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Endocrine Abstracts (2020) 70 EP72 | DOI: 10.1530/endoabs.70.EP72

ECE2020 ePoster Presentations Bone and Calcium (65 abstracts)

Hypophosphatemia: Collateral damage in parenteral iron administration

Georgiana Cristina Taujan , Felicia Baleanu , Rafik Karmali & Laura Iconaru


Endocrinology, CHU Brugmann, Bruxelles, Belgium


Introduction: Iron-induced hypophosphatemia is a well-known adverse effect in patients receiving parenteral iron supplementation. Initially thought to be transient and mild, it seems that in certain cases, especially in patients who require repeated intravenous iron administrations, it can lead to spectacular symptomatology and serious complications.

Case report: A female patient, aged 61 was referred for intense muscle and bone pain, severe impaired mobility, vertigo and headaches. She has been known with Rendu–Osler syndrome which led to recurrent severe epistaxis and anemia requiring repeated administrations of intravenous ferric carboximaltose for the last 2 years. Laboratory results revealed severe hypophosphatemia (0.49 mmol/l) with hyperphosphaturia (Tmp/GFR 0.21 mmol/l) and an elevated FGF23 level (137 pg/ml). Two months before presentation, the patient was also diagnosed with vitamin D deficiency and secondary hyperparathyroidism (25 OH vitamin D 7 µg/l, PTH 114 ng/l, corrected calcium 2.01 mg/dl) which further increased phosphate renal leak. The correction of hypophosphatemia in this case was achieved after changing the parenteral formula from ferric carboximaltose to saccharated ferric oxide, oral phosphate and vitamin D supplementation confirming the literature according to which a greater risk for hypophosphatemia is associated with ferric carboximaltose through an increase of FGF23.

Discussion: Beyond the major impact on patient’s quality of life, chronic and severe hypophosphatemia may lead to other serious complications such as hemolytic anemia, osteomalacia and fragility bone fractures, cardiac and pulmonary dysfunctions, delirium, seizures and coma. The mechanism in this situation seems to be a decrease in phosphate renal reabsorption and inhibition of renal 1-alpha hydroxylation due to an increase in FGF23 level, which is reported to reach a maximum in the first week after parenteral iron administration. Apparently, the risk of phosphate depletion is related to several risk factors like iron formulation, frequency of administration, renal function, previous vitamin D deficiency or hyperparathyroidism.

Conclusion: Hypophosphatemia should be sought in patients with recurrent parenteral iron administration, with monitoring of phosphate levels during 2–6 weeks after the iron administration. In addition, in order to avoid hypophosphatemia, it seems preferable to use an iron formulation devoid of ferric carboximaltose.

Volume 70

22nd European Congress of Endocrinology

Online
05 Sep 2020 - 09 Sep 2020

European Society of Endocrinology 

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