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 pla...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). Material and 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.展开更多
文摘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). Material and 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.
