Nephrology Dialysis Transplantation, Vol 13, Issue 11 2867-2872, Copyright © 1998 by Oxford University Press
D Tarng and T Huang
Background: Functional iron deficiency may develop and
cause erythropoietin resistance in haemodialysis patients with iron
overload. Controversy remains as to whether intravenous iron medication can
improve this hyporesponsiveness due to decreased iron availability, or
whether iron therapy will aggravate haemosiderosis. Intravenous
administration of ascorbic acid has been shown to effectively circumvent
resistant anaemia associated with iron overload in a small preliminary
study. To elucidate further the possible mechanisms of this resistance, a
parallel, comparative study was conducted to compare the effects of
intravenous iron and ascorbate therapies in iron-overloaded haemodialysis
patients. Methods: Fifty haemodialysis patients with
serum ferritin of >500 &mgr;g/l were randomly divided into two
protocols. They were further stratified into controls (Control I, n=11) and
intravenous iron group (IVFE, n=15) in protocol I; and into controls
(Control II, n=12) and intravenous ascorbic acid group (IVAA, n=12) in
protocol II. Controls had a haematocrit of >30% and did not receive
any adjuvant therapy. IVFE and IVAA patients were hyporesponsive to
erythropoietin and functionally iron deficient. Ferric saccharate (100 mg
dose) was administered intravenously post-dialysis on five consecutive
dialysis sessions in the first 2 weeks; and ascorbic acid (300 mg dose)
thrice a week for 8 weeks. Red cell and iron metabolism indices were
examined before and following therapy. Results: Mean
values of haematocrit and transferrin saturation were significantly lower,
and erythropoietin dose was higher in IVFE and IVAA patients compared to
controls. Intravenous iron therapy neither improved erythropoiesis nor
reduced erythropoietin dose during 12 weeks. Iron metabolism indices
significantly increased at 2 and 6 weeks, but decreased at 12 weeks
returning to the baselines. In contrast, mean haematocrit significantly
increased from 25.8±0.5 to 30.6±0.6% with a
concomitant reduction of 20% in erythropoietin dose after 8 weeks of
ascorbate therapy. Serum ferritin modestly fell but with no statistical
significance. The enhanced erythropoiesis paralleled a rise in transferrin
saturation from 27±3 to 48±6% and serum iron from
70±11 to 107±19 &mgr;g/dl (P<0.05).
Conclusions: Short term intravenous iron therapy
cannot resolve the issue of functional iron deficiency in haemodialysis
patients with iron overload. Intravenous administration of ascorbic acid
not only facilitates iron release from storage sites, but also increases
iron utilization in the erythron. Our study draws attention to a potential
adjuvant therapy, intravenous ascorbic acid, to treat
erythropoietin-hyporesponsive anaemia in iron-overloaded patients.
Key words: erythropoietin hyporesponsiveness;
functional iron deficiency; haemodialysis; intravenous ascorbic acid; iron
overload
ORIGINAL ARTICLES
A parallel, comparative study of intravenous iron versus intravenous ascorbic acid for erythropoietin-hyporesponsive anaemia in haemodialysis patients with iron overload
Institute of Clinical Medicine, National Yang-Ming University, Taiwan; Corresponding author at: No 201, Section 2, Shih-Pai Road, Division of Nephrology, Department of Medicine, Veterans General Hospital, Taipei, 11217, Taiwan
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