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Endocrine Abstracts (2023) 91 WF10 | DOI: 10.1530/endoabs.91.WF10

Western General Hospital, Edinburgh, United Kingdom


A 66 year old woman was referred to endocrinology in January 2023 with severe hypercalcaemia of 4.7mmol/ladjusted (2.2-2.6mmol/l) and low normal PTH of 1.8 pmol/l(1.6-6.9 pmol/l). She presented with one week of cough, breathlessness and fatigue, and 3-4 days of nausea and vomiting. She had commenced Furosemide 40 mg for bloating symptoms one month prior. She had a history of breast cancer treated with mastectomy and lymph node clearance in 2019, with subsequent Letrozole (ongoing) and six monthly Zolendronic acid (last given November 2021). Other past medical history included well controlled COPD and previous TIA. Drug history included Adcal D3 (Calcium Carbonate 750 mg + Colecalciferol 200units) two tablets twice daily. Admission investigations revealed she was Influenza A positive with WCC 14 and CRP 27 mg/l. She had a severe acute kidney injury (Urea 19mmol/l, Creatinine 200umol/l- previously normal) with hypokalemia (2.8mmol/l) and severe hypercalcaemia (4.7mmol/l). Phosphate was normal at 1.23mmol/l(0.8-1.4) and Magnesium was just above the normal range at 1.03mmol/l(0.7-1.0mmol/l). Vitamin D level was replete at 96nmol/l(50-139nmol/l). Furosemide and Adcal D3 were stopped on admission. She was initially treated with intravenous fluids with a reduction in adjusted Calcium to 3.03mmol/lafter 72 hours. As she had ongoing symptomatic hypercalcaemia over 3mmol/l, she was given Zolendronic Acid infusion on day four of admission with rapid resolution of Calcium to the normal range. Due to the low normal PTH level and history of recent breast cancer she was investigated with CT head, chest, abdomen and pelvis which showed no evidence of malignancy. Myeloma screen was negative. Further review revealed a milk rich diet and alkalosis on admission with a pH of 7.47 and elevated total bicarbonate of 43mmol/l(22-30mmol/l). Adcal D3 was discontinued and switched to Cholecalciferol. Bloods on discharge showed an appropriate rise of PTH to 5.0 pmol/lwith a corresponding decline in Calcium to 2.32mmol/l. Follow up Calcium levels in the community have remained normal. We believe this case is in keeping with Milk-Alkali syndrome given the combination of hypercalcaemia, metabolic alkalosis, acute kidney injury and use of calcium supplements, likely precipitated by dehydration secondary to Influenza A infection and recent diuretics. Milk Alkali syndrome is thought to be the third most common presentation of hypercalcaemia after malignancy and primary hyperparathyroidism and should be considered in people presenting with hypercalcaemia on calcium carbonate containing supplements, especially if bicarbonate is raised in the context of renal failure.

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