Allergic rhinitis and rhinoconjunctivitis — short-answer questions

This stem concerns a typical seasonal allergic rhinoconjunctivitis presentation in an atopic school-aged child, illustrating classification, mechanism and stepwise management. [1]

Question 1 (10 marks)

a) Give the most likely diagnosis, classify it using the ARIA framework, and outline the IgE-mediated pathophysiology. (6 marks) [1]

The most likely diagnosis is seasonal allergic rhinoconjunctivitis — an IgE-mediated inflammation of the nasal and conjunctival mucosa driven by grass-pollen exposure, supported by the classic quartet of sneezing, itch, rhinorrhoea and congestion, the itchy eyes, and the positive grass-pollen skin-prick test. [1]

By the ARIA framework, the duration is persistent because symptoms occur on most days of the week for the duration of the pollen season (more than four consecutive weeks), and the severity is moderate-to-severe because sleep and school concentration are disturbed. The trigger pattern is seasonal, with a perennial dust-mite sensitisation likely contributing background symptoms. [1]

The pathophysiology has two phases. In sensitisation, inhaled pollen is taken up by antigen-presenting cells, presented to naïve CD4-positive T cells, which polarise to a T-helper-2 phenotype and release interleukin-4 and interleukin-13; these cytokines drive B-cell immunoglobulin class-switching to grass-pollen-specific IgE, which coats mast cells via Fc-epsilon-RI receptors. On re-exposure, pollen cross-links adjacent IgE complexes, triggering mast-cell degranulation with release of histamine and leukotrienes that produce immediate sneeze, itch and rhinorrhoea, followed by a late-phase eosinophil infiltration that sustains congestion. [3]

b) Describe four characteristic physical signs and state how you would confirm sensitisation. (4 marks) [3]

The four characteristic signs are the allergic salute with a transverse nasal crease, pale violaceous boggy inferior turbinates with clear rhinorrhoea, allergic shiners with Dennie-Morgan infraorbital folds, and conjunctival injection with watery discharge. [3]

Sensitisation is confirmed by skin-prick testing — a wheal at least 3 mm larger than the negative control at 15 to 20 minutes demonstrates allergen-specific IgE bound to skin mast cells — with serum-specific IgE reserved for when skin-prick testing is contraindicated or uninterpretable. [3]

Question 2 (10 marks)

a) Outline your stepwise management according to the ARIA ladder and explain why intranasal corticosteroids are first-line for this child. (6 marks) [5]

Management follows the ARIA stepwise ladder. Step zero is allergen avoidance and education: pollen-avoidance advice during the season, saline nasal irrigation, dust-mite-impermeable covers and a written management plan. Step one adds an oral second-generation antihistamine such as cetirizine or loratadine for rapid control of itch, sneeze and rhinorrhoea. [1]

Because this child has moderate-to-severe persistent disease with sleep and school impairment, he should start at step two with an intranasal corticosteroid such as fluticasone or mometasone, which is the most effective single pharmacotherapy and reduces total nasal symptom scores more than antihistamines, with onset over hours and a full effect after about two weeks of continuous use. [5]

Intranasal corticosteroids are first-line for moderate-to-severe disease because they target the underlying Th2-driven nasal inflammation, have minimal systemic bioavailability at paediatric doses with no clinically meaningful effect on the hypothalamic-pituitary-adrenal axis, and improve the congestion that antihistamines alone do not adequately control. Correct spray technique — directing the nozzle away from the septum — minimises local adverse effects. [5]

b) Discuss the role of allergen immunotherapy and when it would be indicated in this child. (4 marks) [10]

Allergen immunotherapy, delivered subcutaneously (SCIT) or sublingually (SLIT), is the only disease-modifying therapy for allergic rhinitis and works by inducing immune tolerance to the specific allergen through regulatory T-cell and IgG4 responses. A three-to-five-year course produces sustained symptom reduction and medication sparing in a proportion of treated children, and sublingual therapy is increasingly preferred in children because of its superior safety profile and home-based convenience. [10]

Immunotherapy is indicated for this child if his symptoms remain uncontrolled on optimised intranasal corticosteroid and antihistamine therapy with documented IgE sensitisation to a clinically relevant allergen, if he has unacceptable side effects from pharmacotherapy, or if he wishes to prevent progression along the atopic march to asthma. Referral to a paediatric allergist is the appropriate step before initiating either route. [10]