Food allergies in children: signs and treatment

Food allergy in children is not a "reaction to food in general," but an immune response to specific proteins: milk (casein), egg (ovomucoid), peanut (Ara h 2), tree nuts, fish (paravalbumin), crustaceans (tropomyosin), wheat, soy, and sesame. Most children have immunoglobulin E mechanisms—rapid symptoms lasting minutes to hours; less common are non-IgE forms (e.g., FPIES) and mixed forms (e.g., eosinophilic esophagitis). [1]

In recent years, the approach to early nutrition has changed dramatically: introducing peanuts early, at 4-6 months, to at-risk children is a proven prevention strategy with effects extending into adolescence. This is supported by data from the long-term LEAP follow-up (LEAP-Trio, 2024) and real-world field studies: the incidence of peanut allergies in infants has significantly decreased since the change in recommendations. [2]

A diagnosis cannot be made "by testing everything at once." The process is always the same: clinical interview → confirmation of sensitization (skin tests/specific immunoglobulin E, and, if available, component diagnostics) → if necessary, oral challenge using a standardized protocol. This eliminates overdiagnosis and excessive dieting. [3]

Treatment isn't just about "not eating anything." The foundation is education and avoidance of the trigger, plus preparedness for anaphylaxis (adrenaline). There are methods that change the prognosis: oral peanut immunotherapy (a standardized drug) and—for the first time since 2024—anti-IgE therapy with omalizumab, which reduces the risk of reactions to one or more food allergies in children from 1 year of age. [4]

ICD-10 and ICD-11 codes

ICD-10 uses a combination of codes based on the clinical phenotype: T78.0 - anaphylactic shock due to food reaction; T78.1 - other adverse food reactions; K52.2 - allergic/dietary gastroenteritis and colitis (with severe gastrointestinal manifestations); L27.2 - dermatitis from ingested food. There is no separate "universal" code for "food allergy in children" - the syndrome is coded.

In ICD-11, allergic conditions are better organized: 4A84.0 - anaphylaxis due to food allergy; 4A85.2 - food hypersensitivity (with target organ specifications). This improves the accuracy of reporting and data comparability in pediatrics.

Table 1. Frequently used codes for documentation

Situation	ICD-10	Comment	ICD-11	Comment
Anaphylaxis to food	T78.0	In case of systemic reaction	4A84.0	Clarifies the external cause
Other adverse food reaction	T78.1	When the mechanism is not yet clarified	4A85.2	There are subtypes by organs.
Allergic/dietary gastroenteritis	K52.2	For severe gastrointestinal symptoms	4A85.2 (Gastrointestinal tract)	Contains food for hypersensitivity.
Food dermatitis	L27.2	For skin phenotype	4A85.2 (leather)	Similar to ICD-11

Epidemiology

According to confirmed data, true food allergies in children occur in approximately 2-10% of cases, while self-reported figures are inflated (up to 9-10% and higher). Epidemiology varies greatly by region and confirmation method (skin tests/specific immunoglobulin E/provocations). [5]

The allergen profile changes with age: milk and eggs are the most common allergens in toddlers, eggs/peanuts in preschoolers, and peanuts, tree nuts, fish, and seafood in schoolchildren and adolescents. Some children outgrow milk/egg by school age, while peanuts/tree nuts and seafood are more likely to persist. [6]

The change in complementary feeding recommendations has already changed the picture at the population level: after the introduction of early peanut introduction, a decrease in peanut allergy diagnoses in children aged 0-3 years by approximately 27% was recorded, as well as a decrease in overall IgE-mediated food allergies in real-world pediatric practices. This confirms the "LEAP effect" outside of clinical trial settings. [7]

The long-term LEAP-Trio study showed that the protective effect of early peanut introduction persists up to age 12, even if the child ate peanuts irregularly after age 5. This is an important argument in favor of early prevention. [8]

Table 2. Approximate prevalence estimates

Allergen	Prevalence assessment	Comment
Milk	0.5-7.5% (infants/preschoolers)	Often disappears before school
Egg	~1-3% in <5 years	"Baked" forms are often portable
Peanut	~1-2%	Often persists
Fish/seafood	~0.5-3%	Tendency to preserve

Reasons

The cause is an immune response to specific food proteins: binding of immunoglobulin E to high-affinity receptors on mast cells/basophils and the release of mediators upon repeated contact (histamine, leukotrienes, prostaglandins). "Component" allergology helps understand the risk: Ara h 2 (peanuts), ovomucoid Gal d 1 (egg), casein Bos d 8 (milk) are associated with more persistent reactions. [9]

Not all food reactions are allergies: there are FPIES (non-IgE enterocolitis), eosinophilic esophagitis (mixed mechanism), celiac disease (autoimmunity to gluten), enzyme deficiencies (lactase), toxic infections and histamine intolerance - they have different algorithms. [10]

A combination of skin → mouth factors: a defective skin barrier in atopic dermatitis and early skin contact with food proteins increase the risk of sensitization, while oral administration of proteins in the “immunotolerogenic window” conversely trains the immune system to tolerance. [11]

Cross-reactions are also important: pollen-food syndrome in schoolchildren (birch → apple/nuts/carrots) causes itching in the mouth and usually rare systemic reactions; in young children this is less common, but with age it becomes more significant. [12]

Risk factors

High risk - early severe atopic dermatitis; familial atopy increases the likelihood, but is not a diagnosis in itself. In infants with severe eczema, early introduction of peanuts (if necessary, after screening by an allergist) reduces the risk of allergy. [13]

Delayed introduction of major allergens (especially peanuts) increases the likelihood of sensitization. Conversely, early introduction of peanuts (4-6 months) in at-risk groups reduces the risk by 70-80%, and this effect persists into adolescence. [14]

Environmental factors (urbanization, air pollution, smoking, microbiota) influence a child's immune landscape and modify risk, although the magnitude of their contribution varies. A family diet with low diversity and "sterile" eating practices in early childhood also play a role. [15]

Certain medications and physical activity may act as cofactors for anaphylaxis in older children (for example, with nuts/fruits in combination with sports), but this is not a reason for a total ban on food - the decision is made based on history and tests. [16]

Pathogenesis

IgE-mediated allergy is triggered by antigen presentation, polarization of the Th2 response, and the production of immunoglobulin E, which "primes" mast cells and basophils. Repeated exposure to the protein results in rapid degranulation and clinical symptoms ranging from urticaria to anaphylaxis. "Components" help predict heat tolerance and the risk of severe reactions. [17]

Non-IgE forms (FPIES) are realized through cellular mechanisms with delayed symptoms (vomiting, lethargy after 1-4 hours), and eosinophilic esophagitis is a chronic eosinophilic inflammation of the mucosa, which requires different tactics (topical steroids/biological drugs). [18]

Oral tolerance is an active process. Introduction of allergens in infancy trains the regulatory mechanisms to "tolerate" the food; the window of opportunity is the first few months, so delaying it is both futile and harmful. [19]

Symptoms

Skin and mucous membranes: itching, blisters, redness, angioedema of the lips/eyelids; itching in the mouth, especially with the "pollen-food" phenotype in schoolchildren. Symptoms begin to worsen within minutes to a couple of hours after eating. [20]

Gastrointestinal: nausea, vomiting, cramping, diarrhea; in non-IgE forms - delayed multiple vomiting and lethargy (FPIES). Infants may experience blood/mucus in the stool due to cow's milk protein - separate formula protocols apply here. [21]

Respiratory and systemic: sneezing, wheezing, chest tightness, drop in blood pressure, fainting - anaphylaxis, requiring immediate administration of adrenaline. Antihistamines and glucocorticosteroids are not a substitute for adrenaline. [22]

Delayed reactions of 3-8 hours are a “red flag” for α-gal syndrome (to red meat) in adolescents in tick-endemic areas – rare in preschool children, but important to know. [23]

Classification, forms and stages

By mechanism: IgE-mediated; non-IgE (FPIES, etc.); mixed (eosinophilic esophagitis). By source: milk, egg, peanut, tree nuts, wheat, soy, fish, crustaceans/mollusks, sesame. [24]

By severity: local reactions → systemic without hypotension → anaphylaxis (WAO/AAAAI). By course: transient (milk/egg) and persistent (peanuts/nuts/seafood). [25]

Based on the thermal stability of the target protein: thermolabile (baking tolerance) vs. thermostable (casein, Ara h 2, paravalbumin, tropomyosin). This explains why baked forms are sometimes acceptable. [26]

Complications and consequences

The main acute complication is anaphylaxis. The risk is higher in asthma and sensitization to heat-stable "storage" proteins (Ara h 2, etc.). Children at risk require two epinephrine autoinjectors and an action plan. [27]

Chronic consequences include anxiety, school/kindergarten restrictions, and excessive diets with the risk of deficiencies (calcium, vitamin D, protein, iodine). Dietary support is not "optional," but rather based on indications. [28]

Untreated eosinophilic esophagitis results in dysphagia and strictures; self-treatment with strict diets results in growth/weight failure. We evaluate the risks and benefits of any exceptions. [29]

When to see a doctor

Immediately - if signs of anaphylaxis occur: wheezing/difficulty breathing, hoarseness, multiple vomiting/diarrhea with lethargy, drop in blood pressure, widespread hives with dizziness - immediately inject adrenaline into the thigh and call an ambulance. [30]

In the near future - with recurring skin/gastrointestinal episodes after meals, with swelling of the lips/eyelids, with suspected FPIES (vomiting 1-4 hours after milk/rice porridge/oats) and with dysphagia/food impaction (eosinophilic esophagitis). [31]

Separately - for children with severe atopic dermatitis before starting complementary feeding: discuss early introduction of peanuts/eggs and the need for screening. [32]

Table 3. Red flags and what to do

Situation	Actions
Anaphylaxis	Adrenaline, ambulance, observation
Vomiting after 1-4 hours in an infant	Suspected FPIES → see an allergist/inpatient provocations
Dysphagia/food impaction	Exclude eosinophilic esophagitis (endoscopy, biopsy)
Repeated reactions to baked forms	Components (casein/ovomucoid), dietary revision

Diagnostics

Step 1. History. What exactly, in what quantity and form (raw/baked), how long before symptoms began, how they were relieved; concomitant asthma, dermatitis, cofactors (stress/NSAIDs). This filters out "non-allergies." [33]

Step 2. Sensitization tests. Skin prick tests and/or specific immunoglobulin E to extracts. In complex cases, components (Ara h 2, Bos d 8, Gal d 1, etc.) and, if available, a basophil activation test. Tests assess risk and do not make a diagnosis alone. [34]

Step 3. Oral challenge (OC). "Gold standard": step doses at 20-30 minute intervals, protein-specific protocols; separate regimens for FPIES/skin phenotypes. Safety is an absolute priority. [35]

Step 4. Verification of the systemic response. In a severe episode, serum tryptase (in the "window" and baseline levels). In case of dysphagia, endoscopy with biopsy for eosinophilic esophagitis. [36]

Table 4. Diagnostic tools

Test	What does it give?	When needed	Restrictions
Skin tests/specific immunoglobulin E	Confirmation of sensitization	Almost always	Not equal to clinical allergy
Components (Ara h 2, Bos d 8, Gal d 1…)	Severity/thermostability prognosis	Complex cases/crossovers	Availability/cost
BAT	Functional activity	In case of dispute	An expert laboratory is needed
General physical training	Clinical reactivity	In case of doubt/assessment of tolerance	Resource-intensive, there is a risk
Tryptase	Confirmation of anaphylaxis	After the event	Narrow "window"

Differential diagnosis

Celiac disease (autoimmunity to gluten) is not an IgE allergy: tTG-IgA markers and biopsy; treatment is a lifelong gluten-free diet. Lactose intolerance is an enzyme deficiency with gas/diarrhea without an immune phase; a hydrogen breath test is helpful. [37]

FPIES in infants - vomiting/lethargy 1-4 hours after milk/rice porridge/oats, immunoglobulin E is often negative; diagnosis - clinical + in-hospital provocations. Eosinophilic esophagitis - dysphagia/reflux-like symptoms, confirmation - biopsy. [38]

Pollen-food syndrome in schoolchildren/adolescents – itching of the mouth/lips after eating raw fruits/vegetables/nuts without systemic symptoms; often controlled by cooking. Foodborne illnesses and histamine toxicosis (spoiled fish) mimic allergies, but the mechanisms are different. [39]

Table 5. How to distinguish common "masks"

State	Start	Immune mechanism	Key tests	Therapy-base
IgE allergy	Minutes-hours	IgE	Skin/specific immunoglobulin E, OFP	Avoidance, adrenaline, ICU/anti-IgE
FPIES	1-4 hours	non-IgE	Clinic ± provocation	Diet, infusions in acute
Eosinof. esophagitis	Chronic	mixed	Endoscopy + biopsies	Diet/topical steroids/bio
Celiac disease	Chronic	autoimmune	tTG-IgA, biopsy	Gluten-free diet

Treatment

The basics are avoiding the offending product, teaching label reading and managing cross-contamination (at home, kindergarten/school, and restaurants). In the EU, 14 allergens are mandatory, while in the US, the "Big Nine" (sesame has been added since 2023) are. However, labeling doesn't eliminate the risk of traces and errors—I teach families to ask the "right questions." [40]

Emergency preparedness: For a child at risk of a systemic reaction, keep two epinephrine autoinjectors on hand and a written action plan (parents, caregivers, and teachers know the protocol). Epinephrine is the first-line drug for anaphylaxis; antihistamines and glucocorticosteroids are adjuvant. I teach injection technique and early warning signs. [41]

Symptomatic therapy: non-sedating antihistamines for skin itching/urticaria; intranasal steroids for rhinitis; bronchodilators according to the asthma plan. For eosinophilic esophagitis - "swallowed" steroids/budesonide suspensions and, if indicated, biological therapy. We do not "treat" allergies with antihistamines - they mask the symptoms. [42]

Peanut oral immunotherapy (OIT): A standardized preparation (peanut allergen powder, Palforzia) is approved for children 4-17 years old to reduce the risk of accidental exposure; this is not an "allergy reliever," but rather a threshold raiser. Treatments are performed in experienced centers, with selection and long-term maintenance. For milk and eggs, OIT is available in specialized programs (off-label). [43]

Sublingual immunotherapy (SLIT) with peanut is an option with lower systemic reactogenicity and moderate efficacy; it is chosen by some families, especially for infants or those with contraindications to ICU. The decision is individualized, with realistic goals: "raising the threshold" rather than allowing freedom to "do everything at once." [44]

Anti-IgE therapy with omalizumab (Xolair): FDA-approved on February 16, 2024, for use in children 1 year and older and adults with one or more food allergies to reduce severe reactions following accidental exposure. This is the first approved "broad-spectrum" drug; it does not eliminate avoidance but improves safety in daily living and can be used as monotherapy or as a "shield" around the ICU. [45]

Epicutaneous immunotherapy (EPIT) with peanut (Viaskin Peanut) is on the horizon: a regulatory program in the US is being promoted for infants; further decisions are awaited. In real-world practice, this is a potential "gentle" alternative, but does not yet replace OIT/anti-IgE where indicated. [46]

"Baked forms" of milk/egg: Some children tolerate them and may accelerate tolerance development. Tolerability should be tested only by provocation in a clinical setting; home experiments are prohibited. If tolerance is confirmed, introduce them according to protocol. [47]

Nutrition without deficiencies: elimination diets without a nutritionist are a direct path to calcium/vitamin D/iodine/protein deficiencies. For infants with milk allergies, the choice of therapeutic formula (extensively hydrolyzed/amino acid formulas) is individualized; for older children, complete replacements and growth/weight monitoring are recommended. At the same time, I teach my family how to correctly read the menu at preschool/school. [48]

School/kindergarten: written plan (who to call, where to find the adrenaline, who knows how to administer it), staff training, and a "standby kit" (two adrenalines, an antihistamine, and instructions). This is enough to mitigate most risks without keeping a child under a "glass window." [49]

Table 6. Comparison of strategies

Approach	Target	Pros	Cons/risks	Status
Avoidance + learning	Safety every day	Available	The Burden of Family	Standard
Adrenaline auto-injector	Reduction in mortality	Fast and efficient	Requires training	Standard
OIT peanuts	↑ reaction threshold	Proven	Reactions, visits	Approved for 4-17 years
SLIT peanuts	↑ threshold, softer	Less reactions	Weaker effect	Used in centers
Omalizumab	↓ reactions to 1+ allergens	The first "broad" drug	Injections, cost	FDA 2024

Prevention

Early introduction of peanuts: 4-6 months – for children with severe eczema/egg allergy after consultation; for others – as soon as the child is ready for solids. This reduces the risk by 70-80% and, as new data have shown, the effect lasts into adolescence. [50]

Other allergens (egg, milk, wheat): early introduction does not increase risk; there are signs of benefit for egg, but they are weaker than for peanuts. Breastfeeding is beneficial for many reasons, but is not a "vaccine" against food allergies; maternal allergen avoidance during pregnancy/lactation is not recommended for prevention. [51]

Hydrolyzed formulas as "allergy prevention" are no longer recommended: there is insufficient high-quality evidence. The focus is on a varied diet during the first year and proper skin barrier care for children with atopic dermatitis. [52]

Table 7. What parents should do at 4-12 months

Task	How	Comment
Introducing peanuts	Purees/pastes/"puffs", not whole nuts	Risk groups - according to the NIAID scheme
Inserting the egg	Well heat-treated forms	Provocations - only in the clinic
Dietary diversity	Several new products every week	No delays for up to 12 months
Skin in AD	Daily emollients, anti-inflammatory control	Reducing the risk of transdermal sensitization

Forecast

Milk and eggs are often eliminated by school age (especially if baked goods are tolerated), while peanuts/nuts/seafood are often retained. Periodic reassessment (specific immunoglobulin E/OFP) is essential to avoid keeping a child on a "perpetual" diet. [53]

The ICU and anti-IgE have expanded the possibilities: more and more children are living with normal activity and less fear of accidental contact. But there is no "universal allergy shot" yet—nothing is possible without adrenaline and an action plan. [54]

Effective prevention in infancy is already changing the population picture – fewer new cases and fewer hospitalizations. This is a case where "earlier is better." [55]

Allergen Labeling: What Parents Need to Know

In the EU, the Consumer Information Act (Regulation 1169/2011) requires the identification of 14 allergens – gluten-containing cereals, crustaceans, eggs, fish, peanuts, soy, milk, tree nuts, celery, mustard, sesame, sulfur dioxide/sulfites, lupine, and shellfish – and information is also required for unpackaged products. In the US, the FALCPA/FASTER regulations cover the "Big Nine": milk, eggs, fish, crustaceans, tree nuts, peanuts, wheat, soy, and sesame (mandatory on the label since 01.01.2023). [56]

Table 8. "EU-14" and "US-9" in one list

Jurisdiction	Scroll
EU	14 allergens (including celery, mustard, lupine, sulfites)
USA	9 allergens (including sesame since 2023)

FAQ

Do you need to have a blood test for all foods?
No. Tests are done based on your medical history and specific suspicions. A positive test without clinical evidence does not necessarily indicate an allergy; sometimes a general physical examination is necessary. [57]

Is it possible to "outgrow" an allergy?
Common allergies include milk/eggs, and less common ones include peanuts/nuts/fish. We check periodically to avoid sticking to the diet longer than necessary. [58]

Is it true that early peanut
introduction is dangerous? When done correctly, it actually protects at-risk groups. This has already been confirmed by long-term data up to age 12 and real-world pediatric practice. [59]

Will anti-IgE "cure" allergies?
No. Omalizumab reduces the risk of severe reactions during accidental contact and can serve as a "shield" around the ICU. Avoidance and adrenaline remain. [60]

How can children attend kindergarten/school?
With an anaphylaxis plan, two autoinjectors, and trained staff. This allows for life without a "glass dome." [61]

Should a mother avoid allergens during pregnancy/breastfeeding for prevention?
No. Such restrictions have not been shown to be beneficial. The key is early, correct introduction of allergens to the child. [62]