Iron Deficiency and Anaemia in Heart Failure: Understanding the FAIR-HF Trial

José González-Costello; Josep Comín-Colet

Disclosures

Eur J Heart Fail. 2010;12(11):1159-1162. 

In This Article

Treatment of Iron Deficiency

The FAIR-HF trial demonstrated that IV iron therapy in patients with CHF and ID improves their functional status and increases haemoglobin in those that were also anaemic.[16] One may wonder whether oral iron, which is cheaper, could have achieved similar results. We think that most likely the answer is no, because the absorption of oral Fe(II) iron preparations in the anaemia of chronic disease is blocked by hepcidin;[23] these preparations are poorly tolerated, mainly due to gastrointestinal side-effects; and a number of drug interactions may occur, such as with proton pump inhibitors.[20] Also, even if oral iron was absorbed, hepcidin would impair iron delivery to the bone marrow, which is why the anaemia of chronic disease does not respond to oral iron.[23] Intravenous iron, on the other hand, is provided as carbohydrate complexes with iron in its Fe-III form.[20] They are cleared from the bloodstream and taken into the reticuloendothelial system within a few hours of administration. The majority of the dose is deposited in long-term storage, but a portion of this iron is rapidly bound to transferrin and available for transport to the bone marrow,[28] bypassing the restrictions on iron release imposed by hepcidin. In all the clinical trials, large amounts of iron were delivered over minutes or hours as pulse therapy. This could lead to poor utilization of this iron with tissue deposition, free radical formation, and increased risk of infection because of a decrease in cellular immunity and promotion of bacterial growth.[23] However, there was no increase in the risk of infection or cardiovascular events in the FAIR-HF trial.[16] Also, in contrast to dextran iron, currently used IV iron preparations, such as ferric saccharate, ferric gluconate, or ferric carboxymaltose are well tolerated and do not require a test dose as they have fewer hypersensitivity reactions.[29] The total iron dose required for iron repletion in the FAIR-HF trial was calculated according to Ganzoni's formula[30] and was administered as ferric carboxymaltose in weekly doses of 200 mg as an intravenous bolus injection. This is an advantage over the administration of 200 mg of ferric saccharate, which is normally given over a period of 1–2 h, as higher doses can cause hypotension.[29] After this correction phase, a maintenance phase was started, in which 200 mg of iron was given monthly until Week 24. Measures of iron metabolism and haemoglobin were performed every 2 months in the maintenance phase. If the ferritin level exceeded 800 µg/L or was between 500 and 800 µg/L with a TSAT of more than 50%, or if the haemoglobin level was higher than 160 g/L, IV iron was discontinued.[16] It is important to monitor these parameters to avoid iron overload and avoid IV iron in the presence of a suspected infection.

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