Pathophysiology of severe asthma: We’ve only just started

Abstract

Severe asthma is defined by the high treatment requirements to partly or fully control the clinical manifestations of disease. It remains a problem worldwide with a large burden for individuals and health services. The key to improving targeted treatments, reducing disease burden and improving patient outcomes is a better understanding of the pathophysiology and mechanisms of severe disease. The heterogeneity, complexity and difficulties in undertaking clinical studies in severe asthma remain challenges to achieving better understanding and better outcomes. In this review, we focus on the structural, mechanical and inflammatory abnormalities that are relevant in severe asthma.

Contemporary Concise Review 2018: Asthma and chronic obstructive pulmonary disease

“…King et al . reviewed the structural and inflammatory mechanisms that contribute to the pathophysiology of severe asthma . Greater degrees of ventilation heterogeneity and airway closure typify severe asthma with involvement of both small and large airways.…”

“…Increased airway smooth muscle, goblet cell hyperplasia, fibrosis and increased vascularity all contribute to airway wall thickening, and this exaggerates the sequelae of smooth muscle contraction. While inflammation and remodelling are closely related, evidence for a causal relationship is controversial …”

“…Moreover, the pattern of airway inflammation in severe asthma is highly variable, and recognizing this is important with the development of biological agents that target specific cytokines . Heterogeneity is present even within type 2 inflammation, with particular monoclonal antibodies targeting IgE, the IL‐5 pathway and the IL‐4/IL‐13 receptor working in some patients but not in others.…”

Severe asthma: We can fix it? We can try!

“…King et al . discuss the structural, mechanical and inflammatory abnormalities relevant to severe asthma . King et al .…”

“…King et al . eloquently describe how our understanding of the pathogenesis of severe asthma has been limited by the heterogeneity and complexity of disease processes and the difficulty performing studies in relevant clinical populations …”