The reciprocal influences of asthma and obesity on lung function testing, ahr, and airway inflammation in prepubertal children

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Abstract

Although asthma and obesity are among the major chronic disorders their reciprocal or independent influences on lung function testing, airways hyperresponsiveness (AHR) and bronchial inflammation has not been completely elucidated.

In 118 pre-pubertal Caucasian children anthropometric measurements functional respiratory parameters (flow/volume curves at baseline and after 6-minute walk test [6MWT]) together with bronchial inflammatory index (FeNO) were assessed. The study population was divided into four groups according to BMI and the presence or absence of asthma: Obese asthmatic (ObA) Normal-weight asthmatic (NwA), Obese non-asthmatic (Ob), non-asthmatic normal-weight children (Nw).

Baseline PEF and MEF75 (%-expected) were significantly different across the four groups with significantly lower values of MEF75 in ObA and Ob children when compared to Nw children (P = 0.004 and P = 0.0001, respectively) and this independent role of obesity on upper respiratory flows was confirmed by multiple analysis of covariance.

After 6 MWT respiratory parameters decreased only in ObA and NwA children and 12 children presented a positive fall in FEV1, in contrast no changes of respiratory function testing were detected in Ob and Nw children, and only 2 Ob children presented a significant fall in FEV1.

FeNO analysis demonstrated significantly higher values in ObA and NwA children when compared to Ob (P = 0.008 and P = 0.0002, respectively) and Nw children (P = 0.0001 and P = 0.0003, respectively), although a significant difference was found between Ob and Nw children (P = 0.0004). Multiple analysis of covariance confirmed an independent role of asthma on this parameter.

In conclusion while AHR and airway inflammation are clearly associated with an asthmatic status, obesity seems to induce reduction of upper airways flows associated with a certain degree of pro-inflammatory changes. Pediatr Pulmonol. 2010;45:1103–1110. © 2010 Wiley-Liss, Inc.

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