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Asthma is a chronic condition that usually develops after environmental exposures in genetically predisposed individuals.1 It is considered an inflammatory disease leading to airway structural changes (remodelling), both of these processes being involved in the development of airway hyper-responsiveness (AHR) and variable airway obstruction.2 When inflammation and remodelling increase to a sufficient degree, symptomatic asthma occurs.3
Although asthma has been recognised for a very long time as a heterogeneous condition, recent efforts have been devoted to better characterising its various phenotypes.4 The term ‘phenotype’ refers to ‘a set of observable characteristics of an individual or group resulting from the interaction of its genotype with its environment’. Although these phenotypes may overlap or possibly vary over time, their characterisation may help to identify the predominant mechanisms involved and specific patterns of clinical presentation, predict clinical outcomes and may guide treatment. There is still, however, a lack of data in this field.
Various classification systems have been proposed for asthma phenotypes.4 Currently, these phenotypes are usually defined according to their inducers, physiological characteristics, clinical features or—particularly since the development of non-invasive measures of airway inflammation—by their inflammatory characteristics.5–7 The main categories of airway inflammatory phenotypes identified in subjects with asthma are the eosinophilic and non-eosinophilic types, with the latter including neutrophilic and paucigranulocytopenic subtypes. A mixed form also exists in which both eosinophils and neutrophils are increased. These inflammatory phenotypes can be observed in children as well as in adults.8 9
A frequently encountered phenotype of asthma is the eosinophilic type. It is associated with allergic or occupational asthma, steroid withdrawal, aspirin intolerance/nasal polyps and a subset of severe asthma.6 10–12 An increase in airway neutrophils has been observed in subgroups of individuals with occupational or severe asthma,11 13 14 smokers,15 16 …
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Linked articles 126722.
Competing interests None.
Provenance and peer review Commissioned; not externally peer reviewed.