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Asthma guidelines around the world urge healthcare professionals to use the lowest dose of inhaled corticosteroid (ICS) to achieve asthma control, normally defined as achievement of best lung function, reduction in symptoms and reduction of future exacerbation risk.1 At first glance, this approach seems sensible. Long-term ICS use has appreciable side effects and there is evidence that targeting symptoms with increased ICS doses results in improved outcomes. This approach already forms the backbone of the budesonide/formoterol or beclometasone/formoterol as maintenance and reliever therapy (SMART/FMART), and more recently quadrupling ICS doses during a period of worsening symptoms has been shown to lead to improved outcomes in adults.2
However, life is rarely that simple. One of the main physiological effects of ICS, reduced eosinophilic airway inflammation, is not firmly linked to key asthma parameters namely variable airflow obstruction, airway hyper-responsiveness and symptoms.3 This heterogeneity in asthma mechanisms and a call to redefine how we classify airway disease, is well covered in the recent Lancet Commissions article. In this article, the authors suggest that ICS treatment is not escalated unless biomarkers of type 2 inflammation are increased.4 The two most readily available biomarkers are blood or sputum eosinophil counts and the fraction of nitric oxide in exhaled breath (FeNO).5
With this in mind, Petsky and colleagues6 enter the arena with a systematic review and meta-analysis of tailoring asthma treatment on markers of eosinophilic inflammation. They synthesised the evidence from 3 Cochrane reviews and 22 randomised controlled studies, across a range of patient populations, where asthma treatment was tailored using FeNO or sputum eosinophil counts and outcomes compared with a control population. The main outcome was asthma exacerbations as defined …
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