Abstract
The objective of this symposium was to provide an overview of Type 2 inflammation in asthma. The speakers covered the pathophysiology of Type 2 asthma, its heterogeneity, the associated economic burden, and methods for recognising Type 2 inflammation in severe asthma patients in clinical practice.
Asthma is a heterogenous disease and multiple phenotypes are common among patients. Type 2 asthma is so named because it is associated with Type 2 inflammation and typically includes allergic asthma and moderate-to-severe eosinophilic asthma, Prof Canonica explained. By contrast, non-Type 2 asthma commonly has an older age of onset and is often associated with obesity and neutrophilic inflammation.
Prof Diamant highlighted the scale and severity of uncontrolled persistent asthma. Globally, an estimated 420,000 people die of asthma every year, and many more have uncontrolled disease, putting them at risk of persistent airway inflammation and eventual lung decline. Patients may not recognise that their disease is uncontrolled, despite exacerbations and the impact of their asthma on daily activities. Prof Diamant described the impairments to health-related quality of life and the associated costs of uncontrolled asthma.
Prof Dahlén outlined how new predictive biomarkers will be needed to identify the type of asthma an individual patient has. No single biomarker will provide sufficient information, and as such, in the future, profiles of many markers will need to be integrated to produce subgroup-specific profiles for use in personalised medicine. He described ongoing research into protein arrays and lipid mediators in urine, and how cluster analysis and pattern recognition, with the aid of artificial intelligence, will form the basis of future diagnostic tools. Prof Canonica explained that an understanding of the mechanisms of asthma is important in achieving better symptom control. IL-4 and IL-13 are key players in the pathobiology of uncontrolled persistent asthma (IL-4 in inflammation and IL-13 in airway remodelling), but their roles overlap. The heterogenous nature of Type 2 asthma can make it difficult to diagnose; therefore, focussing on a single biomarker is likely to leave some patients sub-optimally controlled.