Iron deficiency and its management in patients undergoing lipoprotein apheresis. Comparison of two parenteral iron formulations.
OBJECTIVE
There is evidence of iron deficiency (ID) in patients treated with lipoprotein apheresis. Aim of this study was to assess ID in apheresis patients and to study its management comparing safety and efficacy of two approved intravenous (i.v.) iron formulations.


METHODS
Inclusion criteria were defined as a) serum ferritin < 300 μg/l and transferrin saturation < 20%, b) ferritin < 100 μg/l. Both iron deficient alone and ID anemic (IDA) patients were included. Other causes for anemia were ruled out by thorough history-taking and examination/blood tests. Patients were treated with six different lipoprotein apheresis methods: DALI, Liposorber D, TheraSorb LDL, HELP, MONET and Lipidfiltration. 50 patients were randomized to either ferric carboxymaltose (FCM, 500-1000 mg as single shot infusion over 20 min) or ferric gluconate (FG, 62.5 mg once weekly).


RESULTS
50 of 67 patients of our Lipoprotein Apheresis Center showed iron deficiency. Both i.v. iron formulations studied were equally safe (no serious adverse events (SAEs), 6 patients/group showed adverse events (AEs)) and both effective (clinically and with respect to laboratory data) in lipoprotein apheresis patients, however FCM led to a more rapid and steeper rise of iron parameters.


CONCLUSIONS
ID and IDA are common findings in lipoprotein apheresis patients. The pathogenesis remains yet poorly understood and is probably multifactorial. Differential diagnosis of ID/IDA is as essential as differential therapy. Handled with care, older i.v. iron preparations like FG appear to be safe and effective in lipoprotein apheresis patients. However, novel formulations like FCM can be administered rapidly at higher doses due to high complex stability, allowing faster filling of iron stores. Newer laboratory parameters (Reticulocyte-He, low/medium/high fluorescence reticulocytes (LFR/MFR/HFR)) assessing iron status may be helpful in early detection of ID and in monitoring iron replacement therapy.
Department of Internal Medicine III, University Hospital Carl Gustav Carus Dresden, Fetscherstrasse 74, 01307 Dresden, Germany. Ulrike.Schatz@uniklinikum-dresden.de
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Schatz
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Arneth
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Siegert
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Siegels
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Fischer
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Julius
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Bornstein
D000368:Aged; D018798:Anemia, Iron-Deficiency / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy* / Q000209:etiology; D015415:Biomarkers / Q000097:blood; D001781:Blood Component Removal / Q000009:adverse effects; D002626:Chemistry, Pharmaceutical; D004334:Drug Administration Schedule; D050171:Dyslipidemias / Q000097:blood / Q000175:diagnosis / Q000628:therapy*; D005260:Female; D005290:Ferric Compounds / Q000008:administration & dosage* / Q000009:adverse effects / Q000737:chemistry; D005293:Ferritins / Q000097:blood; D005858:Germany; D006397:Hematinics / Q000008:administration & dosage* / Q000009:adverse effects / Q000737:chemistry; D006801:Humans; D007262:Infusions, Intravenous; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008320:Maltose / Q000008:administration & dosage / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000737:chemistry; D008875:Middle Aged; D013997:Time Factors; D014168:Transferrin / Q000378:metabolism; D016896:Treatment Outcome
D015415:Biomarkers; D005290:Ferric Compounds; D006397:Hematinics; D008074:Lipoproteins; D014168:Transferrin; C522335:ferric carboxymaltose; D008320:Maltose; D005293:Ferritins; C035552:ferric gluconate