title: [Comparison of intravenous ascorbic acid versus intravenous iron for functional iron deficiency in hemodialysis patients].
abstract: The effect of intravenous ascorbic acid was compared with that of intravenous iron in the treatment of functional iron deficiency, as defined as serum ferritin levels over 300 ng/ml and serum iron levels below 50 microg/dl, in patients on chronic hemodialysis. Thirteen patients on chronic hemodialysis with functional iron deficiency received intravenous injections of ascorbic acid, 100 mg, three times a week, after hemodialysis. The therapy was continued until serum ferritin decreased to below 300 ng/ml (3 months at the maximum). The iron and control group were composed of patients who had serum iron levels below 50 microg/dl within 3 months after serum ferritin rose to over 300 ng/ml. Seven patients with the iron group received more than a total of 10 intravenous injections of saccharated ferric oxide (40 mg/dose) after hemodialysis, and seven patients with the control group received no iron preparation during the 3 months. In the ascorbic acid group, while hemoglobin did not change from 10.9 +/- 0.5 g/dl (mean +/- SE) during the three-month period, serum iron increased significantly from 37 +/- 4 microg/dl to 49 +/- 4 microg/dl after one month (p<0.01), and remained elevated until the end of the three-month period. Serum ferritin decreased significantly from 607 +/- 118 ng/ml to 354 +/- 30 ng/ml after 3 months (p<0.01). In the iron group, hemoglobin and serum iron increased significantly from the respective pre-treatment levels during the 2-month period, and serum ferritin rose significantly after 3 months. In the control group, hemoglobin, serum iron and ferritin levels decreased significantly from the respective pre-treatment levels during the 3 months. The recombinant erythropoietin dose remained stable for three months in the ascorbic acid, iron, and control groups, respectively. These results suggest that in hemodialysis patients with a functional iron deficiency, treatment with intravenous ascorbic acid can prevent iron overload due to treatment with intravenous iron, and provide a useful adjuvant means of maintaining hemoglobin and serum iron levels.
authors.affiliation: Department of Medicine, Fuji Hospital, Shizuoka, Japan.
authors.forename: Makoto
authors.initials: M
authors.lastname: Ogi
authors.forename: Tomohide
authors.initials: T
authors.lastname: Horiuchi
authors.forename: Ryoetsu
authors.initials: R
authors.lastname: Abe
authors.forename: Masanori
authors.initials: M
authors.lastname: Wakabayashi
authors.forename: Tsunemichi
authors.initials: T
authors.lastname: Wakabayashi
mesh_terms: D000368:Aged; D018798:Anemia, Iron-Deficiency / Q000175:diagnosis / Q000188:drug therapy* / Q000209:etiology*; D001205:Ascorbic Acid / Q000008:administration & dosage*; D015415:Biomarkers / Q000097:blood; D005260:Female; D005290:Ferric Compounds / Q000008:administration & dosage*; D000077605:Ferric Oxide, Saccharated; D005293:Ferritins / Q000097:blood; D005937:Glucaric Acid; D006801:Humans; D007501:Iron / Q000097:blood; D007676:Kidney Failure, Chronic / Q000150:complications; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis / Q000009:adverse effects*; D012189:Retrospective Studies; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D005290:Ferric Compounds; D005293:Ferritins; D007501:Iron; D000077605:Ferric Oxide, Saccharated; D001205:Ascorbic Acid; D005937:Glucaric Acid