title: Effects of ferrous sulphate and non-ionic iron-polymaltose complex on markers of oxidative tissue damage in patients with inflammatory bowel disease.
abstract: BACKGROUND
  Iron deficiency is a common complication of inflammatory bowel disease. Oral iron therapy may reinforce intestinal tissue injury by catalyzing production of reactive oxygen species.
  
  
  OBJECTIVE
  To compare the effects of ferrous sulphate and non-ionic iron-polymaltose complex on markers of oxidative tissue damage and clinical disease activity in patients with inflammatory bowel disease.
  
  
  METHODS
  Forty-one patients with inflammatory bowel disease and iron deficiency were randomized to treatment with ferrous sulphate 100 mg twice a day or iron-polymaltose complex 200 mg once a day for 14 days.
  
  
  RESULTS
  Following ferrous sulphate, plasma malondialdehyde increased (P = 0.02), while urine 8-isoprostaglandin F(2alpha) and plasma antioxidants did not change significantly. Iron-polymaltose complex did not change plasma malondialdehyde, urine 8-isoprostaglandin F(2alpha) or plasma antioxidants. Comparing the two treatments, changes in plasma malondialdehyde tended to differ (P = 0.08), while urine 8-isoprostaglandin F(2alpha) and plasma antioxidants did not differ. Neither ferrous sulphate nor iron-polymaltose complex altered clinical disease activity indices.
  
  
  CONCLUSIONS
  Ferrous sulphate increased plasma malondialdehyde, a marker of lipid peroxidation. Comparing treatment with ferrous sulphate and iron-polymaltose complex, changes in plasma malondialdehyde tended to differ. Clinical disease activity was unchanged after both treatments.
authors.affiliation: Department of Medicine, University of Bergen, Bergen, Norway. kari.erichsen@helse-bergen.no
authors.forename: K
authors.initials: K
authors.lastname: Erichsen
authors.forename: R J
authors.initials: RJ
authors.lastname: Ulvik
authors.forename: T
authors.initials: T
authors.lastname: Grimstad
authors.forename: A
authors.initials: A
authors.lastname: Berstad
authors.forename: R K
authors.initials: RK
authors.lastname: Berge
authors.forename: T
authors.initials: T
authors.lastname: Hausken
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000975:Antioxidants / Q000032:analysis; D015415:Biomarkers / Q000097:blood; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D005260:Female; D005290:Ferric Compounds / Q000008:administration & dosage*; D005296:Ferrous Compounds / Q000008:administration & dosage*; D006397:Hematinics / Q000008:administration & dosage*; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000188:drug therapy*; D000090463:Iron Deficiencies; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D010084:Oxidation-Reduction / Q000187:drug effects; D018384:Oxidative Stress / Q000502:physiology; D011446:Prospective Studies; D017382:Reactive Oxygen Species / Q000008:administration & dosage; D013607:Tablets; D014662:Vasoconstrictor Agents / Q000652:urine
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D005290:Ferric Compounds; D005296:Ferrous Compounds; D006397:Hematinics; D017382:Reactive Oxygen Species; D013607:Tablets; D014662:Vasoconstrictor Agents; C075750:8-epi-prostaglandin F2alpha; C020748:ferrous sulfate; D008315:Malondialdehyde; D015237:Dinoprost; C013276:teferrol