Synopsis
Recognise immune-mediated lung disease from inhaled antigens, build a credible exposure diagnosis and prioritise safe exposure control, multidisciplinary assessment and progression surveillance.
- Hypersensitivity pneumonitis is an immune-mediated parenchymal and small-airway response to inhaled antigen in a susceptible person; exposure alone is not disease.
- Use non-fibrotic and fibrotic phenotypes because older acute, subacute and chronic labels overlap and can obscure behaviour.
- Sources include birds, mouldy hay or buildings, compost, metalworking fluids, humidifiers and other aerosolised biological material; the antigen is sometimes never identified.
- Ask where, when and how symptoms change: improvement away from work or home and relapse after return can be more useful than a generic allergy history.
- HRCT may combine ground glass, centrilobular nodules, mosaic attenuation and expiratory air trapping; fibrosis adds reticulation, traction change or honeycombing.
- Serum antigen-specific IgG indicates exposure and immune recognition, not causation, severity or a stand-alone diagnosis.
- Bronchoalveolar lavage lymphocytosis can support non-fibrotic disease but no universal threshold proves or excludes hypersensitivity pneumonitis.
- Avoidance is the central intervention, yet vague advice to 'avoid mould' is ineffective without identifying sources and involving occupational or environmental expertise.
- Corticosteroids may accelerate early improvement in selected inflammatory disease but have uncertain long-term benefit and require specialist, infection-aware decisions.
- Fibrotic disease can continue after exposure removal; monitor behaviour and consider progressive-fibrosis pathways rather than assuming avoidance guarantees stability.
Key red flags
Marked tachypnoea, hypoxaemia, diffuse opacities and systemic illness after exposure can mimic infection or oedema and requires emergency hospital care rather than outpatient antigen testing.
Similar symptoms among co-workers or improvement during holidays suggests a shared aerosol, commonly metalworking fluid, agricultural material or contaminated process, and warrants occupational-health escalation.
Investigation priorities
Identify a biologically plausible inhaled antigen and temporal relationship.
Management branches
Clinical or HRCT features raise hypersensitivity pneumonitis.
- Use a structured home, occupational and hobby history to map antigen contact against symptom onset, weekends, holidays, moves and process changes.
- Obtain protocolled HRCT, complete physiology and cause-directed tests; use antigen-specific IgG as exposure support, not as diagnostic proof.
- Discuss confidence at an ILD MDT and decide whether lavage or tissue would materially distinguish HP from IPF, CTD-ILD, sarcoidosis or infection.
- Record the suspected antigen, uncertainty and an achievable control plan, including the teams responsible for workplace or housing action.
Key medicines
Prednisolone for selected inflammatory HPNo universal UK regimen exists; an ILD specialist chooses a time-limited daily induction and response-guided taper according to severity, infection evaluation and the current local protocol.It cannot replace source removal and its long-term disease-modifying benefit is uncertain. Screen for infection and monitor glucose, blood pressure, mood, bone and ocular effects; prolonged courses require steroid-protection planning.
Nintedanib for eligible progressive fibrosisSpecialist initiation is normally 150 mg orally twice daily around twelve hours apart with food, with 100 mg twice daily, interruption or cessation for intolerance according to the SmPC.This does not remove antigen or treat inflammatory episodes. Check liver function, diarrhoea and weight, bleeding and arterial-event risk, gastrointestinal perforation risk, interactions and pregnancy precautions under specialist supervision.