Allergic Bronchopulmonary Aspergillosis (ABPA)

📋 Key Information Summary

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Allergic Bronchopulmonary Aspergillosis (ABPA) is a complex hypersensitivity reaction to Aspergillus fumigatus colonising the airways, most commonly complicating asthma and cystic fibrosis (CF).
Diagnostic criteria require the presence of underlying asthma or CF, elevated total serum IgE (≥1,000 IU/mL), Aspergillus sensitisation (positive skin prick test or specific IgE), and characteristic imaging findings (central bronchiectasis, mucus plugging).
Eosinophilia (≥500 cells/µL), precipitating antibodies to Aspergillus, and pulmonary infiltrates on chest X-ray or CT support the diagnosis.
ABPA is classified into stages: Acute, Response (remission), Exacerbation, Corticosteroid-dependent, and Fibrotic — guiding treatment intensity and monitoring intervals.
First-line treatment is oral prednisolone 0.5–0.75 mg/kg/day for 2 weeks, then taper over 3–6 months to control the inflammatory response and prevent progression to fibrosis.
Itraconazole 200 mg BD (or voriconazole if intolerant/resistant) is the antifungal adjunct of choice, reducing fungal burden and enabling corticosteroid tapering.
Serial total serum IgE is the single most useful biomarker: a ≥50% fall from baseline confirms treatment response; a ≥100% rise signals an exacerbation.
Pulmonary function tests (spirometry with DLCO) and high-resolution CT (HRCT) chest are performed at diagnosis and repeated at regular intervals to monitor disease progression.
ABPA exacerbations are defined by clinical deterioration plus a ≥100% rise in total IgE from the treatment nadir or new pulmonary infiltrates.
The fibrotic stage (ABPA-S/CB with progressive fibrosis) is largely irreversible and requires long-term antifungal therapy with minimal corticosteroid use to avoid further immunosuppression.
Omalizumab (anti-IgE) is an emerging option for steroid-dependent or frequently relapsing ABPA, though PBS access in Australia requires authority application.
Aboriginal and Torres Strait Islander peoples living in remote communities may face delayed diagnosis due to limited access to specialist respiratory services, IgE testing, and HRCT imaging.
Lifelong monitoring is essential — patients in apparent remission may relapse, and the fibrotic stage can develop insidiously over years.

Introduction & Australian Epidemiology

Allergic Bronchopulmonary Aspergillosis (ABPA) is a pulmonary hypersensitivity disorder caused by a complex immune response to Aspergillus fumigatus colonising the airways. Unlike invasive aspergillosis, ABPA does not involve tissue invasion; rather, it represents a Th2-mediated inflammatory cascade with eosinophilic infiltration, mucus hypersecretion, and progressive airway damage that may culminate in proximal bronchiectasis and pulmonary fibrosis.

ABPA occurs almost exclusively in patients with pre-existing asthma or cystic fibrosis (CF). The prevalence of ABPA in the general asthma population is estimated at 1–2%, rising to 2–15% in patients with difficult-to-treat or severe asthma, and 2–9% in CF cohorts. In Australia, the exact national incidence is not well defined, but tertiary respiratory centres in Sydney, Melbourne, Brisbane, and Perth regularly manage these patients. A 2019 study from a Melbourne tertiary centre estimated that ABPA complicates approximately 2.5% of adult asthma referrals to severe asthma clinics.

Australia's warm, humid climate in northern Queensland, the Northern Territory, and parts of Western Australia provides an environment conducive to Aspergillus spore proliferation, particularly in decomposing vegetation, air-conditioning systems, and agricultural settings. Aboriginal and Torres Strait Islander communities in tropical and subtropical regions may face additional exposure risks due to housing conditions and environmental factors, though data specific to ABPA prevalence in Indigenous Australians remain limited.

⚠️

Under-diagnosis is common. ABPA is frequently misdiagnosed as poorly controlled asthma or recurrent pneumonia. Any patient with asthma and unexplained pulmonary infiltrates, bronchiectasis, or persistently elevated IgE should be investigated for ABPA.

The International Society for Human and Animal Mycology (ISHAM) working group has proposed updated diagnostic criteria and classification that form the basis of current Australian practice. This guideline synthesises ISHAM, British Thoracic Society (BTS), Cystic Fibrosis Foundation (CFF), and Australian expert consensus recommendations.

Diagnosis — Criteria & Investigations

ISHAM Diagnostic Criteria (2013, updated in practice)

Diagnosis of ABPA requires fulfilling a combination of predisposing conditions, obligatory criteria, and supportive criteria. The following table summarises the current classification adopted by most Australian respiratory units:

Criterion Category	Component	Threshold / Detail
Predisposing condition	Asthma	Any severity, including mild intermittent
Predisposing condition	Cystic fibrosis	Any genotype
Obligatory criteria (both required)	Elevated total serum IgE	≥1,000 IU/mL (direct IgE immunoassay)
Obligatory criteria (both required)	Aspergillus sensitisation	Positive Aspergillus-specific IgE (>0.35 kU/L) or positive skin prick test (SPT) to A. fumigatus extract (≥3 mm wheal)
Supportive criteria (≥2 of 3 in parenchymal ABPA; ≥1 in serological ABPA)	Eosinophilia	≥500 cells/µL (may be absent if on corticosteroids)
	Radiographic pulmonary infiltrates	Fleeting opacities, mucus plugging, consolidation on CXR or HRCT
	Central bronchiectasis	Bronchiectasis predominantly in the proximal (medial) two-thirds of lung fields on HRCT (high-attenuation mucus [HAM] is highly specific)
	Positive Aspergillus precipitins / IgG	Precipitating antibodies or elevated A. fumigatus-specific IgG (>40 mg/L by ImmunoCAP)

ABPA Classification (ISHAM Phenotypes)

Phenotype	Abbreviation	Features
ABPA with central bronchiectasis	ABPA-CB	Mandatory criteria + central bronchiectasis on HRCT
ABPA with serology only (no bronchiectasis)	ABPA-S	Mandatory criteria met, HRCT normal or shows infiltrates without bronchiectasis — earlier stage, potentially reversible
ABPA-CB with high-attenuation mucus	ABPA-CB-HAM	Central bronchiectasis + hyperdense mucus plugging on HRCT — associated with higher relapse rates and more severe disease

Investigations

Essential

Total serum IgE

Immunoturbidimetric or nephelometric assay. Must be ≥1,000 IU/mL for diagnosis. Serial monitoring is the cornerstone of disease tracking. Available through all Australian pathology services (Medicare-rebated).

Essential

Aspergillus-specific IgE and IgG

ImmunoCAP (Thermo Fisher). Specific IgE >0.35 kU/L confirms sensitisation. IgG >40 mg/L supports active immune response. Available at major Australian laboratories (e.g., Pathology Queensland, Melbourne Pathology, Douglass Hanly Moir).

Essential

Aspergillus skin prick test (SPT)

Using A. fumigatus extract (e.g., Hollister-Stier or ALK). ≥3 mm wheal after 15 minutes. Performed in specialist allergy/respiratory clinics. Superseded by specific IgE in many centres.

Essential

Full blood count with differential

Eosinophil count ≥500 cells/µL is supportive. May be normal in steroid-treated patients. Available universally (Medicare-rebated).

Available

High-resolution CT (HRCT) chest

Gold standard for demonstrating central bronchiectasis, mucus plugging (including high-attenuation mucus), tree-in-bud opacities, and consolidation. Available at all major radiology practices and public hospitals. MBS Item 5630 (CT chest).

Available

Chest X-ray (CXR)

PA and lateral views. May show fleeting infiltrates, tram-track sign, ring shadows. Less sensitive than HRCT but useful for initial screening and acute exacerbation monitoring. MBS Item 58502.

Available

Spirometry with diffusion capacity (DLCO)

FEV₁, FVC, FEV₁/FVC ratio, DLCO. Obstructive pattern typical; restrictive pattern suggests fibrotic stage. DLCO decline may precede spirometric changes. MBS Item 11506. Available at respiratory function laboratories.

Available

Sputum culture for Aspergillus species

Expectorated or induced sputum. Positive culture supports colonisation but is neither sensitive nor specific for ABPA. Species identification and antifungal susceptibility testing recommended if isolated. Available at all microbiology labs.

Referral

Aspergillus precipitins (immunodiffusion)

Classic precipitin testing (Ouchterlony). Being replaced by ImmunoCAP IgG in most centres. Refer to specialist mycology/immunology laboratories if ImmunoCAP unavailable.

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Do not rely on total IgE alone. Total IgE can be elevated in atopic disease, parasitic infection, and allergic bronchopulmonary mycoses caused by non-Aspergillus fungi. Always correlate with Aspergillus-specific IgE/IgG and imaging to confirm ABPA.

Differential Diagnosis

Severe eosinophilic asthma (without fungal sensitisation)
Allergic bronchopulmonary mycosis (ABPM) — caused by Candida, Curvularia, Bipolaris
Chronic pulmonary aspergillosis (CPA) — typically in immunocompetent patients with pre-existing structural lung disease
Eosinophilic granulomatosis with polyangiitis (EGPA / Churg-Strauss)
Hypersensitivity pneumonitis
Cystic fibrosis pulmonary exacerbation (in CF patients)

Staging & Classification

ABPA follows a characteristic clinical trajectory through defined stages. Understanding the current stage guides treatment decisions, monitoring intensity, and prognosis. Patients may not progress sequentially — they may present at any stage and may oscillate between stages.

Stage I

Acute ABPA

Active disease with elevated IgE (≥1,000 IU/mL), positive Aspergillus sensitisation, eosinophilia, new or worsening pulmonary infiltrates, and/or worsening respiratory symptoms. Requires initiation of corticosteroids ± antifungal therapy.

Setting: Outpatient specialist or inpatient if severe

Stage II

Response / Remission

Clinical and radiographic improvement following treatment. IgE falls ≥50% from peak. Infiltrates resolve. Steroids tapered or ceased. Maintain antifungal therapy. Monitor every 1–3 months.

Setting: Respiratory specialist outpatient

Stage III

Exacerbation

Defined as a ≥100% rise in total IgE from the remission nadir (minimum value achieved during treatment), with or without new infiltrates or clinical deterioration. Occurs in ~25–40% of patients. May require re-intensification of therapy.

Setting: Respiratory specialist review within 2 weeks

Stage IV

Corticosteroid-Dependent ABPA

Persistent or relapsing disease requiring ongoing corticosteroids to maintain control. Attempts to taper steroids result in clinical or serological relapse. Consider antifungal optimisation, omalizumab, or combination immunomodulation.

Setting: Specialist respiratory/immunology centre

Stage V

Fibrotic ABPA

End-stage characterised by progressive pulmonary fibrosis, fixed airflow obstruction, declining DLCO, and honeycombing on HRCT. Bronchiectasis is often widespread and irreversible. May require long-term oxygen therapy and lung transplant evaluation.

Setting: Tertiary respiratory/transplant centre

Serial Monitoring Framework by Stage

Stage	Total IgE	Spirometry	HRCT	Clinical Review
I — Acute	Every 2–4 weeks during induction	Baseline + 6 weeks	Baseline; repeat at 3–6 months to assess response	Every 2–4 weeks
II — Remission	Every 2–3 months for 1 year, then 3–6 monthly	Every 3–6 months	At 12 months; earlier if clinical concern	Every 3–6 months
III — Exacerbation	Every 2–4 weeks until new nadir established	At presentation + 6 weeks post-treatment	At relapse to document infiltrates	Every 2–4 weeks
IV — Steroid-dependent	Every 1–3 months (titrate to treatment decisions)	Every 3 months	Annually or if clinical decline	Every 1–3 months
V — Fibrotic	Every 3–6 months (IgE may be less informative)	Every 3–6 months	Annually; assess progression of fibrosis	Every 1–3 months

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Treatment nadir IgE. Always record the lowest total IgE achieved during or after treatment. This "nadir" value is the benchmark against which all future IgE results are compared. A doubling of IgE from the nadir (even if still below 1,000 IU/mL) warrants investigation for relapse.

Treatment

The goals of ABPA treatment are (1) suppression of the allergic inflammatory response, (2) reduction of Aspergillus antigenic load in the airways, (3) prevention of progressive bronchiectasis and fibrosis, and (4) minimisation of corticosteroid-related adverse effects. Treatment is stage-dependent and tailored to individual disease severity.

First-Line: Systemic Corticosteroids

Corticosteroids remain the cornerstone of acute ABPA treatment, targeting the Th2-mediated eosinophilic inflammation and immune complex deposition responsible for tissue damage.

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Prednisolone

Panafcortelone® · Solone® · Sone® · Corticosteroid

Adult dose (Acute ABPA) 0.5–0.75 mg/kg/day PO (typically 30–50 mg/day) for 2 weeks, then taper over 3–6 months. Aim for total duration of 3–6 months. Taper example: reduce by 5 mg every 2 weeks to 20 mg, then by 2.5 mg every 2 weeks.

Paediatric dose 0.5–1 mg/kg/day PO (max 40 mg/day) for 2 weeks, then taper over 3–6 months as per response

Route / Frequency Oral, once daily (morning)

Duration 3–6 months total for acute episodes; longer for steroid-dependent disease (use lowest effective dose)

Renal adjustment No specific dose adjustment; monitor fluid retention in CKD

Hepatic adjustment No adjustment required

Key adverse effects Hyperglycaemia, osteoporosis, adrenal suppression, weight gain, cataracts, psychosis — co-prescribe calcium/vitamin D and bone protection if prolonged

PBS status ✔ PBS General Benefit

Adjunctive Antifungal Therapy

Antifungal agents reduce the airway Aspergillus burden, decrease antigenic stimulation, and facilitate corticosteroid tapering. They are recommended for all ABPA patients alongside corticosteroids in the acute phase and as monotherapy during remission maintenance.

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Itraconazole

Sporanox® · Itrafungol® · Triasporin® · Azole antifungal

Adult dose 200 mg PO BD (capsules taken with food for optimal absorption). Therapeutic drug monitoring (TDM): target trough 1–5 µg/mL (measured after 2 weeks of therapy).

Paediatric dose 5 mg/kg/day PO in 1–2 divided doses (oral solution preferred in children <12 years)

Route / Frequency Oral, BD

Duration Minimum 6 months; continue until in remission (≥2 consecutive normal IgE readings, ≥6 months apart). Steroid-dependent patients may need long-term (≥12–24 months).

Renal adjustment Capsules: no adjustment. Oral solution (cyclodextrin): avoid if CrCl <30 mL/min (cyclodextrin accumulation).

Hepatic adjustment Use with caution; monitor LFTs at baseline, 1 month, 3 months, then 3-monthly. Discontinue if ALT/AST >3× ULN.

Key interactions CYP3A4 inhibitor — avoid with simvastatin, certain benzodiazepines, tacrolimus, cyclosporine. Reduces metabolism of many drugs. Requires TDM of interacting agents.

PBS status ⚑ PBS Authority Required (ABPA-specific authority through PBS/RPBS)

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Voriconazole

Vfend® · Azole antifungal (second-line for ABPA)

Adult dose 200 mg PO BD (after 400 mg BD loading on day 1). TDM: target trough 1–5 µg/mL. Monitor for visual disturbances, hepatotoxicity, and photosensitivity.

Paediatric dose 7 mg/kg PO BD (max 200 mg BD). Not recommended <2 years without specialist guidance.

Route / Frequency Oral, BD (IV for severe cases)

Duration 6–12 months minimum; similar remission criteria as itraconazole

Renal adjustment Oral: no adjustment. IV formulation: avoid if CrCl <50 mL/min (cyclodextrin vehicle).

Hepatic adjustment Reduce dose by 50% in Child-Pugh A/B. Avoid in Child-Pugh C. Monitor LFTs closely.

Key adverse effects Visual disturbances (30%), photosensitivity (risk of squamous cell carcinoma with prolonged use), hepatotoxicity. Use SPF 50+ and protective clothing.

PBS status ⚑ PBS Authority Required

Second-Line / Steroid-Sparing Therapy

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Omalizumab

Xolair® · Anti-IgE monoclonal antibody

Indication Corticosteroid-dependent ABPA or frequent exacerbations despite optimised itraconazole therapy (off-label for ABPA in Australia)

Adult dose 150–375 mg SC every 2–4 weeks, dosed by body weight and baseline IgE (per severe asthma dosing table). Requires specialist initiation.

Paediatric dose As per weight-based dosing; ≥6 years. Limited ABPA-specific paediatric data.

Monitoring Observe for 2 hours after first injection, 1 hour thereafter. Monitor for anaphylaxis (risk <0.1%). Total IgE rises with omalizumab — use free IgE or clinical markers for monitoring.

PBS status ✘ Not PBS-listed for ABPA (PBS-listed for severe allergic asthma with authority; ABPA use is off-label)

Treatment Algorithm — Acute ABPA

1

Confirm diagnosis

Total IgE ≥1,000 IU/mL + Aspergillus sensitisation + imaging/serological criteria met.

2

Initiate prednisolone + itraconazole

Prednisolone 0.5–0.75 mg/kg/day + itraconazole 200 mg BD. Record baseline IgE as the "peak" value.

3

Assess response at 6 weeks

Repeat total IgE. Target: ≥50% reduction from peak. Repeat spirometry. If response, begin steroid taper.

4

Taper corticosteroids

Reduce prednisolone by 5 mg every 2 weeks to 20 mg, then by 2.5 mg every 2 weeks. Continue itraconazole for ≥6 months.

5

Define remission

Total IgE normalised or stable at new nadir, no infiltrates, stable FEV₁, off corticosteroids ≥3 months. Record the nadir IgE for future comparison.

⚠️

Itraconazole therapeutic drug monitoring (TDM). Oral bioavailability of itraconazole capsules is highly variable and food-dependent. Trough levels must be checked after 2 weeks of therapy. If trough <1 µg/mL, consider switching to the oral solution (better bioavailability), increasing the dose, or changing to voriconazole.

Management of Refractory or Steroid-Dependent ABPA

If disease relapses during steroid tapering (≥100% IgE rise from nadir) or requires ongoing corticosteroids to maintain control, the following escalation strategy is recommended:

Optimise antifungal therapy — confirm TDM levels, switch from itraconazole to voriconazole if trough inadequate.
Add or switch to omalizumab — specialist initiation at a tertiary respiratory/immunology centre.
Consider posaconazole (200 mg PO BD) or isavuconazole (200 mg PO daily) — limited ABPA data but may be used under specialist guidance when first-line azoles fail.
Intravenous immunoglobulin (IVIg) — anecdotal evidence in steroid-dependent ABPA; reserved for highly refractory cases.
Lung transplant evaluation — for Stage V fibrotic ABPA with progressive respiratory failure.

Monitoring

Biomarker Monitoring

Serial total serum IgE is the primary biomarker for tracking disease activity, treatment response, and relapse. All other monitoring modalities are adjunctive.

Parameter	Frequency	Target / Significance
Total serum IgE	Every 2–4 weeks (acute); every 1–3 months (remission)	≥50% fall from peak = response. ≥100% rise from nadir = exacerbation. A gradual rise over 6–12 months may precede overt relapse.
Aspergillus-specific IgE/IgG	At diagnosis; every 6–12 months	Decline in specific IgG correlates with reduced fungal burden. Less responsive to treatment than total IgE.
Full blood count / eosinophils	Every 4–8 weeks (acute); every 3–6 months (remission)	Eosinophil count normalises with corticosteroid therapy. Persistent eosinophilia may indicate inadequate treatment or alternative diagnosis.
Spirometry (FEV₁, FVC, FEV₁/FVC)	At diagnosis; every 3 months (acute); every 6 months (remission)	FEV₁ improvement ≥10% suggests treatment response. Progressive decline suggests fibrotic transition.
DLCO	At diagnosis; annually or if clinical decline	DLCO decline is an early marker of fibrotic progression, even before FEV₁ deteriorates.
HRCT chest	At diagnosis; at 3–6 months to assess treatment response; annually or if new symptoms	Resolution of infiltrates and mucus plugging. New or worsening bronchiectasis/fibrosis warrants treatment intensification.
Sputum culture	Every 3–6 months or during exacerbations	Persistent Aspergillus growth may necessitate prolonged or intensified antifungal therapy. Monitor for non-fumigatus species.
Itraconazole / voriconazole trough levels	After 2 weeks of therapy; with dose changes; every 3–6 months; if suspected treatment failure	Target trough: 1–5 µg/mL (both agents). Below 1 µg/mL — likely subtherapeutic. Above 5 µg/mL — toxicity risk.
Liver function tests	Baseline; 1 month; 3 months; then 3-monthly during azole therapy	Hepatotoxicity is a class effect of azole antifungals. Discontinue if ALT/AST >3× ULN or symptomatic hepatotoxicity.

Treatment Duration & Discontinuation

Corticosteroids should be tapered and discontinued over 3–6 months once clinical and serological improvement is confirmed (Stage I/II disease).
Itraconazole is continued for a minimum of 6 months and ideally until the patient has been in remission for ≥6 months with stable IgE and no corticosteroid requirement.
There is no consensus on the optimal total duration of antifungal therapy. Many experts continue for 12–24 months in the first episode, and longer for recurrent disease.
In steroid-dependent ABPA (Stage IV), long-term antifungal therapy (potentially indefinite) may be required.

Recurrence Prevention

✅

Maintain optimal asthma or CF therapy to minimise airway inflammation and mucosal damage that facilitates Aspergillus colonisation.
Environmental exposure reduction: advise patients to avoid compost, mulch, mouldy hay, and poorly ventilated spaces with visible mould. Consider HEPA filtration in the home if feasible.
Adherence to antifungal therapy — non-adherence is a leading cause of relapse. Address pill burden, cost (PBS authority), and side effects proactively.
Corticosteroid-sparing strategies — early introduction of itraconazole or omalizumab to avoid prolonged corticosteroid exposure and its associated morbidities.
Long-term surveillance: even patients in apparent remission should have total IgE checked at least every 6 months for a minimum of 5 years after treatment cessation.

Special Populations

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Paediatric

ABPA in CF children

ABPA complicates CF in 2–9% of paediatric patients. Diagnostic criteria are the same as adults, but total IgE thresholds may need interpretation in the context of atopy. Baseline IgE >500 IU/mL with Aspergillus sensitisation in a CF child warrants investigation even without typical imaging.

Corticosteroid dosing

Prednisolone 0.5–1 mg/kg/day (max 40 mg/day). Shorter taper durations may be appropriate with close monitoring. Growth monitoring is mandatory — refer to paediatric endocrinology if growth faltering occurs.

Itraconazole

5 mg/kg/day in 1–2 divided doses. Oral solution preferred in children <12 years due to capsule absorption variability. Monitor for hepatotoxicity. TDM is essential — target trough 1–5 µg/mL.

Voriconazole

7 mg/kg PO BD (max 200 mg BD). Not recommended <2 years without specialist guidance. Photosensitivity counselling and regular skin checks required with prolonged use.

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Pregnancy & Breastfeeding

Corticosteroids

Prednisolone is considered relatively safe in pregnancy (Category A). It is extensively metabolised by the placenta. Use the lowest effective dose. Monitor for gestational diabetes.

Itraconazole / Voriconazole

Contraindicated in pregnancy. Both are Category D (teratogenic in animal studies — skeletal, craniofacial, and cardiac malformations). Effective contraception required during and for 2 months after azole therapy. Discuss risk–benefit with the patient and consider deferring antifungal therapy if disease is mild.

Omalizumab

Category B1. Limited human data in pregnancy. May be continued if the benefit outweighs risk in steroid-dependent ABPA. Discuss with obstetric medicine.

Breastfeeding

Prednisolone: compatible (low transfer to milk, especially if taken 4 hours prior to feeding). Itraconazole/voriconazole: present in breast milk — avoid or use alternative feeding.

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Elderly

Corticosteroid caution

Higher risk of osteoporotic fractures, hyperglycaemia, cataracts, and adrenal suppression. Co-prescribe calcium 500 mg + vitamin D 800 IU daily. Consider bisphosphonate (alendronate 70 mg PO weekly, PBS General Benefit) if prolonged steroid course anticipated. DEXA scan at baseline.

Drug interactions

Polypharmacy is common in elderly patients. Itraconazole (CYP3A4 inhibitor) has significant interactions with statins, anticoagulants (warfarin), calcium channel blockers, and benzodiazepines. Review all medications before starting azole therapy.

Renal function

Ensure CrCl estimation. Voriconazole IV cyclodextrin vehicle is nephrotoxic — use oral formulation if CrCl <50 mL/min.

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Renal Impairment

Itraconazole

Capsules: no dose adjustment. Oral solution (cyclodextrin vehicle): avoid if CrCl <30 mL/min — cyclodextrin accumulates and is nephrotoxic.

Voriconazole

Oral formulation: no dose adjustment. IV formulation: avoid if CrCl <50 mL/min (cyclodextrin). Always prefer oral route in CKD.

Prednisolone

No specific dose adjustment. Monitor fluid and electrolyte balance closely. Consider shorter courses to minimise renal sodium retention.

🫁

Hepatic Impairment

Azole antifungals

Itraconazole: use with caution, monitor LFTs monthly. Voriconazole: reduce dose by 50% in Child-Pugh A/B; avoid in Child-Pugh C. Both agents are hepatotoxic and hepatometabolised.

Monitoring

Baseline LFTs and at 1, 3, and 6 months. Discontinue azole if ALT/AST >3× ULN or bilirubin >2× ULN.

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Immunocompromised

CF patients on immunosuppression

CF patients on systemic corticosteroids (for ABPA) are at increased risk of non-tuberculous mycobacterial (NTM) infection and Pseudomonas colonisation. Screen sputum for NTM (acid-fast bacilli culture, PCR) before initiating prolonged corticosteroid therapy.

Iatrogenic immunosuppression

Patients on biologics (e.g., mepolizumab, benralizumab for severe eosinophilic asthma) may mask eosinophil counts. Total IgE and Aspergillus-specific markers remain informative.

Azole drug interactions

Itraconazole and voriconazole are potent CYP inhibitors. Avoid concurrent tacrolimus, cyclosporine (or monitor TDM intensively). If on immunosuppressants post-transplant, azole choice and dosing must be managed by the transplant team.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Epidemiological context

Aboriginal and Torres Strait Islander Australians experience a disproportionate burden of respiratory disease, including higher rates of chronic suppurative lung disease, bronchiectasis, and asthma. While ABPA-specific prevalence data for Indigenous Australians are lacking, the high prevalence of poorly controlled asthma, housing overcrowding, and environmental mould exposure in some communities suggests potential under-recognition.

Diagnostic barriers

Access to specialist respiratory services, HRCT imaging, Aspergillus-specific IgE testing, and skin prick testing is limited in remote and very remote communities. Many patients require aeromedical retrieval or fly-in-fly-out (FIFO) specialist clinics to access diagnostic investigations. Point-of-care IgE testing is not yet widely available in rural/remote settings.

Environmental and housing factors

Overcrowded housing, inadequate ventilation, and mould-affected dwellings increase Aspergillus spore exposure. Government programmes (e.g., National Partnership on Remote Housing, Northern Territory Remote Aboriginal Investment — Housing) aim to improve housing stock, but implementation gaps persist. Health workers can advocate for environmental assessments and remediation.

Medication access

Itraconazole requires PBS Authority approval, which may be challenging for remote prescribers without specialist support. Remote Area Aboriginal Health Services (RAAHS) and community pharmacies may not stock itraconazole on the formulary — early communication with the Remote Pharmacist and Aboriginal Health Practitioner is essential. Prednisolone is widely available through PBS General Benefit.

Monitoring and follow-up

Serial IgE monitoring, spirometry, and HRCT require laboratory and imaging services that may be hundreds of kilometres from patients' homes. Point-of-care spirometry (portable devices) can be used by trained Aboriginal Health Workers, but quality assurance programmes must be in place. Telehealth respiratory specialist consultations (MBS Items 99, 105, 106, 2884) are vital for bridging access gaps.

Cultural safety

Engage Aboriginal and Torres Strait Islander Health Workers and Health Practitioners in ABPA education, medication adherence support, and chronic disease management. Ensure culturally safe communication, use plain language and visual aids, and respect preferences around gender of health provider and family involvement in consultations. Acknowledge the strengths of Indigenous knowledge systems and community-controlled health organisations (e.g., AIDA, VACCHO).

Co-morbidity management

Aboriginal and Torres Strait Islander Australians with ABPA often carry concurrent diagnoses including chronic obstructive pulmonary disease (COPD), bronchiectasis, rheumatic heart disease, diabetes, and chronic kidney disease. ABPA management must be integrated into holistic chronic disease care models under Aboriginal Community Controlled Health Organisations (ACCHOs), with attention to corticosteroid effects on glycaemic control and renal function.

📚 References

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