Focus: chronic aspergillosis, allergic Aspergillus disease, and long-term lung damage
This week’s papers are especially relevant to people living with Allergic Bronchopulmonary Aspergillosis (ABPA), allergic bronchopulmonary mycosis, and Chronic Pulmonary Aspergillosis (CPA). The strongest themes are the potential value of Immunoglobulin E (IgE) as a marker of future lung decline, the growing role of biologic therapies in steroid-sparing care, and improved tools for diagnosing CPA in people with previous tuberculosis.
Acute invasive aspergillosis papers are included lower down for context, but this update prioritises chronic and longer-term disease.
Chronic and allergic Aspergillus disease
High total serum IgE level at diagnosis was associated with a progressive decline in lung function in asthmatic patients with allergic bronchopulmonary mycosis
Kodama Y, Takaoka S, Nakashima T, Matsunaga K, Terada K, Yamashita Y, Masumitsu H, Miyasaka A, Muraoka T, Masumoto N, Kaneko T, Watanabe M, Tsurikisawa N.
Allergy Asthma Clin Immunol. 2026 Mar 8. doi: 10.1186/s13223-026-01024-2.
PMID: https://pubmed.ncbi.nlm.nih.gov/41796390/
Why this matters
This is one of the most important chronic-disease papers in this batch. It suggests that very high total IgE at diagnosis may not just reflect current disease activity, but may also predict future lung damage.
Key points
Patients with allergic bronchopulmonary mycosis (ABPM), including many with Allergic Bronchopulmonary Aspergillosis (ABPA), who had higher IgE levels at diagnosis showed a more progressive decline in lung function over time.
This raises the possibility that baseline IgE could help identify patients at higher risk of long-term airway damage.
It supports the idea that some patients may need closer monitoring and earlier treatment escalation rather than waiting for repeated flare-ups.
Relevance
For patients and clinicians, this paper reinforces that IgE is not just a number to follow during treatment. A very high starting IgE may signal the need for more careful long-term planning, especially in people with asthma, mucus plugging, recurrent exacerbations or bronchiectasis.
Biologics Use in Eosinophilic Lung Disease: Controversies and Consensus
Pérez de Llano L, Rivas DD, Pavord I, Aslam MMS, Lugogo N.
J Allergy Clin Immunol Pract. 2026 Mar;14(3):583-596.e12. doi: 10.1016/j.jaip.2026.01.022.
PMID: https://pubmed.ncbi.nlm.nih.gov/41786384/
Why this matters
This review is highly relevant to current ABPA care because biologics are increasingly being used to reduce reliance on oral corticosteroids, especially in people with severe asthma and recurrent eosinophilic inflammation.
Key points
The review discusses biologics including omalizumab, mepolizumab, benralizumab, dupilumab and tezepelumab.
It highlights growing evidence that biologics may help some patients with ABPA by reducing steroid burden, improving asthma control and lowering exacerbation frequency.
The authors also stress that evidence in ABPA is still developing and remains less robust than in severe eosinophilic asthma.
Relevance
This is a useful overview of where the field is heading. For many patients with ABPA, the major clinical problem is not only fungal sensitisation but the long-term harm caused by repeated steroid courses. Biologics are becoming an increasingly important part of steroid-sparing strategy, though patient selection remains crucial.
Differential Diagnosis of Eosinophilic Lung Diseases
Emmi G, Bass J, Baratella E, Akuthota P, Loscocco GG.
J Allergy Clin Immunol Pract. 2026 Mar;14(3):542-557. doi: 10.1016/j.jaip.2026.01.027.
PMID: https://pubmed.ncbi.nlm.nih.gov/41786383/
Why this matters
ABPA is still often missed, mislabelled or diagnosed late. This review is useful because it places ABPA in the wider context of eosinophilic lung disease, where several conditions can look similar.
Key points
The paper compares ABPA with other eosinophilic lung diseases such as chronic eosinophilic pneumonia, eosinophilic granulomatosis with polyangiitis, and drug-related eosinophilic lung disease.
It emphasises the importance of combining history, imaging, blood eosinophils, total IgE, fungal sensitisation and radiology.
The review underlines how easily overlap can occur, especially in people with severe asthma.
Relevance
For patients, this matters because getting the diagnosis right affects treatment. Not every eosinophilic lung disease is ABPA, and not every worsening in an asthma patient with high eosinophils is due to fungus. For clinicians, it is a helpful reminder to keep a broad differential diagnosis.
Chronic Pulmonary Aspergillosis
Performance of the LDBio Aspergillus ICT lateral flow assay and western blot for diagnosing chronic pulmonary aspergillosis in post-tuberculosis patients: a prospective study from South India
Samaddar A, Pramanik P, Voleti H, Akshata JS, Nagarathna S, Thennarasu K, Nagraja C.
Microbiol Spectr. 2026 Mar 6:e0384725. doi: 10.1128/spectrum.03847-25.
PMID: https://pubmed.ncbi.nlm.nih.gov/41789940/
Why this matters
This is the key CPA paper in this week’s list. It focuses on a major real-world problem: how to diagnose CPA more effectively in people left with lung damage after tuberculosis.
Key points
The study found that the LDBio Aspergillus immunochromatographic test (ICT) performed well in diagnosing CPA in post-tuberculosis patients.
Western blot also performed strongly, and combining the tests improved diagnostic confidence.
The results support the use of simpler, more accessible serology in settings where advanced imaging or specialist fungal laboratories may be limited.
Relevance
CPA after tuberculosis remains underdiagnosed worldwide. This paper is especially important because it supports the use of practical, lower-complexity diagnostics that may help identify patients earlier. That has implications far beyond India, particularly in regions where post-tuberculosis lung disease is common.
Host susceptibility and chronic disease risk
Oncostatin M receptor deficiency as a novel candidate genetic cause of autosomal recessive hyper-IgE syndrome
Andersen S, Assing K, Jensen J, Rasmussen LD, Laursen CB, Dellgren CD, Hinke DM, Degn SE, Mogensen TH.
J Hum Immun. 2026 Mar 3;2(3):e20250119. doi: 10.70962/jhi.20250119.
PMID: https://pubmed.ncbi.nlm.nih.gov/41783139/
Why this matters
Some patients develop chronic or severe Aspergillus disease because of an underlying immune problem that may not be obvious at first. This paper adds a possible new genetic explanation.
Key points
The authors describe a patient with very high IgE, eczema, bone fractures and Chronic Pulmonary Aspergillosis (CPA).
They identified a rare variant in the oncostatin M receptor (OSMR) gene.
The paper proposes OSMR deficiency as a possible new cause of autosomal recessive hyper-IgE syndrome.
Relevance
Although rare, studies like this help explain why a small number of people develop unusual susceptibility to chronic fungal disease. Over time, this kind of work may improve genetic diagnosis, immune work-up and personalised management in patients with recurrent or unexplained Aspergillus disease.
Important diagnostic lesson
Peripheral T-cell lymphoma-NOS presenting with cavitary lung lesions mimicking invasive aspergillosis
Lopez Ventosa J, Rodriguez A, Garcia N, Tirado M, Nieves Rivera J.
BMJ Case Rep. 2026 Mar 4;19(3):e268805. doi: 10.1136/bcr-2025-268805.
PMID: https://pubmed.ncbi.nlm.nih.gov/41781006/
Why this matters
Although this is not a chronic aspergillosis paper, it is worth noting because it highlights a key problem in lung medicine: cavities and positive biomarkers do not always equal Aspergillus infection.
Key points
A patient with cavitary lung lesions and a positive serum galactomannan was initially treated for presumed aspergillosis.
Tissue biopsy did not support fungal infection.
The final diagnosis was peripheral T-cell lymphoma.
Relevance
This is a valuable reminder that malignancy, tuberculosis and other diseases can mimic CPA or invasive aspergillosis, and that tissue diagnosis remains important when the picture does not fit cleanly.
Acute invasive aspergillosis: important context papers
How to safely discontinue antifungal treatment in invasive pulmonary aspergillosis? – Clinical considerations in haematology
Stemler J, Sprute R, Koehler P, Cornely OA.
Clin Microbiol Infect. 2026 Mar 6:S1198-743X(26)00106-0. doi: 10.1016/j.cmi.2026.03.001.
PMID: https://pubmed.ncbi.nlm.nih.gov/41796963/
25 years of improvement in mortality in invasive aspergillosis in haematology patients: will it be sustained or is it under threat?
Maertens JA, Vanbiervliet Y, Mercier T, Aerts R, Lagrou K, Slavin MA.
J Antimicrob Chemother. 2026 Mar 4;81(4):dkag077. doi: 10.1093/jac/dkag077.
PMID: https://pubmed.ncbi.nlm.nih.gov/41790511/
Invasive aspergillosis in liver transplant recipients in France (2007-21): a nationwide, retrospective, matched case-control study
Le Hyaric C, Melenotte C, Lefebvre F, Saliba F, Botterel F, El-Domiaty N, Dumortier J, Persat F, Do R, Pasquier G, Camus C, Gangneux JP, Kamar N, Iriart X, Monsel A, Fekkar A, Conti F, Vuotto F, Loridant S, Durand F, Bonnal C, Barbaz M, Chesnay A, Vignals C, Lefranc M, Guerin R, Moniot M, Weil D, Bellanger AP, Decaens T, Maubon D, Lebossé F, Artzner T, Morel G, Letscher-Bru V, Herbrecht R, Ader F, Lortholary O, Lefort A, Guichon C, Danion F.
Lancet Microbe. 2026 Mar 2:101272. doi: 10.1016/j.lanmic.2025.101272.
PMID: https://pubmed.ncbi.nlm.nih.gov/41785881/
Treatment Monitoring and Outcome Prediction in Invasive Aspergillosis using Immunologic Markers
Pereira A, Scott J, Sarlea A, Sprute R, Aerts R, Lass-Flörl C, Mikulska M, Sedik S, Garcia-Vidal C, Gangneux JP, Giacobbe DR, Prattes J, Grothe J, Biswas S, Monzo-Gallo P, Bassetti M, Maertens J, Kumar V, Koehler P, Cunha C, Netea MG, Carvalho A, Hoenigl M.
J Infect Dis. 2026 Mar 4:jiag140. doi: 10.1093/infdis/jiag140.
PMID: https://pubmed.ncbi.nlm.nih.gov/41778487/
Latest News posts
News archive