Abstract
BackgroundThe 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).MethodsWe 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.ResultsBefore 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.ConclusionsWeight 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.
Highlights
The concurrence of obesity and bronchial asthma has become an increasing worldwide major public health problem [1, 2]
Weight loss induced by Bariatric surgery (BS) was the key independent factor associated to airway hyperresponsiveness (AHR) improvement
AHR to mannitol is highly prevalent in obesity, and it is largely abolished by BS
Summary
The concurrence of obesity and bronchial asthma has become an increasing worldwide major public health problem [1, 2]. The mechanisms of the relationship between obesity, AHR, and asthma are not sufficiently established [4, 5], and the impact of its underlying low-grade chronic systemic inflammation on AHR remains unsettled [6]. Bariatric surgery (BS) is the most efficacious therapeutic strategy to achieve major and sustained weight loss in morbidly obese subjects [11] and is associated with improved systemic inflammation [12]. There have been very few studies in obese subjects, mostly in asthmatics, to assess AHR using methacholine [13] before and after effective weight loss with discrepant results [14,15,16,17]. The relationship between airway hyperresponsiveness (AHR) and obesity, a low-grade systemic inflammatory condition, remains largely unknown.
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