CORRESPONDENCE: LETTER TO THE EDITOR
Reply
John N. Nanas, MD, PhD, FESC*,
Charis Matsouka, MD and
Maria I. Anastasiou-Nana, MD, FESC
* 24 Makedonias, 10433 Athens, Greece (Email: jnanas{at}ath.forthnet.gr).
We thank Dr. Ezekowitz and Dr. Westenbrink et al. for their interest in our recent study (1). In general, their letters raise issues and questions that only further research can answer. Our study design did not allow the drawing of conclusions regarding the prevalence of anemia, and the only apparent explanation for the under-representation of women (2 of 37 patients) is that far fewer women than men are admitted to our hospital. Our study focused on patients with "clinically significant" anemia (hemoglobin content <12 g/dl in men and <11.5 g/dl in women) who not only needed to be treated, but also had to undergo extensive diagnostic tests, including bone marrow aspiration.
A ferritin concentration <30 ng/ml, used instead of <17 ng/ml as an indication of depleted iron stores, is associated with a higher positive predictive value for iron-deficiency anemia (2). However, using this higher ferritin concentration increased the number (proportion) of patients from 2 (7.4%) to only 5 of 27 (18.5%) patients. Thus, ferritin remains an unreliable marker of iron deficiency in patients suffering from heart failure. Unfortunately, we did not measure their saturation index.
We agree that our study does not provide insights into the mechanism(s) of iron deficiency. However, in our discussion we do emphasize that "iron deficiency anemia in these desperately ill patients... seems to be multifactorial and at least partially the result of a defective release of iron from cells," although we do not have the data to support this hypothesis.
Although it is, indeed, likely that some iron accumulates in storage sites of the reticulo-endothelial system in these patients, this accumulation would not be limited to the liver and spleen, and would include macrophages in the bone marrow. Smears of the latter are stained for iron with standard Prussian blue and are counterstained with safranin. With this stain, the hemosiderin granules appear as blue/green and the cells are purple/red. In iron-deficiency anemia, by definition, hemosiderin granules are not detected by photomicroscopy either in the macrophages of the bone marrow or in the erythroblasts (3). Such was the case in 25 patients whose iron stores were depleted (grade 0) out of 27 patients included in our study. In addition, patients presenting with chronic heart failure respond to intravenous iron replacement (4) supporting the hypothesis of a central role played by iron deficiency in this clinical setting.
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References
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- Nanas JN, Matsouka C, Karageorgopoulos D, et al. Etiology of anemia in patients with advanced heart failure J Am Coll Cardiol 2006;48:2485-2489.[Abstract/Free Full Text]
- Mast AE, Blinder MA, Gronowski AM, et al. Clinical utility of the soluble transferrin receptor and comparison with serum ferritin in several populations Clin Chem 1998;44:45-51.[Abstract/Free Full Text]
- Lee GR. Wintrobe’s Clinical Hematology. 10th edition. Baltimore, MD: Lippincott, Williams & Wilkins; 1999927.
- Bolger AP, Bartlett FR, Penston HS, et al. Intravenous iron alone for the treatment of anemia in patients with chronic heart failure J Am Coll Cardiol 2006;48:1225-1227.[Abstract/Free Full Text]
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