Ask the Expert

Treatment

Q1. For "inflammatory block," do we always assume that they will be resistant to erythropoietin?

A1. By NAAC Surgeon Richard K. Spence, MD. Posted 8/24/03.
The vast majority of patients with inflammatory-mediated decreases in red blood cell production will respond to iron and erythropoietin therapy. Those who do not respond may have an invasive process that compromises the bone marrow or a disease, such as myelofibrosis. The few nonresponders should undergo bone marrow examination and full hematological evaluation to look for the answer.

Q2. Why do we see the hemoglobin drop within 48 hours of erythropoietin therapy when iron saturation was <20% before the dose was initiated?

A2. By NAAC Surgeon Richard K. Spence, MD. Posted 6/20/03.
The iron saturation will range from normal to abnormal in patients with anemia of chronic disease. The problem is a functional rather than an absolute deficiency. Having said that, it is not unusual to see iron levels decrease shortly after erythropoietin therapy is given because the iron is being incorporated into new red cells. Hemoglobin (Hb) levels should not drop as a result of iron and erythropoietin therapy, so you need to look for another reason. The most common cause of anemia in the hospitalized patient is iatrogenic blood loss. Make sure you are not decreasing red cell mass through unnecessary phlebotomy. Hb and hematocrit (Hct) are not the best measures of the initial success of iron and erythropoietin therapy -- reticulocyte counts are. Measure these before starting therapy and again in 2 to 3 days. By then you should see an increase in the reticulocyte count without any change in Hb and Hct. Resist the urge to draw more blood and let the therapy do its job. Hb and Hct will rise within 5 to 7 days.

Q3. What is the preferred treatment for autoimmune hemolytic anemia?

A3. By NAAC Hematologist/Oncologist John W. Adamson, MD. Posted 5/14/03.
The treatment depends on the type of antibody causing the hemolysis. If it is a typical warm-reacting antibody, then the first line of treatment is high-dose corticosteroids. This will usually elicit a clinical response. However, the response may not be durable, and other interventions may be necessary, such as a splenectomy.

Q4. How much iron sucrose or gluconate can be given IV push and over what period of time?

A4. By NAAC Hematologist/Oncologist Jerry L. Spivak, MD. Posted 10/24/02.
Iron gluconate can be given up to 125 mg IV slow push over 10 minutes. Iron sucrose can be given up to 100 mg IV infusion over 1 hour.

Q5. Should all patients with anemia of chronic disease be placed on epoetin?

A5. By NAAC Hematologist/Oncologist Jerry L. Spivak, MD. Posted 10/24/02.
The anemia of chronic disease is always a consequence of the underlying illness and resolves with successful treatment of the underlying disease. If the underlying illness cannot be corrected, then treatment with recombinant erythropoietin is indicated because anemia is an adverse risk factor with respect to survival in many of these illnesses, and correction of anemia also improves quality of life.

Q6. Why are there no longer any affordable and readily available parenteral iron supplements for anemic patients? It makes life as a small-town family practitioner even tougher.

A6. By NAAC Hematologist/Oncologist Jerry L. Spivak, MD. Posted 9/19/02.
The newer intravenous iron saccharide compounds such as Ferrlecit have proved to be well tolerated and effective when given at doses of 125 mg weekly and are recommended for individuals who cannot tolerate or absorb oral iron or who have a large iron deficit that would take too long to replenish orally.

Q7. Does the etiology of the anemia, other than chronic blood loss, affect the response to erythropoietin and duration of response?

A7. By NAAC Hematologist/Oncologist Jerry L. Spivak, MD. Posted 9/9/02.
The etiology of anemia has a profound influence on the response to recombinant erythropoietin. If the anemia is due to a lack of an essential nutrient such as iron, folic acid, vitamin B_12, or pyridoxine, the anemia will not be corrected by erythropoietin therapy. Hemolytic anemias are not usually responsive to erythropoietin therapy unless there is impaired endogenous erythropoietin production. Thalassemia and sickle cell anemia do not usually respond to erythropoietin if renal disease is not present. Myelofibrosis, leukemia, and aplastic anemia are other situations where erythropoietin therapy is usually ineffective, and when infection or inflammation is sufficiently severe, the response to erythropoietin will be blunted. Many patients with myelodysplasia or HIV infection will also not be responsive to erythropoietin.

Q8. Have you found any correlation between low testosterone levels and anemia? Do they respond well to androgen replacement or should other treatments be tried as well?

A8. By NAAC Hematologist/Oncologist Jerry L. Spivak, MD. Posted 8/15/02.
Men and women differ with respect to their hemoglobin (Hb) and hematocrit (Hct) levels yet have the same mean serum erythropoietin concentration. Androgen production in men accounts for the discrepancy in Hb and Hct between men and women. Suppression of androgen production in men results in a decline in their Hb and Hct values without a change in the serum erythropoietin level; restoration of androgen production or androgen replacement therapy reverses this decline. Before considering androgen replacement therapy, the cause of the androgen insufficiency must be established. For example, it may be the consequence of a pituitary tumor, in which case therapy needs to be directed to the cause not its consequence. In addition, androgen replacement therapy can cause prostatic hypertrophy, fluid retention, and, if excessive, erythrocytosis.

Q9. Does dilutional anemia need treatment?

A9. By NAAC Hematologist/Oncologist Jerry L. Spivak, MD. Posted 8/1/02.
Dilutional anemia, such as that associated with splenomegaly and portal hypertension or pregnancy, does not usually require treatment. In these situations, with respect to oxygen delivery, the reduction in blood viscosity due to the increase in plasma volume offsets the reduction in hematocrit. The difficulty is in determining when anemia is dilutional as opposed to absolute.

Q10. Is there evidence that vitamin C improves the effectiveness of oral iron treatment?

A10. By NAAC Hematologist/Oncologist Jerry L. Spivak, MD. Posted 7/18/02.
Vitamin C is one of the compounds that chelate nonheme food (ferric) iron in the acidic environment of the stomach for absorption in the alkaline environment of the duodenum. When there is normal gastric function, adequate vitamin C is available for this purpose and exogenous vitamin C adds no benefit. When there is achlorhydria, it is unlikely that vitamin C not chelated to ferric iron will enhance its absorption. Iron pills containing vitamin C offer no specific advantage over iron preparations lacking this vitamin.

Q11. Do you have to start all patients with anemia of chronic disease with erythropoietin supplementation? If so, at what level of hematocrit do you start?

A11. By NAAC Vice President and Hematologist/Oncologist Lawrence T. Goodnough, MD. Posted 7/2/02.
For too long, anemia has been viewed as simply an abnormal laboratory value associated with chronic diseases. Recent knowledge gained indicates that anemia is not only associated with increased morbidity and mortality but that its relationship with adverse outcomes is causal and that successful anemia management results in improved patient outcomes.

The impact of anemia on outcomes has perhaps best been defined in patients with chronic kidney disease. Studies have demonstrated that treatment of anemia is associated with not only improved quality of life but also reduced morbidity and improved survival. These findings have led the National Kidney Foundation to recommend that patients in this setting be maintained at hemoglobin (Hb) levels of 11 g/dL to 12 g/dL (Am J Kid Dis. 2001;37:S182-S238).

Additionally, cancer patients undergoing radiation therapy or chemotherapy are recognized to benefit from management of their anemia, as well as patients infected with HIV. These clinical conditions are each recognized in the labeled indications for initiation of erythropoietin therapy. There is also increasing recognition that patients with anemia associated with congestive heart failure (J Am Coll Cardiol. 2001;37:1776-1779) or with ischemic heart disease (N Engl J Med. 2001;345:1230-1236) also have improved outcomes with treatment of anemia.

The level of Hb at which erythropoietin should be started depends on the individual patient’s condition. The generally accepted threshold for asymptomatic patients currently is 10 g/dL, although this is currently undergoing reevaluation based on the studies cited above. Treatment should be implemented at higher levels if the patient has symptoms related to anemia, if the patient has chronic kidney disease, or if the patient is undergoing radiation therapy. Clinical trials to address the level of Hb necessary for optimal radiation therapy are currently ongoing.

Q12. What are the major side effects of recombinant human erythropoietin?

A12. By NAAC Hematologist/Oncologist Jerry L. Spivak, MD. Posted 6/18/02.
The major side effects of recombinant human erythropoietin are the induction of de novo hypertension or exacerbation of pre-existing hypertension, both of which are most commonly observed in patients with kidney disease; excessive elevation of the red cell mass if the hematocrit is not monitored regularly; and enlargement of the spleen or liver in patients with a myelodysplastic or myeloproliferative disorder. If body iron stores are low, the increase in red cell mass induced by recombinant erythropoietin can deplete these stores and reduce responsiveness to the hormone until they are replenished.

Last Updated: February 24, 2010