FENO measurements greater than 47 ppb provide a means of predicting steroid response in patients with undiagnosed respiratory symptoms. Assessing airway inflammation is of more practical value than diagnostic labeling when considering the potential usefulness of inhaled antiinflammatory therapy.
The link between obesity and asthma is unlikely to be explained by enhancement of the "classical" forms of airway inflammation resulting from the systemic inflammatory effects of obesity itself. Other mechanisms, possibly related to innate immunity, may explain the relationship between obesity and asthma.
Genetic variation of the ADRB2 does not influence the immediate response to inhaled beta2-agonist. The confounding effect of tolerance resulting from regular beta2-agonist use must be controlled when assessing the pharmacogenetic influences on clinical outcomes with beta2-agonists.
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