MON-491 Persistent Isolated Hypophosphatemia after Intravenous Ferric Carboxymaltose Infusion in a Patient with Total Gastrectomy

Introduction: Intravenous ferric carboxymaltose infusion has been reported by the FDA to cause hypophosphatemia in 2.1% of patients, with transient low phosphorus level (<2mg/dL) observed in 27% of patients. We present a case of persistent hypophosphatemia where intravenous iron appeared to be a significant contributing cause. Clinical case: A 45 year old woman presented with generalized weakness at an outpatient visit and was discovered to have hypophosphatemia with a lab value of 0.9 mg/dL (ref 2.7 – 4.5 mg/dL). She has a history significant for Non-Hodgkin’s Lymphoma (non-Burkitt’s) at age 16 (s/p chemotherapy at age 18),gastroparesis requiring a jejunostomy tube followed by a total gastrectomy 4 months before admission and reactive hypoglycemia from late dumping syndrome due to gastrectomy. Her nutritional intake consisted of small frequent meals along with tube feedings with no recent change in her diet and taking adequate calcium and vitamin D supplements. Nine days prior to this admission, she had a IV ferric carboxymaltose infusion and a phosphorus level of 0.9 mg/dL discovered on outpatient labs. Before the infusion, she had a normal phosphorus level of 3.2 mg/dL, calcium 9.2 mg/dL (ref 8.5-10.5mg/dL) and magnesium 2.3 mg/dL (ref1.6-2.6mg/dL). Blood tests during admission (two weeks after infusion and one week after initial 0.9 mg/dL level) showed phosphorus level 1.3mg/dL, calcium 9.0 mg/dL, magnesium 2.5 mg/dL and albumin 4.6 (ref 3.4-4.8mg/dL). Further in hospital work-up showed intact PTH 111 (ref 11-95 pg/mL), prealbumin 14.5 (ref 14-38 mg/L), Vitamin D 25(OH)-D3 24 (ref20-100 ng/mL) and Vitamin D 1,25(OH)2 15 (ref 18-72 pg/ml) and increased FGF23 204 (ref <180 RU/mL). A 24 hour urine collection was notable for increased urinary phosphorus of 1343 mg(ref<1100mg/day). Phosphorus was repleted with IV potassium phosphate during admission and she was discharged on oral potassium phosphate 500mg PO BID which was later increased to TID. She was also advised to eat a diet high in phosphorus. She was followed as an outpatient and her phosphorus levels remained <2.1 mg/dL for 4 weeks after the IV ferric carboxymaltose infusion returning to normal thereafter. Conclusion: Although gastrectomy with poor nutrition may cause hypophosphatemia, it is worth considering other etiologies in the setting of persistently low phosphorus levels. With correlative evidence of high urinary phosphorus excretion in the setting of low serum phosphorus and elevated FGF23, we believe that IV ferric carboxymaltose infusion may have been a major contributor to hypophosphatemia in our patient. FGF23 is known to be a “phosphatonin” and ferric carboxymaltose may inhibit FGF23 degradation in osteocytes leading to an increase in its levels. Phosphate levels should be monitored before and after parenteral ferric carboxymaltose infusion, which can persist for weeks.