SAT-796 - Not All Hypophosphatemia Is PTH-Driven: A Case of Ferrous Carboxymaltose-Induced Phosphate Wasting

Background:
Hypophosphatemia is a recognized but often underappreciated complication of intravenous iron therapy, particularly ferrous carboxymaltose (FCM), mediated by fibroblast growth factor 23 (FGF23). In patients with competing etiologies for phosphate wasting, diagnosis may be delayed or misattributed.

Clinical

Case:
A 63-year-old woman with early T-ALL in remission on Ruxolitinib, nonfunctioning pituitary macroadenoma, and recent zoledronic acid exposure presented with myalgia, generalized weakness, and fever. Laboratory evaluation revealed severe hypophosphatemia (phosphate < 0.8 mg/dL), hypocalcemia (7.1 mg/dL), and markedly elevated parathyroid hormone (PTH 784 pg/mL). Differential diagnosis for hypophosphatemia included secondary hyperparathyroidism related to bisphosphonate use, vitamin D or PTH resistance, and/or impaired intestinal phosphate absorption from PPI use. Further evaluation demonstrated elevated urinary phosphate excretion, increased FGF23 levels, and elevated 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D concentrations. Medication review revealed intravenous FCM administration several weeks prior to presentation, consistent with a delayed adverse effect. Although zoledronic acid–induced secondary hyperparathyroidism was initially considered, the severity of hypophosphatemia, disproportionate elevation of FGF23, temporal relationship to FCM administration, and dissociation between phosphate and PTH recovery were most consistent with FCM-induced FGF23-mediated renal phosphate wasting.

Discussion:
FCM has been shown to increase intact FGF23 through impaired proteolytic cleavage, resulting in renal phosphate wasting. This case illustrates a diagnostic pitfall in which severe hypophosphatemia was initially attributed to elevated PTH following bisphosphonate exposure.

Conclusion:
This case highlights the importance of recognizing FCM as a cause of severe hypophosphatemia, particularly in patients with overlapping risk factors. Early identification and avoidance of repeat exposure are critical to prevent recurrent metabolic complications.

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