E-Poster Presentation ESA-SRB-ANZBMS 2021

An under-recognised association: hypocalcaemia and intravenous iron polymaltose (#366)

Lauren Burrage 1 , Amanda Love 1 , Syndia Lazarus 1
  1. Department of Endocrinology and DIabetes, Royal Brisbane and Women's Hospital, Brisbane, QUEENSLAND, Australia

We present two cases of hypocalcaemia post intravenous iron polymaltose infusion. Hypophosphataemia is a well-recognised phenomenon following intravenous iron,1,2 however hypocalcaemia has been rarely documented.3,4

Case 1 is a 62-year-old female who presented with symptomatic hypocalcaemia ten days after intravenous iron polymaltose infusion with a nadir calcium of 1.80mmol/L. Hypophosphataemia preceded hypocalcaemia by five days. She was vitamin D deficient; parathyroid hormone (PTH) and FGF-23 were significantly elevated; 1,25-dihydroxyvitamin D was low. Cholecalciferol and calcitriol (0.5mcg twice daily) were commenced at presentation and calcitriol was subsequently weaned over four weeks. Two months after calcitriol cessation, calcium and phosphate had normalised and PTH had significantly reduced (see Table 1).

Case 2 is a 59-year-old female who developed symptomatic hypocalcaemia seven days after intravenous iron polymaltose with a nadir calcium of 1.82mmol/L. She had a background of glucocorticoid-induced osteoporosis treated with denosumab with the last dose four months prior to presentation, as well as vitamin D deficiency treated with high dose oral cholecalciferol. Vitamin D level was normal and PTH and FGF-23 were significantly elevated (see Table 1). Calcitriol 0.75mcg daily was commenced and subsequently weaned. Calcium normalised three months later.

Parenteral iron is complexed with carbohydrate moieties including carboxymaltose and polymaltose, which prevent the degradation of FGF-23.5,6 Hypophosphataemia therefore develops due to excess FGF-23 inhibiting phosphate reabsorption in the renal tubules.7 FGF-23 also inhibits calcitriol production which reduces intestinal absorption of phosphate and calcium, thus exacerbating hypophosphataemia and potentially causing hypocalcaemia.7

We hypothesise that hypocalcaemia develops primarily in patients with additional risk factors such as vitamin D deficiency or denosumab exposure, as described above. We are conducting a retrospective audit to assess the frequency of hypocalcaemia post intravenous iron infusion, as this complication may be under-recognised. Meanwhile, these cases highlight the need for clinicians to be cognisant of this association.

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