Prolonged Hypophosphatemia Following Intravenous Ferric Carboxymaltose: An Impact on Phosphate Homeostasis Not to be Ignored. A Case Report
Presentation Number: SUN-468
Date of Presentation: March 18, 2018, 2018
K Sri Karpageshwary, MBBS (Singapore), Joan Joo Ching Khoo, MBBS (Singapore), MRCP (UK), MMed (Internal Medici.
Changi General Hospital, Singapore, Singapore.
Intravenous iron is increasingly being favored over oral iron for treatment of iron deficiency anemia, due to its increased efficacy, improved compliance and fewer gastrointestinal side effects. Hypophosphatemia, which can be asymptomatic but nevertheless increases the risk of myocardial depression, seizures and proximal myopathy, is a known complication of parenteral iron treatment, mediated by increased serum concentration of fibroblast growth factor 23 (FGF-23) which inhibits calcitriol synthesis and induces phosphaturia. The nadir of serum phosphate is usually reached within 2-4 weeks after administration of intravenous iron and typically lasts 4-8 weeks, though hypophosphatemia may last as long as 3-6 months. We report the case of a patient who developed hypophosphatemia after administration of Ferric Carboxymaltose (FCM), which persisted for more than 2 months after its administration.
Madam P, a 74-year-old Chinese female was incidentally found to be hypophosphatemic (serum PO4 0.47 mmol/L, 0.65-1.65) on post-operative day 3 after undergoing a right hemicolectomy for tubulovillous adenoma on the 31/08/2017. She had received 2 doses of IV FCM 1000 mg preoperatively on the 15/08/2017, for iron deficiency anemia. Her renal and liver functions were normal and hemoglobin was 8.5 g/dl. Serum phosphate normalized with intravenous replacement and ergocalciferol 50000 units/week was prescribed for the initial impression of Vitamin D deficiency (25-hydroxyvitamin D 6.4 μg/L) with secondary hyperparathyroidism (PTH levels 9.62 pmol/L 1.30-7.6). At the clinic review 2 months later, she was asymptomatic but persistently hypophosphatemic (0.39 mmol/L) despite improved vitamin D levels at 20.9 μg/L and was admitted to the endocrinology unit for further investigations. Her 24-hour urine phosphate was at the upper limit of normal (21.35 mmol/day, 8.10- 22.6) with inappropriately low renal tubular reabsorption of phosphate (TmP/GFR) 0.136mmol/L, indicating renal phosphate wasting. Serum phosphate normalized after IV replacement and she was maintained on oral Fleet 2 ml TDS (24 mmol of phosphorus) and calcitriol 0.25 mcg daily.
Madam P’s case highlights the under-reported risk of prolonged hypophosphatemia that IV FCM poses, particularly in patients with co-existing vitamin D deficiency. Repletion of phosphate and calcitriol, in addition to maintenance of oral phosphate replacement with monitoring of serum phosphate levels (if abnormal 2 weeks after IV FCM) should be continued for at least 2 months after IV FCM. Doing the above via a department based protocol would ensure that electrolyte levels particularly that involving the bone- kidney- phosphate axis is monitored and appropriate follow-up is ensued post IV FCM administration.
K.S. Karpageshwary: None. J.J. Khoo: None.