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1.
Inflamm Bowel Dis ; 13(12): 1545-53, 2007 Dec.
Article in English | MEDLINE | ID: mdl-17985376

ABSTRACT

Anemia is a common complication of inflammatory bowel diseases. An international working party has formed and developed guidelines for evaluation and treatment of anemia and iron deficiency that should serve practicing gastroenterologists. Within a total of 16 statements, recommendations are made regarding diagnostic measures to screen for iron- and other anemia-related deficiencies regarding the triggers for medical intervention, treatment goals, and appropriate therapies. Anemia is a common cause of hospitalization, prevents physicians from discharging hospitalized patients, and is one of the most frequent comorbid conditions in patients with inflammatory bowel disease. It therefore needs appropriate attention and specific care.


Subject(s)
Anemia/diagnosis , Anemia/therapy , Inflammatory Bowel Diseases/complications , Blood Transfusion , Female , Hematinics/therapeutic use , Humans , Iron/therapeutic use , Male , Vitamins/therapeutic use
2.
Drug Target Insights ; 2: 221-8, 2007.
Article in English | MEDLINE | ID: mdl-21901076

ABSTRACT

BACKGROUND: Intestinal microbiota seems to play an essential role in the development of inflammatory bowel diseases (IBD). We hypothesised that an oral vaccine based on live Salmonella typhi would be well tolerated and could even attenuate dextran sulfate sodium (DSS) induced colitis in rats, an animal model of IBD. METHODS: Nine male Wistar rats was used for an initial tolerance study, in which we used 3 dose-levels of Salmonella Ty21a, 0.5 × 10(9), 1 × 10(9), and 2 × 10(9)CFU, each dose being tested in 3 rats. Four treatment groups consisting of 8 male Wistar rats per group: 1) control group given standard food and water, 2) control group given four daily administrations of Salmonella Ty21a 1 × 10(9) CFU, 3) water with 5% DSS the last 7 days, 4) four daily administrations of Salmonella Ty21a before water with 5% DSS the last 7 days. The Salmonella Ty21a was administered by gastric gavage on day 1, 3, 5 and 16, while DSS was given with the drinking water from day 15 to 22. The animals were sacrificed and colonic tissue removed for analysis 22 days after gavage of the first vaccine dose. RESULTS: The animals in the tolerance study got no signs of disease. In the treatment study, all animals receiving DSS had histologic indications of colitis, particularly in the distal part of the colon. Administration of Salmonella Ty21a had no significant effect on crypt and inflammation scores (p > 0.05). CONCLUSION: Gastric administration of live vaccine strain Salmonella Ty21a was well tolerated, but did not provide any significant protection against development of DSS induced colitis in rats.

3.
Scand J Gastroenterol ; 40(9): 1058-65, 2005 Sep.
Article in English | MEDLINE | ID: mdl-16165718

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). 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.


Subject(s)
Colitis, Ulcerative/drug therapy , Crohn Disease/drug therapy , Ferric Compounds/administration & dosage , Ferrous Compounds/administration & dosage , Administration, Oral , Adolescent , Adult , Antioxidants/metabolism , Biomarkers/metabolism , C-Reactive Protein/metabolism , Chromatography, High Pressure Liquid , Colitis, Ulcerative/metabolism , Crohn Disease/metabolism , Cross-Over Studies , Feces/chemistry , Female , Ferric Oxide, Saccharated , Follow-Up Studies , Glucaric Acid , Humans , Injections, Intravenous , Leukocyte L1 Antigen Complex/analysis , Male , Malondialdehyde/blood , Middle Aged , Severity of Illness Index , Treatment Outcome
4.
Inflamm Bowel Dis ; 11(8): 744-8, 2005 Aug.
Article in English | MEDLINE | ID: mdl-16043990

ABSTRACT

BACKGROUND: Oral ferrous iron therapy may reinforce intestinal inflammation. One possible mechanism is by catalyzing the production of reactive oxygen species. We studied the effects of low-dose oral ferrous fumarate on intestinal inflammation and plasma redox status in dextran sulfate sodium (DSS)-induced colitis in rats. METHODS: Forty male Wistar rats were divided into 5 groups: no intervention, sham gavage (distilled water), ferrous fumarate, DSS, and ferrous fumarate + DSS. Ferrous fumarate was dissolved in distilled water (0.60 mg Fe/kg per day) and administered by gavage on days 1 to 14. All rats were fed a standard diet. Colitis was induced by 5% DSS in drinking water on days 8 to 14. Rats were killed on day 16. Histologic colitis scores, fecal granulocyte marker protein, plasma malondialdehyde, plasma antioxidant vitamins, and plasma aminothiols were measured. RESULTS: DSS significantly increased histologic colitis scores (P < 0.001) and fecal granulocyte marker protein (P < 0.01). Ferrous fumarate further increased histologic colitis scores (P < 0.01) in DSS-induced colitis. DSS + ferrous fumarate decreased plasma vitamin A compared with controls (P < 0.01). Otherwise, no changes were seen in plasma malondialdehyde, plasma antioxidant vitamins, or plasma aminothiols. CONCLUSION: Low-dose oral ferrous iron enhanced intestinal inflammation in DSS-induced colitis in rats.


Subject(s)
Colitis, Ulcerative/drug therapy , Colitis, Ulcerative/pathology , Ferrous Compounds/adverse effects , Ferrous Compounds/pharmacology , Intestinal Mucosa/drug effects , Administration, Oral , Analysis of Variance , Animals , Biopsy, Needle , Confidence Intervals , Dextran Sulfate , Disease Models, Animal , Dose-Response Relationship, Drug , Immunohistochemistry , Intestinal Mucosa/pathology , Male , Oxidative Stress/physiology , Probability , Random Allocation , Rats , Rats, Wistar , Reference Values , Sensitivity and Specificity
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