Related Experiment Video
Updated: Jun 7, 2025
05:23
Continuous Manual Exchange Transfusion for Patients with Sickle Cell Disease: An Efficient Method to Avoid Iron Overload
Published on: March 14, 2017
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[Muscle weakness after intravenous iron replacement]
Laura Giezendanner1,2, Franziska Vogler1, Andrea Hausammann1
1Klinik für Allgemeine Innere Medizin/Hausarztmedizin und Notfallmedizin, Kantonsspital St. Gallen Rorschacherstrasse 95, 9007 St. Gallen.
Praxis
|November 12, 2024
Summary
Intravenous iron infusion can cause severe hypophosphatemia, a condition marked by low phosphate levels. This occurs due to elevated Fibroblast Growth Factor 23 (FGF23), impacting kidney and intestinal phosphate absorption.
Area of Science:
- Endocrinology
- Nephrology
- Hematology
Background:
- Iron-deficiency-anemia requires treatment with intravenous iron infusions.
- Severe hypophosphatemia developed in a young female patient post-infusion.
- Associated symptoms included mild muscle weakness.
Purpose of the Study:
- To investigate the link between ferric carboxymaltose infusion and hypophosphatemia.
- To understand the role of Fibroblast Growth Factor 23 (FGF23) in this condition.
- To highlight potential diagnostic challenges.
Main Methods:
- Case report analysis.
- Biochemical analysis of serum phosphate and FGF23 levels.
- Assessment of renal phosphate handling.
Main Results:
- Diagnosis of hypophosphatemia attributed to ferric carboxymaltose.
- Elevated serum FGF23 levels confirmed.
- Evidence of renal phosphate wasting observed.
Conclusions:
- Ferric carboxymaltose can induce hypophosphatemia.
- Elevated FGF23 is a key mechanism.
- Awareness is crucial as symptoms may be masked by iron repletion.
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