Comprehensive characterisation of difficult-to-treat asthma reveals near absence of T2-low status
Comprehensive characterisation of difficult-to-treat asthma reveals near absence of T2-low status
Background: asthma is conventionally stratified as type 2-inflammation (T2) high or T2-low disease. Identifying T2-status has therapeutic implications for patient management but real-world understanding of this T2 paradigm in difficult-to-treat/ severe asthma remains limited.
Objectives: to identify prevalence of T2-high status in difficult-to-treat asthma patients using a multicomponent definition and compare clinical and pathophysiological characteristics between patients classified as T2-high and T2-low.
Methods: 388 biologic naïve patients from the Wessex Asthma Cohort of difficult asthma (WATCH) study, United Kingdom, were evaluated. T2-high asthma was defined as fractional exhaled nitric oxide (FeNO)≥20ppb and/or peripheral blood eosinophils (PBE) ≥150 cells/ul and/or need for maintenance oral corticosteroids and/or clinically allergy-driven asthma.
Results: this multicomponent assessment identified T2-high asthma in 93% (360/388) of patients. Body Mass Index, inhaled corticosteroid dose, asthma exacerbations and common comorbidities did not differ by T2-status. Significantly worse airflow limitation was found in T2-high compared to T2-low patients (FEV1/FVC 65.9% vs 74.6%). 75% patients defined as T2-low asthma had raised PBE within the preceding 10-years, leaving only 7 patients (1.8%) who never had T2-signals. Incorporation of sputum eosinophilia ≥2% into the multicomponent definition in a subset of 117 patients with induced sputum data similarly found that 96% (112/117) met criteria for T2-high asthma of which 50% (56/112), had sputum eosinophils ≥2%.
Conclusions: amost all patients with difficult-to-treat asthma have T2-high disease with <2% of patients never displaying T2-defining criteria. This highlights a need to comprehensively assess T2 status in clinical practice before labelling a patient with difficult-to-treat asthma as T2-low.
Difficult-to-treat asthma, Eosinophils, Phenotypes, T2 inflammation, T2-low asthma
2812-2821.e4
Rupani, Hitasha
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Kyyaly, Mohammed Aref
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Azim, Adnan
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Freeman, Anna
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Dennison, Paddy
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Howarth, Peter
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Djukanovic, Ratko
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Vijayanand, Pandurangan
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Seumois, Gregory
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Arshad, Syed Hasan
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Haitchi, Hans Michael
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Kurukulaaratchy, Ramesh J.
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Abadalkareem, Rana
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September 2023
Rupani, Hitasha
ed650f59-d273-46e9-ac34-0cd179f494ca
Kyyaly, Mohammed Aref
7bd69b33-fec8-405c-9f40-b7157f0242f0
Azim, Adnan
87c31e0e-c9bf-4258-9ae9-889e2382e7ba
Freeman, Anna
b5f45a0d-f9e4-4a91-9af0-40efb6730787
Dennison, Paddy
837dcc21-e806-4c76-92f6-c5b6c0a8e4d9
Howarth, Peter
ff19c8c4-86b0-4a88-8f76-b3d87f142a21
Djukanovic, Ratko
d9a45ee7-6a80-4d84-a0ed-10962660a98d
Vijayanand, Pandurangan
79514f33-66cf-47cc-a8fa-46bbfc21b7d1
Seumois, Gregory
0be7d3d6-5526-458c-aa5c-cce52410a2ed
Arshad, Syed Hasan
ea51da7d-a0ee-4d31-b443-69b3b929e5eb
Haitchi, Hans Michael
68dadb29-305d-4236-884f-e9c93f4d78fe
Kurukulaaratchy, Ramesh J.
9c7b8105-2892-49f2-8775-54d4961e3e74
Abadalkareem, Rana
10895b08-b25b-4077-8381-86ba37d4523c
Rupani, Hitasha, Kyyaly, Mohammed Aref, Azim, Adnan, Freeman, Anna, Dennison, Paddy, Howarth, Peter, Djukanovic, Ratko, Vijayanand, Pandurangan, Seumois, Gregory, Arshad, Syed Hasan, Haitchi, Hans Michael, Kurukulaaratchy, Ramesh J. and Abadalkareem, Rana
(2023)
Comprehensive characterisation of difficult-to-treat asthma reveals near absence of T2-low status.
Journal of Allergy and Clinical Immunology: In Practice, 11 (9), .
(doi:10.1016/j.jaip.2023.05.028).
Abstract
Background: asthma is conventionally stratified as type 2-inflammation (T2) high or T2-low disease. Identifying T2-status has therapeutic implications for patient management but real-world understanding of this T2 paradigm in difficult-to-treat/ severe asthma remains limited.
Objectives: to identify prevalence of T2-high status in difficult-to-treat asthma patients using a multicomponent definition and compare clinical and pathophysiological characteristics between patients classified as T2-high and T2-low.
Methods: 388 biologic naïve patients from the Wessex Asthma Cohort of difficult asthma (WATCH) study, United Kingdom, were evaluated. T2-high asthma was defined as fractional exhaled nitric oxide (FeNO)≥20ppb and/or peripheral blood eosinophils (PBE) ≥150 cells/ul and/or need for maintenance oral corticosteroids and/or clinically allergy-driven asthma.
Results: this multicomponent assessment identified T2-high asthma in 93% (360/388) of patients. Body Mass Index, inhaled corticosteroid dose, asthma exacerbations and common comorbidities did not differ by T2-status. Significantly worse airflow limitation was found in T2-high compared to T2-low patients (FEV1/FVC 65.9% vs 74.6%). 75% patients defined as T2-low asthma had raised PBE within the preceding 10-years, leaving only 7 patients (1.8%) who never had T2-signals. Incorporation of sputum eosinophilia ≥2% into the multicomponent definition in a subset of 117 patients with induced sputum data similarly found that 96% (112/117) met criteria for T2-high asthma of which 50% (56/112), had sputum eosinophils ≥2%.
Conclusions: amost all patients with difficult-to-treat asthma have T2-high disease with <2% of patients never displaying T2-defining criteria. This highlights a need to comprehensively assess T2 status in clinical practice before labelling a patient with difficult-to-treat asthma as T2-low.
Text
T2 disease manuscript JACI-IP accepted
- Accepted Manuscript
Text
1-s2.0-S2213219823005664-main
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More information
Accepted/In Press date: 17 May 2023
e-pub ahead of print date: 26 May 2023
Published date: September 2023
Additional Information:
Funding Information:
The Wessex Asthma Cohort of difficult asthma (WATCH) study has been supported by the National Institute for Health and Care Research Southampton Biomedical Research Centre and Clinical Research Facility at University Hospital Southampton National Health Service Foundation Trust, United Kingdom. The WATCH study itself is not externally funded. Funding assistance for database support for the WATCH study was initially obtained from a nonpromotional grant from Novartis (£35,000). Funding assistance for sputum assessment was provided within a nonpromotional investigator-led grant from Boehringer-Ingelheim. Funding assistance for patient costs (eg, parking) was initially provided by a charitable grant (£3,500) from the Asthma, Allergy & Inflammation Research Charity.
Publisher Copyright:
© 2023 The Authors
Keywords:
Difficult-to-treat asthma, Eosinophils, Phenotypes, T2 inflammation, T2-low asthma
Identifiers
Local EPrints ID: 477586
URI: http://eprints.soton.ac.uk/id/eprint/477586
ISSN: 2213-2198
PURE UUID: 2c58383b-4617-4db8-8ba3-3795d3e1daab
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Date deposited: 08 Jun 2023 16:56
Last modified: 18 Mar 2024 02:32
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Contributors
Author:
Hitasha Rupani
Author:
Adnan Azim
Author:
Anna Freeman
Author:
Paddy Dennison
Author:
Pandurangan Vijayanand
Author:
Gregory Seumois
Author:
Syed Hasan Arshad
Author:
Rana Abadalkareem
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