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PLoS One. 2016 Dec 1;11(12):e0167146. doi: 10.1371/journal.pone.0167146. eCollection 2016.

Choice of High-Dose Intravenous Iron Preparation Determines Hypophosphatemia Risk.

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Medical University of Innsbruck, Department of Medicine II, Gastroenterology and Hepatology, Anichstr. Innsbruck, Austria.
Central Institute for Medical and Chemical Laboratory Diagnosis, Innsbruck University Hospital, Anichstr. Innsbruck, Austria.
Medical Research Council (MRC) Human Nutrition Research, Elsie Widdowson Laboratories, Fulbourn Road, Cambridge, United Kingdom.
Medical University of Innsbruck, Department of Medicine I, Gastroenterology, Endocrinology and Metabolism, Anichstr. Innsbruck, Austria.
Medical University of Vienna, Department of Pathology, Währingergürtel, Vienna, Austria.



Ferric carboxymaltose (FCM) and iron isomaltoside 1000 (IIM) are increasingly used because they allow correction of severe iron deficiency in a single infusion. A transient decrease in serum phosphate concentrations is a frequent side effect of FCM.


To characterize this adverse event and search for its predictors in a gastroenterology clinic patient cohort.


Electronic medical records of patients attending the University Hospital of Innsbruck were searched for the keywords ferric carboxymaltose or iron isomaltoside. Eighty-one patients with documented administration of FCM or IIM with plasma phosphate concentrations before and after treatment were included.


The prevalence of hypophosphatemia (<0.8 mmol/L) increased from 11% to 32.1% after treatment with i.v. iron. The hypophosphatemia risk was greater after FCM (45.5%) compared with IIM (4%). Severe hypophosphatemia (<0.6 mmol/L) occurred exclusively after FCM (32.7%). The odds for hypophosphatemia after i.v. iron treatment were independently determined by baseline phosphate and the choice of i.v. iron preparation (FCM vs. IIM-OR = 20.8; 95% CI, 2.6-166; p = 0.004). The median time with hypophosphatemia was 41 days, but prolonged hypophosphatemia of ≥ 2 months was documented in 13 of 17 patients in whom follow-up was available. A significant increase in the phosphaturic hormone intact FGF-23 in hypophosphatemic patients shows that this adverse event is caused by FCM-induced hormone dysregulation.


Treatment with FCM is associated with a high risk of developing severe and prolonged hypophosphatemia and should therefore be monitored. Hypophosphatemia risk appears to be substantially lower with IIM.

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