A 23-year-old Rwandan lady was 27 weeks pregnant and reported feeling non-specifically unwell for 3 days followed by 24 h of diarrhoea and vomiting. She denied fever, rash, polyuria, polydipsia, weight loss or foreign travel. She has sickle cell trait with no other past medical history. Laboratory glucose at 16 weeks gestation was 5.1 mmol/l.
On admission she looked unwell and was tachycardic and dehydrated. Her capillary blood glucose was 17.9 mmol/l and urine dipstick was positive for ketones and protein. A metabolic acidosis was confirmed on arterial blood gases (pH 7.2, bicarbonate 12 mmol/l) with elevated inflammatory markers (CRP 328, WCC 13.4), a normochromic normocytic anaemia and mild renal impairment.
A diagnosis of metabolic acidosis secondary to sepsis with gestational diabetes was made and sliding scale intravenous insulin and broad spectrum antibiotics were commenced. The chest radiograph was normal and urine and blood cultures were negative.
Hypercalcemia was noted 24 h later (CorrectedCa2+ 2.98 mmol/l, phosphate 0.66 mmol/l). A retrospective admission calcium was 3.28 mmol/l with a suppressed parathyroid hormone (PTH). A renal ultrasound scan showed a cyst in the left kidney.
Intermittent pyrexia, thrombocytopenia and raised haemolytic markers prompted a malaria screen and falciparum malariae was detected.
Subcutaneous insulin was commenced and the malaria was treated with chloroquine. The hypercalcaemia improved with fluid replacement and the PTH became detectable. She was noted to be vitamin D deficient, PTH-related peptide (PTHrp) was undetectable and HTLV 1 serology was negative.
She improved clinically but a mildly elevated corrected calcium persisted (<2.7 mmol/l). She was monitored closely throughout pregnancy and had a spontaneous vaginal delivery at term.
1. Can hypercalcaemia be attributed to malaria? What is the mechanism?
2. What other investigations may elucidate the cause for her persistent mild hypercalcaemia?
3. Would you manage her differently in pregnancy?