Synopsis
Recognise eosinophilic granulomatosis with polyangiitis across asthma, eosinophilic tissue disease and vasculitis, exclude parasitic, drug and clonal eosinophilia, detect cardiac and neurological emergencies, and match induction and biologic treatment to organ severity.
- Suspect EGPA when adult-onset asthma and chronic rhinosinusitis accompany eosinophilia, migratory lung infiltrates, purpura, neuropathy, cardiac, renal or gastrointestinal disease.
- Check the absolute eosinophil count before high-dose steroid when safe, because glucocorticoid can normalise it rapidly and obscure phenotype.
- MPO-ANCA supports a vasculitic subset but most patients can be ANCA-negative; never use a negative test to dismiss eosinophilic myocarditis or neuropathy.
- Exclude Strongyloides and other exposure-related parasites, ABPA, drug reaction, clonal eosinophilia and hypereosinophilic syndrome using travel, medicine, IgE, microbiology, film and molecular or marrow tests when indicated.
- Obtain ECG, troponin, NT-proBNP and echocardiography at baseline; use cardiac MRI for suspected myocarditis because cardiac disease can be clinically subtle and prognostically dominant.
- Organ-threatening heart, nerve, kidney, lung or gut disease needs high-dose glucocorticoid plus cyclophosphamide or selected rituximab; an anti-IL-5 biologic does not replace urgent induction.
- Benralizumab 30 mg subcutaneously every four weeks is NICE-recommended for eligible adults with relapsing or refractory non-organ-threatening EGPA and can reduce steroid exposure.
- Mepolizumab 300 mg every four weeks is licensed for adult EGPA, but NICE TA845 did not make an NHS recommendation; severe-asthma funding must not be assumed to cover EGPA.
- Monitor asthma, sinus, eosinophil, vascular, nerve, cardiac and steroid-toxicity domains separately; worsening wheeze does not automatically mean vasculitic relapse.
- Before immunosuppression address vaccines, TB and hepatitis as agent-relevant, Strongyloides risk, Pneumocystis prevention, bone health, fertility and pregnancy.
Key red flags
Chest pain, syncope, arrhythmia, troponin rise, ventricular dysfunction or unexplained dyspnoea may indicate eosinophilic myocarditis even without striking CRP.
New painful asymmetric sensory loss, foot drop or wrist drop indicates nerve infarction and should not be attributed to asthma medication.
Severe abdominal pain, bleeding or peritonism may represent mesenteric vasculitis and requires urgent imaging and surgical review.
Hypoxia with diffuse opacity, falling haemoglobin or renal active sediment suggests pulmonary-renal capillaritis rather than uncomplicated asthma.
Marked eosinophilia requires rapid review of helminths, medicines, haematological neoplasm and hypereosinophilic syndrome before immunosuppression obscures evidence.
Acute painful asymmetric sensory loss and foot or wrist drop is a classic organ-threatening vasculitic feature.
Chest pain, arrhythmia, troponin elevation, heart failure or MRI inflammation may occur particularly in ANCA-negative eosinophilic disease.
Investigation priorities
Confirm eosinophilia before steroid and identify clonal or reactive haematological clues.
Management branches
Asthma or sinus disease accompanies eosinophilia and systemic organ features.
- Record the pre-steroid eosinophil count, travel, medicines, atopy, asthma trajectory and skin, nerve, heart, lung, renal and gut findings.
- Send ANCA, urine, renal, cardiac and lung tests and a phenotype-directed parasite, fungal and clonal-eosinophilia screen.
- Biopsy the safest active site and begin urgent treatment before pathology only when myocarditis, neuropathy or another organ is threatened.