**Adrenal Insufficiency & Steroid Tapering:

A Complete Patient Guide**

People taking long-term steroids (prednisolone, methylprednisolone, hydrocortisone, dexamethasone) can develop adrenal insufficiency because their adrenal glands “go to sleep” and stop making cortisol.
During tapering, the body must slowly “wake up” again — and this needs careful monitoring.

This guide explains the symptoms, tests, warning signs, and emergency precautions to keep you safe.

⭐ 1. Why adrenal insufficiency happens

Long-term steroid use suppresses the HPA axis (hypothalamus–pituitary–adrenal system).
When daily steroid doses are reduced, your body must produce more of its own cortisol. This takes time.

If the steroid reduction is too quick, or the body is under stress, low cortisol symptoms appear.

⭐ 2. Symptoms to watch for during steroid tapering

These are early signs that your body may not be keeping up with the reduction.

✔ Early, mild symptoms

  • Fatigue / sudden exhaustion

  • Muscle weakness

  • Dizziness when standing

  • Nausea or reduced appetite

  • Flu-like aching

  • Low mood, anxiety, irritability

  • Brain fog

  • Feeling unusually cold

  • Worsening joint or muscle pain

These often improve if the taper is slowed or paused.

⭐ 3. More serious symptoms of low cortisol

These symptoms suggest steroid levels are too low and the taper needs urgent review:

  • Vomiting

  • Persistent dizziness

  • Very low blood pressure

  • Severe fatigue (unable to function normally)

  • Salt cravings

  • Ongoing nausea preventing eating

  • Faintness or near-collapse

These require medical advice (same day).

⭐ 4. Emergency symptoms — possible adrenal crisis

Call 999 or go to A&E immediately if you develop:

  • Severe vomiting or diarrhoea

  • Collapse or inability to stand

  • Severe dehydration

  • Confusion

  • Sudden severe abdominal or back pain

  • Pale, clammy skin

  • Rapid breathing

  • Loss of consciousness

This is a medical emergency.
Patients normally receive 100 mg hydrocortisone IM/IV, but patients allergic to hydrocortisone require a pre-agreed emergency alternative — your endocrinologist must document this clearly.

⭐ 5. Symptoms that mean you may need a temporary “stress dose” of steroids

Your cortisol requirement increases during physical stress.
If you have adrenal suppression, your body cannot produce this extra cortisol.

You may need a temporary increase in dose if you have:

✔ Illness

  • Fever

  • Chest infection

  • Flu-like illness

  • COVID

  • Urinary infection

  • Gastroenteritis

  • Diarrhoea

  • Persistent nausea

✔ Physical stress

  • Injury

  • Significant fall

  • Severe pain

  • Dental surgery

  • Medical or surgical procedures

✔ Emotional stress

  • Bereavement

  • Panic attacks

  • Trauma

If vomiting prevents taking steroids → seek emergency help immediately.

⭐ 6. Tests used to monitor adrenal function during tapering

Doctors rely on a combination of symptoms and laboratory tests.

✔ Morning cortisol (8–9 am)

A key test to assess recovery.

Typical interpretation:

  • > 400–500 nmol/L → likely normal function

  • 150–350 nmol/L → recovering / borderline

  • < 100 nmol/L → adrenal insufficiency

(Exact thresholds vary.)

✔ ACTH level

Shows whether the pituitary is trying to stimulate the adrenals.

  • Low ACTH → still suppressed

  • High ACTH → trying to wake adrenals

  • Normal ACTH + low cortisol → gland slow to respond

✔ Short Synacthen Test (SST)

Gold standard.
A small ACTH injection tests whether your adrenal glands can produce cortisol.

Used when:

  • taper reaches low doses

  • symptoms appear

  • deciding if steroids can be stopped

✔ Electrolytes (U&Es)

Low cortisol may cause:

  • Low sodium

  • High potassium (less common in steroid-induced insufficiency)

✔ Blood pressure monitoring

Low cortisol → low BP, dizziness, faintness.

✔ Glucose levels

Low-normal glucose and shakiness may occur during withdrawal.

✔ Clinical symptom review

Symptoms are sometimes more sensitive than tests.

Doctors track:

  • fatigue

  • appetite

  • dizziness

  • illness triggers

  • salt cravings

  • mental state

  • recovery after small dose increases

⭐ 7. How tapering decisions are made

Tapering depends on:

  • how long steroids have been taken

  • current dose

  • symptoms

  • test results

  • presence of illness

  • rate at which symptoms develop

  • allergy restrictions (pred/hydrocortisone allergy requires specialist handling)

General principles (not schedules):

  1. Higher doses can reduce more quickly.

  2. Taper slows dramatically near physiological levels
    (~4–6 mg pred-equivalent).

  3. If symptoms appear → pause, slightly increase, or slow taper.

  4. SST is used near the end to confirm recovery.

⭐ 8. When to contact your medical team

Same day advice needed

  • worsening dizziness

  • persistent nausea

  • new vomiting

  • symptoms appear with each taper step

  • fainting

  • new severe fatigue

  • any infection (urinary, chest, flu)

Urgent / A&E

  • collapse

  • severe vomiting/diarrhoea

  • confusion

  • severe abdominal pain

  • unable to take oral steroids

  • suspected adrenal crisis

⭐ 9. What patients should do to stay safe

  • Carry a Steroid Emergency Card at all times

  • Keep emergency instructions from your endocrinologist

  • Know your Sick Day Rules

  • Ensure A&E or ambulance crews know about corticosteroid allergy

  • Keep a written record of tapering plan

  • Never stop steroids suddenly

  • Be cautious during illness

  • Know your emergency steroid plan (alternative if allergic to hydrocortisone)

⭐ Final reassurance

Adrenal insufficiency during tapering is common, manageable, and often reversible.
By monitoring symptoms, using regular blood tests, and following specialist guidance, tapering can be done safely.

You are not alone — your endocrine team will guide every step, especially if allergies (to prednisolone or hydrocortisone) make your case more complex.

With careful observation and a clear emergency plan, serious complications are rare and preventable.

by GAtherton

🧩 NAC Aspergillosis Research Digest — Focus: Chronic Aspergillosis (October 2025: week 42)

🧬 Focus Review — Chronic Aspergillosis (October 2025)

Here are peer-reviewed papers on chronic aspergillosis published in the last month:

1. Improving Diagnostic Sensitivity Using Species-Specific IgG (Sep 2025)

  • This study investigated better blood tests to diagnose CPA by measuring IgG antibodies not just to Aspergillus fumigatus but also to other common Aspergillus species.

  • They found adding antibodies against non-fumigatus species identified more CPA cases that would have been missed by the standard A. fumigatus test alone.

  • The treatment results were similar regardless of which Aspergillus species was involved.

  • This means broader antibody testing improves diagnosis without changing expected outcomes.

  • Read full paper on PubMed

2. Prevalence and Impact of Bacterial Co-infections in CPA (April 2025)

  • This study looked at how often bacterial infections occur alongside CPA and their effect on patients.

  • About 21% of CPA patients had bacterial co-infections.

  • However, having a bacterial co-infection did not significantly change mortality rates compared to those without.

  • This highlights the need to assess for bacteria but suggests it may not worsen long-term outcomes.

  • Read full paper on PMC

3. Non-invasive Monitoring Using Serology and HRCT Imaging (June 2025)

  • Researchers combined blood antibody tests and high-resolution chest CT scans to identify active Aspergillus infections in chronic lung disease patients.

  • This method distinguished active infections from colonization without invasive procedures.

  • It supports using combined non-invasive tests to decide who needs further invasive diagnostics or antifungal treatment.

  • This approach helps avoid unnecessary treatments and invasive tests.

  • Read full paper on Frontiers

In short: these studies improve how doctors diagnose and monitor CPA — by expanding antibody testing beyond classic targets, recognizing the role but limited impact of bacterial co-infections, and using combined non-invasive testing strategies to guide management safely and effectively.

by GAtherton

🔍 Aspergillosis: Recent Highlights & Key Publications October 2025 (Week 41)

Revised ISHAM-ABPA working group guidelines (2024)

  • Scope & criteria: Codifies ABPA diagnosis around mandatory Aspergillus sensitisation (specific IgE or SPT) plus total IgE ≥ 500 IU/mL, with supporting features (Aspergillus-specific IgG/precipitins, eosinophilia, imaging with central bronchiectasis/mucus plugging). Distinguishes ABPA vs. ABPM (other fungi) and sets clinical states (acute, response, exacerbation, remission).

  • Treatment pathways: For acute ABPA, permits oral corticosteroids or itraconazole as first-line; combination is reasonable in severe disease or frequent relapsers. Provides steroid-sparing strategies (itraconazole/voriconazole/posaconazole) and practical taper schedules.

  • Biologics & monitoring: Positions omalizumab/mepolizumab/dupilumab for recurrent/exacerbation-prone ABPA. Recommends multidimensional response criteria (symptoms, exacerbations, lung function, IgE kinetics, radiology) rather than IgE alone.

  • Paper (Eur Respir J) · PubMed · OA summary (PMC).

BTS Clinical Statement on Aspergillus-Related Chronic Lung Disease (2025)

  • Who it’s for: UK-focused guidance to help respiratory teams manage CPA, aspergilloma, chronic airway disease with Aspergillus, and allergic phenotypes in secondary care.

  • CPA approach: Emphasises radiology over time (HRCT), microbiology/Aspergillus-IgG, and exclusion of mimics (NTM, malignancy). Advises long-term azoles (with TDM & LFTs), and when to consider surgery (haemoptysis/aspergilloma).

  • Service model: Encourages early referral/MDT (radiology, mycology, thoracic surgery, interventional radiology), signposts NAC pathways, and sets pragmatic follow-up intervals (clinical, radiology, serology).

  • BTS page · News item · (access via Thorax from BTS page).

Consensus guidelines for invasive aspergillosis (ECMM/ISHAM CAPA; 2021)

  • Definitions: Introduces proven/probable/possible CAPA using clinical + mycological evidence (BAL/TA culture or PCR, GM thresholds, imaging).

  • ICU nuance: Acknowledges non-neutropenic ICU patients (COVID/influenza) can develop IA with atypical imaging and lower fungal burdens; endorses combined biomarker strategies (BAL GM/PCR ± serum GM).

  • Therapy: Positions voriconazole/isavuconazole as first-line; L-AmB where resistance or intolerance suspected. Flags early initiation on high suspicion to improve outcomes.

  • Paper (Lancet Infect Dis) · PubMed · ECMM guideline hub.

Epidemiology & Clinical Cohorts

Marseille 2-year retrospective cohort — CPA & ABPA insights (2025)

  • Design: Single-centre retrospective study applying ESCMID CPA criteria and modified ISHAM ABPA criteria to consecutive referrals.

  • Findings: High rate of diagnostic overlap (allergy + chronic infection features). Delays to diagnosis common, especially where IgG negative/indeterminate but GM/BAL/PCR positive.

  • Implication: Supports multimodal testing (serology, GM/PCR, serial imaging) and repeat sampling in indeterminate cases; highlights value of centre-based MDT.

  • PubMed · (preprint/alt copies if needed: SSRN/other listing, ResearchGate record).

Invasive aspergillosis in ICU settings (2025 review)

  • Epidemiology: IA increasingly reported in severe viral pneumonias (COVID, influenza); mortality ~40–50% depending on definition and antifungal timing.

  • Diagnostics: BAL GM outperforms serum GM in non-neutropenic ICU; PCR adds sensitivity but needs pre-test probability framing to avoid over-calling colonisation.

  • Care points: Advocate protocolised screening (e.g., twice-weekly BAL GM/PCR in high-risk ventilated patients) and earlier empiric therapy when criteria met.

  • Open access review (Frontiers, 2025) · (alt listing: ResearchGate record).

Review: Invasive aspergillosis — scope & new species (2024)

  • Landscape: Expands on non-fumigatus Aspergillus species, cryptic species with distinct susceptibility patterns, and emerging hosts (advanced COPD, cirrhosis, ICU).

  • Resistance: Summarises azole resistance mechanisms (cyp51A variants, TR34/L98H, TR46/Y121F/T289A) and notes environmental selection via triazole fungicides.

  • Practice: Reinforces susceptibility testing and situational use of L-AmB or isavuconazole where resistance is likely.

  • Review (ScienceDirect).

Diagnostics: Biomarkers, Molecular, Imaging & Novel Methods

GM antigen & Aspergillus IgG negative “escape” cases

  • Problem: In suspected CPA/airway disease, Aspergillus-IgG can be false-negative early or in immunomodulated hosts.

  • Finding: High GM titres (especially BAL) can help “rescue” such cases, prompting treatment or further invasive sampling.

  • Clinical use: In IgG-negative but high-suspicion scenarios, pair BAL GM + PCR and repeat serology; avoid reliance on single negative IgG.

  • OA study (2025) · PubMed. (See also general GM/BDG performance review: Medicine 2024).

Molecular diagnosis, qPCR & NGS advances (2025 review)

  • Performance: qPCR improves sensitivity vs culture/microscopy; specificity hinges on contamination control and clinical context.

  • Best practice: Combine qPCR with GM/BDG in high-risk patients; consider cycle thresholds and duplicate positivity to support true infection.

  • NGS: Useful for broad pathogen screens or resistant/cryptic species; needs standardisation and careful interpretation.

  • OA review (Front Cell Infect Microbiol, 2025). British Thoracic Society

Microscopy, GM, PCR comparative pilot (2025)

  • Design: Head-to-head assay comparison across serum/BAL/sputum against a composite clinical reference.

  • Takeaway: No single test is definitive; dual-modality (e.g., BAL GM + PCR) yields best balance. Microscopy remains specific but insensitive.

  • Study (ScienceDirect). ERS Publications

Emerging spectroscopy / imaging techniques (TERS)

  • What it is: Tip-enhanced Raman spectroscopy mapping conidial wall components (melanin, polysaccharides, proteins) at nanoscale.

  • Why it matters: Potential to differentiate strains or track resistance-linked wall changes; currently preclinical, not diagnostic.

  • AIP Applied Physics Letters (2025) · arXiv preprint.

Therapeutics, Resistance & New Drugs

Olorofim (F901318) — Phase IIb results (2025)

  • Population: Refractory invasive mould disease (including azole-resistant Aspergillus), many salvage scenarios.

  • Efficacy: Global response ~29% (D42) and ~27% (D84); when counting stable disease, success rises to ~75% (D42) and ~63% (D84).

  • Safety: Transaminase elevations ~10%, mostly reversible with dose interruption/adjustment; no treatment-related deaths reported.

  • Use case: Salvage/compassionate therapy where standard options fail or resistance limits choices; monitor LFTs and DDIs.

  • PubMed · Lancet Infect Dis abstract. (Trial record: NCT03583164).

Review of olorofim in aspergillosis

  • MoA: Inhibits dihydroorotate dehydrogenase (DHODH), blocking de novo pyrimidine synthesis (novel class, no cross-resistance with azoles/echnocandins/AmB).

  • Signals: Case series in azole-resistant disease (incl. CGD) report clinical/radiologic remission; combination strategies under study.

  • Caveats: Access via trials/managed access; need phase III data and resistance surveillance under use pressure.

  • epocrates.com

Pipeline and alternative antifungals

  • Fosmanogepix (Gwt1 inhibitor): Oral/IV; activity against Candida/Aspergillus; CNS penetration promising; phase II positive signals.

  • Rezafungin (long-acting echinocandin): Weekly IV dosing enables OPAT; emerging real-world data in invasive disease and step-down.

  • Ibrexafungerp (tricohalose class/β-glucan): Oral; Aspergillus data limited (better for Candida), but combinations explored.

  • New azoles (isavuconazole real-world/TDM): Use where voriconazole intolerance or QT issues exist.

  • (See contemporary reviews; real-world rezafungin data below.)

Rezafungin (real-world, 2025) — OPAT-friendly weekly echinocandin; emerging safety/utility data.

Azole resistance & clinical implications

  • Drivers: Agricultural triazoles select environmental cyp51A mutations; patients can acquire primary resistant strains.

  • Practice changes: Where resistance prevalence is ≥10%, consider empiric L-AmB or isavuconazole until susceptibility known; always request AFST when feasible.

  • Nature Communications 2024 · Review PubMed.

Therapeutic drug monitoring & combination strategies

  • TDM: Essential for voriconazole/posaconazole (target troughs, avoid toxicity). Isavuconazole TDM less routine, but consider in extremes.

  • Combinations: Azole + echinocandin in refractory disease or high burden IA; AmB-based combos when resistance suspected. Evidence heterogeneous—use in expert-guided salvage.

  • (Covered within recent IA/therapy reviews above.)

Immunology, Host Responses & Biologics

Immunopathogenesis review (2023)

  • Pathways: Th2-skewed responses drive ABPA/SAFS (IgE/eosinophilia); defects in phagocyte function (neutropenia, CGD, high-dose steroids) predispose to invasive disease.

  • Mediators: Roles for IFN-γ, IL-5/IL-13, mucus hypersecretion, and airway remodelling; supports biologic targeting in allergic phenotypes.

  • OA review (Front Immunol 2023).

Biologics in ABPA / severe asthma

  • When to use: Relapsing ABPA, frequent steroid bursts, or steroid toxicity despite azole therapy.

  • Agents & effects: Omalizumab (anti-IgE) reduces exacerbations/steroid need; mepolizumab/benralizumab (anti-IL-5/IL-5R) tackle eosinophilia; dupilumab (anti-IL-4Rα) addresses Th2 axis and mucus/plugging.

  • Integration: Keep antifungal therapy for fungal burden; use biologics to control inflammation/exacerbations and spare steroids; monitor IgE dynamics and radiology.

  • ISHAM ABPA paper · PubMed.

by GAtherton

Side Effects, New Medicines, and Safety Reporting: What Every Patient Should Know

Modern medicines, including antifungals used for aspergillosis, can be life-saving. But they can also have powerful side effects. One patient recently described developing nerve damage (neuropathy) while on treatment, but never mentioned it to their doctor, because they didn’t know it could be a side effect. Sadly, by the time it was recognised, the damage was permanent.

This story shows why patients and doctors need to work together in partnership to spot and report side effects early — especially when medicines are new and real-world safety data is still limited.

1. From passive role to partnership

In the past, healthcare was one-way: the doctor gave instructions, the patient followed. Today the NHS encourages shared responsibility:

  • Doctors bring their expertise about the illness and treatments.

  • Patients bring their daily experience of living with the condition.

  • Together they can make safer, better-informed decisions.

This partnership is essential for powerful drugs like antifungals, where side effect monitoring depends on both sides working together.

2. Why side effect statistics can be misleading

Leaflets list side effects as “common” or “rare,” often with percentages. But these figures don’t always reflect real life because:

  • Trials are limited – only a few thousand people take part, often younger and healthier than typical NHS patients.

  • Under-reporting is common – doctors and patients often fail to report side effects, especially mild ones.

  • Bias exists – severe or unusual reactions are reported more often than everyday ones.

👉 Bottom line: leaflets tell us what can happen, not always how often it happens.

3. The Yellow Card system

The UK’s main tool for detecting safety issues is the Yellow Card Scheme, run by the MHRA.

  • Anyone can report: doctors, nurses, pharmacists, patients, or carers.

  • Reports are vital: patterns in these reports may reveal risks not seen in trials.

  • Action is taken: if needed, leaflets are updated, warnings issued, or drugs restricted/withdrawn.

You can report suspected side effects at yellowcard.mhra.gov.uk.

4. Why reporting matters

Poor reporting leads to harm:

  • Delayed warnings – e.g. photosensitivity with voriconazole took years to be recognised.

  • Biased safety data – drugs may seem safer than they are.

  • Preventable harm – patients may suffer permanent injury before action is taken.

For new medicines (marked with a ▼ black triangle in the BNF and leaflets), the MHRA asks for all side effects to be reported, no matter how small.

5. Extra protections for new medicines

When a drug is new, safety systems are stronger than usual:

  • Black triangle (▼) – signals “additional monitoring” so all suspected ADRs should be reported.

  • Specialist prescribing – new antifungals are usually limited to centres like NAC.

  • Closer monitoring – frequent blood tests, drug levels, eye or skin checks depending on risk.

  • Risk Management Plans – agreed with regulators, spelling out what to watch for.

  • Post-marketing studies – Phase 4 trials track safety in real-world patients.

These safeguards are extensive, but not fool-proof. Rare or long-term effects may still emerge only after years of wider use.

6. The NHS challenge

Despite the systems:

  • Only a small percentage of doctors file Yellow Card reports each year.

  • Most GPs never prescribe brand-new drugs — so reporting falls heavily on specialist centres like NAC.

  • Under-reporting risks harm, increases NHS costs, and erodes trust.

7. Who sets the rules?

Several organisations provide guidance on reporting and safety:

  • MHRA (UK regulator): runs Yellow Card, monitors new and established drugs, and issues safety updates.

  • BNF (British National Formulary): highlights side effects, black triangle drugs, and links to reporting tools.

  • GMC (General Medical Council): obliges doctors to report serious ADRs and all reactions to ▼ drugs.

  • EMA (European Medicines Agency): operates EudraVigilance, pooling reports from across Europe.

  • Global standards: the UK follows international rules (ICH E2B) so data is shared worldwide.

8. What patients can do

You are central to this safety net:

  • Be observant – notice anything new or unusual.

  • Keep a record – note when it started, how often, and any changes with medication.

  • Report promptly – tell your team and consider submitting a Yellow Card yourself.

  • Ask questions – “What side effects should I look out for? Which are urgent? How will we monitor this drug?”

  • Use trusted sources – NHS.uk, bnf.nice.org.uk, NAC, or your pharmacist.

9. The reality of side effects

For many, side effects are not “minor inconveniences.” They can mean:

  • Permanent disability (e.g. nerve or vision damage).

  • Loss of independence or mobility.

  • Social isolation and depression.

That’s why side effect monitoring is not just bureaucracy — it’s about protecting real lives.

Key message

The systems around new medicines are extensive but not fool-proof. That’s why patients and doctors must work as partners.

👉 If you notice something new, strange, or worrying while on antifungal medication — however small — tell your healthcare team and consider reporting it. Your report may be the missing piece that protects you and others.

by GAtherton

Damp, Cold, and Poor Housing – Why It Matters for Lung Health

This briefing from the House of Commons Library (2025) looks at how poor housing conditions—especially damp, mould, and cold homes—affect health and what’s being done about it in the UK.

Main Points

  • Health risks are serious
    Living in damp or mouldy homes increases the risk of respiratory problems, particularly for people with existing lung disease like aspergillosis, asthma, COPD, or bronchiectasis.

  • Children and vulnerable adults
    Young children, older adults, and people with weakened immune systems are most affected. Damp and mould can trigger flare-ups, worsen breathing symptoms, and increase infection risk.

  • Mental health impact
    Poor housing is linked to stress, anxiety, and depression. Worrying about your home can also worsen physical symptoms, especially if you avoid using rooms with mould or limit heating to save costs.

  • Cold homes add to the problem
    Cold airways can make breathing more difficult, weaken the immune system, and increase the chance of winter infections.

  • Wider health effects
    Damp and cold can also affect heart health, bone/joint pain, and overall wellbeing.

What’s Being Done

  • Legal responsibilities: Landlords must keep homes safe and fit to live in under UK law. This includes dealing with serious damp and mould.

  • Government programmes:

    • Funding for improving insulation and heating in social housing.

    • Advice services for tenants.

    • Local councils can take action if landlords fail to address hazards.

  • Public health guidance now recognises the link between housing and chronic illness, with stronger advice for early intervention.

What This Means for Aspergillosis Patients

  • Stay alert to symptoms: If your cough, breathlessness, or fatigue worsen at home, check for damp, mould, or poor heating.

  • Act early: Report problems to your landlord or council quickly—prolonged exposure can worsen lung damage.

  • Medical link is recognised: You are more likely to be taken seriously now, as official guidance acknowledges the health risks.

  • Keep records: Photos, symptom diaries, and GP notes can support housing complaints.

For full details see https://commonslibrary.parliament.uk/research-briefings/cdp-2025-0096/

by GAtherton

📘 What is CPA? (Chronic Pulmonary Aspergillosis)

Patient handout for A&E staff who are not aware of aspergillosis.

What is CPA?

CPA is a chronic fungal infection of the lungs caused by Aspergillus, most often in people who already have damaged lungs from conditions like tuberculosis, COPD, lung cancer, or sarcoidosis.

Unlike ABPA, CPA is a true infection, not an allergic reaction. It is not contagious but can slowly destroy lung tissue if not treated.

Symptoms

  • Chronic cough, often with mucus

  • Coughing up blood (haemoptysis)

  • Fatigue, low-grade fever

  • Unexplained weight loss

  • Breathlessness

  • Recurrent chest infections not responding to antibiotics

Diagnosis

  • CT scan of the chest showing cavities, nodules, or fungus balls (aspergillomas)

  • Aspergillus IgG antibody (usually raised)

  • Positive sputum PCR or culture for Aspergillus

  • Exclude TB and malignancy

Treatment

  • Long-term antifungal therapy (e.g. itraconazole, voriconazole, posaconazole)

  • Monitor blood levels and liver function

  • Surgery or embolisation if severe bleeding occurs

  • Supportive care: oxygen, nutrition, physiotherapy

Key Points for A&E:

✅ CPA is a progressive fungal infection, not a typical bacterial pneumonia
✅ May present with haemoptysis, respiratory distress, or systemic illness
✅ Review current antifungal treatment and potential drug interactions
✅ Consider urgent chest CT and specialist referral if patient is unwell

📍 For specialist support:

National Aspergillosis Centre (NAC)
🏥 Wythenshawe Hospital, Manchester University NHS Foundation Trust
🌐 NAC homepage on MFT website  https://mft.nhs.uk/wythenshawe/services/infectious-diseases/national-aspergillosis-centre/
🌐 www.aspergillosis.org

📞 Daytime contact: 0161 291 2891 or 0161 291 4362
📞 Urgent out-of-hours: Call Wythenshawe switchboard on 0161 998 7070
📢 Ask for the on-call Infectious Diseases Consultant

by GAtherton

📘 What is ABPA? (Allergic Bronchopulmonary Aspergillosis)

Patient handout for A&E staff who ask what aspergillosis is.

What is ABPA?

ABPA is an allergic lung condition caused by the immune system overreacting to the fungus Aspergillus. It mainly affects people with asthma or cystic fibrosis.

When Aspergillus spores are inhaled, most people clear them without issue. In ABPA, the immune system sees these spores as dangerous and mounts a strong inflammatory response. This leads to asthma-like symptoms, mucus plugging, and can result in permanent lung damage (bronchiectasis) if left untreated.

Symptoms

  • Worsening breathlessness

  • Wheezing, chest tightness

  • Coughing up thick, often brown mucus

  • Fever, fatigue, or feeling generally unwell

  • Unintentional weight loss (advanced cases)

Diagnosis

  • History of asthma or cystic fibrosis

  • High IgE levels and positive Aspergillus-specific IgE

  • Eosinophilia (raised white blood cells)

  • Sputum culture or PCR positive for Aspergillus

  • Chest imaging showing mucus plugging or bronchiectasis

Treatment

  • Oral corticosteroids (e.g. prednisolone) to reduce inflammation

  • Antifungal medication (e.g. itraconazole) to lower fungal burden

  • Biologic therapies (e.g. omalizumab or benralizumab) in some patients

  • Regular monitoring by respiratory or infectious diseases specialists

Key Points for A&E:

✅ ABPA is an allergic lung disease, not a classical infection
✅ Can present with severe asthma, mucus plugging, or type 2 respiratory failure
✅ Requires early recognition and often systemic steroids and antifungal therapy
✅ Take bloods (IgE, eosinophils, CRP), consider chest imaging, and review oxygen status

📍 For specialist support:

National Aspergillosis Centre (NAC)
🏥 Wythenshawe Hospital, Manchester University NHS Foundation Trust
🌐 NAC homepage on MFT website https://mft.nhs.uk/wythenshawe/services/infectious-diseases/national-aspergillosis-centre/
🌐 www.aspergillosis.org

📞 Daytime contact: 0161 291 2891 or 0161 291 4362
📞 Urgent out-of-hours: Call Wythenshawe switchboard on 0161 998 7070
📢 Ask for the on-call Infectious Diseases Consultant

by GAtherton

🤐 Why It's Important Not to Share Your Clinical Trial Experience — Until It’s Over

If you have chronic pulmonary aspergillosis (CPA), you may be invited to take part in a clinical trial for a new antifungal medication like rezafungin. That’s exciting — and could help improve treatment for many people in future.

Naturally, people want to support each other by sharing experiences, especially in online support groups. But when it comes to clinical trials, there’s a really important reason why we shouldn’t talk about how we’re feeling while we’re still in the trial.

Here’s why.

🧪 What Are Clinical Trials For?

Clinical trials help doctors and researchers answer important questions like:

  • Does this new treatment work?

  • Is it better than the current treatment?

  • What side effects might it cause?

To get accurate answers, the trial needs to be fair and unbiased — meaning that personal expectations and outside influences shouldn’t affect how people report their symptoms or progress.

📣 The Problem With Sharing During a Trial

If you’re taking part in a trial and say something like:

“I feel great — this new drug is working for me!”
or
“This is making me feel worse than ever — don’t join!”

...other people may change how they think and feel based on your comment.

This is called bias. It can:

  • Make others expect the same good (or bad) result

  • Affect how people rate their own symptoms

  • Cause people to drop out or not join at all

  • Make the trial results less accurate or even unusable

Even well-meaning comments can damage the study, especially if the trial is small (like most CPA studies are).

🕵️‍♀️ What If It’s a Blinded Trial?

Some trials are "blinded", meaning you don’t know whether you're getting the new treatment or a standard one (or placebo).

But if people start guessing or posting:

“I’m sure I’m on the real drug — I feel amazing!”

...then other people might also guess, or feel disappointed — which again, affects how results are reported.

🚦When Is It Safe to Share?

💬 After the trial is over and the results are published, you can talk freely about your experience.

In fact, patient voices are vital at that stage — they help others understand what it’s like to be part of a trial and whether new treatments are helpful in real life.

💡 What You Can Say During the Trial

You can still help raise awareness without compromising the study. For example:

  • ✅ “I’m taking part in a CPA trial – ask your doctor if you might be eligible.”

  • ✅ “There’s a study on a new antifungal — here’s the link to the official trial page: clinicaltrials.gov/study/NCT06794554”

  • ✅ “I’m proud to be contributing to research — happy to share my experience once the trial ends.”

Just don’t talk about how the treatment is affecting you until the trial is complete.

🙏 Why This Matters

By keeping quiet during the trial, you're:

  • Protecting the integrity of the study

  • Helping future patients get trustworthy answers

  • Supporting the research team who need clear, unbiased data

You’re not just taking part in a trial — you’re helping build evidence that others will depend on for years to come.

🧭 Summary

✅ Do ❌ Don’t
Tell people a trial exists Share how the treatment is affecting you
Encourage others to talk to their doctor Post guesses about which drug you’re on
Wait until the trial ends to share experiences Influence others to join based on your results

If you're ever unsure, ask your clinical trial team or group moderator — they'll be glad to help. Your role in research is important, and your silence now is a powerful act of support for science, fairness, and future care.

by GAtherton

Other forms of Aspergillosis: 🔬 Acute Invasive Aspergillus Sinusitis (AIAFS)

⚠️ A rare and severe fungal sinus infection — seen almost exclusively in people with severely weakened immune systems

🧾 What is it?

Acute Invasive Aspergillus Sinusitis (AIAFS) is a rapidly progressing fungal infection of the sinuses, caused by Aspergillus species (typically A. fumigatus). It leads to tissue invasion, destruction, and potentially fatal complications if not treated urgently.

🛡️ Who is at Risk of Acute Invasive Aspergillus Sinusitis?

Acute Invasive Aspergillus Sinusitis (AIAFS) is very rare, and affects people who are significantly immunocompromised — meaning their immune systems are unable to control even common environmental fungi.
However, “immunocompromised” is not always black-and-white. There are different degrees of vulnerability, and it's important to understand who is at greatest risk.

🔴 High-risk (severe immunosuppression)

These individuals are at the greatest risk for AIAFS:

  • Profound neutropenia (especially <500 neutrophils/μL for >10 days)

  • Acute leukaemia or stem cell transplantation

  • Solid organ transplant recipients on strong immunosuppressive regimens

  • High-dose corticosteroids (e.g. ≥20 mg prednisolone/day for ≥2 weeks)

  • Uncontrolled HIV/AIDS with low CD4 counts (<200)

  • Diabetic ketoacidosis or severe metabolic acidosis

🟠 Intermediate-risk (chronic or moderate immunosuppression)

Patients in this category may not be at risk of AIAFS, but may still be more vulnerable to chronic or allergic forms of aspergillosis or other infections:

  • Long-term oral corticosteroids at lower doses (e.g. <10 mg/day)

  • Biologic therapies for asthma (e.g. anti-IL-5, anti-IgE), which may subtly modulate immunity

  • Genetic susceptibility (e.g. subtle immune pathway deficiencies identified in CPA or ABPA)

  • COPD, bronchiectasis or severe asthma with impaired local defence

  • Malnutrition or poorly controlled diabetes

These patients are not typically at risk of invasive sinus aspergillosis, but may experience worsening of fungal conditions or atypical presentations of infection.

🟢 Low-risk (normal immune function)

People with normal immune function — even those with:

  • Allergic rhinitis

  • Chronic rhinosinusitis

  • Mild asthma or occasional infections

…are not at risk of developing AIAFS. Everyday exposure to Aspergillus spores is harmless to most people.

💬 Key Clarification:

Having aspergillosis does not automatically mean you are at risk of invasive sinus infection.
Many patients with CPA, ABPA, or SAFS are immunologically “fragile,” but not severely immunocompromised.
AIAFS typically only occurs in people with a combination of immune suppression and a very specific set of risks — especially when white blood cell function is severely impaired.

📋 Symptoms and Signs (typically <4 weeks onset)

  • Fever that does not respond to antibiotics

  • Facial pain or pressure, often severe and one-sided

  • Nasal congestion, discharge (often bloody or blackish)

  • Dark scabs (eschar) on the nasal mucosa or palate

  • Eye swelling, visual changes, or cranial nerve symptoms (if spread to the orbit or brain)

  • Altered mental state, seizures (in advanced cases)

🧪 Diagnosis

AIAFS is diagnosed based on:

  • Clinical suspicion in a high-risk patient

  • Endoscopic examination with biopsy and histology (showing hyphal invasion of tissue)

  • CT/MRI imaging to assess spread (bone, orbit, brain)

  • Culture and molecular testing of sinus material

  • Aspergillus PCR or galactomannan testing may help, but are not definitive alone

💊 Treatment Approach

Treatment must begin urgently, ideally within hours of suspicion.

1. Systemic antifungal therapy

  • First-line: Voriconazole or Isavuconazole

  • Alternatives: Liposomal Amphotericin B

  • Combination therapy may be considered in some cases

  • Therapeutic drug monitoring is essential (especially for voriconazole)

2. Surgical debridement

  • Prompt and aggressive endoscopic surgery is critical

  • Repeat procedures may be needed to remove necrotic tissue

3. Immunological support

  • Reversal of neutropenia if possible (e.g. G-CSF)

  • Reduction or withdrawal of immunosuppressive drugs

  • Management of underlying condition (e.g. glycaemic control in diabetes)

📈 Prognosis

  • Mortality is high (>50%) if not recognised and treated early

  • With rapid antifungal therapy and surgery, survival improves significantly

  • Regular monitoring, follow-up imaging, and immune recovery are crucial to long-term outcomes

🧠 Key Points to Remember

✅ This is a medical emergency, but
✅ It is extremely rare, and
✅ Almost exclusively affects those with profound immune suppression
✅ Not a risk to the general public or people with typical sinus infections

📣 Summary for Patient Awareness

Acute Invasive Aspergillus Sinusitis is very rare.
It is a fast-moving sinus infection caused by a fungus called Aspergillus, but it only happens in people with very weak immune systems, like those having chemotherapy or organ transplants.
It needs urgent treatment with antifungal medicine and sometimes surgery.
If your immune system is normal, this infection is not a risk to you.

by GAtherton

Patient Guide: Understanding Aspergillus-Related Chronic Pulmonary Disease

Based on new international guidance (2024)

What is Aspergillus and Why Is It Important?

Aspergillus is a common type of fungus found in the environment. Most people breathe it in every day without any problem. However, if you have a lung condition or a weakened immune system, Aspergillus can cause serious problems. It can:

  • Trigger allergic reactions in the lungs
  • Infect damaged lung tissue
  • Worsen symptoms like coughing, wheezing, or breathlessness

Until recently, doctors treated each type of aspergillus-related lung disease as a separate condition. But new guidance recognises that many patients may have more than one form or sit on a spectrum.

What Conditions Are Included?

The term "aspergillus-related chronic pulmonary disease" covers a range of conditions:

Condition What it means
ABPA (Allergic Bronchopulmonary Aspergillosis) An allergic reaction to Aspergillus, usually in asthma or cystic fibrosis patients
CPA (Chronic Pulmonary Aspergillosis) A slow-developing fungal infection, often in people with pre-existing lung damage
Aspergillus bronchitis A fungal infection in the airways, often in people with bronchiectasis
Overlap syndromes Some people show features of more than one of the above

What Are the Symptoms?

Symptoms can vary, but common signs include:

  • Persistent cough (sometimes with mucus or blood)
  • Wheezing or breathlessness
  • Fatigue and low energy
  • Weight loss or loss of appetite
  • Repeated chest infections

If you experience these symptoms and have an underlying lung condition, it’s important to ask whether Aspergillus might be involved.

How Is It Diagnosed?

Doctors now use a combination of tests to get a clearer picture:

  • Chest CT scan – to look for signs of lung damage or fungal balls
  • Sputum samples – to check for the presence of Aspergillus
  • Blood tests – to detect allergic antibodies (IgE), immune responses (IgG), or fungal antigens
  • Bronchoscopy (sometimes) – to collect samples directly from the lungs

These tests help doctors decide whether it’s an allergic reaction, an infection, or both.

How Is It Treated?

Treatment depends on your symptoms and test results. The aim is to:

  • Reduce inflammation
  • Clear fungal infection
  • Prevent further lung damage

Common treatment options include:

Treatment Purpose
Steroids (e.g. prednisolone) Reduce allergic inflammation (especially in ABPA)
Antifungal drugs (e.g. itraconazole, voriconazole) Treat fungal infection and reduce fungal burden
Biologic therapies (e.g. omalizumab, dupilumab) Used in difficult-to-treat allergic cases
Nebulised antibiotics If other infections (like Pseudomonas) are also present
Surgery (rarely) To remove fungal balls or damaged tissue in severe CPA

What Has Changed in the 2024 Guidance?

  • Doctors are now encouraged to look for overlapping features, not just one diagnosis.
  • More emphasis is placed on early detection and preventing lung decline.
  • Guidelines promote the use of multidisciplinary teams (MDTs) for complex cases.
  • Newer treatments, including biologics, are being recommended more often.
  • Patients with symptoms but unclear diagnoses should be re-evaluated regularly.

What Can You Do as a Patient?

  • Know your diagnosis – Ask your team whether your current label still fits your symptoms
  • Track your symptoms – Keep a log of cough, breathlessness, fatigue, and infections
  • Ask about specialist referral – For example, to a National Aspergillosis Centre
  • Stay informed – Visit aspergillosis.org for up-to-date guidance
  • Take medications as prescribed and report any side effects promptly

Support and Information

  • Patient support groups can help you connect with others
  • Pulmonary rehabilitation and breathing therapy can improve quality of life
  • Annual reviews and regular scans can help spot problems early

For more information, leaflets, and help getting the right care, visit: aspergillosis.org

You don’t have to manage this alone.

by GAtherton