Endocrine Abstracts

Background: Phosphate plays an important role in bone mineralisation. Hypophosphataemia is a common electrolyte abnormality which can result from poor intestinal absorption, increased renal loses (secondary to renal disease, alcohol abuse or drugs) or intracellular phosphate shift (often secondary to septicaemia or glucose or insulin treatment). This case showcases the importance of identifying the underlying cause of hypophosphataemia to guide subsequent treatment.

Case History: We present a case of a 41-year-old Afro-Caribbean woman referred to the inpatient endocrinology team with severe hypophosphataemia. She had been admitted a month prior, presenting with a life-threatening asthma exacerbation. Her medical history included brittle asthma with frequent exacerbations managed with steroids, Ehlers-Danlos Syndrome, type 2 diabetes mellitus, osteopenia and thalassaemia trait. During her prolonged admission, the patient was managed for her asthma exacerbation (with aminophylline infusions, intravenous hydrocortisone, nebulisers) and anaemia (with intravenous ferric carboxymaltose).

Investigations: The patient’s admission bone profile was normal. Phosphate levels became abnormal three weeks into the admission and reached a nadir of 0.25 mmol/l (normal rage 0.8-1.5). At this time, the patient was also symptomatic with weakness and muscle cramps. Investigations showed a persistently elevated PTH level (23.6 pmol/l, normal 1.6 - 6.9) and a raised 24-hour urinary phosphate output (56.2 mmol/24 hour, normal 15 – 50), with a reduced 24-hour urinary calcium output (2.3 mmol/24hour, normal 2.5–7.5). Other investigations, including renal and liver function, serum vitamin D, metanephrines and gut hormones, were normal. A DEXA scan post-discharge showed generalised osteopenia.

Results and treatment: This patient had several risk factors for developing serum hypophosphataemia secondary to increased urinary phosphate excretion, inducing frequent corticosteroid use and treatment with ferric carboxymaltose. As the phosphate level was normal for several weeks after admission despite treatment with hydrocortisone and its nadir happened seven days after intravenous ferric carboxymaltose administration, it was deemed that this was the likely precipitant. The patient was commenced on a 12-week course of oral phosphate replacement. Subsequent blood tests revealed a normal phosphate level, even once oral supplementation was completed.

Conclusions and points for discussion: This is not the only documented case of severe hypophosphataemia secondary to ferric carboxymaltose. A recent analysis showed ferric carboxymaltose is associated with over 50 times increased risk of hypophosphataemia than other intravenous iron preparations. It is thought that ferric carboxymaltose leads to an increase of biologically active FGF23 levels, subsequently inducing pathophysiological renal phosphate wasting and secondary hyperparathyroidism, leading to hypophosphataemia.