Asthma, atopy and airway inflammation in obese children.

The concurrent increased prevalence of asthma and obesity in adults as well in children has led investigators to consider a possible correlation between the 2 conditions. However, mechanisms underlying this association have not been completely explained.1 A recent study of a large population-based cohort assessed at age 32 years showed that adiposity is associated with asthma and airflow obstruction in women but not in men.2 The authors also demonstrated the absence of a significant association between body fat and airway inflammation in both sexes. Results suggested that being overweight or obese might cause asthma symptoms and airflow limitation in women. Nevertheless, this was not likely originated by an increase in airway inflammation. These findings encouraged us to develop a pilot study aimed at exploring the association among adiposity and asthma symptoms, lung function, atopy, and airway inflammation, as indicated by exhaled nitric oxide (eNO) levels in a group of obese children. Patients were recruited from those attending the Obesity Unit, Department of Pediatrics, Federico II University, Naples, Italy. The patients consisted of 50 children with a body mass index (BMI) >95th percentile for age and sex reference values [28 males; median age, 12.2 years (range, 8-16.8); 34 showing signs of initial or advanced pubertal stage]. A questionnaire was administered to patients and their families to obtain information about any physiciandiagnosed respiratory disease. Atopy was defined as a positive response to 1 or more aeroallergens during skin prick testing. Median FEV1 (% predicted), and percent change in FEV1 after albuterol were obtained. We measured eNO by the single-breath on-line method (NIOX, Aerocrine, Sweden). Patients had not had asthma or rhinitis symptoms or signs, nor did they take inhaled or nasal steroids in the 4 weeks prior to the study. No patient was an active smoker. We also measured eNO levels in 50 age- and sex-matched healthy nonatopic controls. The BMI z score was computed in both obese and healthy children. Because eNO distribution was skewed, analyses were performed with log-transformed data. Comparisons were made using the Student t test. A stepwise regression analysis evaluated the contribution to eNO of all subjectspecific variables in obese children, including age, sex, BMI, BMI z score, FEV1, atopy, and asthma. The level of significance was determined asP<.05. The Institutional Review Board approved the study, and informed consent was obtained from the parent or legal guardian of each child. In obese children, median BMI and BMI z scores were 34.5 kg/m2 (range, 23-54.7) and 2.51 (range, 1.81-4.08), respectively. Fifty-four percent and 42% of the cases were classified as severely or moderately obese because they had a BMI z score 2.5 or 2, respectively.3 Eighteen (36%) and 11 (22%) children had previously received a diagnosis of asthma or seasonal rhinitis, respectively. Among subjects with asthma, 6 (12% of the whole population) had current asthma defined as physician-diagnosed asthma in the previous year. Skin prick test results were positive in 29 cases (58%). Thirteen atopic children had asthma. In all obese children, median FEV1 and percent change in FEV1 after albuterol were 114% predicted (range, 81-168) and 4% (range, 28.8-13.1), respectively. In healthy controls, median BMI and BMI z scores were 18.9 kg/m2 (range, 14.6-24.6) and 0.46 (21.58-1.61), respectively. In obese children, eNO geometric mean (95% CI) was 12.5 ppb (10.4-15.1) and did not appear significantly different from eNO levels of healthy controls [10.8 ppb (9.6-12.2); P 5 .2; 95% CI of the difference, 20.03-0.2]. No significant difference in eNO was found in obese children with a BMI z score <2.5 or 2.5 [12.8 ppb (9.4- 17.3) vs 12.3 ppb (9.7-15.8); P 5 .8; 95% CI of the difference, 0.7-1.5]. In obese children,eNOwas not significantly different between boys and girls [13 ppb (10.2-16.7) vs 11.9 ppb (8.8-16.2); P 5 .6; 95% CI of the difference, 0.7-1.6], between asthmatics and nonasthmatics [11.6 ppb (7.8-17.2) vs 13.1 ppb (10.7-16.1); P 5 .5; 95% CI of the difference, 0.6-1.3], and between atopic and nonatopic subjects [12.3 ppb (9.6-15.9) vs 12.8 ppb (9.5-17.3); P5.8;95%CI of the difference, 0.7-1.4], respectively (Fig 1). In the 13 children with atopic asthma, eNO was not significantly different from the remaining 37 subjects [14.8 ppb (9.3-23.5) vs 11.8 (9.7-14.5);P5.3;95%CI of the difference, 0.8-1.9]. No differences in BMI were found between asthmatics and nonasthmatics [35.2 kg/m2 (range, 24.1-42.1) vs 33.2 kg/m2 (range, 23-54.7); P 5 .6; 95% CI of the difference, 24.8-2.6], and between atopic and nonatopic subjects [34.4 kg/m2 (range, 23-54.7) vs 34.9 kg/m2 (range, 25.5-42.3); P5.6; 95% CI of the difference, 22.7-4.8]. The BMI z score was not different between asthmatics and nonasthmatics [2.49 (range, 1.81-2.83) vs 2.52 (range, 2.05-4.08); P 5 .1; 95% CI of the difference, 20.4-0.05] and between atopic and nonatopic patients [2.53 (range, 1.81-4.08) vs 2.5 (range, 2.09-2.95); P 5 .7;95%CI of the difference,20.2-0.2]. In the linear regression model, none of the subject-specific variables (age, sex, BMI, BMI z score, FEV1, atopy, and asthma) showed a significant association with eNO (P > .05)