Recent changes in the drug treatment of allergic asthma

Abstract

Asthma is a heterogeneous condition with multiple phenotypes that respond to treatments in different ways. Allergic asthma is an important phenotype and although currently available treatments are effective, about 5% of affected patients have severe, treatment-refractory disease. Despite advances in our understanding of the disease, there remains an unmet need in this group of patients. The most recent and significant advance in treatment has been anti--immunoglobulin E (IgE) therapy, which improves symptoms and quality of life in patients with severe allergic asthma. Clinical trials are ongoing with novel biologic agents that demonstrate potential efficacy; determining the subsets of patients for which they are suitable will be crucial to ensure cost effectiveness. Personalised medicine and targeted therapies may hold the key to long-term control in this group of patients.

Keywords: Allergic asthma; Th2; phenotype; treatment.

Fig 1.

Inflammatory pathways of interleukins currently involved in asthma clinical trials. Inhaled allergens (such as pollen, dust mites and animal dander) can activate mast cells and basophils. This can trigger an acute inflammatory response in sensitive individuals, resulting in airway inflammation and airways hyper-responsiveness. Allergens are recognised and processed by dendritic cells, which drive T helper (Th) 2 differentiation and secretion of multiple cytokines, including interleukin 4 (IL-4), IL-5, IL-9, IL-13 and IL-17. IL-4 and IL-13 induce B cells to produce immunoglobulin E (IgE), IL-13 induces epithelial cells to secrete periostin (a biomarker of airway eosinophilia) and IL-5 promotes the proliferation, differentiation, recruitment and survival of eosinophils. FcϵR = Fc receptors for immunoglobulin E; IG = immunoglobulin; IL = interleukin; Treg cell = regulatory T cell. Reproduced with permission from Gibeon and Menzies-Gow (2012).