Case report reveals severe hypocalcemia and hypophosphatemia after ferric carboxymaltose in a gastric bypass patient, highlighting the need for post-treatment monitoring.
Iron deficiency anemia is commonly treated with intravenous iron when oral therapy is ineffective, poorly tolerated, or inadequately absorbed.Ferric carboxymaltose (FCM) is an effective intravenous iron formulation but is increasingly recognized to cause hypophosphatemia through fibroblast growth factor 23 (FGF23)-mediated renal phosphate wasting.Although FCM-induced hypophosphatemia is well described, concurrent clinically significant hypocalcemia is less commonly reported.We present the case of a 39-yearold woman with a history of Roux-en-Y gastric bypass, iron deficiency anemia, and vitamin D deficiency who developed severe symptomatic hypocalcemia and hypophosphatemia following a course of FCM.She presented with generalized muscle cramps, paresthesia, perioral numbness, blurry vision, and fatigue and required repeated hospitalization and intensive electrolyte replacement.Laboratory evaluation demonstrated severe hypocalcemia and hypophosphatemia, elevated C-terminal FGF23, secondary hyperparathyroidism, and inappropriate urinary phosphate loss.Her previous bariatric surgery and vitamin D deficiency likely increased her susceptibility to FCM-associated disturbances in mineral metabolism.This case highlights the importance of identifying patients at increased risk before FCM administration and considering biochemical monitoring after treatment, particularly in individuals with altered gastrointestinal anatomy or pre-existing nutritional deficiencies.
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Elhassan et al. (2026) studied this question.
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