319 Bronchial Hyperresponsiveness in Obese Adolescents

considerably associated with BA severity (R 1⁄4 0.4) and IgE-autoreactivity only in obese asthmatics (R 1⁄4 0.58; P 1⁄4 0.01), which showed raised IgEautoAbs to keratin (11.6 6 2 IU/mL) and collagen III (1.03 6 0.3 IU/mL) in comparison with preobese (6.7 6 1.5 IU/mL, 0.3 6 0.01 IU/mL) and nonobese patients. The levels of total IgE in all groups showed no association with BMI and serum leptine concentration. Leptine level correlated with CRP (R 1⁄4 0.59) and BMI (R 1⁄4 0.4) and appeared to be overproduced in obese (57 6 7.1 ng/mL) via non-obese (23 6 6 ng/mL) asthmatics, as compared with AR patients and healthy subjects independently from BMI (6.1 6 0.3 ng/mL) and therefore was associated with BA but not atopy in overweight patients. Conclusions: In obese patients with atopy the adipose mass represents an important source of inflammatory cytokines whereas it’s mediators, such as leptine appears to impact especially in pathogenesis of BA in comparison with AR. Obesity is attended with higher generation of autoIgE-Abs, which elevated levels can indicate the disturbance of normal immune regulation. So asthmatics with higher BMI, show a special phenotype of disease which needs to be managed and treated distinctly.