0
Correspondence |

Can Omalizumab Be Effective in Chronic Eosinophilic Pneumonia?Anti-IgE Against Eosinophil-Associated Disorders FREE TO VIEW

Christian Domingo, MD; Xavier Pomares, MD
Author and Funding Information

From the Servei de Pneumologia, Corporació Parc Taulí, Departament de Medicina, Universitat Autònoma de Barcelona.

Correspondence to: Christian Domingo, MD, Servei de Pneumologia, Corporació Parc Taulí, Parc Taulí1, 08208 Sabadell, Barcelona, Spain; e-mail: cdomingo@tauli.cat


Funding/Support: The authors’ research was partially supported by Beca FUCAP 2008.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;143(1):274. doi:10.1378/chest.12-2035
Text Size: A A A
Published online
To the Editor:

We have recently read with interest the article by Kaya et al1 in CHEST (August 2012) reporting on a patient suffering from chronic eosinophilic pneumonia (CEP) who responded successfully to omalizumab. Five years ago, we attended a 43-year-old nonsmoking man who complained of cough, fever, dyspnea, and wheezing. On the basis of his clinical presentation, peripheral blood and BAL eosinophilia, and the presence of bilateral peripheral infiltrates on the chest radiograph, the diagnosis of CEP was made. As in the Kaya et al1 case, oral corticosteroids (OCs) were started with an initial successful response. After 3 months of therapy, the dose of OCs was progressively tapered. When the dose reached 10 mg prednisolone, a relapse occurred that forced us to increase the dose of OCs. The patient improved, and bronchospasm and chest infiltrates disappeared.

During the process of OC tapering, a new relapse occurred, bronchospasm being the most relevant clinical symptom that forced us to increase again the dose of OCs. A skin prick test was performed that was positive for mite dust. Total blood IgE level was 253 IU/mL. Omalizumab treatment was started at the dose calculated according to the patient’s weight and IgE concentration. The patient progressively improved, and after 18 months of treatment (6 months to check clinical response followed by 12 months of stabilization), according to our decreasing-dose protocol of omalizumab,2 the dose of omalizumab was progressively tapered by 50% every 6 months. The patient’s tolerance was excellent, and omalizumab treatment could be safely quit 12 months later. The patient has remained free of symptoms of CEP for >2 years, requiring only two short courses of OCs for his asthma.

The IgE-dependent inflammatory phenomena have been studied in depth and are clearly recognized in atopic subjects, and the anti-IgE blocking effect of omalizumab has been clearly shown. Additional benefits can be provided by the findings of Kalesnikoff et al,3 who observed that by binding to its high-affinity receptor, FcεRI, IgE was able to induce intracellular signaling pathways, resulting in the production of cytokines and the enhancement of mast-cell survival on its own, without cross-linking by allergens. In addition, IgE can directly bind and activate receptors present on eosinophils, neutrophils, and monocytes. As a result, the rationale for the use of omalizumab in diseases other than allergy is based on its blocking effect on IgE, which inhibits part of the T helper cell type 2 immune response, thus, reducing recruitment and activation of effector cells of the inflammatory process, including eosinophils. Because IgE effector cells (ie, mast cells and basophils) are a source of proinflammatory molecules, anti-IgE therapy may have antiinflammatory properties that reduce circulating and tissue eosinophils4; indeed, this role has been suggested in other diseases, such as eosinophil-associated GI disorders.5 More recently, Noga et al4 demonstrated an increase in eosinophil apoptosis and a decrease in granulocyte-macrophage colony-stimulating factor. All this information can help to explain the benefits of omalizumab in CEP.

In their report, Kaya et al1 communicate that their patient remains free of symptoms 15 months after omalizumab treatment began, but they do not state future treatment options. We believe some of these patients can benefit from a decreasing dose protocol.2

Acknowledgments

Role of sponsors: The sponsor had no role in the design of the study, the collection and analysis of the data, or in the preparation of the manuscript.

Kaya H, Gümüş S, Uçar E, et al. Omalizumab as a steroid-sparing agent in chronic eosinophilic pneumonia. Chest. 2012;142(2):513-516. [CrossRef] [PubMed]
 
Domingo C, Pomares X, Casabon J, Garcia A, Veigas C, Monton C. Decreasing dose protocol for omalizumab treatment in oral corticosteroid allergic asthma patients. Paper presented at: European Respiratory Society Annual Congress; September 24-28, 2011; Amsterdam, The Netherlands.
 
Kalesnikoff J, Huber M, Lam V, et al. Monomeric IgE stimulates signaling pathways in mast cells that lead to cytokine production and cell survival. Immunity. 2001;14(6):801-811. [CrossRef] [PubMed]
 
Noga O, Hanf G, Kunkel G. Immunological and clinical changes in allergic asthmatics following treatment with omalizumab. Int Arch Allergy Immunol. 2003;131(1):46-52. [CrossRef] [PubMed]
 
Foroughi S, Foster B, Kim N, et al. Anti-IgE treatment of eosinophil-associated gastrointestinal disorders. J Allergy Clin Immunol. 2007;120(3):594-601. [CrossRef] [PubMed]
 

Figures

Tables

References

Kaya H, Gümüş S, Uçar E, et al. Omalizumab as a steroid-sparing agent in chronic eosinophilic pneumonia. Chest. 2012;142(2):513-516. [CrossRef] [PubMed]
 
Domingo C, Pomares X, Casabon J, Garcia A, Veigas C, Monton C. Decreasing dose protocol for omalizumab treatment in oral corticosteroid allergic asthma patients. Paper presented at: European Respiratory Society Annual Congress; September 24-28, 2011; Amsterdam, The Netherlands.
 
Kalesnikoff J, Huber M, Lam V, et al. Monomeric IgE stimulates signaling pathways in mast cells that lead to cytokine production and cell survival. Immunity. 2001;14(6):801-811. [CrossRef] [PubMed]
 
Noga O, Hanf G, Kunkel G. Immunological and clinical changes in allergic asthmatics following treatment with omalizumab. Int Arch Allergy Immunol. 2003;131(1):46-52. [CrossRef] [PubMed]
 
Foroughi S, Foster B, Kim N, et al. Anti-IgE treatment of eosinophil-associated gastrointestinal disorders. J Allergy Clin Immunol. 2007;120(3):594-601. [CrossRef] [PubMed]
 
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543