17].

3.3. Non-IgE-Mediated Allergies and Their Presentations

In contrast to the immediate and cutaneous nature of IgE-mediated food allergies, non-IgE-mediated food allergies involve a delayed, cell-mediated immune response and primarily present with gastrointestinal symptoms. Cutaneous manifestations are less common, but subtle or indirect signs may offer diagnostic clues. One of the most studied non-IgE food allergies, food protein-induced enterocolitis syndrome (FPIES), is described as repetitive emesis, lethargy, and diarrhea after ingestion of a trigger [18,19]. Symptoms typically appear 1–4 h after ingestion, with possible diarrhea occurring within 24 h [19]. The most common trigger is cow’s milk, though grains, fish, and other foods have also been implicated [18,20]. With repeated exposure, chronic FPIES may develop. Chronic FPIES is described as diarrhea with occasional emesis. While classic allergic skin findings are typically absent, pallor is a frequently reported sign, likely secondary to systemic inflammation or dehydration. Pallor was observed in 89.2% of acute cases in a multicenter retrospective study [20]. Rarely, reports may describe atypical cutaneous findings. A perianal rash and a generalized papular rash were described in one case, and urticaria in another case, both presenting with the gastrointestinal symptoms of FPIES and resolving with elimination of the triggering food [21]. Because no biomarkers exist for FPIES, diagnosis relies on clinical presentation and resolution of symptoms with removal of the suspected trigger.

Food protein-induced allergic proctocolitis (FPIAP) typically presents within the first 6 months of life as hematochezia and is most commonly triggered by cow’s milk [22]. While it can affect both breastfed and formula-fed infants, it appears to be more common amongst exclusively breastfed infants [23]. Moreover, those who are not exclusively breastfed tend to present with the symptoms of FPIAP later. In terms of cutaneous signs, a significant subset of infants present with coexisting atopic eczema and/or a family history of allergic diseases.

Eosinophilic esophagitis is a mixed-IgE- and non-IgE-mediated condition, with non-IgE mechanisms predominant, defined clinically by symptoms such as dysphagia and regurgitation, and on histologic exam of the esophagus, greater than 15 eosinophils per high-powered field [24,25]. Younger children may present with symptoms of feeding difficulties, vomiting, and delayed growth [25]. Eosinophilic esophagitis is strongly associated with asthma, allergies, and atopy. A significant portion of those affected demonstrated low levels of specific IgE antibodies to milk, wheat, and peanuts, with sensitization to cow’s milk especially high in pediatric populations [26]. Additionally, there is a large overlap between eosinophilic esophagitis and concurrent atopic dermatitis [27]. The physical signs of atopic conditions may support diagnosis.

Together, these non-IgE-mediated food allergies demonstrate that while cutaneous manifestations may not present as hallmark features, associated skin findings and comorbid atopic conditions can provide valuable diagnostic context.

4. Discussion

4.1. Diagnosis of Cutaneous Food Allergy

Food allergies can manifest as IgE, non-IgE, or mixed reactions. IgE-mediated reactions commonly involve acute urticaria and angioedema, often triggered by common allergens such as eggs, milk, and peanuts, and can escalate to life-threatening anaphylaxis. Atopic dermatitis (AD) frequently coexists with food allergies, with significant evidence linking the severity of AD to increased risk of developing food allergies. While food allergies may not directly cause AD, they can exacerbate symptoms through immune-mediated inflammation and skin barrier disruption. Non-IgE-mediated allergies, such as FPIES, FPIAP, and eosinophilic esophagitis, are most often present with delayed gastrointestinal symptoms. Cutaneous changes are less consistent and, to our knowledge, there are no highly specific skin findings unique to these conditions. Reported nonspecific features include pallor, mottling, perioral erythema, transient maculopapular eruptions, and, less commonly, diaphoresis [6]. In the appropriate clinical context, these findings may help support suspicion for a non-IgE-mediated mechanism. Diagnosis is primarily clinical, though allergy testing may assist in guiding management when used judiciously. These findings underscore the complexity of pediatric food allergies and the importance of recognizing varied clinical patterns to inform diagnosis, treatment, and long-term care.

The diagnosis of food allergies in pediatric patients presents several challenges due to the reliance on clinical history and limitations of current diagnostic tools. A detailed clinical history and physical examination remain foundational. Important factors to ask about include, but are not limited to, symptom onset, timing, correlations with specific food(s), dietary exposures, and personal or family history of atopic diseases. IgE-mediated food allergy reactions often present with the acute onset of urticaria and possibly angioedema, flushing, and pruritus shortly after ingestion [28,29]. In contrast, non-IgE-mediated food allergies may present with concurrent skin conditions, such as atopic dermatitis or eczema, or pallor in the case of FPIES [29].

Diagnostic testing includes skin prick testing (SPT), serum-specific IgE (sIgE) testing, and oral food challenge (OFC). SPT is typically first-line for suspected IgE-mediated food allergies [30]. It should be noted that a positive result reflects sensitization and not necessarily clinical allergy, and testing is contraindicated in high-risk patients (those with high risk of anaphylaxis or with uncontrolled asthma) [28]. sIgE testing can complement or, with an inconclusive or contraindicated SPT, substitute for SPT. Notably, IgE sensitization to foods may be observed in eosinophilic esophagitis despite its predominant non-IgE mechanism [25]. The OFC, especially when performed as a double-blind, placebo-controlled test, remains the diagnostic gold standard for both IgE-mediated and non-IgE-mediated food allergies [29]. It can also determine threshold doses and be used to test or reintroduce foods in sensitized patients. However, the test can be costly, resource-intensive, and comes with the inherent risks of inducing reactions.

Allergy testing in AD should be considered when there is high suspicion of an inciting source based on a thorough history and physical exam findings of urticaria and angioedema. Testing should also be performed if there is a clear temporal relationship between exposure and allergic symptoms or in severe cases of AD where disease persists despite adequate management. If allergen testing is performed, it should be limited to the most common food allergies (milk, eggs, peanuts) in children under 5 due to false positives from sensitization [16]. False positives may lead to excessive food restriction at a time when children would benefit from a varied diet.

Furthermore, determining when to involve allergy versus dermatology specialties can add complexity. While allergies may focus on identifying triggers and guiding diagnostic testing, dermatologists are suited to manage acute and chronic cutaneous symptoms. A study found that atopic dermatitis patients evaluated in a combined dermatology-allergy clinic were more likely to undergo diagnostic testing and receive appropriate medications than those seen by either specialty alone, suggesting a synergistic benefit in diagnosis and treatment [31]. Given the intricacies of diagnosing food allergies, it is recommended to integrate clinical judgment with targeted testing and multidisciplinary care.

4.2. Management Strategies

Management of pediatric food allergies hinges on diagnosing the allergy and tailoring treatment accordingly. Foods associated with IgE-mediated food allergies and atopic dermatitis vary considerably by age and geographic region. In a systematic review of global anaphylaxis data, Baseggio Conrado et al. reported that in children, common triggers include cow’s milk, egg, and peanuts, while adults more frequently react to shellfish, tree nuts, and fruits. Regional patterns were also evident: for example, peanut and tree nut allergies are more prevalent in Western countries, whereas shellfish and wheat are more common triggers in parts of Asia [1]. These findings underscore the importance of tailoring diagnostic and management strategies to the local allergen profile and the patient’s age group.

In IgE-mediated food allergies, the primary approach involves strict allergen avoidance and usage of antihistamines or epinephrine for acute reactions. Addressing the systemic inflammatory response generally leads to improvement in associated cutaneous symptoms.

There is currently no cure for either FA or AD, and guidelines from the American Academy of Dermatology recommend avoidance of allergens if there is a true IgE-mediated allergy, use of topical corticosteroids, and use of topical emollients to protect the skin barrier [16]. While there is a strong association between the two diseases, there is no direct evidence of a mechanism for food allergies to trigger the development of AD. However, food allergies can exacerbate AD, either via immune cell activity and histamine release or the accompanying intense pruritus leading to scratching and potential breaks in the skin barrier. Reducing the rate of food allergy incidence has been trialed in the LEAP (Learning Early about Peanut Allergy) study which compared avoidance and early introduction of peanuts in infants with AD and/or egg allergies. Findings noted that early introduction greatly reduced peanut allergy incidence but had no effect on AD trajectory [17].

In non-IgE-mediated conditions, avoidance of the trigger food(s) remains essential. In FPIAP, the allergen should also be eliminated from the maternal diet if the infant is breastfed. However, up to 20% of breastfed infants experience spontaneous resolution of FPIAP without dietary changes [32]. It is thus suggested to proceed with a 1 month “watch and wait” period before initiating dietary elimination [33].

In terms of long-term care, many of the common IgE-mediated pediatric food allergies are outgrown during childhood, after which food may be reintroduced to the diet [8].

In recent years, biologic therapies and allergen immunotherapy (AIT) have emerged as promising adjuncts in the management of pediatric food allergies, particularly in cases of severe IgE-mediated reactions or coexisting atopic dermatitis. Dupilumab, a monoclonal antibody targeting the IL-4 receptor alpha subunit and inhibiting IL-4 and IL-13 signaling, has been FDA-approved for children aged 6 months and older with moderate-to-severe atopic dermatitis. Studies have shown that dupilumab not only improves eczema but may also modulate the allergic immune response, potentially reducing food allergen sensitivity over time [34]. On the other hand, AIT, including oral immunotherapy (OIT) and epicutaneous immunotherapy (EPIT), involves gradual exposure to increasing doses of an allergen to induce desensitization. In a phase 3 trial of AR101, a standardized peanut protein formulation, participants who received OIT were significantly more likely to tolerate peanut exposure compared to placebo [35]. Though still under investigation for long-term efficacy and safety, peanut OIT has been approved for children aged 4 to 17 years. Omalizumab, an anti-IgE monoclonal antibody, is another biologic that has been investigated for its role in facilitating oral immunotherapy (OIT) by decreasing the risk of anaphylaxis during food reintroduction. FDA-approved in 2024 for food allergy in children, omalizumab has shown promise in clinical trials as a co-therapy with peanut OIT [36]. Even so, OIT carries a risk of adverse reactions and requires close monitoring by allergy specialists. Overall, these therapies represent a shift from strict avoidance toward immune modulation, offering hope for more durable tolerance in select patients.

A study in Korea found that cow’s milk FPIES typically resolved in children by age 2 and soy FPIES by age 14 months, though lower rates of resolution have been reported in studies from the United States [32,37]. Foods may be reintroduced with OFC under supervision. In FPIAP, reintroduction may occur at home 6 months after elimination of the trigger food(s) [32]. For eosinophilic esophagitis, it is a chronic condition, which may require long-term allergen avoidance and medical management with proton pump inhibitors [25].

Table 1. Long-Term Course and Recommendations for Food Allergies.

	IgE-Mediated Food Allergies	FPIES	FPIAP	Eosinophilic Esophagitis
Characteristics	Urticaria, angioedema, flushing, pruritus, wheezing, SOB	Repetitive emesis, lethargy, diarrhea, pallor	Hematochezia	Feeding difficulty, dysphagia, regurgitation
Long-term course	May resolve during childhood, can consider dupilumab or omalizumab	May resolve during early years	Majority resolve during infancy	Chronic condition
Recommendations for dietary reintroduction	Inpatient OFC	Inpatient OFC	At home 6 months after dietary elimination	--

summarizes the discussed food allergies and their long-term management.

5. Conclusions and Future Directions

Cutaneous manifestations are often the earliest clinical indicators of pediatric food allergies. In particular, AD is strongly associated with food sensitization and allergy, both as a comorbidity and as a potential contributor to disease development through impaired skin barrier function. Food allergies can exacerbate AD symptoms, highlighting the bidirectional relationship between the skin and immune response. As such, interdisciplinary collaboration between dermatology and allergy specialists is essential for comprehensive care, earlier diagnosis, and better quality of life in affected children.

Currently, diagnostic approaches rely heavily on detailed history and clinical examination, supported by tests such as skin prick or serum-specific IgE testing. However, these tools are limited by issues such as false positives and lack of predictive value for clinical reactivity. Most treatment remains supportive, emphasizing allergen avoidance and symptom control, though emerging therapies show promise for immune modulation and desensitization.

Future research should focus on refining diagnostic criteria to better distinguish between sensitization and true food allergy, particularly in the context of atopic dermatitis. Improved biomarkers and predictive tools would aid in risk stratification and treatment personalization. Additionally, as Kulis et al. describe, the route and form of allergen exposure, such as cutaneous or inhalational contact with raw versus processed food proteins, may influence sensitization risk and merit further investigation in pediatric populations [5]. While this review centers on cutaneous manifestations, other contributors to food allergy development, including genetic predisposition, food quality, and degree of processing, are important and should be addressed in broader multidisciplinary research.

In particular, future studies could investigate whether the composition and sourcing of foods—such as organic versus GMO products, or wild-caught versus farm-raised proteins—play a role in allergy development or symptom expression. Although these factors fall beyond the scope of this review, they represent promising avenues for future investigation, especially in the context of cutaneous disease triggered by dietary antigens.