Severe Asthma and Biologics: Managing Complex Patients

J Investig Allergol Clin Immunol. 2023 Jun 15;33(3):168-178. doi: 10.18176/jiaci.0856. Epub 2022 Sep 5.

Abstract

Bronchial asthma is a chronic inflammatory disease of the respiratory tract that varies in terms of clinical presentations (phenotypes) and distinct underlying pathophysiological mechanisms (endotypes). The definition of phenotype/endotype is crucial, given the availability of novel biologic agents for patients who do not respond to conventional therapies. Although patients with type 2 severe asthma benefit significantly from treatment with biologics, nonresponders have been identified. Comorbidities worsen the symptoms of asthma and complicate management of the disease. The assessment and treatment of comorbidities is a crucial step, and appropriate management may improve asthma symptoms and morbidity. Among comorbidities, those with a marked negative impact on control despite appropriate treatment include chronic rhinosinusitis with nasal polyps, obesity, bronchiectasis, and immune deficiency. Although asthma is frequently characterized by increased blood eosinophils that release mediators and cytokines and are involved in inflammation of the airway wall, in patients with very high blood eosinophil levels, we must differentiate between isolated severe eosinophilic asthma and asthma in eosinophilic granulomatosis with polyangiitis. In addition, hypereosinophilia may result from specific biological treatment, as in the case of dupilumab. We outline the clinical features of patients with severe asthma whose disease is complex to manage.

Keywords: Biologics; Dupilumab-induced hypereosinophilia; Severe asthma.

Publication types

  • Review

MeSH terms

  • Asthma* / diagnosis
  • Asthma* / drug therapy
  • Biological Products* / therapeutic use
  • Chronic Disease
  • Churg-Strauss Syndrome*
  • Cytokines
  • Granulomatosis with Polyangiitis* / drug therapy
  • Humans
  • Pulmonary Eosinophilia* / drug therapy

Substances

  • Biological Products
  • Cytokines