Alimentary Pharmacology & Therapeutics · 2005 · 72 citations · 27 references
MedicineBiochemistryNutritional SciencesInflammationIron Metabolism DisordersMicronutrient DeficiencyInflammatory Bowel DiseaseIron Chelation TherapyIron DeficiencyIron Deficiency DisordersIron MetabolismOxidative Stress In InflammationAntioxidantsIron Deficiency TreatmentLipid Peroxidation MarkersMalondialdehyde FormationOral Iron SupplementationOxidative Damage BiomarkersReactive Oxygen Species GenerationReactive Oxygen Species Injury
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. AIM: 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.
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Development of a Crohn's Disease Activity Index
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