Asthma

Asthma is a chronic inflammatory disease of the airways characterised by variable expiratory airflow limitation, bronchial hyperresponsiveness and structural remodelling over time. Diagnosis rests on a compatible symptom pattern plus objective evidence of variable obstruction, usually bronchodilator reversibility on spirometry. The most important shift in modern management is that short-acting beta agonist monotherapy is no longer acceptable. GINA now recommends that every adult and adolescent with asthma receive inhaled corticosteroid-containing treatment, because SABA-only use is associated with more exacerbations and death even in apparently mild disease. Anti-inflammatory reliever therapy with combined budesonide-formoterol reduced severe exacerbations substantially in the SYGMA and Novel START trials. Phenotype matters. Type 2 high asthma, driven by eosinophils and IL-4, IL-5 and IL-13 signalling, responds well to corticosteroids and to biologics such as mepolizumab, benralizumab and dupilumab in severe cases. Non-type 2 asthma, more common in obesity and smoking-related disease, responds less predictably and benefits more from weight loss and comorbidity management. Supplements are adjunctive at best. Vitamin D reduces exacerbation rates in Cochrane analysis, with the effect concentrated in those with baseline levels below 25 nmol/L. Omega-3 and antioxidant claims have not held up in trials, and high-dose vitamin C has no meaningful preventive role. Magnesium is genuinely useful, but as intravenous therapy in acute severe asthma in hospital, not as an oral supplement.

• •Wheeze, particularly on expiration
• •Breathlessness that varies over time and with triggers
• •Chest tightness
• •Cough, often dry and worse at night or early morning
• •Symptoms provoked by exercise, cold air, allergens or infection
• •Waking at night from breathlessness — a marker of poor control

• •Atopy and allergic sensitisation
• •Family history of asthma or eczema
• •House dust mite, pet dander, pollen and mould exposure
• •Tobacco smoke, including in utero exposure
• •Air pollution and traffic-related particulates
• •Respiratory viral infections in early childhood
• •Occupational sensitisers such as flour, isocyanates and latex
• •Obesity
• •Aspirin and NSAID sensitivity in a subset

Asthma arises from gene-environment interaction: atopic predisposition and family history, early-life respiratory viral infection, allergen and house dust mite sensitisation, air pollution and tobacco smoke exposure, occupational sensitisers, and obesity, which produces a distinct less steroid-responsive phenotype. Aspirin-exacerbated respiratory disease and gastro-oesophageal reflux are important contributing patterns in adults.