6.2 Allergic Disease & Atopy

Allergic Disease & Atopy

The Atopic March

The atopic march describes the classic temporal sequence in which allergic disease tends to appear across childhood: atopic dermatitis (eczema) in infancy, followed by food allergy, then allergic rhinitis, then asthma, typically emerging later in childhood. Not every atopic child follows the full sequence, but the pattern is a favorite exam concept because it links seemingly separate organ-system diseases to one underlying process.

The leading explanation is the "outside-in" (epidermal barrier) hypothesis: loss-of-function mutations in the filaggrin gene weaken the skin barrier, allowing environmental allergens to penetrate the skin and prime a Th2-skewed immune response before oral tolerance has a chance to develop through the gut. Infants with early-onset, severe eczema -- especially with a filaggrin mutation or a positive family history of atopy -- carry the highest risk of progressing along the march. This is why early, effective eczema control and early allergen-introduction strategies (below) are active areas of prevention research.

Food Allergy

IgE-mediated food allergy produces rapid-onset reactions, from minutes up to two hours after ingestion: urticaria, angioedema, vomiting, and wheeze, up to anaphylaxis (full emergency management of anaphylaxis is covered separately in the Emergencies chapter). Non-IgE-mediated reactions are delayed and include food protein-induced enterocolitis syndrome (FPIES) -- profuse, delayed vomiting and lethargy hours after ingestion, sometimes with hypotension -- and eosinophilic esophagitis, which presents with chronic dysphagia or feeding difficulty.

The "top 9" allergens account for most reactions: cow's milk, egg, peanut, tree nuts, soy, wheat, fish, shellfish, and sesame. Milk and egg allergy are usually outgrown by school age; peanut, tree nut, and shellfish allergy more often persist into adulthood.

Diagnosis

Skin prick testing and serum allergen-specific IgE identify sensitization, not necessarily clinical allergy -- many sensitized children tolerate the food on challenge. The oral food challenge (OFC), performed under medical supervision with resuscitation equipment available, remains the gold standard for diagnosis.

Management

Strict avoidance of the confirmed allergen, caregiver education on food-label reading, dietitian involvement to prevent nutritional deficiency from a restricted diet, a written emergency action plan, and prescription of an epinephrine auto-injector for any child with IgE-mediated food allergy. Periodic re-testing is appropriate for allergens commonly outgrown, such as milk, egg, soy, and wheat.

Prevention -- a key exam trap

The LEAP (Learning Early About Peanut Allergy) trial changed practice. Current guidance favors early introduction of peanut-containing foods around 4-6 months of age, including in high-risk infants (severe eczema and/or egg allergy) after appropriate evaluation, because early introduction reduces the risk of developing peanut allergy. This reverses older advice to delay peanut until age 3, which the exam may present as a distractor.

Urticaria and Angioedema

Acute urticaria presents as transient, intensely pruritic wheals lasting less than 6 weeks, most often triggered by viral illness, medications (especially beta-lactam antibiotics), or foods. Angioedema is deeper dermal/submucosal swelling affecting the lips, tongue, eyelids, or genitalia. When urticaria or angioedema occurs without accompanying respiratory compromise, hypotension, or multisystem involvement, management is second-generation oral antihistamines (cetirizine, loratadine) at standard or doubled doses; short courses of oral corticosteroids may be used for severe, refractory flares. Do not confuse isolated angioedema with anaphylaxis -- absence of bronchospasm and stable blood pressure supports outpatient antihistamine therapy rather than epinephrine. Hereditary angioedema (C1 esterase inhibitor deficiency) causes recurrent, non-pruritic, non-pitting swelling without urticaria and does not respond to antihistamines or corticosteroids; it is treated with C1 inhibitor concentrate or bradykinin-pathway agents, not epinephrine.

Allergic Rhinitis

Allergic rhinitis is IgE-mediated nasal mucosal inflammation from inhaled allergens, classified as seasonal (pollens) or perennial (dust mite, pet dander, mold). Symptoms are clear rhinorrhea, nasal congestion, sneezing, and itchy eyes, nose, and palate.

Stepwise Management

Allergen avoidance first; second-generation, non-sedating oral antihistamines (cetirizine, loratadine) for mild intermittent symptoms; intranasal corticosteroids are the single most effective therapy and first-line for persistent or moderate-to-severe disease; leukotriene receptor antagonists (montelukast) as an adjunct, particularly with comorbid asthma; allergen immunotherapy for confirmed, refractory IgE-mediated disease.

Atopic Dermatitis (Eczema)

Atopic dermatitis is a chronic, relapsing, intensely pruritic inflammatory skin condition and usually the first step of the atopic march. Distribution changes with age:

• Infants (2 months to 2 years): face, scalp, and extensor surfaces of the limbs; the diaper area is characteristically spared.
• Older children and adolescents: flexural surfaces -- antecubital and popliteal fossae, neck, wrists, and ankles.

Pruritus drives an itch-scratch cycle that perpetuates barrier breakdown and inflammation. Diagnosis is clinical, based on morphology, distribution, chronicity, and a personal or family history of atopy -- no specific laboratory test is required.

Stepwise Management (the exam favors an asthma-style stepped approach)

1. Foundation, all severities: liberal emollient/moisturizer use (thick ointments preferred over lotions), lukewarm short baths, fragrance-free products, and trigger avoidance (harsh soap, wool, overheating).
2. Mild-to-moderate flares: low-to-mid potency topical corticosteroids applied to affected skin, tapered once controlled; lower-potency preparations are used on the face, skin folds, and groin because thinner skin there is more prone to steroid-induced atrophy.
3. Steroid-sparing/sensitive areas: topical calcineurin inhibitors (tacrolimus, pimecrolimus) do not cause skin atrophy, making them preferred for the face, eyelids, and long-term maintenance therapy.
4. Moderate-to-severe/refractory disease: wet-wrap therapy, treatment of secondary bacterial infection (impetiginized eczema, usually Staphylococcus aureus), phototherapy, or systemic immunomodulators/biologics (for example, dupilumab, an IL-4/IL-13 receptor blocker) in recalcitrant cases.

Complication to Recognize

Eczema herpeticum is disseminated herpes simplex virus infection superimposed on eczematous skin, presenting with punched-out vesicles/erosions and systemic illness. It is a dermatologic emergency treated with intravenous acyclovir and must not be mistaken for a routine flare.