Speaker's Highlight

• Don Sin University of British Columbia, St. Paul Hospital (Canada)
  Kenneth R. Chapman Toronto General Hospital Research Institute (Canada)
• Parameswaran Nair McMaster University (Canada)
  Carolyn Calfee UCSF (U.S.A.)
• Gregory P. Downey University of Colorado School of Medicine (U.S.A.)
  David A. Schwartz University of Colorado School of Medicine (U.S.A.)
• Neil Schluger Tuberculosis Control Branch, California Department of Public Health (U.S.A.)
  Nick Kim Critical Care & Sleep Medicine, University of California San Diego (U.S.A.)
• Nicola Hananiah Baylor College of Medicine (U.S.A.)
  Jae-Joon Yim Seoul National University College of Medicine (Republic of Korea)
• Koichiro Asano Tokai University School of Medicine (Japan)
  Diahn-Warng Perng Taipei Veterans General Hospital (Taiwan)
• Konstantinos Kostikas University of Ioannina (Greece)
  Karin Klooster University Medical Center Groningen (Kingdom of the Netherlands)

• Corticosteroid-sparing advances in eosinophilic granulomatosis

  Eosinophilic granulomatosis with polyangiitis (EGPA), historically called Churg–Strauss syndrome, combines eosinophilic inflammation, asthma and small- to medium-vessel vasculitis. Cardiac, renal and neurological involvement can be fatal, while prolonged glucocorticoids cause infection, metabolic, bone and psychiatric complications. Rapid disease control and steroid withdrawal therefore need to advance together.

  For the clinical audience of APSR 2022, the major change is a more selective use of steroid-sparing drugs. Trial evidence supports rituximab for severe disease and interleukin-5 pathway blockade in selected patients. Treatment still depends on organ involvement, relapse risk, comorbidity, regulatory status and the ability to monitor disease and drug toxicity.

  Why steroid toxicity drives treatment choices

  Glucocorticoids remain the fastest way to suppress the acute inflammatory cascade, and severe EGPA may still begin with pulse or high-dose oral methylprednisolone or prednisolone. The therapeutic aim is to use the smallest effective dose for the shortest feasible period while another agent takes effect and consolidates control.

  Cumulative exposure is associated with diabetes, hypertension, obesity, osteoporosis, cataract, mood disturbance, infection and adrenal suppression. These harms can be as disabling as vasculitis itself. Steroid-sparing treatment is therefore a toxicity-reduction strategy, not simply a convenience or a substitute for careful assessment of disease activity.

  The evolving treatment hierarchy

  Methotrexate, azathioprine and mycophenolate remain useful for non-organ-threatening disease or maintenance. Cyclophosphamide has a role in selected organ-threatening presentations, although its toxicity, fertility effects and infection risk reserve it for situations where the expected benefit outweighs those harms. Oral glucocorticoids remain part of many regimens, usually at a lower dose once remission is secure.

  Rituximab depletes CD20-positive B cells and has strong guideline support for severe active EGPA; observational and trial data show substantial remission and steroid-sparing rates, although response varies. Mepolizumab, benralizumab and reslizumab target the interleukin-5 pathway, reducing eosinophils and improving asthma control. Placebo-controlled data for mepolizumab and benralizumab support higher remission rates and lower steroid requirements, especially in eosinophilic disease, but no agent has established universal superiority across every EGPA phenotype.

  Matching biological therapy to disease phenotype

  Treatment selection begins with phenotype. Eosinophilic asthma, chronic rhinosinusitis and nasal polyps form a respiratory-predominant illness; neuropathy, glomerulonephritis, skin vasculitis or myocarditis indicate systemic vasculitis requiring close organ assessment. ANCA positivity may help stratify renal and neurological risk, while ANCA-negative disease more often has prominent eosinophilic features and relapse, but ANCA alone cannot guide treatment.

  Interleukin-5 blockade is attractive when asthma and eosinophilic tissue disease dominate. Severe cardiac, renal or neurological vasculitis still requires urgent specialist management, and rituximab or conventional induction therapy may be needed even when eosinophils fall. Comorbid asthma, coronary disease, osteoporosis and infection risk should be incorporated into the induction choice rather than treated as separate afterthoughts.

  Biomarkers, tapering and relapse prevention

  No single laboratory result reliably confirms remission. Eosinophil count, C-reactive protein, ESR, ANCA titre and organ-specific tests support interpretation, yet circulating eosinophils can fall with steroids while disease persists, and ANCA may remain positive after control. Clinical review remains central: respiratory symptoms, new neuropathy, pulse or blood-pressure changes, urine abnormalities, rash and exercise tolerance should prompt renewed assessment.

  Once control is secure, tapering should be planned rather than improvised. Many protocols reduce glucocorticoids over three to six months, with slower steps after prolonged high-dose treatment and rapid reversal if relapse emerges. Each review should include blood count, liver and renal function, blood pressure, glucose and bone protection, alongside infection symptoms and vaccination needs. Influenza, pneumococcal, COVID-19 and shingles vaccination are reviewed before immunosuppression or B-cell depletion, using current Australian guidance.

  Australian access and delivery of specialist care

  Australian prescribing sits within a specific regulatory and reimbursement framework. Under the Therapeutic Goods Act 1989, the TGA assesses a product before inclusion in the Australian Register of Therapeutic Goods and publishes an Australian Public Assessment Report. PBS subsidy then depends on the indication and listing; an asthma listing does not automatically establish subsidy for EGPA. Specialist PBS pathways and public-hospital formularies may provide access to high-cost therapy when standard conditions are met.

  Specialist services are concentrated in Melbourne, Sydney, Brisbane, Adelaide and Perth. Medicare-supported telehealth allows a patient in rural or remote Australia to link a metropolitan rheumatologist or respiratory physician with a local GP, laboratory service and community pharmacist. The congress news area also contains non-clinical promotional items, including a mobile casino update, which is a useful reminder to check sponsorship and context before treating a web link as clinical evidence.

  Australian community chemists commonly manage repeat dispensing and PBS scripts, but complex biologics still require infusion or injection capacity and a reliable specialist review process. Holiday travel and regional pharmacy stock can interrupt treatment, so prescriptions, monitoring dates and a contact for medication problems should be coordinated. Seasonal pollen in Melbourne, Sydney and Adelaide may also complicate asthma assessment, making symptom timing and inhaler technique part of the local review.

  A practical shared-care framework

  A workable Australian pathway starts with multidisciplinary assessment that includes rheumatology, respiratory medicine, immunology and the organ specialties needed for the individual presentation. Diagnostic review should consider alternative causes of eosinophilia and asthma before labelling relapse. A written record should state the steroid dose, taper date, blood tests, vaccine status and the features that require escalation.

  Shared care then distributes surveillance: the specialist controls induction and major treatment changes, while the GP, local laboratory and pharmacist support monitoring, vaccination and medication supply. Patients who live far from tertiary centres can use telehealth for stable reviews and local services for blood collection or administration. New breathlessness, chest pain, neurological change, fever or a rapidly spreading rash warrants urgent assessment rather than waiting for the next appointment.

  The practical takeaway is to pair disease control with the lowest glucocorticoid exposure that remains safe, using a predefined taper, reliable laboratory surveillance, early management of drug toxicity and an accessible plan for relapse; for many patients, that means treating EGPA as a coordinated respiratory–rheumatology condition rather than switching between isolated symptom pathways.

  Richard Russell Nuffield Department of Clinical Medicine, University of Oxford (United Kingdom)
• Mona Bafadhel King’s College London (United Kingdom)
  David Jackson Guy’s and St Thomas’ Hospital, King’s College London (United Kingdom)
• James Chalmers University of Dundee (United Kingdom)
  David Price University of Aberdeen (United Kingdom)