In New Zealand, allergic Asthma is managed by allergy & immunologists. Allergic asthma is the most common phenotype of asthma, defined by chronic airway inflammation driven by Type 2 immune responses to inhaled allergens such as house dust mite, animal dander, mould, and pollen. Roughly 60-80% of children and 50-60% of adults with asthma have an allergic phenotype, and globally an estimated 260 million people live with asthma overall (GBD 2021).
Allergic asthma (ICD-10: J45.0), also called atopic or extrinsic asthma, is a chronic inflammatory disease of the airways triggered by IgE-mediated and Type 2 immune responses to inhaled aeroallergens. Inhaled allergen binds IgE on mast cells and triggers degranulation, releasing histamine, leukotrienes, and prostaglandins that produce immediate bronchospasm. A second, late-phase response 4-8 hours later recruits eosinophils, T-helper 2 lymphocytes, and innate lymphoid cells, releasing interleukins IL-4, IL-5, IL-13, and thymic stromal lymphopoietin (TSLP). Chronic inflammation thickens the airway smooth muscle, increases mucous gland mass, and causes basement membrane fibrosis (airway remodelling).
The key symptoms of Allergic Asthma are: Episodic dry cough, especially at night or in the early morning, often the first and only symptom in milder allergic asthma., Audible wheeze on exhalation, sometimes also on inspiration, produced by narrowed airways and turbulent airflow., Chest tightness, described as a band or weight on the chest, often worse during exacerbations., Breathlessness on exertion, with cold air, or after laughing — exercise-induced bronchoconstriction occurs in 70-90% of patients., Symptoms triggered or worsened by specific allergens (house dust mite, cat or dog dander, mould, tree, grass, or weed pollen, cockroach)., Seasonal pattern of symptoms matching pollen calendars (spring tree, summer grass, autumn weed, year-round perennial allergens)., Coexisting allergic rhinitis (sneezing, itchy nose, blocked nose, watery eyes) in 70-80% of patients with allergic asthma..
Diagnosis combines a typical history with objective evidence of variable airflow obstruction. The classic history includes episodic wheeze, cough, chest tightness, or breathlessness triggered by allergens, exercise, viral infection, or cold air, with day-to-day variability and a personal or family history of atopy. Spirometry is the primary lung function test: a post-bronchodilator increase in FEV1 of 12% and 200 mL (children: 12%) confirms reversible airflow obstruction. If baseline spirometry is normal, alternative objective tests include peak flow variability (more than 10% in adults, 13% in children over two weeks), bronchial challenge with methacholine or mannitol (PC20 <8 mg/mL is positive), or exercise challenge for exercise-induced bronchoconstriction. Type 2 biomarkers refine the phenotype and guide biologic eligibility: blood eosinophils above 150/µL, fractional exhaled nitric oxide (FeNO) above 25 ppb in adults (35 ppb in children 5-12), and total IgE above 30 IU/mL. Allergy assessment with skin-prick testing or serum specific IgE to common aeroallergens identifies modifiable triggers and informs allergen avoidance and allergen immunotherapy. A chest X-ray excludes alternative diagnoses (pneumonia, cardiac failure, malignancy) in adults with new wheeze. Differential diagnoses include COPD, vocal cord dysfunction, hyperventilation syndrome, eosinophilic granulomatosis with polyangiitis, allergic bronchopulmonary aspergillosis, and cardiac failure.
Most patients with mild to moderate allergic asthma achieve good control on inhaled corticosteroid-formoterol with rare exacerbations and normal life expectancy. About 50% of children with allergic asthma improve substantially or enter clinical remission by adolescence, although airway hyperresponsiveness often persists. Severe allergic asthma now responds to targeted biologic therapy in 60-80% of well-phenotyped patients, with halving of severe exacerbations, halving of oral corticosteroid use, and substantial quality-of-life improvement. Asthma-related mortality has fallen substantially in countries with widespread access to inhaled corticosteroids — UK and US rates now around 1.5 per 100,000 — but remains higher among lower-income and minority populations. The major modifiable risk factors for poor prognosis are non-adherence, smoking, persistent allergen exposure, and untreated comorbid rhinitis or obesity.
Patients with frequent exacerbations (more than two per year), persistent symptoms despite medium-dose ICS-LABA, FEV1 below 70% predicted, oral corticosteroid dependence, or features of Type 2 inflammation should be referred to an allergist or respiratory physician for phenotyping and biologic assessment. Children with frequent symptoms or poor inhaler response benefit from paediatric allergy review.
Find specialists →Symptomatic improvement begins within hours of initiating ICS-formoterol. FEV1 and FeNO improve over 6-8 weeks. Biologic therapy effects are usually apparent by 4-12 weeks with maximal exacerbation reduction by 6 months. Allergen immunotherapy requires 3-5 years for long-lasting benefit. Step-down to lower controller doses can be considered after 3 months of good control.
Regular aerobic exercise (150 minutes per week) improves cardiovascular fitness and asthma control. Use a 10-15 minute warm-up to reduce exercise-induced bronchoconstriction; pre-exercise inhaled corticosteroid-formoterol or salbutamol can be added when needed. Swimming in chlorinated pools may benefit some patients but worsens others — try alternatives if symptoms develop after swimming.
Choose a clinician with subspecialty training in asthma and allergy who has access to spirometry, FeNO, allergy testing, and biologic prescribing. Ask whether the clinic offers a severe asthma multidisciplinary team review including respiratory physiotherapy, allergy nurse specialist, and clinical psychology, and whether they use validated outcome measures (ACT, ACQ).
Medically reviewed by AIHealz Medical Editorial Board · May 13, 2026
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