Background: Calcium-alkali syndrome is an increasingly recognised cause for hospital presentations with non-PTH-mediated hypercalcaemia, characterised by hypercalcaemia, metabolic alkalosis and acute kidney injury.¹ Historically associated with milk and alkali therapy for peptic ulcer disease, contemporary cases reflect widespread calcium carbonate use in antacids and supplements.

Case: A 73-year-old woman presented after an unwitnessed fall with four days of drowsiness, slurred speech, anorexia and constipation. Her history included hypertension and gout, treated with candesartan and hydrochlorothiazide. Initial biochemistry demonstrated extreme hypercalcaemia (adjusted calcium 5.56 mmol/L), acute kidney injury, metabolic alkalosis, hypokalaemia and profound hypophosphataemia. PTH was detectable at 2.0 pmol/L. The extreme hypercalcaemia, hypophosphataemia and incompletely suppressed PTH raised concern for malignancy-associated hypercalcaemia, including a PTHrP-mediated process.

Management and outcome: She received intravenous saline and calcitonin infusion before transfer for urgent haemodialysis. Intravenous pamidronate was administered, followed by hypocalcaemia during recovery. Investigations including serum free light chains, electrophoresis, PET imaging, QuantiFERON testing and PTHrP did not identify an alternative cause. Once delirium improved, targeted history revealed substantial calcium carbonate ingestion for gastritis. Initially described as “a few” Rennie tablets daily, consumption equated to approximately 4.9 g elemental calcium per day.

Discussion: Calcium-alkali syndrome is traditionally considered to cause mild-to-moderate hypercalcaemia; however, this case represents the severe extreme of its spectrum. Extreme hypercalcaemia, profound hypophosphataemia and incompletely suppressed PTH may mimic a PTHrP-mediated process. Modern calcium-alkali syndrome differs from the historical form associated with milk and absorbable alkali therapy: it more commonly results from calcium carbonate-containing antacids or supplements, affects older patients with reduced renal calcium clearance, and is often compounded by dehydration or thiazide exposure.^1,2 Hypophosphataemia is also more characteristic of modern cases, reflecting lower phosphate intake and calcium carbonate-mediated phosphate binding.¹ Targeted quantification of elemental calcium intake is essential, as unnecessary antiresorptive therapy may contribute to prolonged hypocalcaemia.²