title: Oral ferrous fumarate or intravenous iron sucrose for patients with inflammatory bowel disease.
abstract: OBJECTIVE
  Iron therapy may reinforce intestinal inflammation by catalysing production of reactive oxygen species. The effects of oral ferrous fumarate and intravenous iron sucrose on clinical disease activity and plasma redox status were investigated in patients with inflammatory bowel disease (IBD).
  
  
  METHODS
  Nineteen patients with iron deficiency anaemia and Crohn's disease (11) or ulcerative colitis (8) were included in a crossover study. The patients were randomly assigned to start treatment with ferrous fumarate (Neo-fer) 120 mg orally once daily or iron sucrose (Venofer) 200 mg intravenously 3 times during a period of 14 days. Clinical disease activity assessment and blood and faecal analysis were performed on days 1 and 15.
  
  
  RESULTS
  Following oral ferrous fumarate clinical disease activity (p=0.037), general well-being score (i.e. patients felt worse) (p=0.027) and abdominal pain score (p=0.027) increased, while no changes were seen following iron sucrose treatment. C-reactive protein (CRP) and faecal calprotectin were unchanged after both treatments. As compared with iron sucrose, ferrous fumarate increased Crohn's disease activity index (CDAI) scores of general well-being (p=0.049), whereas alterations in clinical disease activity (p=0.14) and abdominal pain score (p=0.20) did not differ. Ferrous fumarate did not significantly alter plasma malondialdehyde (MDA) or plasma antioxidants. Iron sucrose increased plasma MDA (p=0.004) and decreased plasma vitamin C (p=0.017) and betacarotene (p=0.008).
  
  
  CONCLUSIONS
  Oral ferrous fumarate, but not intravenous iron sucrose, increased clinical disease activity in IBD patients. Intravenous iron sucrose increased intravascular oxidative stress.
authors.affiliation: Department of Medicine, Haukeland University Hospital, Bergen, Norway. kari.erichsen@helse-bergen.no
authors.forename: Kari
authors.initials: K
authors.lastname: Erichsen
authors.forename: Rune J
authors.initials: RJ
authors.lastname: Ulvik
authors.forename: Gunnar
authors.initials: G
authors.lastname: Nysaeter
authors.forename: Jack
authors.initials: J
authors.lastname: Johansen
authors.forename: Jens
authors.initials: J
authors.lastname: Ostborg
authors.forename: Arnold
authors.initials: A
authors.lastname: Berstad
authors.forename: Rolf K
authors.initials: RK
authors.lastname: Berge
authors.forename: Trygve
authors.initials: T
authors.lastname: Hausken
mesh_terms: D000284:Administration, Oral; D000293:Adolescent; D000328:Adult; D000975:Antioxidants / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D002851:Chromatography, High Pressure Liquid; D003093:Colitis, Ulcerative / Q000188:drug therapy* / Q000378:metabolism; D003424:Crohn Disease / Q000188:drug therapy* / Q000378:metabolism; D018592:Cross-Over Studies; D005243:Feces / Q000737:chemistry; D005260:Female; D005290:Ferric Compounds / Q000008:administration & dosage*; D000077605:Ferric Oxide, Saccharated; D005296:Ferrous Compounds / Q000008:administration & dosage*; D005500:Follow-Up Studies; D005937:Glucaric Acid; D006801:Humans; D007275:Injections, Intravenous; D039841:Leukocyte L1 Antigen Complex / Q000032:analysis; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D012720:Severity of Illness Index; D016896:Treatment Outcome
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D005290:Ferric Compounds; D005296:Ferrous Compounds; D039841:Leukocyte L1 Antigen Complex; D008315:Malondialdehyde; D002097:C-Reactive Protein; D000077605:Ferric Oxide, Saccharated; D005937:Glucaric Acid; C031621:ferrous fumarate