Obesity-associated severe asthma represents a distinct clinical phenotype: analysis of the British Thoracic Society Difficult Asthma Registry Patient cohort according to BMI.
BACKGROUND
Obesity has emerged as a risk factor for the development of asthma and it may also influence asthma control and airway inflammation. However, the role of obesity in severe asthma remains unclear. Thus, our objective was to explore the association between obesity (defied by BMI) and severe asthma.


METHODS
Data from the British Thoracic Society Difficult Asthma Registry were used to compare patient demographics, disease characteristics, and health-care utilization among three BMI categories (normal weight: 18.5-24.99; overweight: 25-29.99; obese: 30) in a well-characterized group of adults with severe asthma.


RESULTS
The study population consisted of 666 patients with severe asthma; the group had a median BMI of 29.8 (interquartile range, 22.5-34.0). The obese group exhibited greater asthma medication requirements in terms of maintenance corticosteroid therapy (48.9% vs 40.4% and 34.5% in the overweight and normal-weight groups, respectively), steroid burst therapy, and short-acting b 2 -agonist use per day. Significant differences were seen with gastroesophageal reflux disease (53.9% vs 48.1% and 39.7% in the overweight and normal weight groups, respectively) and proton pump inhibitor use. Bone density scores were higher in the obese group, while pulmonary function testing revealed a reduced FVC and elevated carbon monoxide transfer coefficient. Serum IgE levels decreased with increasing BMI and the obese group was more likely to report eczema, but less likely to have a history of nasal polyps.


CONCLUSIONS
Patients with severe asthma display particular characteristics according to BMI that support the view that obesity-associated severe asthma may represent a distinct clinical phenotype.
Royal Brompton Hospital, London, England; Airway Disease Section, Respiratory Division, National Heart & Lung Institute, Imperial College, London, England.
David
D
Gibeon
Department of Computing, Imperial College, London, England.
Kannangara
K
Batuwita
Department of Computing, Imperial College, London, England.
Michelle
M
Osmond
Centre for Infection and Immunity, Queen's University of Belfast, Belfast, Northern Ireland.
Liam G
LG
Heaney
University of Leicester, Leicester, England.
Chris E
CE
Brightling
The University of Manchester and University Hospital of South Manchester, Manchester, England.
Rob
R
Niven
Birmingham Heartlands Hospital, University of Birmingham, Birmingham, England.
Adel
A
Mansur
Gartnavel General Hospital, University of Glasgow, Glasgow, Scotland.
Rekha
R
Chaudhuri
Glasgow Royal Infirmary, Glasgow, Scotland.
Christine E
CE
Bucknall
Department of Computing, Imperial College, London, England.
Anthony
A
Rowe
Department of Computing, Imperial College, London, England.
Yike
Y
Guo
Airway Disease Section, Respiratory Division, National Heart & Lung Institute, Imperial College, London, England.
Pankaj K
PK
Bhavsar
Royal Brompton Hospital, London, England; Airway Disease Section, Respiratory Division, National Heart & Lung Institute, Imperial College, London, England.
Kian Fan
KF
Chung
Royal Brompton Hospital, London, England. Electronic address: a.menzies-gow@rbht.nhs.uk.
Andrew
A
Menzies-Gow
D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D058666:Adrenergic beta-2 Receptor Agonists / Q000627:therapeutic use; D000328:Adult; D001249:Asthma / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology*; D015992:Body Mass Index; D015331:Cohort Studies; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000150:complications*; D010641:Phenotype; D012042:Registries; D012129:Respiratory Function Tests; D012720:Severity of Illness Index; D012955:Societies, Medical; D006113:United Kingdom
D000305:Adrenal Cortex Hormones; D058666:Adrenergic beta-2 Receptor Agonists