Iron, anaemia, and inflammatory bowel diseases

C Gasche, M C E Lomer, I Cavill, G Weiss, C Gasche, M C E Lomer, I Cavill, G Weiss

Abstract

Iron deficiency anaemia is one of the most common disorders in the world. Also, one third of inflammatory bowel disease (IBD) patients suffer from recurrent anaemia. Anaemia has significant impact on the quality of life of affected patients. Chronic fatigue, a frequent IBD symptom itself, is commonly caused by anaemia and may debilitate patients as much as abdominal pain or diarrhoea. Common therapeutic targets are the mechanisms behind anaemia of chronic disease and iron deficiency. It is our experience that virtually all patients with IBD associated anaemia can be successfully treated with a combination of iron sucrose and erythropoietin, which then may positively affect the misled immune response in IBD.

Figures

Figure 1
Figure 1
Iron and erythropoiesis in chronic disease. When erythropoiesis is suppressed, iron which is released at the end of the red cell lifespan and which would normally have been recycled into new haemoglobin is diverted into iron stores. As a result, serum ferritin levels are increased. Iron absorption is driven mainly by erythropoiesis. When this is suppressed, iron absorption is likewise decreased.
Figure 2
Figure 2
Response to iron sucrose in ulcerative colitis and Crohn’s disease. A total of 2 g of iron sucrose were given intravenously within eight weeks: 400 mg/week during the first two weeks and 200 mg/week thereafter. Response was defined as increase in haemoglobin of equal to or above 2 g/dl. Data were collected from two trials.
Figure 3
Figure 3
Iron sucrose versus ferrous sulphate for inflammatory bowel disease associated anaemia. Two controlled studies, both of which were demonstrating the effect of erythropoietin (Epo) in IBD associated anaemia, are outlined. Baseline haemoglobin levels and total Epo dosage were identical. In one trial (A), ferrous sulphate was used for iron supplementation and in the other (B) iron sucrose was given. On ferrous sulphate alone, 100 mg/day, mean haemoglobin level dropped over the 12 week study period. In contrast, iron sucrose caused a considerable haemoglobin increase that was faster and larger when combined with Epo.
Figure 4
Figure 4
Adjusting therapy to the degree of anaemia. The place of oral iron therapy is mainly prevention of iron deficiency anaemia. In patients with normocytic or microcytic anaemia, iron sucrose demonstrates the best efficacy and tolerability. The amount of iron needed relates to the degree of anaemia and can be estimated using the approximation that an increase of 1 g/dl haemoglobin (Hb) requires about 200 mg of intravenous iron. It is recommend that iron therapy is suspended in cases of acute infection (for example, abscess) or at a transferrin saturation >50%. *Instead of transferrin, the soluble transferrin receptor (below 50 nmol/l) or erythropoietin concentration (below 100 U/l) can be applied.

Source: PubMed

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