Background: Recently, it has been shown that increasing body mass index (BMI) in asthma is associated with reduced exhaled NO. Our objective in this study was to determine if the BMIrelated changes in exhaled NO differ across asthmatics and controls, and to determine if these changes are related to increased airway oxidative stress and systemic levels of leptin and adiponectin.

Asthma and obesity are frequently associated, and obesity has been considered a factor contributing to both an increase in severity of asthma and to its development. The present document summarizes the proceedings of a symposium held in Montreal, Quebec, on November 2, 2006, under the auspices of the Réseau en santé respiratoire du Fonds de la recherche en santé du Québec in collaboration with the McGill University - Strauss Severe Asthma Program, Université Laval (Quebec City) and Université de Montréal. It includes an overview of the various aspects of the relationships between asthma and obesity with regard to animal models; genetic, hormonal and physiological determinants; influence of comorbidities (eg, sleep apnea syndrome); epidemiology; clinical and psychological features; and management of asthma in the obese population.

IntroductionTo understand the mechanisms by which obesity is associated with increased risk for asthma, we determined the association of body mass index (BMI) with airway mechanics and exhaled nitric oxide (NO) with adipocyte-related cytokine levels in subjects with moderate to severe persistent asthma.MethodsWe recruited patients, who were nonsmokers, with moderate to severe asthma during baseline conditions. Blood samples were obtained from all subjects in a fasting state to determine serum levels of inflammatory markers. The Raw (airway resistance) change in response to a DI (deep inhalation) was measured to determine airway hysteresis. Subsequently, we determined the levels of eNO, spirometry, and FRC.ResultsWe recruited 34 African American patients with a mean age of 50 years (range 25-68) of which 79% were female. The mean BMI was 34 (range 21-55). Sixty-eight percent were obese and 32% were overweight. Obese participants had higher mean leptin levels (1.72 mg/mL; 95% CI 0.11-2.33) compared to overweight (0.78 mg/mL; 95% CI 0.24-1.33) participants (p < .05). Obese subjects had nonsignificant lower mean levels of adiponectin (308.44 mg/mL; 95% CI 23-385) compared to overweight (331.58 mg/mL; 95% CI 26-405) subjects (p = .64). The mean post-DI Raw was higher in the obese (16.2 cmH2O/L/sec; 95% CI 13-20) compared to overweight (13.0 cmH2O/L/sec; 95% CI 6-20) subjects (p < .05). The log-transformed values of eNO in the obese (2.62 ppb) were lower when compared to overweight (3.31 ppb) participants (p < .05). We found nonsignificant correlations between leptin and log-eNO (r = 2.17, p = .4), and log-eNO and adiponectin (r = .14, p = .4).ConclusionsIn moderate to severe asthma, BMI was associated with increased leptin levels, increased Raw after a DI, and eNO. Exhaled eNO levels and airway hysteresis were not associated with adipocyte-related cytokines.