Ferric carboxymaltose increases fracture risk in patients and reduces bone formation in mice with iron deficiency anemia

S Sonja A. Wagner (1Christian Doppler Laboratory for Iron and Phosphate Biology, Medical University of Innsbruck, Innsbruck, Austria) M Marlene Panzer (1Christian Doppler Laboratory for Iron and Phosphate Biology, Medical University of Innsbruck, Innsbruck, Austria) E Elke Pertler S Stefan Redl M Martina Saretto (2Department of Internal Medicine I, Medical University of Innsbruck, Innsbruck, Austria) B Benedikt Schaefer L Lorenz M. Pammer (2Department of Internal Medicine I, Medical University of Innsbruck, Innsbruck, Austria) L Laura Obholzer (2Department of Internal Medicine I, Medical University of Innsbruck, Innsbruck, Austria) M Maria R. Troppmair M Michael W. Hess (Institute of Histology and Embryology, Medical University of Innsbruck) W Willi Salvenmoser (5Institute of Zoology, Leopold-Franzens University of Innsbruck, Innsbruck, Austria) G Gerald Degenhart M Marisa Grossgut (1Christian Doppler Laboratory for Iron and Phosphate Biology, Medical University of Innsbruck, Innsbruck, Austria) H Heribert Talasz (7Institute of Medical Biochemistry, Protein Core Facility, Biocenter, Medical University of Innsbruck, Innsbruck, Austria) K Klaus Faserl B Bettina Sarg (Institute of Medical Biochemistry, Protein Core Facility, Biocenter, Medical University of Innsbruck) R Roland Haubner (8Department of Nuclear Medicine, Medical University of Innsbruck, Innsbruck, Austria) M Markus A. Hartmann (91st Medical Department, Ludwig Boltzmann Institute of Osteology at Hanusch-Hospital of Oesterreichische Gesundheitskasse and Allgemeine Unfallversicherungsanstalt Trauma Centre Meidling, Hanusch Hospital, Vienna, Austria) S Stéphane Blouin (91st Medical Department, Ludwig Boltzmann Institute of Osteology at Hanusch-Hospital of Oesterreichische Gesundheitskasse and Allgemeine Unfallversicherungsanstalt Trauma Centre Meidling, Hanusch Hospital, Vienna, Austria) V Verena Petzer P Petra Gronich-Wondrak (2Department of Internal Medicine I, Medical University of Innsbruck, Innsbruck, Austria) A Andreas Kronbichler C Claudia Manzl (12Institute of Neuropathology and Neuromolecular Pathology, Medical University of Innsbruck, Innsbruck, Austria) B Bernhard Glodny (6University Clinic for Radiology, Core Facility MicroCT, Medical University of Innsbruck, Innsbruck, Austria) H Herbert Tilg A Andre Franke M Myles Wolf (14Weill Department of Medicine, Weill Cornell Medical College, New York, NY) M Michel V. Hadjihannas (13Institute of Clinical Molecular Biology, University Hospital Schleswig-Holstein, Christian Albrecht University Kiel, Kiel, Germany) H Heinz Zoller

Abstract

Abstract Modern IV iron formulations allow treatment of iron deficiency anemia (IDA) with 1 or 2 infusions. Ferric carboxymaltose (FCM) is a widely used IV iron, which causes hypophosphatemia in most of the patients. Osteomalacia and fractures are increasingly recognized after repeated infusions of FCM. It is unknown why ferric derisomaltose (FDI) rarely causes hypophosphatemia. In this study, we compare the effects of FCM and FDI on fracture risk and investigate potential underlying mechanisms explaining the different effects on bone and mineral metabolism. For this aim, fracture rate and osteomalacia were assessed in a cohort of 357 patients treated with either drug, who reported a significantly higher rate of incident osteomalacia or fracture after FCM. These findings were validated in >20 000 patients from the TriNetX database, where FCM treatment was independently associated with a higher fracture risk compared with FDI. The underlying mechanisms were investigated in a mouse model of IDA treated with FCM or FDI, an osteocyte model, and biochemically. FCM caused lower expression of collagen and ossification genes, associated with significantly higher bone iron concentrations than FDI. Electron microscopy showed iron-loaded vesicles in osteoblasts and early osteocytes. FCM but not FDI inhibited the binding of dentin matrix protein 1 to αVβ3-integrin on osteocytes. This is a potential mechanism for reduced bone formation and higher levels of intact fibroblast growth factor 23 after FCM. Our data report that IDA and FCM treatment can directly impair bone formation and increase fracture risk.

Article Details

Journal Blood
Volume / Issue Vol. 148, Issue 1
Published July 02, 2026
Pages 15-30
ISSN 0006-4971
Publisher Elsevier BV

Journal Info

Blood

Elsevier BV

ISSN: 0006-4971 Health Sciences

Authors (29)

S

Sonja A. Wagner

1Christian Doppler Laboratory for Iron and Phosphate Biology, Medical University of Innsbruck, Innsbruck, Austria

M

Marlene Panzer

1Christian Doppler Laboratory for Iron and Phosphate Biology, Medical University of Innsbruck, Innsbruck, Austria

E

Elke Pertler

S

Stefan Redl

M

Martina Saretto

2Department of Internal Medicine I, Medical University of Innsbruck, Innsbruck, Austria

B

Benedikt Schaefer

L

Lorenz M. Pammer

2Department of Internal Medicine I, Medical University of Innsbruck, Innsbruck, Austria

L

Laura Obholzer

2Department of Internal Medicine I, Medical University of Innsbruck, Innsbruck, Austria

M

Maria R. Troppmair

M

Michael W. Hess

Institute of Histology and Embryology, Medical University of Innsbruck

W

Willi Salvenmoser

5Institute of Zoology, Leopold-Franzens University of Innsbruck, Innsbruck, Austria

G

Gerald Degenhart

M

Marisa Grossgut

1Christian Doppler Laboratory for Iron and Phosphate Biology, Medical University of Innsbruck, Innsbruck, Austria

H

Heribert Talasz

7Institute of Medical Biochemistry, Protein Core Facility, Biocenter, Medical University of Innsbruck, Innsbruck, Austria

K

Klaus Faserl

B

Bettina Sarg

Institute of Medical Biochemistry, Protein Core Facility, Biocenter, Medical University of Innsbruck

R

Roland Haubner

8Department of Nuclear Medicine, Medical University of Innsbruck, Innsbruck, Austria

M

Markus A. Hartmann

91st Medical Department, Ludwig Boltzmann Institute of Osteology at Hanusch-Hospital of Oesterreichische Gesundheitskasse and Allgemeine Unfallversicherungsanstalt Trauma Centre Meidling, Hanusch Hospital, Vienna, Austria

S

Stéphane Blouin

91st Medical Department, Ludwig Boltzmann Institute of Osteology at Hanusch-Hospital of Oesterreichische Gesundheitskasse and Allgemeine Unfallversicherungsanstalt Trauma Centre Meidling, Hanusch Hospital, Vienna, Austria

V

Verena Petzer

P

Petra Gronich-Wondrak

2Department of Internal Medicine I, Medical University of Innsbruck, Innsbruck, Austria

A

Andreas Kronbichler

C

Claudia Manzl

12Institute of Neuropathology and Neuromolecular Pathology, Medical University of Innsbruck, Innsbruck, Austria

B

Bernhard Glodny

6University Clinic for Radiology, Core Facility MicroCT, Medical University of Innsbruck, Innsbruck, Austria

H

Herbert Tilg

A

Andre Franke

M

Myles Wolf

14Weill Department of Medicine, Weill Cornell Medical College, New York, NY

M

Michel V. Hadjihannas

13Institute of Clinical Molecular Biology, University Hospital Schleswig-Holstein, Christian Albrecht University Kiel, Kiel, Germany

H

Heinz Zoller