Severe Concurrent Hypocalcemia and Hypophosphatemia Following Ferric Carboxymaltose After Roux-en-Y Gastric Bypass: A Comparative Two-Patient Case Series

Ferric carboxymaltose (FCM) can cause hypophosphatemia through fibroblast growth factor 23 (FGF23)associated renal phosphate wasting.Patients who have undergone Roux-en-Y gastric bypass may be particularly vulnerable because calcium and vitamin D homeostasis may already be impaired.We describe two women with previous Roux-en-Y gastric bypass who developed severe symptomatic concurrent hypocalcemia and hypophosphatemia after FCM.Both had preexisting mineral vulnerability, and the findings are therefore interpreted as a multifactorial interaction rather than evidence that FCM alone caused the hypocalcemia.The first patient, aged 39 years, received FCM 500 mg weekly for five weeks (cumulative dose approximately 2,500 mg) and developed calcium 5.3 mg/dL and phosphate 0.8 mg/dL, with elevated Cterminal FGF23 and inappropriate urinary phosphate excretion during hypophosphatemia.The second patient, aged 37 years, received FCM 500 mg weekly for two doses (cumulative dose 1,000 mg) and presented approximately seven weeks later with calcium 5.9 mg/dL and a subsequent phosphate nadir of 1.3 mg/dL.Her C-terminal FGF23 was measured during early biochemical recovery and remained elevated; urinary phosphate excretion remained measurable during the hypophosphatemic/repletion period, although interpretation was limited by concurrent treatment.Both required prolonged mineral replacement, and the second patient required multiple admissions and repeated IV calcium.These cases suggest that FCMassociated phosphate disturbance may act as an additional metabolic stressor in post-bariatric patients with reduced calcium and vitamin D reserve, producing a severe combined mineral phenotype rather than isolated hypophosphatemia.