• Asthma
• asthma mechanisms
• eosinophil biology
• exhaled airway markers
• neutrophil biology

There are important aspects of the study design that cast doubt on the claim of Cowan et al that ‘modified responses’ to corticosteroids occur in patients with non-eosinophilic asthma.1

First, the population recruited was more likely to include patients who experienced loss of control of their asthma after steroid withdrawal than those who remained stable or improved. This increases the potential for regression to the mean as well as identifying a particularly steroid-responsive population. Secondly, it is not possible to make any firm claims about the efficacy of inhaled corticosteroids in either population as the intervention was not placebo controlled. In the only placebo-controlled trial, Berry et al2 showed no evidence of a response to inhaled corticosteroids in patients with non-eosinophilic asthma.

A more reasonable interpretation of the authors' findings is that there is a much greater response to re-introduction of inhaled corticosteroids in patients classified as eosinophilic compared with non-eosinophilic. This reinforces the view that the presence of sputum eosinophilia is a strong predictor of steroid responsiveness. The apparent relationship between the fraction of exhaled nitric oxide (FE_NO) and improvement in airway responsiveness after re-introduction of inhaled steroids in the non-eosinophilic patients is interesting. One possible explanation is that an increased FE_NO is an early marker of returning eosinophilic airway inflammation. The concept that non-eosinophilic asthma can be subclassified into a group that is non-eosinophilic as a result of treatment and a group where eosinophilic inflammation is not a component of the disease is supported by a recent study investigating the presence of eosinophilic proteins in airway macrophages.3