Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2011:4:49-59.
doi: 10.2147/JAA.S14520. Epub 2011 Jun 13.

Update on optimal use of omalizumab in management of asthma

Affiliations

Update on optimal use of omalizumab in management of asthma

Girolamo Pelaia et al. J Asthma Allergy. 2011.

Abstract

Omalizumab is a humanized monoclonal anti-IgE antibody recently approved for the treatment of severe allergic asthma. This drug inhibits allergic responses by binding to serum IgE, thus preventing interaction with cellular IgE receptors. Omalizumab is also capable of downregulating the expression of high affinity IgE receptors on inflammatory cells, as well as the numbers of eosinophils in both blood and induced sputum. The clinical effects of omalizumab include improvements in respiratory symptoms and quality of life, paralleled by a reduction of asthma exacerbations, emergency room visits, and use of systemic corticosteroids and rescue bronchodilators. Omalizumab is relatively well-tolerated, and only rarely induces anaphylactic reactions. Therefore, this drug represents a valid option as add-on therapy for patients with severe persistent allergic asthma inadequately controlled by high doses of standard inhaled treatments.

Keywords: anti-IgE; omalizumab; severe asthma.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Mechanism of action of omalizumab. Omalizumab binds to IgE, thus forming immune complexes that reduce levels of circulating free IgE and prevent their interactions with high-affinity IgE receptors (FcɛRI) expressed by dendritic cells, mast cells, basophils, and eosinophils. As a consequence, IgE-dependent antigen presentation, mast cell/basophil degranulation, and eosinophil infiltration are inhibited. Anti-IgE therapy with omalizumab also results in decreased FcɛRI expression. All these effects are responsible for a reduction of allergic airway inflammation, as well as of related asthma symptoms and exacerbations.

References

    1. Holgate ST, Arshad HS, Roberts GC, Howarth PH, Thurner P, Davies DE. A new look at the pathogenesis of asthma. Clin Sci. 2010;118(7):439–450. - PMC - PubMed
    1. Anderson GP. Endotyping asthma: new insights into key pathogenetic mechanisms in a complex, heterogeneous disease. Lancet. 2008;372(9643):1107–1119. - PubMed
    1. Anandan C, Nurmatov U, van Schayck OCP, Skeih A. Is the prevalence of asthma declining? Systematic review of epidemiological studies. Allergy. 2010;65(2):152–167. - PubMed
    1. Masoli M, Fabian D, Holt S, Beasley R. The global burden of asthma: executive summary of the GINA dissemination committee report. Allergy. 2004;59(5):469–478. - PubMed
    1. Bateman ED, Boushey HA, Bousquet J, et al. Can guideline-defined asthma control be achieved? The Gaining Optimal Asthma ControL (GOAL) study. Am J Respir Crit Care Med. 2004;170(8):836–844. - PubMed