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Letter to the Editor |
Address correspondence to Jong Weon Choi, M.D., Ph.D., Department of Laboratory Medicine, Inha University Hospital, 7-206, 3-ga, Shinheung-dong, Jung-gu, Incheon, 400-711, South Korea; tel 82 32 890 2503; fax 82 32 890 2529; e-mail jwchoi{at}inha.ac.kr.
To the Editor:
Serum soluble transferrin receptor (sTfR) concentration reflects the body iron status and erythro-poietic activity [1]. Serum sTfR originates mostly from erythroblasts and to a lesser extent from reticulocytes. In healthy adults, approximately 80% of sTfR molecules are in erythroid precursors in bone marrow [2]. Increased sTfR concentrations are usually observed in iron deficiency anemia (IDA) because iron deprivation induces a synthesis of transferrin receptor (TfR) [3].
Matsuda et al [4] reported that a new indicator, the sTfR-E index, which is the ratio of serum sTfR concentration to total erythroblast count, can reflect the number of TfR molecules on the cell membrane per bone marrow erythroblast. To investigate which parameter is most closely linked to the increased sTfR concentrations in patients with IDA, the sTfR-E index and the erythroblast count were measured.This study also tested the differences in TfR expression and sTfR levels between patients with IDA and those with anemia of chronic diseases (ACD).
Materials and Methods
A total of 45 patients (24 men and 21 women) with a median age of 49 yr (range, 32 to 67 yr) were investigated by measurements of bone marrow erythroblasts, serum sTfR concentration, and sTfR-E index.The subjects were selected from patients who were diagnosed as IDA (n = 16) and ACD (n = 14) based on their bone marrow specimens, serum iron parameters, and clinical profiles.The ACD subjects comprised anemic patients (blood hemoglobin level <12 g/dl) with rheumatoid arthritis (n = 8) or osteoarthritis (n = 6). As a control group, 15 non-anemic individuals with normocellular marrow were used; these subjects showed no evidence of bone marrow involvement when a bone marrow study was undertaken for evaluating malignant tumors.
The degree of TfR synthesis on erythroblasts was assessed by the sTfR-E index.The sTfR-E index was calculated by the following formula: sTfR-E index = serum sTfR concentration (mg/L) / [bone marrow cellularity (%) x bone marrow erythroblasts (%)], as described previously [4].
Serum iron and serum ferritin levels were measured, respectively, with a Hitachi 7600 analyzer (Hitachi, Tokyo, Japan) and a ACS 180 analyzer (Bayer Diagnostics, Tarrytown, NY). Serum sTfR concentrations were analyzed by an enzyme immunoassay (IDeA sTfR, Orion Diagnostica, Espoo, Finland). Reticulocyte maturity index (RMI) was determined by quantitating the subfractions of reticulocytes (R-3000; Sysmex, Kobe, Japan) [5]. Data analysis was performed using Wilcoxon’s rank sum test and Spearman’s correlation coefficient. All p values <0.05 were considered significant.
Results and Discussion
Serum sTfR concentrations in IDA patients were 3.2-fold higher than those in the control group, whereas serum iron and serum ferritin levels were 3.7- and 8.6-fold lower in IDA patients than in the control subjects. However, no significant differences were observed in the erythroblasts and the bone marrow cellularity between the 2 groups. Nor were significant differences observed in total erythroblast counts, which were calculated from the bone marrow cellularity and the relative percentage of erythroblasts.
On the other hand, the sTfR-E index in IDA patients was significantly above the values in control subjects (0.007 ± 0.009 vs 0.002 ± 0.003, p <0.05).These results suggest that the increased sTfR concentration, which is observed in IDA patients, is not attributable to erythroid hyperplasia, but is attributable to enhanced TfR expression on erythroid precursors.
Corrected reticulocyte counts and RMI in IDA patients showed a propensity toward increased values compared to control group, but no statistically significant differences were noted between the 2 groups.These observations differ from the results of our previous study, which demonstrated that immature reticulocyte production was significantly increased in IDA, compared to non-anemic healthy controls [5]. A possible reason is that the present control group was selected, not from normal healthy subjects, but from patients with carcinoma or lymphoma, although they were all non-anemic individuals without any evidence of bone marrow involvement.
As shown in Table 1
, the patients with ACD exhibited significantly lower serum iron levels than the control group (41.2 ± 25.1 vs 109.3 ± 46.8 µg/ dl, p < 0.05). In contrast, there were no significant differences in serum sTfR concentrations and sTfR-E index between the groups.These results imply that the decrease in serum iron levels is not accompanied by an increase in TfR synthesis and serum sTfR levels in patients with ACD.The way that TfR is produced in ACD may differ from that in IDA, although the two diseases are both categorized as microcytic hypochromic anemias.
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). It appears that the relationship of iron markers and hematologic variables versus TfR expression varies according to the type of anemia.
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Acknowledgement
This work was supported by a research grant from Inha University.
References
This article has been cited by other articles:
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  G. C. Bullock, L. L. Delehanty, A.-L. Talbot, S. L. Gonias, W.-H. Tong, T. A. Rouault, B. Dewar, J. M. Macdonald, J. J. Chruma, and A. N. Goldfarb Iron control of erythroid development by a novel aconitase-associated regulatory pathway Blood, July 8, 2010; 116(1): 97 - 108. [Abstract] [Full Text] [PDF]
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