Journal
OBESITY SURGERY
Volume 25, Issue 9, Pages 1666-1671Publisher
SPRINGER
DOI: 10.1007/s11695-014-1564-8
Keywords
Abdominal obesity; Airway inflammation; Bronchial hyperreactivity; Indirect bronchoconstrictor; Systemic inflammation
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Funding
- Fondo de Investigacion Sanitaria (FIS) [PI080311]
- CIBER Enfermedades Respiratorias
- Generalitat de Catalunya [2009SGR00911]
- Almirall
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The relationship between airway hyperresponsiveness (AHR) and obesity, a low-grade systemic inflammatory condition, remains largely unknown. It is established that AHR to indirect stimuli is associated with active airway inflammation. The objectives were to investigate the rate of AHR to mannitol in obese subjects and its changes 1 year after bariatric surgery (BS). We enrolled 58 candidates to BS severely obese (33 nonsmokers and 25 smokers) without history of asthma and 20 healthy, nonobese participants and related AHR to functional findings and serum and exhaled biomarkers. Before surgery, AHR was observed in 16 (28 %) obese with the provocation doses of mannitol to induce a 15 % fall in FEV1 (PD15) of (geometric mean [95 % CI]) 83 (24-145) mg. Compared to control participants, obese participants had lower spirometric values and higher serum and exhaled biomarkers (p < 0.05 each). After surgery, AHR was abolished (p < 0.01) in all but four obese subjects. Weight loss induced by BS was the key independent factor associated to AHR improvement. AHR to mannitol is highly prevalent in obesity, and it is largely abolished by BS.
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