American Journal of Gastroenterology ISSN 0002-9270

C 2005 by Am. Coll. of Gastroenterology doi: 10.1111/j.1572-0241.2005.00250.x
Published by Blackwell Publishing

Intravenous Iron Sucrose versus Oral Iron Supplementation

for the Treatment of Iron Deficiency Anemia in Patients
with Inflammatory Bowel DiseaseA Randomized,
Controlled, Open-Label, Multicenter Study
Oliver Schroder, M.D.,1 Oliver Mickisch, M.D.,2 Ursula Seidler, M.D.,3 Andreas de Weerth, M.D.,4 Axel U.
Dignass, M.D.,5 Hans Herfarth, M.D.,6 Max Reinshagen, M.D.,7 Stefan Schreiber, M.D.,8 Ulrich Junge, M.D.,9
Marc Schrott, PharmD.,1 and Jurgen Stein, M.D., Ph.D.1
1
First Department of Internal Medicine, Division of Gastroenterology, ZAFES, Johann Wolfgang
Goethe-University, Frankfurt, Germany; 2 Private Gastroenterology Practice, Mannheim, Germany;
3
Department of Gastroenterology, Hepatology, and Endocrinology, Hannover Medical School, Hannover,
Germany; 4 Department of Medicine, University Hospital Eppendorf, Hamburg, Germany; 5 Charite Medical
School-Virchow Clinic, Department of Medicine, Division of Hepatology and Gastroenterology, Berlin,
Germany; 6 Department of Internal Medicine I, University of Regensburg, Regensburg, Germany;
7
Department of Medicine I, University of Ulm, Ulm, Germany; 8 First Department of Medicine,
Christian-Albrechts-University, Kiel, Germany; and 9 Municipal Hospitals Bielefeld, Hospital Rosenhohe,
Bielefeld, Germany

OBJECTIVES: Anemia is a frequent complication in patients with inflammatory bowel disease (IBD). The optimal
route for iron supplementation to replenish iron stores has not been determined so far. We therefore
evaluated the efficacy and safety of intravenous iron sucrose as compared with oral iron sulfate for
the treatment of iron deficiency anemia (IDA) in patients with IBD.
METHODS: A randomized, prospective, open-label, multicenter study was performed in 46 patients with anemia
and transferrin saturation 20% and/or serum ferritin concentrations 20 g/L. The intravenous
group received a single dose of iron sucrose of 7 mg iron/kg body weight, followed by five 200 mg
infusions for the following 5 wks. The oral group received iron sulfate 100200 mg per day for 6 wks.
RESULTS: While a comparable increase in hemoglobin was observed for both administration routes (median
increase 0.25 g/L in the intravenous group vs 0.21 g/L in the oral group), only iron sucrose led to a
rise in serum ferritin concentrations. Intractable gastrointestinal adverse events caused permanent
study drug discontinuation in five patients (20.8%) receiving iron sulfate, whereas only one patient
(4.5%) had to be withdrawn because of side effects due to iron sucrose.
CONCLUSIONS: Although being equal in short-term efficacy and overall tolerability our results suggest a better
gastrointestinal tolerability for iron sucrose. Larger trials are mandatory to prove a possible
advantage of iron sucrose in short- and long-term efficacy as well as in tolerability over iron sulfate in
the management of IDA in IBD.
(Am J Gastroenterol 2005;100:25032509)

INTRODUCTION loss from the gut, suppression of erythropoietin production,

Iron deficiency anemia (IDA) is a frequent complication in
inflammatory bowel disease (IBD), with a prevalence rang-
ing from 17% to 70% (14). It has significant impact on the
quality of life (QoL) in affected patients. IDA is not only char-
acterized by a higher score of disease activity, loss of weight,
and impaired physical activity but also by developmental and
cognitive abnormalities in children and adolescents (5). The
causes of IDA in IBD are thought to include chronic blood
and alteration of iron metabolism by proinflammatory cy-
tokines, reactive oxygen metabolites, and nitric oxide (for
review see 6).
Until recently, oral iron supplementation has been the
mainstay therapy for anemia in IBD. However, this treat-
ment is limited by poor absorption and frequent side ef-
fects, thereby straining resources of clinicians and challeng-
ing the patients compliance (7, 8). Moreover, there is a legiti-
mate concern that oral iron may exacerbate inflammation and

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