Severe osteomalacia and insufficiency fractures due to combined iron induced hypophosphataemia and malabsorption-related calcium deficiency in a patient with Crohn's disease: A case report
- 1Department of Geriatrics, UZ Leuven, Leuven, Belgium
- 2Department of Geriatrics, Imeldaziekenhuis, Bonheiden, Belgium
- 3Department of Gastroenterology, Ziekenhuis Oost-Limburg (ZOL), Genk, Belgium
Abstract
Ferric carboxymaltose (FCM) induced hypophosphataemia is increasingly recognized as a clinically relevant adverse effect of intravenous iron therapy. In severe and prolonged cases, phosphate depletion may result in osteomalacia, insufficiency fractures, and significant functional impairment. However, longitudinal bone mineral density outcomes after treatment remain poorly documented.
We report a 32-year-old woman with Crohn's disease and chronic iron deficiency anaemia who developed severe hypophosphataemia following repeated FCM infusions. She presented with profound muscle weakness, diffuse bone pain, wheelchair dependence, multiple atraumatic insufficiency fractures, severe hypophosphataemia (0.24 mmol/L), secondary hyperparathyroidism, and markedly reduced bone mineral density (T-score at femoral neck (FN) and lumbar spine (LS) −3.7 and −3.5 respectively). FCM was discontinued and oral phosphate, calcium, and vitamin D supplementation was initiated, followed by active vitamin D and intravenous calcium. Over follow-up, the patient experienced near-complete functional recovery, progressing from wheelchair dependence to independent ambulation. DXA demonstrated an exceptional skeletal recovery, with femoral neck T-score improving from −3.7 to +3.2 (+186%) and lumbar spine T-score from −3.5 to +1.0 (+128%).
This case highlights the possibility of complete recovery and excellent outcomes if drug-induced hypophosphatemia is appropriately recognized and managed. While iron-induced FGF23-mediated hypophosphataemic osteomalacia likely played a major role, additional contributing factors were present, including calcium malabsorption related to inflammatory bowel disease. The magnitude and rapidity of BMD improvement following treatment largely exceed what is typically reported in FCM-induced or other forms of osteomalacia, and illustrates the remarkable reversibility of severe acquired osteomalacia.
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BibTeX
@article{hellemans2026severe,
title = {{Severe osteomalacia and insufficiency fractures due to combined iron induced hypophosphataemia and malabsorption-related calcium deficiency in a patient with Crohn's disease: A case report}},
author = {Elisabeth Hellemans and Jolan Dupont and Marian Dejaeger and Michaël R. Laurent and Evelien Humblet and Evelien Gielen},
journal = {Bone reports},
year = {2026},
month = oct,
doi = {10.1016/j.bonr.2026.101957},
url = {https://europepmc.org/article/PMC/PMC13722024},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Severe osteomalacia and insufficiency fractures due to combined iron induced hypophosphataemia and malabsorption-related calcium deficiency in a patient with Crohn's disease: A case report
AU - Elisabeth Hellemans
AU - Jolan Dupont
AU - Marian Dejaeger
AU - Michaël R. Laurent
AU - Evelien Humblet
AU - Evelien Gielen
PY - 2026
DA - 2026/10/07
JO - Bone reports
DO - 10.1016/j.bonr.2026.101957
UR - https://europepmc.org/article/PMC/PMC13722024
AB - Ferric carboxymaltose (FCM) induced hypophosphataemia is increasingly recognized as a clinically relevant adverse effect of intravenous iron therapy. In severe and prolonged cases, phosphate depletion may result in osteomalacia, insufficiency fractures, and significant functional impairment. However, longitudinal bone mineral density outcomes after treatment remain poorly documented. We report a 32-year-old woman with Crohn's disease and chronic iron deficiency anaemia who developed severe hypophosphataemia following repeated FCM infusions. She presented with profound muscle weakness, diffuse bone pain, wheelchair dependence, multiple atraumatic insufficiency fractures, severe hypophosphataemia (0.24 mmol/L), secondary hyperparathyroidism, and markedly reduced bone mineral density (T-score at femoral neck (FN) and lumbar spine (LS) −3.7 and −3.5 respectively). FCM was discontinued and oral phosphate, calcium, and vitamin D supplementation was initiated, followed by active vitamin D and intravenous calcium. Over follow-up, the patient experienced near-complete functional recovery, progressing from wheelchair dependence to independent ambulation. DXA demonstrated an exceptional skeletal recovery, with femoral neck T-score improving from −3.7 to +3.2 (+186%) and lumbar spine T-score from −3.5 to +1.0 (+128%). This case highlights the possibility of complete recovery and excellent outcomes if drug-induced hypophosphatemia is appropriately recognized and managed. While iron-induced FGF23-mediated hypophosphataemic osteomalacia likely played a major role, additional contributing factors were present, including calcium malabsorption related to inflammatory bowel disease. The magnitude and rapidity of BMD improvement following treatment largely exceed what is typically reported in FCM-induced or other forms of osteomalacia, and illustrates the remarkable reversibility of severe acquired osteomalacia.
SN - 2352-1872
ER -