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Anemia Management in Oncology and Hematology

^aJohns Hopkins University, School of Medicine, Baltimore, Maryland, USA; ^bMedical Oncology, Hospital Clinic, IDIBAPS, University of Barcelona, Barcelona, Spain; ^cCenter for Oncology and Hematology, Wilhelminen Hospital, Vienna, Austria

Key Words. Anemia • Erythropoiesis-stimulating agents • Quality of life • Blood transfusions • Inflammatory cytokines

Correspondence: Jerry L. Spivak, M.D., Johns Hopkins University School of Medicine, Baltimore, Maryland 21210, USA. Telephone: 410-955-5454; Fax: 410-614-0854; e-mail: jlspivak{at}jhmi.edu

Received March 10, 2009; accepted for publication June 16, 2009.

Disclosures: Jerry L. Spivak: Consultant/advisory role: Amgen, Ortho Biotech, Roche; Pere Gascón: None; Heinz Ludwig: Consultant/advisory role: ESMO; Honoraria: Amgen, Ortho Biotech; Research funding/contracted research: Mundipharma, Janssen-Cilag.

The content of this article has been reviewed by independent peer reviewers to ensure that it is balanced, objective, and free from commercial bias. No financial relationships relevant to the content of this article have been disclosed by the independent peer reviewers.

Anemia is frequent in cancer patients and its incidence increases with chemotherapy. The probability of requiring transfusions also increases with chemotherapy. Anemia negatively impacts survival and accentuates fatigue in cancer patients. Cancer promotes inflammatory cytokine production, which suppresses erythropoiesis and erythropoietin (EPO) production. Erythropoiesis-stimulating agents (ESAs) improve erythropoiesis and reduce transfusion needs in anemic cancer patients receiving chemotherapy. However, meta-analyses have shown an increased risk of thromboembolic (TE) events with ESA use during chemotherapy, but not increased on-study mortality or reduced overall survival. Three reasons have been proposed to explain why ESAs might have adverse effects in anemic cancer patients: tumor progression due to stimulation of tumor cell EPO receptors; increased risk of TE; and reduced survival. However, erythropoietin is not an oncogene, nor is the EPO receptor. It has also been demonstrated that erythropoietin does not stimulate tumor proliferation. Increased TE risk associated with ESAs is probably a consequence of increased blood viscosity due to excessive RBC mass elevation with concomitant plasma volume contraction, nitric oxide scavenging, and endothelial cell activation. Increased ESA dosing may also impact survival negatively because EPO contracts the plasma volume and stimulates inflammatory cytokine production independently of increasing erythropoiesis. Furthermore, transfusions themselves are associated with an increase in TE and plasma volume contraction, and these events are potentiated when ESAs are given with transfusions. An update on the management of anemia in oncology, the potential adverse events of ESAs, the benefits and risks of transfusions, and QoL are discussed in this paper.

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