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Ventilation heterogeneity in asthma could be due to many reasons. Luminal obstruction due to inflammatory cells or mucus, smooth muscle constriction and airway wall thickness could all contribute individually or collectively to ventilation heterogeneity. Interleukin-4 and interleukin-13, acting through the common interleukin-4 receptor, have the potential to modulate all of these features of asthma.1 Inhaled hyperpolarised gas MRI provides a way to regionally visualise and quantify the functional consequence of these features.2 Dupilumab is a fully human monoclonal antibody directed against the alpha-subunit of the interleukin-4 receptor.3 Here, we report a severe asthmatic who showed significant improvement and normalisation of MRI ventilation heterogeneity and associated clinical and physiological variables with dupilumab treatment, suggesting that dupilumab modulated various aspects of luminal airway obstruction.
A 39-year-old atopic woman (total serum immunoglobulin E 1009 kU/L and peripheral blood eosinophils 1200 cells/µL) was seen for asthma in January 2015. She had mixed obstructive and non-obstructive spirometry (forced expiratory volume in one second (FEV1) 1.42 L (44%pred), forced vital capacity (FVC) 1.72 L (44%pred) and total lung capacity (TLC) 3.78 L (71%pred)), with 13% reversibility to salbutamol. Her asthma …
Contributors SS and PN were responsible for the study design and conceived the idea for the case report. SS and RLE were responsible for MRI data collection, analysis and interpretation. EAH was responsible for reviewing CT data sets to generate the CT mucus score and the interpretation of CT data. GP was responsible for MRI acquisition, analysis and interpretation as well as the guarantor of the integrity of the imaging data. PN was responsible for identifying and characterising the patient, clinical interpretation of the data as well as the guarantor of the integrity of the clinical data. SS prepared the first and all revised drafts of the case report. All the authors edited and reviewed the case report and approved the final version.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests PN reports grants from AZ, Novartis, Teva and Sanofi; personal fees from Roche, Teva, Novartis and Knopp; and grants and personal fees from GSK, outside the submitted work.
Patient consent for publication Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.
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