MON-819 - Unintended Consequences: Iron Infusion Related Hypophosphatemia

Ferric carboxymaltose (FCM) is a widely used intravenous iron formulation that is increasingly recognized to cause clinically significant hypophosphatemia. This effect is mediated by elevations in fibroblast growth factor 23 (FGF23), resulting in renal phosphate wasting, reduced calcitriol production, and secondary hyperparathyroidism. Hypophosphatemia may be prolonged and refractory to phosphate replacement alone.

We present a case of a 52-year-old woman with chronic iron deficiency anemia and intolerance to oral iron who developed severe hypophosphatemia following FCM administration. She has a history of longstanding anemia secondary to menorrhagia necessitating intravenous iron therapy and subsequently a hysterectomy. Shortly after an FCM infusion, she developed muscle cramps, upper extremity pain, and chest discomfort. Laboratory evaluation revealed hypophosphatemia to 1.5 mg/dL (2.5-4.5 mg/dL) with parathyroid hormone level of 111.2 pg/mL (14-72 pg/mL) and normal 25-hydroxyvitamin D levels. FGF23 measured several weeks after exposure was mildly elevated at 60 pg/mL ( < 59 pg/mL).

Despite phosphate supplementation, hypophosphatemia persisted, prompting endocrine consultation. Management included discontinuation of further FCM exposure and initiation of calcitriol to address impaired vitamin D activation and secondary hyperparathyroidism. Serum phosphate levels gradually normalized over subsequent weeks, with resolution of symptoms.

This case underscores FCM-associated hypophosphatemia as an important and underrecognized endocrine complication of intravenous iron therapy. Symptoms may be musculoskeletal and nonspecific; onset may be delayed, and treatment with phosphate alone may be insufficient. Recognition of at-risk patients, avoidance of repeat FCM exposure, and use of active vitamin D are key to effective management. Future studies should evaluate the impact of repeated FCM exposure and prolonged hypophosphatemia on bone outcomes, including osteomalacia and fracture risk, and to develop a standardized guide for monitoring after FCM administration.

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