A Case Report of Symptomatic Hypophosphatemia Secondary to Elevated FGF-23 from Parenteral Ferric Carboxymaltose Treatment for Iron Deficiency Anemia

Presentation Number: SAT 314
Date of Presentation: April 1st, 2017

Dinesh Edem, Helena Levitt and Sue Marion Challinor*
UPMC, Pittsburgh, PA


Introduction: Diagnosis of hypophosphatemia is often missed due to non specific symptoms, but it can cause considerable morbidity. Causes of hypophosphatemia include decreased intestinal absorption, internal redistribution, or increased renal excretion. FGF-23 is an osteocyte - derived hormone that maintains normal phosphate levels by decreasing both phosphate reabsorption and plasma calcitriol levels. We present a case of FGF-23 mediated hypophosphatemia caused by treatment with IV Ferric Carboxymaltose (FCM), resulting in severe muscle weakness.

Case: An 81 yr old male with a history of gastric bypass surgery 32 yrs previously, was admitted for evaluation after a 14- month history of progressive back pain, muscle weakness, frequent falls and inability to ambulate coinciding with onset of monthly IV FCM for Iron deficiency anemia. FCM was last given 1 week before admission. Physical exam revealed a wheelchair-bound obese male, L3-L5 point tenderness, decreased motor strength of 4/5 in lower extremities, and difficulty ambulating. CT revealed diffuse osteopenia and compression deformities of L1, L2 and L3. He was found to have a low phosphorus (Phos) level of 1.4 mg/dl (2.5-4.5). Phos was normal at 2.9, 3 yrs before. Further workup revealed elevated urine fractional excretion of phosphate (UFE Phos) of 49% (5-20%), inappropriately normal (nl) 24 hr urine Phos of 540 mg/D (400-1300), nl corrected Ca of 10.0, nl Mg of 1.7, elevated PTH of 194 pg/ml(15-65), nl 25- OH Vitamin (Vit.) D level of 33 ng/ml, and a low 1, 25 OH Vit. D level of 11 pg/ml (18-72). His FGF-23 level was elevated at 269 RU/ml (n<180). Markers of bone resorption were elevated: Alk Phos at 276 IU/L (38-126), Urine NTX at 118 nmol BCG/mmol Cr (9-60), and CTX at 1711 pg/ml (87-345). He was treated with oral Calcitriol 0.25mcg BID, oral 25-OH Vit. D 2000 IU QD, and oral K-Phos 1500 mg TID. IV FCM injections were changed to iron Dextran( DXN). Improvement in muscle weakness correlated with normalization of his Phos levels. Calcitriol and oral Phos supplementation were stopped after discharge at 4 weeks and 10 weeks, respectively. At 2 months after discharge, his FGF-23 level and 1,25 OH Vit. D normalized at 110 and 30, respectively. At 5 months follow-up, he was able to ambulate with use of a cane.

Discussion: Our case is similar to prior reports, indicating that IV iron preparations with carbohydrate moieties like FCM, lead to increased FGF-23 levels and cause hypophosphatemia, low 1,25 OH Vit-D and increased UFE Phos 1-4 . In contrast to FCM, IV iron DXN was not associated with elevated FGF-23 or low Phos in a prospective study which compared the two forms of iron 2. Similarly, our patient maintained a normal Phos after switching to iron DXN treatment. Parenteral iron formulations are increasingly prescribed, hence clinicians should be aware of the risk of significant, symptomatic hypophosphatemia that is a consequence of FCM infusions.


Nothing to Disclose: DE, HL, SMC