Hypereosinophilic Syndrome Medication

  • Author: Venkata Samavedi, MBBS, MD; Chief Editor: Emmanuel C Besa, MD   more...
 
Updated: Jan 10, 2012
 

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications in patients with hypereosinophilic syndrome.

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Corticosteroids

Class Summary

Corticosteroids often cause a rapid reduction in level of the eosinophilia. The mechanisms for this are not entirely clear.

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Prednisone (Deltasone, Meticorten, Orasone)

 

Initial DOC. Once eosinophils are suppressed, the dose may be slowly tapered. Patients whose condition responds to steroids tend to have a better prognosis.

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Antineoplastic Agents

Class Summary

Chemotherapeutic agents may be used in patients whose conditions are refractory to steroid treatment. As a group, antineoplastic agents interfere with the production of eosinophils, but they may also cause toxicity to normal tissues, especially the bone marrow.

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Hydroxyurea (Hydrea)

 

Second line of treatment. Goal is to reduce total white blood cell (WBC) count to < 10,000 cells/µL. One week of therapy may be required before a reduction of the eosinophil count is observed. Anemia and thrombocytopenia are common complications associated with this drug.

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Vincristine (Oncovin, Vincasar)

 

May be instituted in patients whose condition fails or is only partially responsive to hydroxyurea. A response is often observed within 1-3 d. Marrow suppression is less common than with hydroxyurea, but occurrence of neurologic toxicity may limit treatment and closely resemble the neurologic symptoms of hypereosinophilic syndrome.

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Chlorambucil (Leukeran)

 

Primary alkylating agent used in cases in which prednisone fails and in those patients who cannot tolerate hydroxyurea or vincristine. A reasonable alternative for long-term treatment. Bone marrow suppression may be a problem.

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Immunomodulators

Class Summary

Immunomodulators are naturally produced proteins with antiviral, antitumor, and immunomodulatory actions. Alpha, beta, and gamma interferons may be given topically, systemically, and intralesionally. These agents have demonstrated efficacy in small trials.

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Interferon alfa 2a (Roferon-A)

 

Has been reported to effectively suppress eosinophilia in several different patients using several different doses. Some patients have had progression of disease despite therapy.

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Interferon alpha-2b (Intron A)

 

Has been reported to effectively suppress eosinophilia in several different patients using several different doses. Some patients have had progression of disease despite therapy.

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Contributor Information and Disclosures
Author

Venkata Samavedi, MBBS, MD  Internist in Houston, TX

Disclosure: Nothing to disclose.

Coauthor(s)

Ronald A Sacher, MB, BCh, MD, FRCPC  Professor, Internal Medicine and Pathology, Director, Hoxworth Blood Center, University of Cincinnati Academic Health Center

Ronald A Sacher, MB, BCh, MD, FRCPC is a member of the following medical societies: American Association for the Advancement of Science, American Association of Blood Banks, American Clinical and Climatological Association, American Society for Clinical Pathology, American Society of Hematology, College of American Pathologists, International Society of Blood Transfusion, International Society on Thrombosis and Haemostasis, and Royal College of Physicians and Surgeons of Canada

Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching; Talecris Honoraria Board membership

Vincent E Herrin, MD  Associate Professor of Medicine, Divisions of Hematology and Oncology, University of Mississippi School of Medicine

Vincent E Herrin, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine and American Society of Hematology

Disclosure: Nothing to disclose.

Joe C Files, MD  Director, Division of Hematology, Associate Chairman, Professor, Department of Internal Medicine, University of Mississippi Medical Center

Joe C Files, MD is a member of the following medical societies: American Association for Cancer Education, American Association for the Advancement of Science, American College of Physicians, American Federation for Medical Research, American Heart Association, American Medical Association, American Society of Human Genetics, Mississippi State Medical Association, New York Academy of Sciences, and Southern Medical Association

Disclosure: Nothing to disclose.

Youwen Zhou, MD, PhD, FRCP(C)  Associate Professor, Department of Dermatology and Skin Science, University of British Columbia; Director, Hyperhidrosis Specialty Clinic, Co-Director, Psoriasis and Phototherapy Centre, Consulting Physician, Department of Dermatology, Vancouver General Hospital, Co-Director, Vitiligo and Pigmentation Clinic, Oncologist Consultant, Skin Tumor Program, BC Cancer Agency

Youwen Zhou, MD, PhD, FRCP(C) is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Paul Schick, MD  Emeritus Professor, Department of Internal Medicine, Jefferson Medical College of Thomas Jefferson University; Research Professor, Department of Internal Medicine, Drexel University College of Medicine; Adjunct Professor of Medicine, Lankenau Hospital

Paul Schick, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Hematology, International Society on Thrombosis and Haemostasis, and New York Academy of Sciences

Disclosure: Nothing to disclose.

Specialty Editor Board

Antoni Ribas, MD  Assistant Professor of Medicine, Division of Hematology-Oncology, University of California at Los Angeles Medical Center

Disclosure: Nothing to disclose.

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

Troy H Guthrie, Jr, MD  Director of Cancer Institute, Baptist Medical Center

Troy H Guthrie, Jr, MD is a member of the following medical societies: American Federation for Medical Research, American Medical Association, American Society of Hematology, Florida Medical Association, Medical Association of Georgia, and Southern Medical Association

Disclosure: Nothing to disclose.

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.

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Indurated edematous plaques of hypereosinophilic syndrome on a patient's legs.
Erythroderma in a patient with hypereosinophilic syndrome.
 
 
 
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