Clinical record A 35-year-old pregnant woman (gravida 4, para 3) presented in February 2004 at 35 weeks' gestation with a 1-day history of vomiting, abdominal pain and drowsiness. She had no significant past medical history, was not taking any prescription medication, and had had an uncomplicated pregnancy up to that time. Her level of consciousness subsequently deteriorated, and she became responsive only to painful stimuli. She had a blood pressure of 190/110 mmHg, abdominal tenderness and generalised oedema. Urinalysis was positive for protein and leukocytes. Blood biochemical levels included creatinine 0.19 mmol/L (reference range [RR], 0.05-0.09 mmol/L); urea 9.2 mmol/L (RR, 2.5-8.3 mmol/L); ionised calcium 2.64 mmol/L (RR, 1.12-1.3 mmol/L); bicarbonate 32 mmol/L (RR, 22-28 mmol/L); amylase 2397 IU/L (RR, <160 IU/L); lipase 1364 IU/L (RR, <60 IU/L); urate 0.65 mmol/L (RR, 0.2-0.47 mmol/L); and phosphate 0.58 mmol/L (RR, 0.8-1.5 mmol/L). Abdominal ultrasound excluded acute cholecystitis. A fetal cardiotocograph showed reduced variability in fetal heart rate. Pre-eclampsia was diagnosed, and the woman underwent an urgent caesarean section 3 hours after presentation. The pre-eclampsia was managed with magnesium sulfate infusion, intravenous hydralazine and metoprolol. A 2574 g boy was delivered (Apgar score 3 at 1 minute, 9 at 10 minutes). Initially, he had a blood pH of 7.37 and serum calcium level of 4.12 mmol/L (RR, 2.1-2.6 mmol/L). Within 1 week he had made a full recovery from respiratory distress, jaundice and sepsis. Neonatal hypocalcaemia did not occur. Subsequently, a computed tomography (CT) scan of the woman's abdomen confirmed acute pancreatitis, with an oedematous pancreas and fluid in the paracolic gutter (Box 1). Her serum parathyroid hormone (PTH) level on Day 2 was suppressed (0.66pmol/L; RR, 1.3-6.8 pmol/L), with PTH-related protein undetectable (< 1 pmol/L). On Day 7, her serum 25-hydroxy-vitamin D level was inappropriately high (120 nmol/L; RR, 25-108 nmol/L). (On later questioning, she said she had not taken vitamin D supplements.) The level of 1,25-dihydroxyvitamin D was not measured. The serum level of angiotensin-converting enzyme was normal. The patient's hypercalcaemia was managed by intravenous administration of saline, followed by frusemide and pamidronate 90 mg. Over the next few days, her condition improved and her blood pressure and renal function normalised. The hypercalcaemia resolved quickly - to the extent that, by Day 8, she had developed symptomatic hypocalcaemia requiring oral supplementation with calcium carbonate and calcitriol (Box 2). When her delirium had resolved, she reported a 1-month history of severe heartburn, for which she had self-medicated with antacids, taking up to 10 Rennie tablets a day (an over-the-counter [OTC] preparation containing calcium carbonate 680mg and magnesium carbonate 80 mg per tablet) (10 tablets contain about 3 g elemental calcium). She had also been drinking up to three glasses of milk a day. In light of this history, milk-alkali syndrome was diagnosed, and the pancreatitis was attributed to hypercalcaemia. By Day 16, the pancreatitis had resolved and the calcium level normalised. She was discharged home without medication and has remained well.
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