Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2011) 25 P78


Salisbury Foundation NHS Trust, Salisbury, Wiltshire, UK.

A 50-year-old woman with learning difficulties and schizophrenia presented to accident and emergency with 5 days of epigastic pain and vomiting.

Initially, she was peripherally shut down, with a pulse of 120 and blood pressure of 115/80. Chest examination was normal. Abdominal examination showed epigastric tenderness with guarding.

Blood tests confirmed a diagnosis of acute pancreatitis (Amylase 1972 IU/l), with hypercalcaemia (corrected calcium 3.46 mmol/l) and acute renal failure (creatinine 692 mmol/l, urea 31.8 mmol/l).

Initial management included i.v. fluids, i.v. antibiotics and transfer to high dependency unit. The following day her bloods were as follows: Corrected Calcium 2.64 mmol/l, PTH 17.6 pmol/l.

DaysDay 1Day 2Day 3Day 4Day 7Day 44Day 119
Corrected calcium (mmol/l)3.462.641.821.642.452.492.36
PTH (pmol/l)17.63.6
Creatinine (mmol/l)6926275945061856169

Over the coming days she became more unwell and was intubated on intensive care unit. Her calcium plummeted and was managed with calcium infusion. She then slowly recovered and calcium normalised.

On further discussion it was apparent that she had been consuming excessive indigestion remedies (rennes and gaviscon) for years before admission. She has now been started on a proton pump inhibitor and calcium and PTH have both normalised and remained normal.

This is a case of milk–alkali syndrome complicated by severe pancreatitis and renal failure. The raised PTH on day two is due to the huge drop in calcium over the first 24 h.

It is important to still consider milk–alkali syndrome in the differential for severe hypercalcaemia. Measurement of PTH after initial treatment of hypercalcaemia can give a misleading result as in this case and teams should be encouraged to measure PTH at initial assessment in all patients with hypercalcaemia.

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