The Alkaline Trap: Severe Calcium-Alkali Syndrome Secondary to Chronic Calcium Carbonate Ingestion

Calcium-alkali syndrome is an increasingly recognised cause of parathyroid hormone (PTH)-independent hypercalcaemia resulting from excessive calcium and absorbable alkali ingestion, commonly through calcium-containing antacids or supplements. Its clinical presentation may mimic neurological or malignant disease, potentially leading to extensive investigation and delayed diagnosis. A 64-year-old woman presented following a fall with paraparesis and lower back pain. Investigations demonstrated severe hypercalcaemia (adjusted calcium 4.83 mmol/L), suppressed PTH of 1.4 pmol/L, metabolic alkalosis (pH 7.47; bicarbonate 39.8 mmol/L), and mild renal impairment. Extensive investigation for malignant and granulomatous causes was unremarkable. Neurological assessment identified bilateral symmetrical peripheral neuropathy, and severe vitamin B12 deficiency was subsequently identified. Following intravenous fluid resuscitation and a single dose of pamidronate, serum calcium fell to 1.69 mmol/L. Subsequent testing demonstrated severe vitamin D deficiency with an appropriately elevated PTH. Detailed medication review revealed ingestion of 6-12 Rennie® tablets daily for more than two years for chronic indigestion. In the context of excessive calcium carbonate exposure and the characteristic biochemical triad of hypercalcaemia, metabolic alkalosis, and renal impairment, calcium-alkali syndrome was diagnosed. This case highlights the importance of obtaining a detailed over-the-counter medication history when evaluating severe hypercalcaemia. Early recognition of calcium-alkali syndrome can prevent unnecessary investigations, diagnostic delay, and avoidable morbidity.