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Allergic fungal airways disease (AFAD): an under-recognised asthma endotype

期刊

MYCOPATHOLOGIA
卷 186, 期 5, 页码 609-622

出版社

SPRINGER
DOI: 10.1007/s11046-021-00562-0

关键词

ABPA; SAFS; AFAD; Thermotolerant fungi; Fungal sensitisation

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资金

  1. NIHR Leicester Biomedical Research Centre
  2. Midlands Asthma and Allergy Research Association (MAARA)
  3. Academy of Medical Sciences
  4. Wellcome Trust
  5. Government Department of Business, Energy and Industrial Strategy
  6. British Heart Foundation [SBF003\1125]

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Allergic fungal airways disease is defined based on IgE sensitisation to thermotolerant fungi and evidence of fungal-related lung damage. Treatment should focus on fungi capable of growing in the airways and causing chronic allergenic stimuli. Patients with sensitisation to these fungi are at risk for progressive lung damage and should be monitored closely.
The term allergic fungal airways disease has a liberal definition based on IgE sensitisation to thermotolerant fungi and evidence of fungal-related lung damage. It arose from a body of work looking into the role of fungi in asthma. Historically fungi were considered a rare complication of asthma, exemplified by allergic bronchopulmonary aspergillosis; however, there is a significant proportion of individuals with Aspergillus fumigatus sensitisation who do not meet these criteria, who are at high risk for the development of lung damage. The fungi that play a role in asthma can be divided into two groups; those that can grow at body temperature referred to as thermotolerant, which are capable of both infection and allergy, and those that cannot but can still act as allergens in IgE sensitised individuals. Sensitisation to thermotolerant filamentous fungi (Aspergillus and Penicillium), and not non-thermotolerant fungi (Alternaria and Cladosporium) is associated with lower lung function and radiological abnormalities (bronchiectasis, tree-in-bud, fleeting shadows, collapse/consolidation and fibrosis). For antifungals to play a role in treatment, the focus should be on fungi capable of growing in the airways thereby causing a persistent chronic allergenic stimulus and releasing tissue damaging proteases and other enzymes which may disrupt the airway epithelial barrier and cause mucosal damage and airway remodelling. All patients with IgE sensitisation to thermotolerant fungi in the context of asthma and other airway disease are at risk of progressive lung damage, and as such should be monitored closely.

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