TextbookRheumatology & MusculoskeletalEosinophilic Granulomatosis with Polyangiitis

Eosinophilic Granulomatosis with Polyangiitis

ANCA-associated small-vessel vasculitis (formerly Churg-Strauss syndrome) characterised by asthma, eosinophilia, and granulomatous vasculitis. ANCA (p-ANCA/MPO) positive in only 40% of cases. Distinguished from other AAV by prominent eosinophilia and asthma.

Key Facts

EGPA (formerly Churg-Strauss) is characterised by asthma (>95%), peripheral eosinophilia, and vasculitis affecting small-medium vessels p-ANCA (anti-MPO) positive in only ~40%; ANCA-positive patients have more renal and neurological involvement Three phases: prodromal (allergic rhinitis, asthma), eosinophilic (tissue infiltration), vasculitic (systemic vasculitis) Cardiac involvement (cardiomyopathy, pericarditis) is the leading cause of death (~50% of EGPA mortality); often ANCA-negative Five-Factor Score (FFS): predicts prognosis; cardiac, GI, renal involvement = worse outcome Treatment: prednisolone ± cyclophosphamide (if FFS ≥1); mepolizumab (anti-IL-5) is NICE approved for relapsing/refractory EGPA Incidence: ~2 per million/year; rarest of the three AAV types

Overview

Key Facts

EGPA is unique among AAV due to its association with asthma and eosinophilia. The distinction between ANCA-positive and ANCA-negative disease has important implications for organ involvement and treatment.

Epidemiology

  • Incidence: ~2 per million/year
  • Peak age: 40-60; M=F
  • Rarest of the three AAV

Pathophysiology

  • Eosinophilic tissue infiltration + granulomatous inflammation + small-vessel vasculitis
  • IL-5-driven eosinophil activation and survival
  • ANCA-positive: more GN and neuropathy (similar to other AAV)
  • ANCA-negative: more cardiac and pulmonary infiltrates (eosinophil-driven)

Clinical Presentation

Prodromal Phase

  • Allergic rhinitis, nasal polyps
  • Adult-onset asthma (usually severe, steroid-dependent)
  • May last years before vasculitic phase

Eosinophilic Phase

  • Peripheral eosinophilia (often >1.5 × 10⁹/L, sometimes >10 × 10⁹/L)
  • Eosinophilic pulmonary infiltrates: migratory, transient
  • Eosinophilic gastroenteritis: abdominal pain, diarrhoea

Vasculitic Phase

  • Cardiac (leading cause of death): myocarditis, pericarditis, cardiomyopathy, heart failure
  • Nervous system: mononeuritis multiplex (most common neuropathy; 70%), cranial neuropathy
  • Skin: palpable purpura (50%), nodules
  • Renal: crescentic GN (less common than GPA/MPA; ~25%)
  • GI: mesenteric vasculitis, perforation
  • Constitutional: fever, weight loss, fatigue

Red Flags

  • Cardiac involvement → echocardiogram, troponin, cardiac MRI
  • Mononeuritis multiplex → nerve conduction studies
  • GI vasculitis → surgical emergency if perforation

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
GPANo asthma, granulomata in upper airway, PR3-ANCAANCA, CT
MPANo asthma/eosinophilia, MPO-ANCAANCA, biopsy
Hypereosinophilic syndromeEosinophilia, organ damage, no vasculitisFIP1L1-PDGFRA
Allergic bronchopulmonary aspergillosisAsthma, eosinophilia, Aspergillus sensitisationIgE, Aspergillus IgE
Parasitic infectionTravel history, eosinophiliaStool OCP, serology

Diagnosis / Investigation

Bloods

  • FBC: eosinophilia (usually >1.5 × 10⁹/L; often >10)
  • p-ANCA (anti-MPO): positive in ~40%
  • IgE: elevated
  • CRP/ESR: elevated
  • Troponin: cardiac involvement
  • U&Es: renal function

Imaging

  • CT chest: patchy migratory infiltrates, ground-glass opacities
  • Cardiac MRI: myocarditis, fibrosis (most sensitive for cardiac EGPA)
  • Echocardiogram: pericardial effusion, LV dysfunction

Biopsy

  • Tissue biopsy (skin, nerve, lung): eosinophilic infiltration, granulomata, vasculitis
  • Nerve biopsy: vasculitic neuropathy

Neurophysiology

  • Nerve conduction studies/EMG: mononeuritis multiplex pattern

Management

Induction

FFS = 0 (no poor prognosis factors):

  • Prednisolone 1mg/kg/day alone; taper over months

FFS ≥1 (cardiac, GI, renal, CNS):

  • Prednisolone + IV cyclophosphamide (CYCLOPS protocol) OR rituximab

Maintenance

  • Azathioprine 2mg/kg/day or methotrexate
  • Continue low-dose prednisolone (many patients require long-term due to asthma)

Mepolizumab (Anti-IL-5)

  • NICE TA845: approved for relapsing/refractory EGPA
  • MIRRA trial: 300mg SC monthly; reduced relapse by 50%, reduced steroid dose
  • Particularly effective for eosinophil-driven disease

Asthma Management

  • Optimise asthma therapy (inhalers, biologics)
  • Often severe, steroid-dependent asthma
  • Mepolizumab also treats severe eosinophilic asthma

Referral

  • All EGPA → rheumatology
  • Cardiac involvement → cardiology (cardiac MRI)
  • Neuropathy → neurology

Prognosis

  • 5-year survival: 80-90% with treatment
  • Cardiac involvement: major determinant of mortality (~50% of deaths)
  • Five-Factor Score (FFS): higher score = worse prognosis
  • Relapse rate: 25-35% within 5 years
  • Mepolizumab: significantly reduces relapse and steroid requirements
  • ANCA-positive: more renal/neurological; ANCA-negative: more cardiac

Other Relevant Information

Five-Factor Score (FFS) for EGPA

FactorPoints
Cardiac involvement1
GI involvement1
Renal insufficiency (creatinine >141 µmol/L)1
Proteinuria (>1g/day)1
CNS involvement1

FFS 0: good prognosis; FFS ≥1: poor prognosis → immunosuppression required