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Airway smooth muscle as an underutilised biomarker: a case report

BACKGROUND: Severe asthma and chronic obstructive pulmonary disease (COPD) can be challenging to manage, particularly when the clinical features may be similar. With the increased availability of advanced therapies for both entities, it is more important than ever to diagnose and phenotype accuratel...

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Detalles Bibliográficos
Autores principales: Sha, Joy, Rorke, Steuart, Langton, David
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6348684/
https://www.ncbi.nlm.nih.gov/pubmed/30691439
http://dx.doi.org/10.1186/s12890-019-0789-7
Descripción
Sumario:BACKGROUND: Severe asthma and chronic obstructive pulmonary disease (COPD) can be challenging to manage, particularly when the clinical features may be similar. With the increased availability of advanced therapies for both entities, it is more important than ever to diagnose and phenotype accurately to inform appropriate treatment decisions. This case highlights the use of endobronchial biopsies to allow for histological evaluation of airways disease, and in particular the role of airway smooth muscle mass as an additional biomarker that could facilitate the diagnostic process. CASE PRESENTATION: A 65 year old woman presented with a diagnosis of severe COPD on the background of previous smoking and mild childhood asthma. Despite taking maximal inhaled pharmacotherapy, she had frequent exacerbations requiring corticosteroids and remained dyspnoeic on mild exertion. Lung function tests showed severe obstruction on spirometry (forced expiratory ratio 43%, forced expiratory volume in 1 s 47% predicted), and single breath Diffusing Capacity for Carbon Monoxide was moderately reduced at 45% predicted. Computed tomography revealed hyperinflation without marked emphysema. Quantitative CT for emphysema distribution demonstrated a relatively small lung fraction of 9.35% with <− 950 Hounsfield units. Bronchoscopy with endobronchial biopsy was undertaken to further determine the underlying pathology, and airway mucosa histology was consistent with typical findings of asthma. The patient was treated with bronchial thermoplasty as she did not meet prescribing criteria for monoclonal antibodies. Six months post treatment, she had a significant improvement in symptom control and medication usage, without any exacerbations. CONCLUSIONS: Airway smooth muscle histology is an underutilised biomarker that has a valuable role in phenotyping airways disease in the era of individualised medicine.