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Erythropoitin (EPO) for anemia


Medical editor Harald Holte MD
Oncologist
Dag Torfoss MD
Infection Specialist
Oslo University Hospital

General

Anemia with hemoglobin < 11.0 mg/l is normal during chemotherapy. This will often lead to prominent fatigue. Anemia can be treated symptomatically with transfusion of erythrocytes, or bone marrow can be stimulated with erythropoitin (EPO).

Patients with chemotherapy-induced anemia will usually have sufficient iron storage, but some may need iron supplementation. 

Anemia should normally not cause postponement of treatment. It is quickly corrected by an erythrocyte transfusion – and treatment may then be started.

Indication

  • Patients with chemotherapy-induced anemia

Contraindications

  • Hypersensitivity to darbepoetin alfa, r-HuEPO or any of the additional ingredients.
  • Poorly-controlled hypertension
  • Reduced liver function (raised s-bilirubin). EPO is most likely eliminated via the liver. There is presently no toxicity data on patients with reduced liver function.
  • Some studies indicate a detrimental effect on patient survival by the use of EPO in cancer patients, and this treatment should be avoided for anemia in cancer patient for whom there is a curative goal with the treatment.

 

Goal

  • Reach hemoglobin level of 12–13 g/l

Preparation

  • Survey blood status
  • Evaluate iron status

Implementation

  • EPO is given in a dosage of 40,000 IE subcutaneously once daily
  • With use of Aranesp®, one dose of 500 μg subcutaneously is given every third week
  • For hemoglobin of 12 g/l, the dose is reduced by 25–50%, for example 300 μg every third week
  • For hemoglobin of 14 g/l, treatment is stopped until it has fallen to under 12 g/l where treatment is resumed with a 50% dose (for example, 300 μg or lower every third week). Repeated dosage reductions may be necessary. 
  • If the increase in hemoglobin rises above 2 g/dl (1.3 mmol/l) within 4 weeks, the dose should be reduced by 25–50%.

Assurance of efficient erythropoesis

  • Low s-iron and high ferritin implies iron deficiency. It is then recommended to give iron supplementation, for example slow-release iron tablets 100 mg x 2 daily for the first 4 weeks then once daily. If still no effect from this treatment, immediate action should be taken to find the cause.
  • Lack of iron, folic acid, or vitamin B12 reduces the effect of erythropoietin-stimulating drugs and should therefore be treated.
  • In the case of functional iron deficiency, iron storage is not released as needed and iron must be taken parenterally. Functional iron deficiency is characterized by normal or raised ferritin and normal serum iron/TIBC. 
  • Simultaneous infections, inflammatory or traumatic episodes, hidden blood loss, severe aluminum toxicity, or underlying hematological disease or bone marrow fibrosis can also impair erythropoietin response.
  • Reticulocyte count should be monitored as part of the evaluation.
  • If typical causes for no response have been excluded and the patient has reticulocytopenia, a bone marrow examination should be considered. If bone marrow assessment implies erythroaplasia (Pure Red Cell Aplasia – PRCA), testing with anti-erythropoietin antibodies should be done.

Follow-up

Follow-up of hemoglobin under EPO treatment is necessary because overstimulation can lead to polycytemia.


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