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Anker, S.D., Kirwan, B.A., van Veldhuisen, D.J., Filippatos, G., Comin-Colet, J., Ruschitzka, F., Luscher, T.F., Arutyunov, G.P., Motro, M., Mori, C., Roubert, B., Pocock, S.J. and Ponikowski, P. (2018) Effects of Ferric Carboxymaltose on Hospitalisations and Mortality Rates in Iron-Deficient Heart Failure Patients: An Individual Patient Data Meta-Analysis. European Journal of Heart Failure, 20, 125-133.
https://doi.org/10.1002/ejhf.823

has been cited by the following article:

• TITLE: Iron Succinate Increased Ferritin and Transferrin Saturation in Non-Anaemic Patients with Heart Failure and Iron Deficiency—A Pilot Study

  AUTHORS: Kurt Boman, Mona Olofsson

  KEYWORDS: Iron Deficiency, Non-Anemic, Heart Failure, Iron Succinate

  JOURNAL NAME: World Journal of Cardiovascular Diseases, Vol.11 No.1, January 13, 2021

  ABSTRACT: Introduction: Iron deficiency (ID) is often present (32% - 65%) in patients with heart failure (HF). Oral iron absorption in patients with HF is generallypoor. This is the reason why oral treatment is not recommended. Aim: To test whether oral iron succinate significantly increases iron deposits in non-anaaemic patients with HF. Methods: ID was defined as ferritin 2+ plus 100 mg succinate) in the morning and one tablet at bedtime for at least 3 months. Hemoglobin, CRP, ferritin, iron, TSAT, and hepcidin were analyzed before starting treatment, at 6 weeks, and at 3 months end of study (EOS). Results: Five women and 15 men were included in the study. The level of ferritin increased significantly from baseline to 6 weeks (47 to 78 μg/L, p = 0.009) and baseline to EOS (47 to 85 μg/L, p = 0.001). TSAT increased significantly from baseline to 6 weeks (20% to 27%, p = 0.046) and baseline to EOS (20% to 25%, p = 0.043). Hepcidin increased significantly from baseline to 6 weeks (2.5 nmol/L to 4.8 nmol/L, p = 0.006) and baseline to EOS (2.5 to 4.2 nmol/L, p = 0.02). Conclusion: Oral iron succinate significantly increased iron uptake, almost doubling the ferritin levels and increasing the TSAT, in patients with HF. Our findings challenge the opinion that oral iron treatment cannot significantly increase iron deposits in non-anemic patients with ID and HF.