It is well known that corticosteroids improve asthma in a subgroup of patients and that this responder subgroup is invariably large enough to drive statistically significant differences in asthma outcomes when steroids are compared to placebo in unselected patients. The consistency of clinical trial data showing benefit from corticosteroids, especially in less severe patients, is the reason why asthma treatment guidelines consistently advocate their daily use in all but the mildest forms of asthma. Guidelines also typically advocate an empiric approach to corticosteroid dosing in which the dose of corticosteroid is increased as disease severity worsens. Such empiric approaches to treatment are now considered flawed and the emphasis is switching to development of treatment approaches that are guided by mechanism-based molecular endotypes rather than trait-based clinical phenotypes. The reason is simple: asthma traits such as symptoms and airflow limitation result from heterogeneous molecular mechanisms, and a one-size-fits all treatment paradigm to treat these traits does not make sense. Prescribing corticosteroids for asthma based on mechanism-based endotypes rather than trait-based phenotypes
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Dunican et al. (2017) studied this question.
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