Comprehensive Characterization of Difficult-to-Treat Asthma Reveals Near Absence of T2-Low Status
Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved..
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 a real-world understanding of this T2 paradigm in difficult-to-treat and severe asthma remains limited.
OBJECTIVES: To identify the prevalence of T2-high status in difficult-to-treat asthma patients using a multicomponent definition and compare clinical and pathophysiologic characteristics between patients classified as T2-high and T2-low.
METHODS: We evaluated 388 biologic-naive patients from the Wessex Asthma Cohort of difficult asthma (WATCH) study in the United Kingdom. Type 2-high asthma was defined as 20 parts per billion or greater FeNO , 150 cells/μL or greater peripheral blood eosinophils, the need for maintenance oral corticosteroids, and/or clinically allergy-driven asthma.
RESULTS: This multicomponent assessment identified T2-high asthma in 93% of patients (360 of 388). 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 with T2-low patients (FEV1/FVC 65.9% vs 74.6%). Moreover, 75% of patients defined as having T2-low asthma had raised peripheral blood eosinophils within the preceding 10 years, which left only seven patients (1.8%) who had never had T2 signals. Incorporation of sputum eosinophilia 2% or greater into the multicomponent definition in a subset of 117 patients with induced sputum data similarly found that 96% (112 of 117) met criteria for T2-high asthma, 50% of whom (56 of 112) had sputum eosinophils 2% or greater.
CONCLUSIONS: Almost all patients with difficult-to-treat asthma have T2-high disease; less than 2% of patients never display T2-defining criteria. This highlights a need to assess T2 status comprehensively in clinical practice before labeling a patient with difficult-to-treat asthma as T2-low.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2023 |
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| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:11 |
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| Enthalten in: |
The journal of allergy and clinical immunology. In practice - 11(2023), 9 vom: 01. Sept., Seite 2812-2821.e4 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Rupani, Hitasha [VerfasserIn] |
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| Links: |
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| Themen: |
Adrenal Cortex Hormones |
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| Anmerkungen: |
Date Completed 11.09.2023 Date Revised 20.03.2024 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.jaip.2023.05.028 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM357479459 |
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| 245 | 1 | 0 | |a Comprehensive Characterization of Difficult-to-Treat Asthma Reveals Near Absence of T2-Low Status |
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| 500 | |a Date Revised 20.03.2024 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved. | ||
| 520 | |a 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 a real-world understanding of this T2 paradigm in difficult-to-treat and severe asthma remains limited | ||
| 520 | |a OBJECTIVES: To identify the prevalence of T2-high status in difficult-to-treat asthma patients using a multicomponent definition and compare clinical and pathophysiologic characteristics between patients classified as T2-high and T2-low | ||
| 520 | |a METHODS: We evaluated 388 biologic-naive patients from the Wessex Asthma Cohort of difficult asthma (WATCH) study in the United Kingdom. Type 2-high asthma was defined as 20 parts per billion or greater FeNO , 150 cells/μL or greater peripheral blood eosinophils, the need for maintenance oral corticosteroids, and/or clinically allergy-driven asthma | ||
| 520 | |a RESULTS: This multicomponent assessment identified T2-high asthma in 93% of patients (360 of 388). 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 with T2-low patients (FEV1/FVC 65.9% vs 74.6%). Moreover, 75% of patients defined as having T2-low asthma had raised peripheral blood eosinophils within the preceding 10 years, which left only seven patients (1.8%) who had never had T2 signals. Incorporation of sputum eosinophilia 2% or greater into the multicomponent definition in a subset of 117 patients with induced sputum data similarly found that 96% (112 of 117) met criteria for T2-high asthma, 50% of whom (56 of 112) had sputum eosinophils 2% or greater | ||
| 520 | |a CONCLUSIONS: Almost all patients with difficult-to-treat asthma have T2-high disease; less than 2% of patients never display T2-defining criteria. This highlights a need to assess T2 status comprehensively in clinical practice before labeling a patient with difficult-to-treat asthma as T2-low | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Difficult-to-treat asthma | |
| 650 | 4 | |a Eosinophils | |
| 650 | 4 | |a Phenotypes | |
| 650 | 4 | |a T2 inflammation | |
| 650 | 4 | |a T2-low asthma | |
| 650 | 7 | |a Adrenal Cortex Hormones |2 NLM | |
| 700 | 1 | |a Kyyaly, Mohammed Aref |e verfasserin |4 aut | |
| 700 | 1 | |a Azim, Adnan |e verfasserin |4 aut | |
| 700 | 1 | |a Abadalkareen, Rana |e verfasserin |4 aut | |
| 700 | 1 | |a Freeman, Anna |e verfasserin |4 aut | |
| 700 | 1 | |a Dennison, Paddy |e verfasserin |4 aut | |
| 700 | 1 | |a Howarth, Peter |e verfasserin |4 aut | |
| 700 | 1 | |a Djukanovic, Ratko |e verfasserin |4 aut | |
| 700 | 1 | |a Vijayanand, Pandurangan |e verfasserin |4 aut | |
| 700 | 1 | |a Seumois, Gregory |e verfasserin |4 aut | |
| 700 | 1 | |a Arshad, S Hasan |e verfasserin |4 aut | |
| 700 | 1 | |a Haitchi, Hans Michael |e verfasserin |4 aut | |
| 700 | 1 | |a Kurukulaaratchy, Ramesh J |e verfasserin |4 aut | |
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