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Milk-alkali syndrome secondary to abuse and hypocalcaemia: case report A 65-year-old woman developed milk-alkali syndrome following misuse of calcium-carbonate/magnesium-carbonate/ magnesium-trisilicate as an antacid to alleviate reflux symptoms. She subsequently developed hypocalcaemia following treatment with pamidronic-acid for the milk-alkali syndrome. The woman presented with generalised lethargy, anorexia, vomiting, abdominal discomfort, constipation, myalgias and altered mental state for 2 weeks. She did not have fevers, night sweats or unintentional weight loss. Her medical history was remarkable for localised cervical cancer treated with radiotherapy 10 years earlier. At the current presentation, she did not have any other medications. Further investigations revealed ingestion of 12 tablets of the antacid calcium-carbonate/magnesium-carbonate/ magnesium-trisilicate [Quick-Eze] equivalent of 3.6g elemental calcium daily for 1 week to help alleviate reflux symptoms. On investigation, she was stable hemodynamically. Neurological evaluation was grossly intact except acute delirium. She demonstrated dry mucous membranes and no other significant findings were noted on cardiorespiratory and gastrointestinal evaluation. She had marked diffuse tenderness to palpation over her shoulders and hip girdle. Laboratory investigations on admission revealed severe hypercalcaemia, acute kidney injury, hyponatraemia, hypokalaemia and metabolic alkalosis with a partially compensated respiratory acidosis. The intact parathyroid hormone (PTH) was low-normal. The serum 25-hydroxyvitamin D level returned high in the absence of Vitamin D supplementation. The 1,25-dihydroxyvitamin D was performed on day 10, after treatment of hypercalcaemia returned slightly above the normal range. Thereafter, a CT chest/abdomen/ pelvis and pelvic and thyroid ultrasounds were performed, which excluded obvious malignancies or granulomatous processes. Baseline-corrected calcium level 4 years ago was normal. Based on these findings, she was diagnosed with milk-alkali syndrome [time to reaction onset not stated]. The woman initially received crystalloid fluids for the first 48 hours; followed by electrolyte replacement and renally adjusted single dose of IV pamidronic-acid [pamidronate] 30mg. Consequently, her calcium level normalised by day 3 of admission. However, she developed symptomatic hypocalcaemia with acral paraesthesia after 4 days of the pamidronate dose. She had nadir calcium level of 1.96 mmol/L at that time, and PTH was appropriately increased. The hypocalcaemia was treated with calcium carbonate and calcium gluconate. She was then discharged on day 10 when her corrected calcium level had normalised. Later, at follow-up after 5 days of discharge, laboratory investigation revealed normal corrected calcium level and renal function. Subsequently, calcium supplementation was stopped. Wang M, et al. Milk-alkali syndrome: A ’quick ease’ or a ’long-lasting problem’ Endocrinology, Diabetes and Metabolism Case Reports 2020: No. 1, 2020. Availa