COPD biologics in general practice: spot the eosinophilic exacerbator

Why this talk matters now

The chair opened with a striking claim: something like 20% of your COPD patients may be eligible for a biologic. The speaker — Dr Gregory, a respiratory and sleep physician with interest across asthma severities, working across St George, Sutherland Shire, St Vincent’s Private Darlinghurst and other hospitals — is director of the National Asthma Council, on its Guidelines Committee, and affiliated with the Woolcock Institute. The brief was clear: make COPD “sexy” by showing GPs how to spot people who can benefit from targeted therapy rather than more of the same inhalers and prednisone cycles.

Three aims for the session:

• Spot COPD patients who may benefit from a biologic
• Understand the current TGA and PBS situation for COPD biologics
• Refer early — and if it is already late, still refer

Case: Mrs T

Mrs T is 80 years young. She presents with persistent shortness of breath despite triple therapy (ICS + LAMA + LABA), and has needed multiple courses of prednisone for exacerbations, including two hospital admissions for COPD. In older people, hospitalisation carries high morbidity and mortality risk — the speaker shared a heartbreaking anecdote of a patient who, after another exacerbation, said “enough is enough — just let me go.”

• Past asbestos exposure; comorbidities typical of the age group: hypertension, cholesterol, anxiety, osteoporosis — think about oral steroid burden on blood pressure and bones
• No childhood asthma or bronchitis history
• Lives with a friend; has a pet dog
• Sats 93%, no clubbing; chest often sounds “normal” unless wheezing at the time; possible steroid skin/body-shape clues
• Ex-smoker (quit recently, around 2024); exercise tolerance worsening (~200 metres cited); producing sputum

Respiratory physicians are “getting excited about sputum” again — not only as infection, but as a marker of airways inflammation. In asthma on biologics, some patients said their phlegm went away; that taught clinicians that inflammation, not just infection, was driving symptoms and antibiotic courses.

Lung function that supports COPD

• FEV1 ~43% predicted — roughly “one lung instead of two”; normal is roughly 80–120%
• FEV1/FVC ratio ~49% — obstruction
• No bronchodilator reversibility — favours COPD over asthma (note: if they took LABA/triple therapy that morning, reversibility may be masked; ideally test off therapy on the day)
• Low DLCO and KCO — often low in COPD; often normal in asthma — useful when the label is unclear in a smoker

Chest X-ray may be reported as hyperinflated fields “consistent with COPD,” but you cannot diagnose COPD on an X-ray. Clinical diagnosis needs airflow obstruction on lung function. CT changes alone do not equal the clinical diagnosis.

Confirm COPD properly

Australian practice still sits on COPD-X holistic care: pulmonary rehab, vaccination, comorbidity review, weight, then pharmacotherapy from LAMA/LABA up to triple therapy, and reassessment for other causes of breathlessness. This talk focuses on the people who have already stepped to the end — on triple therapy, poorly controlled, exacerbating, and taking the therapy (technique and adherence matter).

Lessons from two decades of severe asthma transfer into COPD: get the inflammatory phenotype right, and biologics can “knock out” a lot of airway inflammation. The speaker described an ~87-year-old COPD patient (with overlapping severe-asthma features) who returned after two months on a biologic, hugged them, and said she could say her morning prayers without stopping for breath, walk the dog, and cook for her grandson — quality of life, not FEV1 points, was what mattered.

Eosinophils: biomarker and treatment signal

Do eosinophils matter in COPD? Yes — in several ways from the talk:

• In exacerbation studies with bronchial washings, eosinophils were the inflammatory cell that rose
• Prednisone suppresses eosinophilic inflammation well — a “prednisone lover” with airways disease should make you hunt for eosinophils
• Higher airway eosinophils associate with worse FEV1 decline over time — a poor prognostic marker that is also a marker of treatment response
• ICS reduce exacerbations versus LABA alone; the higher the eosinophils, the greater the ICS benefit — which is why guidelines add ICS as the step to triple therapy when dual bronchodilators are not enough

How common is eosinophilic COPD? One ICS-treated cohort looked around ~60% eosinophilic (selected population). A GP-practice figure cited was about 35%. Practical ask: for a new COPD patient who might need a biologic, have staff pull the last 12 months of full blood counts from the lab or GP — you often already have the answer.

What the biologics trials showed

Asthma responses are often larger (~50–60% exacerbation reduction). COPD has an irreversible component, but that does not mean outcomes cannot be good.

MATINEE — mepolizumab (anti–IL-5)

• Triple therapy + monthly mepolizumab vs triple therapy alone
• About a 30% reduction in exacerbations
• Greater eosinophilia → better anti–IL-5 response
• Blocking IL-5 (Nucala) lowers blood and airway eosinophils; eosinophils contribute to mucus plugging — clinically, mucus can improve as counts fall

BOREAS — dupilumab (IL-4 / IL-13 pathway)

• Second biologic discussed (familiar from eczema / severe asthma; brand Dupixent)
• Similar order of magnitude: ~30% exacerbation reduction
• Lung-function gains also reported — if FEV1 is ~40% and improves ~20–30%, that can change walking and independence

TGA / PBS — mepolizumab (Nucala)

Until recently, two biologics were TGA-listed for COPD (mepolizumab and a second agent discussed in the IL-4/IL-13 space — dupilumab). PBAC had recommended PBS listing for both. As of the week of the talk — 1 September 2026 — mepolizumab (Nucala) is PBS-listed for severe eosinophilic COPD. Dupilumab remained TGA-listed for COPD at the time of the talk without the same PBS access described for Nucala.

Criteria (speaker’s morning slide after reading the listing — confirm current PBS wording yourself):

How this changes GP practice

• Search your database for COPD + eosinophils ≥300 — the chair suggested exactly this QI exercise
• Confirm diagnosis with lung function; if asthma vs COPD is unclear, get full LFTs including diffusion
• Risk reduction: smoking cessation, vaccination, COPD-X basics
• Optimise device technique and adherence — National Asthma Council how-to videos cover every inhaler
• Step up to triple therapy when indicated; if still exacerbating with the eosinophil signal — refer
• Refer to a local physician who actually uses biologics; referring to someone who does not can add delay via a second hop
• Before you assume “more COPD,” exclude mimics when obstruction is mild–moderate but symptoms are severe: reflux, heart disease, PE, other lung disease

Five takeaways

1. Biologics are not routine for every COPD patient — target eosinophilic exacerbators on steroids.
2. Biologics are controllers, not cures — like reframing severe asthma to a milder lived disease; inhalers usually continue.
3. Mepolizumab (Nucala) is PBS-listed for severe eosinophilic COPD as of 1 Sep 2026; another agent may remain TGA-only — check current listings.
4. Refer to physicians who prescribe biologics to avoid treatment delay.
5. GPs own the front door: confirm diagnosis, optimise basics, gather eosinophil and exacerbation data, refer with the right package.

Magic number to remember: 0.3 (300 cells per microlitre) eosinophils on one occasion in the last twelve months.

Also on the program: AF ablation

After the COPD talk, the same Healthed session moved to atrial fibrillation and earlier referral for ablation (cardiac electrophysiology guidelines). That content is covered separately — see af-ablation-update.drkotha.com rather than duplicating it here.

All Dr Kotha CPD pages · copd-biologics.drkotha.com · crimson theme