[Bronchial asthma in obesity--a distinct phenotype of asthma?]

Abstract

Asthma and obesity have a considerable impact on public health and their prevalence has increased in recent years. Numerous large cross-sectional and prospective studies performed in adults, adolescents, and children throughout the world supports the hypothesis that obesity is an independent risk factor for asthma. The pathogenetic basis for asthma and obesity associations in humans is not well established. Obesity is capable of reducing pulmonary compliance, lung volumes, and the diameter of peripheral respiratory airways, and may influence on airway hyperresponsiveness. The increase of adipose tissue in obese subjects leads to a systemic inflammatory state, which produces a rise in the serum concentrations of several pro-inflammatory cytokines, chemokines and adipokines. The proinflammatory adipokines (leptin, resistin) and antiinflammatory (adiponectin) may be causally associated with asthma, however human studies are inconclusive. Obese asthma patients very often demonstrate increased asthma severity and relative corticosteroid resistance. Some studies suggest improvements in the disease with weight loss in obese asthma patients. Recently published data suggest that obese asthma patients may represent a distinct phenotype of asthma.