# Food Allergy: Prevention, Diagnosis, and Management

## Introduction

Food allergy affects approximately 8% of children and 10% of adults in the United States, with prevalence rising over the past two decades. **IgE-mediated food allergy** represents the most clinically significant form, capable of causing life-threatening **anaphylaxis**. Med-peds physicians must understand evolving paradigms in early allergen introduction, accurate diagnostic strategies, and emergency management across the age spectrum.

## Epidemiology and Risk Factors

The "big nine" allergens account for >90% of reactions: **milk, egg, peanut, tree nuts, wheat, soy, fish, shellfish, sesame**. Childhood prevalence peaks in the first two years of life; milk and egg allergies often resolve by school age. Peanut, tree nut, and shellfish allergies tend to persist into adulthood. Risk factors include **atopic dermatitis**, family history of atopy, and filaggrin gene mutations. The **dual allergen exposure hypothesis** proposes that cutaneous sensitization through disrupted skin promotes allergy, while early oral exposure promotes tolerance.

## Prevention Strategies

### Early Allergen Introduction

The **LEAP trial** demonstrated that early peanut introduction (4-11 months) reduced peanut allergy by 81% in high-risk infants. Current guidelines recommend introducing peanut-containing foods around 4-6 months in infants with severe eczema or egg allergy after evaluation. The **EAT study** supported early introduction of multiple allergens, though adherence was challenging. Breastfeeding is encouraged but is not independently protective against food allergy.

### Role of the Skin Barrier

Aggressive treatment of **atopic dermatitis** with emollients and topical anti-inflammatories may reduce transcutaneous sensitization. Avoidance diets during pregnancy and lactation are no longer recommended for allergy prevention.

![Diagram illustrating the dual allergen exposure hypothesis with cutaneous vs oral routes](illustration-dual-allergen-exposure-hypothesis.jpg)

## Diagnosis

### Clinical History

Detailed history should characterize the **timing** (minutes to hours), **reproducibility**, and **specific symptoms** of reactions. Distinguish **IgE-mediated** (urticaria, angioedema, anaphylaxis) from **non-IgE-mediated** (FPIES, eosinophilic esophagitis) and **mixed** presentations. In adults, consider cofactors such as exercise, alcohol, and NSAIDs that lower the reaction threshold.

### Diagnostic Testing

| Test | Sensitivity | Specificity | Best Use | Limitations |
|------|-------------|-------------|----------|-------------|
| Skin prick test (SPT) | ~90% | ~50% | Initial screening; rapid results | Cannot use with antihistamines; risk of reaction |
| Serum-specific IgE | ~90% | ~50% | When SPT not feasible; trending over time | Does not confirm clinical reactivity |
| Component-resolved diagnostics | Variable | Higher than whole-allergen | Distinguishing true allergy from cross-reactivity | Limited allergens available |
| Oral food challenge (OFC) | Gold standard | Gold standard | Definitive diagnosis; assessing resolution | Requires medical supervision; time-intensive |

**Skin prick testing (SPT)**: High sensitivity (~90%), moderate specificity; a wheal >=3 mm above negative control is positive. **Serum-specific IgE**: Useful when SPT is not feasible; values above predictive decision points increase likelihood of clinical reactivity. **Component-resolved diagnostics (CRD)**: Identifies specific allergenic proteins (e.g., Ara h 2 for peanut) to improve specificity. **Oral food challenge (OFC)**: The gold standard for diagnosis; performed under medical supervision.

![Diagnostic algorithm for suspected IgE-mediated food allergy](illustration-food-allergy-diagnostic-algorithm.jpg)

## Management

### Allergen Avoidance

Strict dietary avoidance remains the cornerstone of management. Educate families on **label reading**, cross-contact risks, and restaurant safety. In pediatric patients, ensure nutritional adequacy with dietitian involvement when eliminating major food groups.

### Emergency Preparedness

All patients with IgE-mediated food allergy should carry **epinephrine auto-injectors** and have an anaphylaxis action plan. Epinephrine dosing: 0.01 mg/kg IM (max 0.3 mg in children <30 kg, 0.5 mg in adults) Train patients, caregivers, and school personnel on device use. Antihistamines treat cutaneous symptoms but do **not** substitute for epinephrine in anaphylaxis.

### Immunotherapy and Emerging Treatments

**Palforzia** (peanut oral immunotherapy) is FDA-approved for ages 4-17 to reduce severity of accidental exposures. **Omalizumab** (anti-IgE) is approved as adjunct therapy for food allergy, reducing reaction severity. Epicutaneous immunotherapy (EPIT) and sublingual immunotherapy (SLIT) are under investigation. Desensitization does not equate to sustained unresponsiveness; ongoing dosing is typically required.

### Special Populations

**FPIES**: Non-IgE-mediated; presents with profuse vomiting 1-4 hours after ingestion; managed with avoidance and ondansetron for acute episodes. **Eosinophilic esophagitis**: Overlaps with food allergy; requires endoscopic evaluation and elimination diets or swallowed topical corticosteroids. **Adult-onset food allergy**: Increasingly recognized; shellfish and tree nuts are common culprits.

![Epinephrine auto-injector technique demonstration](illustration-epinephrine-autoinjector-technique.jpg)

## Clinical Pearls

Early introduction of allergenic foods in high-risk infants is now standard of care and has shifted prevention paradigms. A positive skin prick test or specific IgE alone does not confirm clinical allergy; oral food challenge remains the gold standard. Epinephrine is the first-line treatment for anaphylaxis; delays in administration are associated with fatal outcomes. Oral immunotherapy reduces reaction severity but does not cure food allergy; shared decision-making is essential. Non-IgE-mediated food allergies (FPIES, EoE) require different diagnostic and management frameworks.

## References

1. Du Toit G, Roberts G, Sayre PH, et al. Randomized trial of peanut consumption in infants at risk for peanut allergy (LEAP). *N Engl J Med*. 2015;372(9):803-813.
2. Togias A, Cooper SF, Acebal ML, et al. Addendum guidelines for the prevention of peanut allergy in the United States. *J Allergy Clin Immunol*. 2017;139(1):29-44.
3. Sampson HA, Aceves S, Bock SA, et al. Food allergy: A practice parameter update. *J Allergy Clin Immunol*. 2014;134(5):1016-1025.
4. PALISADE Group. AR101 oral immunotherapy for peanut allergy. *N Engl J Med*. 2018;379(21):1991-2001.