Tezepelumab in real-world clinical practice: our own experience

Severe asthma (SA) is asthma that requires stage V therapy according to the Global Initiative for Asthma (GINA) criteria to achieve control. Attempts to reduce the amount of controller therapy invariably lead to loss of control of asthma symptoms, or asthma remains uncontrolled despite this treatment. Patients with SA have the highest rate of loss of control and exacerbations, making the search for new approaches to SA therapy relevant. Targeted therapy with genetically engineered biological products (biologics) is available for patients with T2-SA (allergic or late eosinophilic). This therapy is aimed at suppressing excessive immune signaling pathways associated with T2 cytokines (IL-5 and IL-5R, IL-4/IL-13) or IgE. This therapy is effective with the correct identification of the patient’s phenotype and selection of biologic agent. However, anti-cytokine biological agents do not produce the expected effect in all patients, which may be due to multiple signaling pathways mediated by different cytokines that may be involved in the pathogenesis of SA. So, a single biologic agent targeting a specific cytokine is insufficient. The phenotypes and endotypes of asthma are known to change over time in some patients, which can make it difficult to determine the phenotype for selecting a specific biologic agent in routine clinical practice. Some patients with SA may simultaneously exhibit features of T2- and non-T2-type inflammation. Therefore, there is a need for a biologic agent capable of targeting multiple cytokine signaling pathways and independent of, or less dependent on, the phenotypes and SA biomarker levels. The aim of this study was to observe the manifestations of severe asthma in patients receiving tezepelumab, a first-in-class biologic agent that inhibits thymic stromal lymphopoietin (TSLP), a key alarmin that plays a central role in the pathogenesis of SA. Conclusion. We present our experience with tezepelumab in adult patients. Its effectiveness in controlling various phenotypes of SA is demonstrated, which may be related to the suppression of the immune cascade at the early stages of inflammation via cytokine signaling pathways.