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Sirs, We read with interest the article of Silva et al.1 concerning the efficacy and tolerability of oral iron therapy in patients with inflammatory bowel disease (IBD). The authors compared patients with anaemia and IBD and patients with other causes of iron deficiency anaemia treated with oral iron in terms of efficacy, side-effects and pro-oxidant actions of iron. They found that intolerance rate did not differ significantly between IBD and non-IBD patients, and that 4 weeks iron supplementation led to significant rises in haemoglobin (Hb) and iron stores. In IBD patients various markers of disease activity, antioxidant capacity and reactive oxygen metabolite production did not change with the iron therapy. The conclusion of this article that ‘oral iron is equally efficacious and well tolerated in IBD and non-IBD patients’ raises several and important questions.

For many years oral iron supplementation was the mainstay therapy for anaemia in IBD. However, this treatment is limited by several problems the most important being gastrointestinal side-effects and the poor iron absorption.2 Moreover, there is evidence that oral iron increases the clinical disease activity in IBD3 and induces oxidative stress at the site of bowel inflammation.2, 3 It has also been demonstrated in several rodent models of colitis that the intestinal inflammation was aggravated during the course of oral iron supplementation.4, 5

The overall poor tolerability and patients incompliance of oral iron supplementation compared with intravenous iron sucrose has led many doctors including us to prefer the administration of intravenous iron sucrose which has been proved to be effective and safe. Refractory to iron therapy cases can be treated with recombinant human erythropoietin or darbepoetin.2, 6

We feel that Silva et al.1 are inaccurate in the conclusions according to the findings of their study especially on the effects of iron therapy on disease activity in IBD patients. Based on the finding of only two (6%) relapses of disease under oral iron they conclude that oral iron supplementation is only rarely associated with increased IBD activity. However, studying the markers of activity they report that the simple colitis clinical activity score in ulcerative colitis (UC) was significantly changed after iron treatment (P = 0.01). Moreover, there were alterations in the other clinical and laboratory markers indicating more active disease after iron treatment. For example, Harvey-Bradshaw index increased from 3.1 to 3.7 (P = 0.1), and C-reactive protein (CRP) levels increased in both diseases [from 5 to 7 mg/dL in UC (P = 0.06); and from 16 to 22 mg/dL in CD (P = 0.4)]. In addition, sigmoidoscopic grading activity of UC increased from 0 (0.5) to 1 (1.5) (P = 0.06) whereas histological grade increased from 2.0 (4.5) to 4.5 (7.5) (P = 0.5). It seems possible that with larger number of patients these differences would have been statistically significant. Moreover, we think that a longer follow-up period is required than the rather short follow-up (1 month) used in this study.

The data of the literature including the results of Silva et al.1 suggest that the efficacy of oral iron for the treatment of anaemia is similar in IBD and non-IBD patients but there are important concerns about the high intolerance rates (35–44% in the study of Silva et al.1) and the possible deterioration of disease activity. Although the most appropriate route for iron supplementation has not been completely determined, recent data3, 7 and our experience6 suggest that intravenous iron sucrose has a better safety profile that might positively influence the compliance of IBD patients and consequently improve their quality of life.

References

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  2. References
  • 1
    Silva AD, Tsironi E, Feakins RM, Rampton DS. Efficacy and tolerability of oral iron therapy in inflammatory bowel disease: a prospective, comparative trial. Aliment Pharmacol Ther 2005; 22: 1097105.
  • 2
    Gasche C, Lomer MC, Cavill I, Weiss G. Iron, anaemia, and inflammatory bowel diseases. Gut 2004; 53: 11907.
  • 3
    Erichsen K, Ulvik RJ, Nysaeter G, et al. Oral ferrous fumarate or intravenous iron sucrose for patients with inflammatory bowel disease. Scand J Gastroenterol 2005; 40: 105865.
  • 4
    Carrier J, Aghdassi E, Platt I, Cullen J, Allard JP. Effect of oral iron supplementation on oxidative stress and colonic inflammation in rats with induced colitis. Aliment Pharmacol Ther 2001; 15: 198999.
  • 5
    Erichsen K, Milde AM, Arslan G, et al. Low-dose oral ferrous fumarate aggravated intestinal inflammation in rats with DSS-induced colitis. Inflamm Bowel Dis 2005; 11: 7448.
  • 6
    Koutroubakis IE, Karmiris K, Makreas S, Xidakis C, Niniraki M, Kouroumalis EA. Effectiveness of darbepoetin alfa in combination with intravenous iron sucrose in patients with inflammatory bowel disease and refractory anemia. A pilot study. Eur J Gastroenterol Hepatol (in press).
  • 7
    Schroder O, Mickisch O, Seidler U, et al. Intravenous iron sucrose versus oral iron supplementation for the treatment of iron deficiency anemia in patients with inflammatory bowel disease – a randomized, controlled, open-label, multicenter study. Am J Gastroenterol 2005; 100: 25039.
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