Eosinophilia Treatment & Management

  • Author: Michaelann Liss; Chief Editor: Emmanuel C Besa, MD   more...
 
Updated: Aug 25, 2011
 

Medical Care

A detailed discussion of therapeutics for the many individual causes of eosinophilia, including parasitic and malignancy-associated forms, are beyond the scope of this article. General guidelines only are addressed here.

Most cases of secondary eosinophilia are treated based on their underlying causes. Allergic and connective tissue disorders may be amenable to corticosteroid treatment. Parasitic and fungal infections can be worsened or disseminated by use of steroids and should be ruled out if they are indicated by patient history.

In patients with primary eosinophilia without organ involvement, no treatment may be necessary. Cardiac function should be evaluated at regular intervals, however, as peripheral eosinophilia does not necessarily correlate with organ involvement. Steroid responsiveness should be evaluated, both for prognosis (steroid-responsive patients do better) and to guide treatment when needed.

Choices for systemic treatment of primary eosinophilia with organ involvement initially include corticosteroids and interferon (IFN)-alpha for steroid resistant disease. Other agents for steroid resistant disease include hydroxyurea, chlorambucil, vincristine, cytarabine, 2-chlorodeoxyadenosine (2-CdA), and etoposide. These agents are usually given as chronic maintenance regimens to control organ involvement.

In the presence of PDGFRA and PDGFRB mutations, imatinib has achieved complete and durable remissions. Jain et al evaluated the use of imatinib in 18 patients with hypereosinophilic syndrome (HES) with known and unknown PDGFRalpha status.[10] The investigators confirmed a low response rate to imatinib in HES patients with unknown or negative PDGFRalpha status. Jain et al concluded that new therapeutic options are needed for hypereosinophilic syndrome (HES).[10]

In refractory cases, many investigational combinations of chemotherapeutic agents, tyrosine kinase inhibitors and monoclonal antibodies are being studied. Nonmyeloablative allogenic hematopoietic stem cell transplantation (HSCT) can also be considered in drug-refractory cases.

A recent study investigated the roles of the prostaglandin D receptor chemoattractant receptor-homologous molecule expressed on Th2 cells, which are 2 distinct receptors of prostaglandin D2. Modified CD16-negative selection was used to isolate eosinophils from human test subjects.[11] Eosinophil migration was measured by Boyden chamber as stimulation both with and without the prostaglandin D receptor agonist was performed. When taken together, the balance of prostaglandin D receptor and chemoattractant receptor-homologous molecule expressed on Th2 cells could influence the degree of prostaglandin D2-induced eosinophil migration, and the prostaglandin D receptor agonist was seen to regulate eosinophil activation.

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Surgical Care

Surgical care may be indicated in patients with eosinophilia, depending on the specific diagnosis.

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Consultations

Consultation with infectious disease and hematology-oncology physicians can help determine the cause and treatment of eosinophilia.

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Contributor Information and Disclosures
Author

Michaelann Liss  DO, Consulting Staff, Department of Hematology/Oncology, The Vancouver Clinic/South West Washington Medical Center

Michaelann Liss is a member of the following medical societies: American College of Physicians, American Medical Association, American Osteopathic Association, American Physical Therapy Association, American Society of Hematology, and Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Erik Zeger, MD  Consulting Staff, Main Line Oncology Hematology Associates

Erik Zeger, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for Cancer Research, and American Society of Hematology

Disclosure: Nothing to disclose.

Daniel R Lucey, MD, MPH  Chief, Fellowship Program Director, Department of Internal Medicine, Division of Infectious Diseases, Washington Hospital Center; Professor, Department of Internal Medicine, Uniformed Services University of the Health Sciences

Daniel R Lucey, MD, MPH is a member of the following medical societies: Alpha Omega Alpha and American College of Physicians

Disclosure: Nothing to disclose.

Palaniandy Kogulan, MBBS, MD  Assistant Director of Internal Medicine, Synergy Medical Education Alliance; Assistant Professor of Medicine, Michigan State University College of Human Medicine

Palaniandy Kogulan, MBBS, MD is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America, and Michigan State Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Pradyumna D Phatak, MBBS, MD  Chair, Division of Hematology and Medical Oncology, Rochester General Hospital; Clinical Professor of Oncology, Roswell Park Cancer Institute

Pradyumna D Phatak, MBBS, MD, is a member of the following medical societies: American Society of Hematology

Disclosure: Novartis Honoraria Speaking and teaching

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Marcel E Conrad, MD  Distinguished Professor of Medicine (Retired), University of South Alabama College of Medicine

Marcel E Conrad, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American Association of Blood Banks, American Chemical Society, American College of Physicians, American Physiological Society, American Society for Clinical Investigation, American Society of Hematology, Association of American Physicians, Association of Military Surgeons of the US, International Society of Hematology, Society for Experimental Biology and Medicine, and Southwest Oncology Group

Disclosure: No financial interests None None

Rajalaxmi McKenna, MD, FACP  Southwest Medical Consultants, SC, Department of Medicine, Good Samaritan Hospital, Advocate Health Systems

Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis

Disclosure: Nothing to disclose.

Chief Editor

Emmanuel C Besa, MD  Professor, Department of Medicine, Division of Hematologic Malignancies, Kimmel Cancer Center, Jefferson Medical College of Thomas Jefferson University

Emmanuel C Besa, MD is a member of the following medical societies: American Association for Cancer Education, American College of Clinical Pharmacology, American Federation for Medical Research, American Society of Clinical Oncology, American Society of Hematology, and New York Academy of Sciences

Disclosure: Nothing to disclose.

References

  1. Spry CJF, ed. Eosinophils: A Comprehensive Review and Guide to the Scientific and Medical Literature. Oxford, UK: Oxford University Press; 1988.

  2. Gotlib J. Molecular classification and pathogenesis of eosinophilic disorders: 2005 update. Acta Haematol. 2005;114(1):7-25. [Medline].

  3. Tefferi A, Patnaik MM, Pardanani A. Eosinophilia: secondary, clonal and idiopathic. Br J Haematol. Jun 2006;133(5):468-92. [Medline].

  4. Weller PF, Bubley GJ. The idiopathic hypereosinophilic syndrome. Blood. May 15 1994;83(10):2759-79. [Medline]. [Full Text].

  5. Bain BJ. Relationship between idiopathic hypereosinophilic syndrome, eosinophilic leukemia, and systemic mastocytosis. Am J Hematol. Sep 2004;77(1):82-5. [Medline]. [Full Text].

  6. Gotlib J, Cools J, Malone JM 3rd, et al. The FIP1L1-PDGFRalpha fusion tyrosine kinase in hypereosinophilic syndrome and chronic eosinophilic leukemia: implications for diagnosis, classification, and management. Blood. Apr 15 2004;103(8):2879-91. [Medline]. [Full Text].

  7. Tefferi A. Modern diagnosis and treatment of primary eosinophilia. Acta Haematol. 2005;114(1):52-60. [Medline].

  8. Fletcher S, Bain B. Eosinophilic leukaemia. Br Med Bull. 2007;81-2:115-27. [Medline]. [Full Text].

  9. Weller PF. Eosinophilia in travelers. Med Clin North Am. Nov 1992;76(6):1413-32. [Medline].

  10. Jain N, Cortes J, Quintas-Cardama A, et al. Imatinib has limited therapeutic activity for hypereosinophilic syndrome patients with unknown or negative PDGFRalpha mutation status. Leuk Res. Jun 2009;33(6):837-9. [Medline].

  11. Chiba T, Ueki S, Ito W, et al. The opposing role of two prostaglandin D2 receptors, DP and CRTH2, in human eosinophil migration. Ann Allergy Asthma Immunol. Jun 2011;106(6):511-7. [Medline].

  12. Allen JN, Davis WB. Eosinophilic lung diseases. Am J Respir Crit Care Med. Nov 1994;150(5 Pt 1):1423-38. [Medline].

  13. Butterfield JH. Success of short-term, higher-dose imatinib mesylate to induce clinical response in FIP1L1-PDGFRalpha-negative hypereosinophilic syndrome. Leuk Res. Aug 2009;33(8):1127-9. [Medline].

  14. Cohen AJ, Steigbigel RT. Eosinophilia in patients infected with human immunodeficiency virus. J Infect Dis. Sep 1996;174(3):615-8. [Medline].

  15. Cortes J, Ault P, Koller C, et al. Efficacy of imatinib mesylate in the treatment of idiopathic hypereosinophilic syndrome. Blood. Jun 15 2003;101(12):4714-6. [Medline]. [Full Text].

  16. Fink SR, Belongie KJ, Paternoster SF, et al. Validation of a new three-color fluorescence in situ hybridization (FISH) method to detect CHIC2 deletion, FIP1L1/PDGFRA fusion and PDGFRA translocations. Leuk Res. Jun 2009;33(6):843-6. [Medline].

  17. Heimall J, Freeman A, Holland SM. Pathogenesis of hyper IgE syndrome. Clin Rev Allergy Immunol. May 19 2009;epub ahead of print. [Medline].

  18. Lucey DR, Clerici M, Shearer GM. Type 1 and type 2 cytokine dysregulation in human infectious, neoplastic, and inflammatory diseases. Clin Microbiol Rev. Oct 1996;9(4):532-62. [Medline]. [Full Text].

  19. [Best Evidence] Nair P, Pizzichini MM, Kjarsgaard M, et al. Mepolizumab for prednisone-dependent asthma with sputum eosinophilia. N Engl J Med. Mar 5 2009;360(10):985-93. [Medline].

  20. Nand R, Bryke C, Kroft SH, et al. Myeloproliferative disorder with eosinophilia and ETV6-ABL gene rearrangement: efficacy of second-generation tyrosine kinase inhibitors. Leuk Res. Aug 2009;33(8):1144-6. [Medline].

  21. Roufosse F, Goldman M, Cogan E. Hypereosinophilic syndrome: lymphoproliferative and myeloproliferative variants. Semin Respir Crit Care Med. Apr 2006;27(2):158-70. [Medline].

  22. Tefferi A, Pardanani A. Imatinib therapy in clonal eosinophilic disorders, including systemic mastocytosis. Int J Hematol. Jun 2004;79(5):441-7. [Medline].

  23. Tostes Oliveira D, Tjioe KC, et al. Tissue eosinophilia and its association with tumoral invasion of oral cancer. Int J Surg Pathol. Jul 2009;17(3):244-9. [Medline].

 
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Indurated edematous plaques of hypereosinophilic syndrome on a patient's legs.
Erythroderma in a patient with hypereosinophilic syndrome.
Granuloma with a central core of eosinophilic debris surrounded by a peripheral palisade of epithelioid histiocytes and eosinophils from a patient with Churg-Strauss syndrome (allergic granulomatosis).
Magnified view of papules and nodules with central necrosis in a patient with Churg-Strauss syndrome (allergic granulomatosis).
High-power photomicrograph of fascia shows heavy inflammatory infiltration with numerous eosinophils, lymphocytes, and occasional plasma cells in a patient with eosinophilic fasciitis.
Lower back part of the legs in a patient with eosinophilic fasciitis shows hypopigmentation, induration, biopsy site, and asymmetric involvement.
Egg of Schistosoma hematobium, with its typical terminal spine.
 
 
 
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