E-Poster Presentation ESA-SRB-ANZBMS 2021

Hypercalcaemia – a basic case in point (#423)

Matthew Sawyer 1 , Caroline Jung 1 2
  1. Department of Endocrinology & Diabetes, St Vincent's Hospital Melbourne, Fitzroy, VIC, Australia
  2. University of Melbourne, Melbourne, VIC, Australia

A 62-year-old man presented with increasing confusion, falls, dysarthria and ataxia. Past medical history included a traumatic brain injury many years ago, with subsequent cognitive impairment and seizures. He resided in a residential care facility.

Initial pathology demonstrated moderate hypercalcaemia of 3.34 mmol/L (2.21-2.63) with an acute kidney injury (eGFR 40 mL/min). There were not thought to be any medications contributing to hypercalcaemia, though it was noted that he was taking colecalciferol 50mcg daily.

Fluid resuscitation was followed by administration of pamidronate 60mg. Subsequent investigations included a low-normal parathyroid hormone level 20 pg/mL (15-68) paired with calcium 2.97 mmol/L, vitamin D 89 nmol/L (>50), 1,25-dihydroxyvitamin D 42 pmol/L (50-190). Screening for solid organ and haematological malignancy was unremarkable. Computed tomography (CT) of the neck/chest/abdomen/pelvis identified a filling defect within the caecum, however a colonoscopy performed with good preparation within one month prior to admission had not demonstrated any abnormality at this site. At the time of discharge, calcium had normalised to 2.47 mmol/L and renal function had partially recovered to eGFR 60 mL/min.

He represented within two weeks of discharge with recurrence of the previous symptoms. Biochemistry was similar to the first presentation. Venous blood gas revealed a pH of 7.39 (7.35-7.45), bicarbonate 42 mmol/L (21-28) and pCO2 69 mmHg (32-48), consistent with a compensated metabolic alkalosis. A careful history identified the frequent ingestion of six to 12 QuickEze tablets per day, each containing calcium carbonate 750mg. Calcium normalised to 2.27 mmol/L with fluid repletion and eGFR recovered to 60 mL/min.

This case highlights the milk-alkali syndrome as an uncommon and under-recognised cause of PTH-independent hypercalcaemia. A high index of suspicion and careful history is needed to elicit potential contributing substances and avoid unnecessary investigations and treatments, while a high bicarbonate level may be useful clue suggesting metabolic alkalosis.

 

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