There was a general consensus that a growing body of compelling data suggests that any patient with asthma, including those with intermittent disease, should receive ICS. Such treatment results in reduced numbers of exacerbations; even patients with mild asthma can have severe exacerbations. However, the long-term effects of intermittent asthma are not known, and there are insufficient data to suggest ICS for all patients.
Many inflammatory markers, such as nitric oxide and leukotrienes, were still believed to be research tools rather than good clinical indicators. However, as asthma is a complex, multifactorial disease and the mechanism of asthma in each patient is likely to be different, it may be that no one marker will be practical.
There was some discussion among the group regarding the potential interaction between LABAs and inhaled corticosteroids as potentiating corticosteroid efficacy, although most believe this requires further investigation. Only US guidelines offer leu-kotriene receptor antagonists as an option in the treatment of asthma, and they are only recommended first-line for those who refuse or cannot tolerate corticosteroids. Fixed combination therapy may be useful in patients with more severe disease and generally follows a trial of ICS monotherapy. Concerns were raised about overuse of combination therapy and overdiagnosis of asthma, particularly in primary care leading to oversimplification of asthma treatment. there
The clinical relevance of remodeling remains controversial. Issues that need to be resolved include whether remodeling is a consequence of inflammation (sequential) or whether they start at the same time (in parallel). It was suggested that high levels of remodeling can occur in patients with the mildest disease, and more studies are required to define its clinical relevance. The literature on inflammation and remodeling suggests the need for ICS treatment in early disease, but a need for more long-term data on airway remodeling was recognized.
In asthma, inflammation occurs throughout the tracheobronchial tree, even in the small airways, and is the underlying component to be treated. Remodeling in the airways results from the chronic inflammation associated with asthma that disrupts the normal repair process.
It involves thickening of the airway walls due to subepithelial fibrosis, myocyte hyperplasia and hypertrophy, myofibroblast hyperplasia, epithelial hypertrophy, and mucus gland and goblet cell hyperplasia. Inflammation and the resultant remodeling of the airways lead to decreased pulmonary function, but early antiinflammatory therapy might limit airway remodeling and has been shown to improve outcomes. Patients with allergic asthma and those with seasonal allergic rhinitis are believed to have minimal persistent inflammation, and the two diseases often occur together. Corticosteroid therapy influences many different inflammatory and structural cell types and continues to be the “gold standard” of therapy in asthma. As inflammation is a persistent component of asthma, ICS treatment should be started early and be continuous to be effective.