This week’s research includes a large real-world study of treatments for ABPA in people with cystic fibrosis, early research into why some people with ABPA may respond differently to biologic treatments, and the start of an important Cochrane review examining antifungal treatment in asthma associated with fungal sensitisation.
Steroids or antifungals for ABPA in cystic fibrosis?
A large real-world study published in CHEST examined treatment of allergic bronchopulmonary aspergillosis (ABPA) in 3,096 people with cystic fibrosis who had received their first ABPA diagnosis between 2006 and 2022.
Researchers compared people initially treated with oral corticosteroids, antifungal drugs, or a combination of the two.
Oral corticosteroid treatment was associated with an improvement in the rate of change in lung function after treatment began. However, adding an antifungal was not associated with significantly better lung function, fewer pulmonary exacerbations or a longer time before ABPA relapse compared with corticosteroids alone.
Why does this matter?
Antifungal drugs such as itraconazole and voriconazole are frequently used in ABPA because reducing Aspergillus in the airways may reduce the stimulus driving inflammation. They can also sometimes reduce the amount of corticosteroid treatment required.
This study suggests that, at a population level in people with cystic fibrosis-associated ABPA, routinely adding an antifungal to corticosteroid treatment may not improve the major respiratory outcomes measured.
However, this was an observational study rather than a randomised clinical trial. Treatment was chosen by clinicians, and people receiving antifungals may have differed from those receiving corticosteroids alone. The results also apply specifically to people with cystic fibrosis and should not automatically be extrapolated to ABPA associated with asthma.
Current international ABPA guidelines recognise both systemic corticosteroids and azole antifungals as treatments for acute ABPA, with treatment tailored to the individual patient.
Read the paper:
Walsh J, Hsu JY, Tully E, Hong G. Comparing the real-world effectiveness of oral corticosteroids and antifungals for the treatment of allergic bronchopulmonary aspergillosis in cystic fibrosis. CHEST. 2026.
https://doi.org/10.1016/j.chest.2026.09.085
Can we predict which people with ABPA will respond to biologic treatment?
Biologic medicines are increasingly being used for people with difficult-to-control or treatment-dependent ABPA.
A new retrospective study investigated people with ABPA receiving omalizumab, a biologic that targets IgE. The researchers looked for clinical characteristics and blood biomarkers associated with failure to respond to omalizumab and explored whether these might help identify people who could benefit from switching to mepolizumab, which targets IL-5 and therefore a different part of the allergic inflammatory pathway.
Why does this matter?
ABPA does not appear to be driven by exactly the same inflammatory mechanisms in every patient.
Omalizumab has the greatest accumulated experience among biologics used for ABPA, but some patients do not respond adequately. Mepolizumab, benralizumab, dupilumab and tezepelumab have also been used, particularly in treatment-dependent disease.
If biomarkers can eventually identify which inflammatory pathway is dominant in an individual patient, they could help clinicians choose the most appropriate biologic rather than relying largely on trial and response.
This study therefore points towards a more personalised approach to biologic treatment of ABPA.
There is an important limitation: this is a retrospective study currently published as a preprint, so its findings have not yet undergone full peer review and should be regarded as preliminary.
Read the preprint:
Wang H, Chen Y, Jing X, Zhang Y, Huang K. Predictors of Omalizumab non-response in ABPA and exploratory biomarkers for switching to mepolizumab: A retrospective cohort study. Research Square. 2026.
https://doi.org/10.21203/rs.3.rs-10727692/v1
Cochrane begins major review of antifungal treatment for fungal-associated asthma
A new Cochrane publication will examine an important and long-running question: do systemic azole antifungals improve outcomes when added to standard treatment for people with asthma and evidence of fungal sensitisation?
The planned review will include people with conditions such as severe asthma with fungal sensitisation (SAFS) and allergic bronchopulmonary aspergillosis/allergic bronchopulmonary mycosis (ABPA/ABPM).
Previous studies have produced mixed results. Some studies of itraconazole have reported improvements in people with severe asthma and fungal sensitisation, while trials of other azoles have not consistently demonstrated benefit.
Why does this matter?
Fungal sensitisation is relatively common in difficult asthma, but sensitisation does not necessarily mean that fungal growth in the airways is contributing sufficiently to disease to make antifungal treatment worthwhile.
Azoles can also cause side effects and have important interactions with other medicines, so identifying the patients most likely to benefit is important.
Cochrane reviews systematically assess all eligible clinical trials using predefined methods and are influential in evidence-based medicine and clinical guidelines.
Importantly, the publication this week is the protocol for the review, not the completed review. It therefore contains no new conclusion about whether azoles are effective. Instead, it shows that this question is now being subjected to a formal systematic assessment.
We will watch for the completed review.
Read the Cochrane protocol:
Fukuda Y, Homma T, Miyamoto Y, Watanabe N. Systemic azoles for asthma with fungal sensitisation. Cochrane Database of Systematic Reviews. 2026;9:CD016394.
https://doi.org/10.1002/14651858.CD016394
Research to watch: understanding azole resistance
Laboratory research continues to reveal that the way azole antifungals affect Aspergillus fumigatus is more complicated than simply blocking production of ergosterol, an essential component of the fungal cell membrane.
Particular attention is being paid to Hmg1, an enzyme involved in the pathway used by the fungus to manufacture ergosterol. Mutations affecting the sterol-sensing region of Hmg1 have previously been identified in azole-resistant clinical isolates of A. fumigatus.
Previous research has shown that azole exposure triggers a feedback system involving Hmg1 and another regulatory protein, InsA. Disruption of this system can reduce susceptibility to azole antifungals.
New preprint research published this week investigates Hmg1 regulation under triazole stress further.
This is basic laboratory research rather than something that changes treatment today, but understanding these additional resistance mechanisms may eventually help researchers develop better antifungal drugs and improve detection of azole resistance.
Because the new work is currently available only as a preprint, its findings should be regarded as preliminary.
Background research:
Rybak JM, Xie J, Martín-Vicente A, et al. A secondary mechanism of action for triazole antifungals in Aspergillus fumigatus mediated by hmg1. Nature Communications. 2024;15.
https://doi.org/10.1038/s41467-024-48029-2
What have we learned this week?
The strongest clinical evidence this week comes from the large cystic-fibrosis study. It provides useful real-world evidence that adding antifungal treatment to corticosteroids does not necessarily produce better outcomes for every person with ABPA.
At the same time, emerging work on biologics illustrates how ABPA treatment may increasingly move in the opposite direction to a “one treatment fits all” approach — towards identifying the particular inflammatory mechanisms operating in an individual patient.
Finally, the new Cochrane protocol highlights an important unresolved question: exactly which patients with fungal-associated asthma benefit from antifungal treatment?
Together, these studies reinforce a recurring theme in aspergillosis research: the presence of Aspergillus, fungal sensitisation and allergic inflammation are related, but they are not interchangeable — and treatment increasingly needs to reflect those differences.
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