Allergic disease in children: integrated approach: SAQ

This boy has multisystem atopic disease: early-onset severe eczema, challenge-or-history-confirmed peanut allergy with prior anaphylaxis, and now asthma and allergic rhinitis. He illustrates the atopic march in a single child, and his poor asthma control in the setting of food allergy places him in the highest-risk group for fatal anaphylaxis. The integrated task is to address all four organs with one coordinated plan, to confirm the peanut diagnosis with a supervised challenge when resolution is plausible, and to ensure he carries an adrenaline autoinjector with a written action plan. ^[5][7]

Question 1 (10 marks)

Classify this child's allergic disease by mechanism and by organ, explain the atopic march, and justify the adrenaline-autoinjector decision. (4 marks for mechanism and organ classification; 3 marks for the atopic march; 3 marks for the autoinjector decision.) ^[4]

By mechanism, his eczema is a non-IgE / mixed Th2-and-barrier disease, his peanut allergy with prior anaphylaxis is an IgE-mediated mast-cell disease, and his asthma and allergic rhinitis are chronic type-2 airway inflammatory diseases. By organ he has skin disease (eczema), gut disease (peanut allergy), lower-airway disease (asthma) and upper-airway disease (rhinitis). The mechanism classification matters because it determines the action plan: the IgE-mediated peanut allergy is the one for which adrenaline belongs in the plan, whereas the non-IgE diseases are not adrenaline-responsive. ^[4]

The atopic march describes the tendency for these diseases to appear in sequence in the same child: eczema and food allergy in infancy followed by allergic rhinitis and asthma in the pre-school and school years. This child is following the march in textbook fashion, beginning with early-onset severe eczema, which is the single strongest predictor of progression. The march is driven by shared type-2 biology: barrier breakdown allows transcutaneous sensitisation, interleukin-4 and interleukin-13 drive immunoglobulin E class switching, and interleukin-5 sustains the eosinophilia that underlies asthma. ^[5]

He should carry an adrenaline autoinjector. The indication is a prior anaphylactic reaction plus ongoing confirmed peanut allergy, and his poorly controlled asthma multiplies his fatality risk because the bronchospasm of anaphylaxis sits on top of a twitchy, undertreated airway. The plan is built around the worst-ever reaction, not the most recent; the prior anaphylaxis at 11 months is the defining event regardless of what has happened since. A written action plan, a loaded autoinjector, and school and carer education are all required. ^[7]