🫁 Understanding Chronic Cough in Aspergillosis
What the latest British Thoracic Society statement means for you
🌬️ Why This Matters
If you live with aspergillosis, Allergic Bronchopulmonary Aspergillosis (ABPA), or bronchiectasis, coughing can dominate your life. It’s tiring, painful, and socially awkward — especially when people assume it means infection.
Doctors used to see cough as just a symptom of another problem, but the British Thoracic Society (BTS) Clinical Statement on Chronic Cough in Adults (2023) recognises something new:
For many people, a cough can become a condition in its own right — caused by airway and nerve hypersensitivity, not just infection.
This matters for aspergillosis patients because fungal allergy and inflammation make the airways especially sensitive.
💡 What Is “Chronic Cough”?
A chronic cough is one lasting eight weeks or more.
It may be:
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Dry – little or no mucus
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Productive – thick sputum (common in bronchiectasis or chronic aspergillosis)
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Triggered by dust, cold air, perfume, or strong scents
For people with aspergillosis, several overlapping causes may exist:
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Fungal colonisation or infection
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Allergic inflammation (ABPA)
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Bronchiectasis and mucus retention
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Reflux or post-nasal drip
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Nerve hypersensitivity
This is why one treatment rarely fixes everything — different “treatable traits” must be addressed together.
🧬 Why It Happens
1️⃣ The Hypersensitive Cough Reflex
People with aspergillosis often develop overactive airway nerves — so normal irritants like dust, scent, or cold air trigger coughing fits.
This “cough reflex hypersensitivity” happens because:
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Ongoing inflammation damages the airway lining.
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Nerve endings in the throat and lungs become over-responsive.
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Even mild triggers set off powerful reflexes.
This is a real physiological process, not psychological.
It’s why cough can continue even when infection is under control.
2️⃣ Treatable Traits – Finding the Real Drivers
| Treatable Trait | What It Means | What Helps |
|---|---|---|
| Airway infection or colonisation | Persistent fungi or bacteria | Antifungal or antibiotic therapy, sputum tests |
| Allergic inflammation | ABPA or asthma-type airway swelling | Corticosteroids, biologics (e.g., mepolizumab, benralizumab) |
| Cough reflex hypersensitivity | Overactive airway nerves | Speech therapy, nerve-modulating medication |
| Airway clearance problems | Mucus that’s hard to shift | Physiotherapy, saline or mucolytic therapy |
| Reflux or postnasal drip | Acid or sinus drainage irritation | Reflux management, ENT care |
Identifying these traits helps your clinician personalise treatment.
💊 Medications That Can Cause or Worsen Cough
The BTS statement highlights that some medicines can trigger or amplify chronic cough — especially in people with already-sensitive lungs.
🔹 ACE Inhibitors (Blood pressure or heart disease)
Examples: Ramipril, Lisinopril, Enalapril, Perindopril
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Can cause a dry, tickly cough due to bradykinin build-up.
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Happens in ~1 in 5 users, sometimes months after starting.
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GP can switch to a similar drug (ARB – e.g., losartan) that doesn’t cause cough.
🔹 Beta Blockers (Heart or migraine medicines)
Examples: Atenolol, Propranolol, Bisoprolol
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May tighten airways, worsening wheeze or cough.
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Safer “lung-selective” versions exist but should still be monitored.
🔹 Inhalers
Examples: Fluticasone, Budesonide, Salbutamol
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Can irritate the throat if used without a spacer or if technique is poor.
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Always rinse or gargle after use, and ask your pharmacist to review inhaler technique.
🔹 Antifungal or Reflux Medicines
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Antifungals (itraconazole, voriconazole) don’t directly cause cough, but reflux or nausea can trigger coughing indirectly.
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PPIs (omeprazole, lansoprazole) usually help reflux-related cough, but long-term use should be reviewed regularly.
🔹 Other Drugs
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Amiodarone, methotrexate, and some biologics can rarely cause cough due to lung inflammation.
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Nasal sprays or lozenges with menthol/alcohol may irritate already-sensitive airways.
💬 If you suspect a medicine is contributing, don’t stop it suddenly — speak to your doctor or pharmacist first.
They can review interactions using the
👉 BNF Interactions Checker – NICE Medicines Guidance.
🔍 How Doctors Assess Chronic Cough
BTS recommends a structured pathway:
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Basic tests: chest X-ray, spirometry, bloods (eosinophils, IgE), FeNO if available.
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Further tests: CT scan, allergy or sputum studies if initial tests are abnormal.
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Trait-based review: identifying overlapping issues — fungal, allergic, nerve-related, or reflux-related.
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Specialist referral: to a Cough Clinic or Aspergillosis Centre if symptoms persist.
🧴 Pharmacists: Your Safety Specialists
Pharmacists — hospital or community — are crucial for managing long-term cough and medication safety:
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Check for cough-inducing drugs or interactions.
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Advise on best timing for antifungal and steroid doses.
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Help switch to fragrance-free personal or cleaning products.
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Liaise with your GP and consultant to fine-tune treatment.
🧭 Regular medication reviews every few months can prevent small problems becoming major triggers.
💬 How It Feels — and Why It’s Misunderstood
People with aspergillosis often describe:
“A tickle that turns into a spasm I can’t stop.”
“People think I’m ill, but it’s just the air or perfume.”
This happens because your airway nerves and immune cells are already primed.
Coughing doesn’t mean you’re infectious — it’s your body’s protective reflex in overdrive.
🩺 What Helps Most
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Optimise your aspergillosis and ABPA treatment.
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Cough-control physiotherapy or speech therapy for nerve-related cough.
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Airway clearance techniques for mucus.
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Identify and avoid irritants: perfume, smoke, strong detergents, cold air.
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Ask about biologics if inflammation remains active despite steroids.
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Use nerve-modulating medicines only under specialist advice.
🧘 Emotional Health Matters Too
Living with a chronic cough can cause anxiety, embarrassment, and isolation.
Support from counsellors, CBT therapists, or patient groups helps manage this stress — and can actually reduce cough frequency through better relaxation and breathing control.
🌱 Key Takeaway
Chronic cough in aspergillosis isn’t “just a symptom” — it’s often a mix of airway inflammation, fungal allergy, nerve hypersensitivity, and sometimes side effects of medicines.
The good news is that every contributing factor is treatable once identified — and cough can improve significantly with the right combination of medical, physical, and environmental care.
🔗 Trusted Resources
💼 Aspergillosis, Scent Sensitivity, and the Workplace
Understanding why everyday environments can trigger coughing — and what you can do about it
🌫️ When the Air Itself Feels Unsafe
Many people living with aspergillosis, Allergic Bronchopulmonary Aspergillosis (ABPA), or severe allergies feel anxious about returning to offices or shared spaces.
It isn’t the job that’s difficult — it’s the environment.
Dusty desks, neglected air vents, cold air-conditioning, and strong perfumes can all trigger coughing or wheezing.
Even a few minutes in a scented or dusty room can leave you coughing for hours — and explaining (again) that you’re not contagious.
If this sounds familiar, you’re not being oversensitive — you’re reacting to real biological triggers.
🧬 Why These Reactions Happen
1️⃣ Chemical Irritants and Perfumes
Perfumes, air fresheners, and cleaning sprays release volatile organic compounds (VOCs) such as limonene, linalool, and formaldehyde.
In sensitive lungs, these cause irritation and inflammation of the airways.
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Research shows VOCs can provoke coughing, wheezing, and chest tightness in people with asthma or allergic airway disease.
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These chemicals also activate airway nerve endings (trigeminal and vagal nerves) that trigger coughing reflexes — even when no infection or allergy is present.
This is known as neurogenic inflammation — a real, measurable process that makes you cough within seconds of exposure.
2️⃣ Damaged or Sensitive Airways
People with aspergillosis, bronchiectasis, or ABPA already have inflamed, scarred, or hypersensitive airways.
The airway lining (epithelium) is fragile and “leaky,” letting irritants trigger inflammation more easily.
Cough receptors are overactive, so small exposures — to scent, dust, or cold air — produce a big response.
Doctors call this airway hyperreactivity or irritant-induced cough reflex hypersensitivity.
It’s not psychological — it’s your lungs doing too good a job of protecting themselves.
3️⃣ Immune System Over-Response
Because aspergillosis and ABPA involve Type-2 immune inflammation (involving eosinophils and Th2 cytokines), your body’s defence cells are already primed.
When you inhale perfumes, dust, or fungal spores, those same immune pathways may flare up — releasing histamine and other inflammatory chemicals.
That’s why even non-allergic triggers can cause coughing or breathlessness.
4️⃣ Combined Triggers
Reactions are often additive.
Dust, perfume, cold air, and low humidity can act together:
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VOCs stick to dust particles and linger.
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Cold air increases nerve sensitivity.
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Mould fragments or Aspergillus spores amplify inflammation.
So what seems like “just perfume” may actually be a cocktail of irritants acting on already-inflamed lungs.
💬 The Social Challenge
Explaining a chronic cough can feel awkward.
Colleagues often assume it means infection — and that’s stressful when you’re already managing symptoms.
You shouldn’t have to justify your condition, but some people find it helps to have a short, calm explanation ready:
“I have a long-term lung condition that makes me cough when the air is dusty or scented — it’s not infectious.”
If you’re comfortable, let HR or Occupational Health know so they can help set expectations and prevent misunderstandings.
🏥 Your Rights and Reasonable Adjustments (UK)
Under the Equality Act 2010, aspergillosis and severe environmental allergies can qualify as a disability because they substantially affect daily life.
That means employers have a legal duty to make reasonable adjustments, such as:
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A clean, fragrance-free workspace
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Portable air purifier or improved ventilation
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Flexible or hybrid working
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Adjusting temperature or airflow
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Asking cleaning teams to use low-VOC products
Occupational Health can formalise these requests confidentially so you’re not seen as a “complainer.”
👉 Equality Act 2010 – Reasonable Adjustments (GOV.UK)
👉 ACAS Guidance on Long-Term Health Conditions
🧴 Pharmacists: The Unsung Safety Specialists
Your hospital or local pharmacist is an important ally.
They can:
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Review all your medicines for interactions or side effects that might worsen coughing.
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Advise how to take antifungals (e.g., with food, not with antacids).
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Suggest fragrance-free personal care or cleaning products.
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Liaise with your GP or hospital consultant if medication changes are needed.
You can also use the official
👉 BNF Interactions Checker (NICE Medicines Guidance)
to look up possible drug interactions — but always confirm findings with your pharmacist.
🏡 Considering Remote or Hybrid Work
If triggers are unavoidable in your current workplace, remote or hybrid work may be a safe and realistic alternative.
A Fit Note from your consultant or GP can recommend home working as a health adjustment.
When searching for jobs, look for roles described as remote, home-based, or flexible — many NHS, charity, and tech employers are now supportive of this.
🧘 Managing the Emotional Side
Anxiety about returning to work is natural.
Many people find that anticipating exposure — and potential misunderstanding — is almost as stressful as the symptoms themselves.
Talking to your consultant or GP about counselling or CBT for health anxiety can help you build confidence and coping strategies.
Peer support from others with chronic respiratory disease can be just as powerful — you’re not alone in feeling this way.
🌱 Key Takeaways
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Reactions to perfume, dust, and cold air are real physiological responses, not oversensitivity.
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They occur because inflamed airways and primed immune systems are hypersensitive to chemical and physical irritants.
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Simple environmental changes — plus understanding from employers and colleagues — can make a huge difference.
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Pharmacists, doctors, and occupational-health teams can help you manage medicines and advocate for a safe workspace.
You deserve an environment that helps you stay well — not one that forces you to prove you’re not sick.
Further Reading
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“Airway Hyperresponsiveness in Asthma: Its Measurement and Clinical Significance” (PMC full-text) — a detailed review of what airway hyper-responsiveness (AHR) is, how it happens, and why it matters. Link
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“Cough Hypersensitivity” (PDF patient leaflet, UK NHS trust) — explains how the airway nerves become too sensitive, what triggers are, and how the cycle of cough can develop. Link
🧠 Article 2: Why Awareness Matters – Staying Safe and Confident on Aspergillosis Treatment
Subtitle: How understanding your medicines can protect you and improve your quality of life.
💬 Awareness Means Safety
For people managing aspergillosis or related lung conditions, awareness isn’t just about learning facts — it’s about staying safe.
Knowing how your treatment works, what to expect, and who to ask for help gives you control and confidence.
1️⃣ Awareness Builds Understanding
Understanding each medicine’s purpose helps you:
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Recognise genuine warning signs early.
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Avoid anxiety over mild or harmless side effects.
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Know when something needs professional advice.
Example: a patient who knows voriconazole can cause brief light sensitivity won’t panic, but they will report a new rash or jaundice straight away.
2️⃣ Awareness Improves Communication
Informed patients are better partners in care.
You can explain symptoms clearly, ask the right questions, and notice how medicines affect you.
This helps doctors and nurses tailor treatment quickly and safely.
3️⃣ Awareness Supports Safer Treatment
Many aspergillosis patients take multiple interacting medicines — antifungals, steroids, antibiotics, and sometimes biologics.
Being aware of potential interactions means you can prevent problems before they happen.
You can check interactions using the official
👉 BNF Interactions Checker – NICE Medicines Guidance
(Free, reliable, and used by UK healthcare professionals.)
💡 Tip: If you find a possible interaction online, don’t stop any medicine yourself. Take a screenshot or note and discuss it with your pharmacist or specialist.
🧴 Awareness Includes Working With Your Pharmacist
Pharmacists — both hospital and community — are a vital part of your care team.
They are medicine specialists who can:
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Review your prescriptions for clashes between antifungals, steroids, and other drugs.
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Advise how to take medicines for best absorption (for example, itraconazole with food, not with omeprazole).
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Explain potential side effects and how to manage them safely.
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Contact your GP or hospital consultant if adjustments are needed.
Whenever you start or stop a medicine — even an over-the-counter painkiller or herbal supplement — let your pharmacist know.
They can quickly check your full medication list using the same professional databases doctors use.
🧭 Remember: Your pharmacist is your first safety checkpoint.
They’re there to protect you, clarify confusion, and help your medicines work safely together.
4️⃣ Awareness Builds Confidence and Control
Long-term illness can feel unpredictable.
Understanding your medicines helps you:
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Manage flare-ups calmly.
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Recognise early changes and act quickly.
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Feel more confident talking with your care team.
Research shows that informed patients have fewer hospital admissions, better symptom control, and improved wellbeing.
⚖️ Balanced Information
Awareness is only helpful if it’s accurate.
Stick to trusted sources such as:
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aspergillosis.org
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Your hospital’s patient information leaflets
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Local or hospital pharmacists who can explain details clearly
Avoid social-media “miracle cures” or alarming headlines that lack evidence.
🌱 The Bottom Line
Awareness doesn’t just make you more knowledgeable — it makes you safer.
Learn what each medicine does, recognise early warning signs, and use trusted resources like the BNF Interactions Checker and your pharmacist to keep your treatment on track.
Awareness turns uncertainty into confidence — and confidence into better health.
🔗 Related Resource
Managing Side Effects of Aspergillosis Treatments » — detailed guide to medicines, monitoring, and how pharmacists and doctors work together to keep you safe.
🩺 Article 1: Managing Side Effects of Aspergillosis Treatments
Subtitle: What to expect, how to recognise problems early, and when to ask for help.
💊 Why This Matters
People living with aspergillosis, bronchiectasis, or Primary Ciliary Dyskinesia (PCD) often take several medicines for months or even years.
These drugs are vital for controlling infection, inflammation, and allergic reactions — but they can also cause side effects or drug interactions.
Being aware of what’s normal, what’s not, and when to seek help helps you stay safe while getting the most from treatment.
⚗️ Antifungal Medicines
Antifungal (azole) drugs are the backbone of treatment for Chronic Pulmonary Aspergillosis (CPA) and Allergic Bronchopulmonary Aspergillosis (ABPA).
They control infection but can affect the liver, heart, or skin, so regular blood monitoring is essential.
Itraconazole (Sporanox® / generic)
Used for long-term control in CPA and ABPA.
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Common: tiredness, nausea, ankle swelling, blurred vision.
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Serious: yellowing skin/eyes, dark urine, shortness of breath.
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Tips:
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Take with a main meal or fizzy drink (acidic stomach aids absorption).
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Avoid taking it with omeprazole or similar acid-reducing drugs, as these block absorption.
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Have regular liver-function and drug-level blood tests.
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Report ankle swelling or jaundice immediately.
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Voriconazole (Vfend®)
Used when itraconazole isn’t effective or tolerated.
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Common: temporary visual flashes or blurred vision, sunlight sensitivity, mild headache.
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Serious: severe rash, blistering, or long-term skin-cancer risk from sunlight.
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Tips:
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Always use SPF 30+ sun cream, even in winter.
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Avoid prolonged sun exposure.
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Report any visual change, rash, or fatigue promptly.
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Blood monitoring checks for safe drug levels.
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Posaconazole (Noxafil®)
Used for resistant infections or as a second-line therapy.
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Common: nausea, diarrhoea, fatigue.
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Serious: liver inflammation, low potassium (causing muscle cramps or irregular heartbeat).
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Tips:
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Take with a main meal or full-fat snack.
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Report unexplained muscle weakness or palpitations.
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Keep up with blood tests.
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Isavuconazole (Cresemba®)
A newer antifungal option that may cause fewer interactions.
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Common: headache, mild nausea, ankle swelling.
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Tips:
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Continue regular liver and kidney checks.
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Report any new swelling, fatigue, or breathlessness.
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💨 Corticosteroids
(Prednisolone, Methylprednisolone, Hydrocortisone)
These reduce inflammation and allergic response in ABPA and asthma.
They are powerful — but long-term use can affect weight, mood, bones, and hormone balance.
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Common: increased appetite, fluid retention, mood swings, difficulty sleeping.
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Long-term: thinning bones, higher blood sugar, adrenal suppression.
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Tips:
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Never stop suddenly — always taper under medical advice.
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Carry a Steroid Emergency Card.
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Ask about bone protection (vitamin D, calcium, bisphosphonates).
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See your GP if you feel very tired, dizzy, or unwell.
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🧬 Biologic Treatments
(Mepolizumab, Benralizumab, Omalizumab)
These injection-based medicines target inflammation or allergic responses in severe asthma or ABPA.
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Common: mild injection-site soreness, tiredness, headache.
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Occasional: mild fever or muscle aches.
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Serious: allergic swelling of lips, tongue, or throat.
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Tips:
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Record any mild reactions.
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If you develop swelling or difficulty breathing, call 999 immediately.
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💊 Long-Term Antibiotics
(Azithromycin, inhaled colomycin, tobramycin)
Used to reduce bacterial infections in bronchiectasis or PCD.
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Common: stomach upset, diarrhoea, mild throat irritation.
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Long-term: tinnitus or hearing loss (especially with azithromycin).
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Tips:
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Have periodic hearing checks.
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Rinse mouth and nebuliser after inhaled antibiotics.
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Report ringing in the ears, severe diarrhoea, or rash.
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⚠️ Drug Interactions
Antifungal medicines (especially azoles) can interfere with many common drugs, including:
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Steroids (e.g., prednisolone, fluticasone) — may increase steroid levels.
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Reflux medicines (e.g., omeprazole, lansoprazole) — reduce antifungal absorption.
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Statins and warfarin — increase risk of side effects or bleeding.
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Some antihistamines and antibiotics — can affect heart rhythm.
These interactions can be complex — always check before starting or stopping any medication.
✅ Check it yourself:
You can use the official BNF Interactions Checker (NICE Medicines Guidance) to see if two medicines are known to interact.
Simply type the names (e.g., itraconazole and prednisolone) and it will show the risk level, what the interaction does, and what clinicians usually recommend.
If unsure, show the result to your GP, pharmacist, or hospital team — they can interpret it for your situation.
🚨 When to Seek Help
Call your specialist or GP urgently if you notice:
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Yellowing of skin or eyes
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Severe rash, blistering, or peeling
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New ankle swelling or breathlessness
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Sudden fatigue or dark urine
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Visual changes or increased photosensitivity
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Ringing in the ears or hearing loss
If you feel acutely unwell, do not stop your medication abruptly — contact your hospital team or emergency services.
🔗 Next read: Why Awareness Matters – Staying Safe and Confident on Aspergillosis Treatment »
⚠️ Omeprazole and PPIs: What’s Behind the Recent Warning?
Recently, several newspapers – including The Mirror – reported that a “BBC doctor” had issued a warning to anyone taking omeprazole, a commonly prescribed drug for acid reflux and heartburn.
So, is this something new, or just another media scare? Let’s look at what the evidence actually says – and what it means if you’re living with aspergillosis, bronchiectasis, or other chronic lung diseases.
💊 What Are PPIs?
Proton Pump Inhibitors (PPIs) such as omeprazole, lansoprazole, and esomeprazole are medicines that reduce stomach acid.
They’re often used to:
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Treat reflux, indigestion, or stomach ulcers
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Protect the stomach from irritation caused by anti-inflammatory drugs or steroids
They’re very effective and widely prescribed — millions of people in the UK take them every day.
⚠️ Why the Headlines?
The recent news stories stem from a discussion on BBC Morning Live, where GP Dr Punam Krishan highlighted the potential long-term side effects of PPIs.
Although these aren’t “new discoveries”, they serve as an important reminder that long-term PPI use should be reviewed regularly.
🧠 What the Evidence Shows
Research over the past decade has shown that taking PPIs for a long time or at high doses can lead to several possible side effects:
| Possible Issue | What Happens | Why It Matters |
|---|---|---|
| Infections | Higher risk of gut infections such as Clostridioides difficile and bacterial overgrowth | Stomach acid normally helps kill harmful bacteria; reducing it alters the balance |
| Changes in gut microbiome | Loss of protective “friendly” bacteria | May influence digestion, immunity, and inflammation |
| Reduced absorption of nutrients | Low magnesium, iron, or vitamin B12 | Can lead to tiredness, cramps, or anaemia |
| Bone health | Slightly higher risk of fractures with very long-term use | May relate to calcium absorption |
| Kidney and heart effects (rare) | Observed in some studies | Still being researched |
Most of these risks are small, and for many people the benefits outweigh them — but it’s still important to make sure you’re taking the lowest effective dose and that your doctor reviews the need for it periodically.
🫁 Why It Matters for Aspergillosis and Lung Conditions
If you have aspergillosis, bronchiectasis, or Primary Ciliary Dyskinesia (PCD), there are extra reasons to think carefully about long-term PPI use:
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Microbiome connections: The gut and lungs are linked through what’s called the gut–lung axis. Disturbances in gut bacteria can affect immune responses elsewhere in the body — possibly including the lungs.
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Infection control: PPIs can slightly increase the risk of bacterial or fungal overgrowth in the gut. While this doesn’t directly cause lung infection, it may influence the body’s balance between helpful and harmful microbes.
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Medication interactions: Some antifungal medicines (like itraconazole or posaconazole) rely on stomach acidity for absorption — so PPIs can reduce their effectiveness. Your specialist will usually time doses or adjust medication accordingly.
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Reflux and aspiration: On the other hand, reflux itself can worsen lung disease if acid is inhaled into the lungs — so stopping PPIs suddenly can make things worse. Always discuss any change with your doctor first.
🩺 What You Can Do
If you take omeprazole or another PPI:
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Check why you’re on it – Is it for reflux, ulcer protection, or another reason?
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Review the dose and duration – Many people can step down to a lower dose or switch to on-demand use once symptoms are controlled.
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Don’t stop suddenly – Stopping PPIs abruptly can cause a rebound in acid production and make symptoms flare.
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Ask about alternatives – Some people can switch to H2-blockers (e.g. ranitidine-type medicines), or use lifestyle changes such as avoiding late meals, raising the bedhead, and reducing caffeine or alcohol.
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Discuss with your specialist team – Particularly if you’re also on antifungal or antibiotic treatments, as interactions can occur.
🧩 Key Takeaway
The recent headlines about omeprazole are not new, but they highlight a genuine issue:
PPIs are very useful drugs — but long-term use should always be reviewed to make sure the benefits outweigh the risks.
For most people, there’s no need to panic.
Just make sure you:
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Use the lowest effective dose
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Review your need for PPIs at least once a year
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Discuss any concerns with your respiratory or gastroenterology team
🔗 Useful References
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NHS Guidance: Proton Pump Inhibitors – Risks and Review Advice
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PrescQIPP PPI Safety Review (UK 2023) – Long-term safety and deprescribing guidance
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Gut (BMJ): Proton pump inhibitors and gut microbiota: cause for concern? (Gut 2016;65:740–748)
🧬 Article 2: When Microbes Turn Hostile – The Evolutionary Pressures Behind Infection
Subtitle: Why stable colonisation sometimes shifts into active disease
Introduction
If microbes can live quietly in the lungs for years, why do they sometimes turn aggressive?
Evolutionary biology and microbiome research show that infection often develops because of environmental pressures — not by design, but as a by-product of survival in a changing ecosystem.
1. Antibiotic Pressure
Repeated antibiotic courses kill sensitive strains and leave behind resistant survivors.
These survivors often produce thicker biofilms and inflammatory molecules, which protect them but also damage airway tissue.
Over time, this selection creates harder-to-treat, more inflammatory strains.
2. Nutrient Competition
Airways are crowded ecosystems.
When nutrients run low, microbes compete by releasing toxins, proteases, and iron-scavenging molecules.
These harm competitors — and incidentally harm the lung.
3. Biofilms and Mutation
Within biofilms, bacteria and fungi evolve quickly.
Mutations can accumulate, producing hypermutator strains that are well adapted to chronic survival but also more inflammatory.
4. Host Factors
Changes in the body — reduced immunity, steroid use, diabetes, or viral infections — relax immune control.
Organisms that were previously contained can now proliferate.
Similarly, damaged or scarred airways provide sheltered niches where microbes thrive.
5. Microbiome Collapse
The healthy lung microbiome helps regulate inflammation and suppress invaders.
When broad antibiotics or infections reduce diversity, opportunists like Pseudomonas or Aspergillus can expand unchecked.
6. Collateral Damage, Not Intent
Most microbes don’t “want” to be pathogenic — they’re simply adapting to survive.
Their survival strategies (biofilms, enzymes, toxins) cause collateral damage to airway tissue.
So, pathogenicity is often an accidental consequence of survival pressure.
7. Cycles of Stability and Flare-Ups
Chronic airway diseases often follow repeating cycles:
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Stable colonisation – coexistence with minimal inflammation
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Disruption – antibiotics, viral infection, or new strain
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Flare-up – inflammation and tissue damage
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Partial recovery – new stable community forms
Each cycle leaves the microbial ecosystem slightly altered — selecting for organisms that can survive stress and immune attack.
Evolutionary Summary
| Pressure | Effect on Microbes | Result for Host |
|---|---|---|
| Antibiotics | Resistant, stress-adapted strains | Harder-to-treat infection |
| Nutrient limitation | Toxin and enzyme producers | Tissue damage |
| Immune suppression | Less control of microbes | Opportunistic growth |
| Microbiome loss | Opportunist expansion | Reduced resilience |
| Biofilm evolution | Genetic drift, persistence | Chronic inflammation |
Key Takeaway
Microbes evolve under pressure from antibiotics, immune stress, and competition.
They don’t plan to harm the host — they adapt to survive.
Unfortunately, those same adaptations often make them more damaging and persistent.
This is why good airway care, careful antibiotic use, and microbiome-friendly approaches are essential to keep the system in balance.
👉 Read also: Colonisation vs Infection in Airways Disease
(Learn how to recognise the difference, when treatment is needed, and how to keep microbial balance.)
🩺 Article 1: Colonisation vs Infection in Airways Disease
Subtitle: Understanding what it means when bacteria or fungi are found in your lungs
Introduction
People with bronchiectasis, Primary Ciliary Dyskinesia (PCD), Allergic Bronchopulmonary Aspergillosis (ABPA), or Chronic Pulmonary Aspergillosis (CPA) often have microbes detected in their sputum samples.
That doesn’t always mean there’s an infection that needs treatment.
Understanding the difference between colonisation and infection helps patients and clinicians make better decisions.
Colonisation
Colonisation means that bacteria or fungi are living in the airways but aren’t currently causing harm.
This happens because mucus clearance is reduced, allowing microbes such as Haemophilus influenzae, Pseudomonas aeruginosa, or Aspergillus fumigatus to persist.
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The microbes are “residents,” not invaders.
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Symptoms stay stable.
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Blood tests for inflammation (like CRP) are usually normal.
Treatment isn’t always needed — instead, care focuses on airway clearance, physiotherapy, hydration, and monitoring through sputum cultures.
Infection
Infection means microbes are actively causing inflammation and tissue irritation.
This happens when microbial numbers rise, new strains appear, or immune defences weaken.
Typical signs:
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Increased cough, sputum, or breathlessness
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Fever or feeling unwell
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Raised inflammatory markers
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New changes on chest X-ray or CT
Treatment involves targeted antibiotics or antifungals based on sputum results and resistance testing.
Why Colonisation Can Turn Into Infection
In chronic airways disease, colonisation and infection exist on a sliding scale — a shift in balance can push the lungs from stable to inflamed.
Common triggers include:
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Growth of a new or resistant strain
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Reduced mucus clearance
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Viral infections (e.g. influenza, COVID-19)
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Immune suppression
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Loss of “friendly” bacteria in the lung microbiome
When this balance is disrupted, inflammation rises and infection takes hold.
The Balance Model
| Factor | Colonisation (Stable) | Infection (Flare-Up) |
|---|---|---|
| Microbial strain | Stable | New or virulent |
| Microbial load | Controlled | Increased |
| Microbiome | Diverse | Reduced diversity |
| Immune status | Balanced | Suppressed or overactive |
| Symptoms | Stable | Worsening |
| CRP / WBC | Normal | Raised |
Key Takeaway
In chronic lung conditions, microbes are often part of daily life. The aim isn’t complete eradication, but balance — keeping numbers low, reducing inflammation, and treating only when infection is active.
👉 Next article: When Microbes Turn Hostile – The Evolutionary Pressures Behind Infection
(Explore how antibiotics, competition, and disrupted microbiomes drive microbes to become more aggressive.)
Living with Primary Ciliary Dyskinesia (PCD) and Bronchiectasis
People living with Primary Ciliary Dyskinesia (PCD) and bronchiectasis often face long-term challenges with their lungs. These conditions can make it difficult to clear mucus effectively, creating a perfect environment for bacteria and fungi to grow — including Aspergillus species and bacteria such as Haemophilus influenzae.
What Is Primary Ciliary Dyskinesia?
Primary Ciliary Dyskinesia is a rare, inherited condition that affects the microscopic hair-like structures (cilia) that line the airways, ears, and sinuses. Normally, cilia move in a coordinated way to sweep mucus, bacteria, and debris out of the lungs.
In PCD, these cilia don’t move properly. As a result, mucus builds up, causing chronic infections and inflammation.
How PCD Leads to Bronchiectasis
Over time, repeated infections and inflammation can damage the airways, leading to bronchiectasis — a condition where the bronchial tubes become widened and scarred. This makes it even harder to clear mucus and allows bacteria and fungi to settle in the lungs more easily.
Common organisms that may persist include:
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Haemophilus influenzae
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Pseudomonas aeruginosa
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Staphylococcus aureus
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Aspergillus fumigatus
The Role of Aspergillus
When Aspergillus spores are inhaled, most people clear them easily.
In PCD and bronchiectasis, however, mucus clearance is reduced and the airways are damaged — so Aspergillus can remain trapped.
Over time, this can lead to sensitisation (as in Allergic Bronchopulmonary Aspergillosis, ABPA) or even chronic infection (Chronic Pulmonary Aspergillosis, CPA).
Both conditions can worsen existing bronchiectasis and make bacterial infections harder to control.
Why Bacteria Like Haemophilus Stick Around
Many patients with PCD or bronchiectasis find that bacteria such as Haemophilus influenzae are always present in their sputum, even when they feel well.
This doesn’t always mean there’s an active infection — it can simply reflect colonisation (the bacteria living there without causing symptoms).
However, when bacterial numbers rise or resistance develops, this can trigger a flare-up with more cough, sputum, or breathlessness.
Managing Persistent Infections
Because eradication is often not possible, the goal is control rather than cure.
Typical strategies include:
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Regular sputum cultures to monitor bacterial and fungal growth and check for antibiotic resistance.
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Targeted antibiotic treatment when symptoms worsen, chosen based on recent resistance results.
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Airway clearance techniques, such as physiotherapy, postural drainage, or devices that help loosen mucus.
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Nebulised saline (often hypertonic) to thin mucus and make it easier to clear.
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Vaccinations (e.g., flu and pneumococcal) to reduce viral triggers.
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Anti-inflammatory and antifungal treatments when fungal infection or allergic sensitisation are part of the problem.
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Regular monitoring with a respiratory specialist to adjust treatment plans.
Living Well with PCD and Bronchiectasis
Many people manage to live active lives by learning what works best for their lungs — combining daily airway clearance, careful infection monitoring, and prompt treatment of flare-ups.
Some also find it useful to join patient support groups, where experiences with long-term bacterial and fungal infections can be shared.
Key Takeaway
For people with PCD and bronchiectasis, infections like Haemophilus influenzae and Aspergillus fumigatus often can’t be completely removed. The focus is on keeping infection levels low, preventing flare-ups, and protecting the lungs for the long term. With good self-management, regular review, and the right treatment plan, symptoms can be controlled and quality of life maintained.
🧬 From Scottish Discovery to American Pharmacy Shelf: The Story of Brensocatib
Sometimes a medicine begins life in one country but reaches patients first in another. The new bronchiectasis drug brensocatib is a perfect example — discovered in Scotland, yet first approved for use in the United States.
Here’s how that happens, and what it tells us about how new treatments make their way to patients.
1️⃣ Discovery in Dundee
At the University of Dundee, scientists in the Drug Discovery Unit (DDU) were studying how certain white blood cells called neutrophils can cause long-term lung damage.
They identified an enzyme, DPP1 (dipeptidyl peptidase I), that activates destructive substances inside these cells.
Blocking DPP1 could calm inflammation without wiping out the body’s defences.
Their research produced a promising new compound — later named brensocatib — which safely switched off this process in lab studies.
2️⃣ Partnering to Go Global
Turning an early discovery into a medicine is an enormous task.
It costs hundreds of millions of pounds and can take 10–15 years.
The Dundee team partnered with Insmed, a biotechnology company based in New Jersey, USA, which had the funding and international trial experience to move brensocatib into large clinical studies.
3️⃣ Worldwide Trials
Insmed led major trials involving hundreds of people with non-cystic fibrosis bronchiectasis in hospitals across North America, Europe, and Asia.
Results showed that brensocatib reduced flare-ups and improved quality of life.
Because Insmed’s main offices and regulatory team are in the U.S., they submitted their results first to the U.S. Food and Drug Administration (FDA).
4️⃣ U.S. Approval
In 2025, the FDA approved brensocatib — the first drug of its kind to treat bronchiectasis.
American patients can now access it while other countries complete their reviews.
5️⃣ What Happens Next in the UK
In the UK, every new medicine goes through two steps:
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The Medicines and Healthcare products Regulatory Agency (MHRA) checks that it is safe and effective.
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Then NICE (the National Institute for Health and Care Excellence) reviews how well it works for its cost and decides whether the NHS should fund it.
NICE is expected to make its decision on brensocatib in July 2026.
Even if approved, it may first be offered to those with the most severe or frequent flare-ups while more real-world data are gathered.
💷 What Dundee Gained from Its Discovery
Although Dundee handed over development to a U.S. company, the university continues to benefit in several ways:
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Financial return: Dundee receives upfront payments, milestone fees for each stage of progress, and royalties on global sales.
These funds support new drug discovery projects, student training, and research facilities. -
Scientific impact: Brensocatib’s success highlights the strength of the Drug Discovery Unit’s model, showing that UK universities can produce world-class medicines.
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Future partnerships: Dundee’s achievement attracts new collaborations and investment, ensuring that more early discoveries have a route to reach patients.
So while the drug is made and sold by Insmed, Dundee’s scientists — and their reinvested funding — continue to play a role in future breakthroughs.
🏭 Manufacturing: Turning Discovery into a Real Medicine
Once a new drug is approved, it still has to be produced safely, at scale, and consistently.
This is often a completely separate operation from the research or licensing stage.
For brensocatib, the chemical process that makes the active ingredient was developed by Dundee and Insmed scientists early on, but large-scale manufacturing is now carried out by specialist pharmaceutical plants under strict international standards known as Good Manufacturing Practice (GMP).
Because brensocatib is a small-molecule oral drug (a tablet, not an injection), it’s made in high-tech chemical manufacturing facilities, not hospitals or biologics plants.
These sites are often in Europe, the U.S., or Asia, depending on where the supply chains, raw materials, and quality-control systems are strongest.
Manufacturing is expensive — it must ensure every tablet is identical in purity, strength, and safety — but it’s also where economies of scale help keep the cost manageable once global production ramps up.
For the NHS and NICE, manufacturing details matter too, because:
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They affect cost-effectiveness (how much the NHS will pay per course of treatment).
-
They influence availability — whether the company can supply enough medicine to meet demand once approved in the UK.
So, while the discovery began in Dundee and the approval started in the U.S., manufacturing is the bridge that makes it real — transforming a scientific idea into a medicine that can be prescribed to patients worldwide.
🌍 Why This Matters
This journey shows how scientific discovery is global.
A breakthrough can start in a Scottish laboratory, be developed with American funding, tested around the world, manufactured across several continents, and eventually come back to help patients in the UK.
It’s a reminder that international collaboration — between researchers, funders, manufacturers, and regulators — is what turns good science into real treatments.
🧩 NAC Aspergillosis Research Digest Aspergillosis (October 2025: week 44)
Highlights
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Pulmonary aspergillosis in chronic lung disease can be severe and life-threatening, especially in patients with underlying interstitial lung conditions. Prompt diagnosis and subtype-targeted treatment are crucial for better outcomes (7).
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Advanced sinus imaging in dogs improves veterinary precision for diagnosing and treating fungal infections such as aspergillosis (1).
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Poultry farms in Turkey are best protected against aspergillosis outbreaks through consistent hygiene and environment management (3).
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Pediatric liver transplant patients remain at high risk of deadly fungal infections, so ongoing immune and drug monitoring is vital (2).
-
New antifungal agents such as isavuconazole are yielding positive results in children, adults, and drug-resistant cases (10).
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Agricultural fungicide use is driving azole resistance in Aspergillus, prompting urgent "One Health" responses across medicine and farming (8).
-
Research is underway to determine the best antifungal prophylaxis for heart transplant recipients (6).
-
Case studies show severe treatment challenges for aspergillosis in post-tuberculosis and cancer patients (5), (9).
Pulmonary Aspergillosis in Lung Disease
Recent research examined the prevalence and outcomes of aspergillosis among patients with interstitial lung disease (ILD) and chronic respiratory disorders. The study highlights three major forms:
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Invasive Pulmonary Aspergillosis (IPA): Occurs in roughly 2% of hospitalised ILD patients, presenting with symptoms such as fever, persistent cough, and rapid decline in lung function. Those prescribed steroids or immunosuppressants and showing certain lung scan features are at greater risk. Estimated 3-month mortality can reach 50%.
-
Chronic Cavitary Pulmonary Aspergillosis (CPA): Represents about 0.6% of cases in target populations, with slower onset but significant respiratory impairment over time. Mortality is lower than IPA but remains notable.
-
Allergic Bronchopulmonary Aspergillosis (ABPA): Occurs in about 3% of studied patients, typically with a better prognosis, though delayed care can worsen outcomes.
Diagnostic strategies involve serology, antigen testing, and imaging to distinguish subtypes and select appropriate antifungal therapy. The study urges multidisciplinary care and more effective protocols for immunosuppressed patients (7).
Veterinary and Animal Health
Advanced radiological mapping now allows veterinarians to better diagnose and treat sinus aspergillosis across various breeds. This enhances surgical accuracy and supports targeted case management (1).
Poultry studies highlight aspergillosis as a leading fungal threat, with hygiene as the most effective control tactic (3).
Human Health: Transplant, Immunosuppression, and Infection
Children undergoing liver transplants require ongoing immune suppression, which increases susceptibility to severe fungal infections like aspergillosis. This underscores the value of rigorous therapeutic monitoring (2).
Current protocols are evaluating which antifungal drugs work best in heart transplant recipients to prevent invasive fungal infections (6)
Clinical Complications and Case Reports
Case studies spotlight life-threatening adrenal crisis and aspergillosis in children recovered from TB and adults with leukaemia. Timely diagnosis and combined therapies are essential for recovery (5), (9)
Transplant patients are vulnerable to bacterial and fungal sinus infections, presenting significant diagnostic challenges (4).
Drug Resistance and Novel Treatments
The rise of azole-resistant Aspergillus, driven by agricultural fungicide use, is making some forms of aspergillosis harder to treat. Integrated medical and environmental interventions are needed to slow resistance (8)
New medications, such as isavuconazole, are being adopted for severe and resistant cases in paediatric and adult populations with positive early results (10).
Reference List
- Cross-Sectional Radiological and Reconstructive Anatomy of the Paranasal Sinuses in Normal Mesaticephalic Dogs
- Pharmacokinetic Monitoring of JAK Inhibitor and Tacrolimus for Safe and Effective Management of Graft-Versus-Host Disease After Pediatric Liver Transplantation
- A Review on Aspergillosis in Turkey: As a Main Fungal Disease in Poultry
- Necrotizing Pseudomonal Sinusitis in a Transplant Patient
- Post‐Tuberculosis Adrenal Crisis in a Young Boy: A Case Report
- Antifungal prophylaxis against invasive Candida and Aspergillus infection in adult heart transplant recipients: protocol for a systematic review and meta-analysis
- Clinical characteristics and prognosis of pulmonary aspergillosis complicating interstitial lung diseases
- Azole fungicides and Aspergillus resistance, five EU agency report highlights the problem for the first time using a One Health approach
- Blinatumomab Along With Combined Antifungal Agents for Refractory Adult Acute Lymphoblastic Leukemia With Invasive Aspergillosis: A Case Report
- Real-life use of isavuconazole in Spanish children and adolescents










