Poster Presentation ESA-SRB-APEG-NZSE 2022

Hypocalcaemia and hypophosphataemia following concurrent denosumab injection and ferric carboxymaltose infusion (#349)

Naomi Szwarcbard 1 , Chloe Dawson 1 , Lai-Ming Kathleen Pak 1 , Kathryn Hackman 1 2
  1. Department of Endocrinology & Diabetes, Alfred Hospital, Melbourne, VIC
  2. Department of Medicine, Monash University, Melbourne, VIC

We present the case of a 29-year-old woman with myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), complicated by recurrent episodes of optic neuritis and an atonic bladder. She had required immunosuppression therapy since diagnosis in 2016, initially with mycophenolate mofetil and azathioprine, followed by the combination of rituximab, methotrexate and prednisolone. In the setting of ongoing flares of optic neuritis the rituximab was transitioned to tocilizumab and she commenced plasma exchange therapy via a right radiocephalic arteriovenous fistula. Given her prolonged high-dose steroid requirement she was commenced on alendronate to reduce her risk of glucocorticoid-induced osteoporosis. This continued from 2017 to 2020, followed by a change to denosumab, which was initiated by her general practitioner in 2021. Two days after her most recent denosumab injection, she received a ferric carboxymaltose infusion for iron deficiency anaemia. She then reported two weeks of perioral and peripheral paraesthesia and muscle spasms, as well as increasing fatigue. Pathology demonstrated a corrected calcium of 1.89 mmol/L (2.15-2.65 mmol/L), an ionised calcium of 1.04 mmol/L (1.15-1.3 mmol/L) and an undetectable phosphate of <0.23 mmol/L (0.75-1.5 mmol/L). Renal function was normal (eGFR >90 ml/min/1.73m2) and vitamin D was 58 nmol/L (>50 nmol/L). The hypocalcaemia was caused by the denosumab injection, which in turn exacerbated hypophosphataemia via a reactive secondary hyperparathyroidism. However, the primary driver of hypophosphataemia was likely the ferric carboxymaltose infusion causing FGF-23 driven phosphaturia. She was commenced on oral electrolyte replacement, requiring a maximum dose of sodium phosphate monobasic 4000mg BD, calcium carbonate 1200mg BD and calcitriol 0.25mcg BD. She reported resolution of her symptoms, however experienced significant diarrhoea associated with high-dose phosphate replacement. Her electrolyte replacements were weaned over a two-month period and then ceased, with maintenance of normal electrolyte levels. She was advised to avoid ferric carboxymaltose infusions in the future.