Endocrine Abstracts (2007) 13 P76

Acute falciparum malaria and parathyroid function

Aparna Pal1, Niki Karavitaki1, John Wass1 & Hugh Simpson2


1Oxford Centre for Diabetes and Endocrinology, Oxford, United Kingdom; 2Centre For Diabetes and Endocrinology, Reading, United Kingdom.


We present a rare case of acute falciparum malaria complicated by hypocalcaemia while having normal renal function.

Case: A 64 year old African lady presented with a 2 week history of lethargy, weakness and oliguria. She had returned from Malawi a fortnight previously and had not taken antimalarial prophylaxis. Her malaria screen was positive for Plasmodium falciparum and she was commenced on quinine. On day 5 of her admission she developed perioral paresthesia and was found to have a corrected calcium of 1.91 mmol/l (2.12–2.65) which dropped further to 1.82; phosphate was 0.73 mmol/l (0.8–1.65). She had a prolonged QT interval on an ECG and positive Chvostek’s sign. She was in acute renal failure on admission (creatinine 447 mmol/l, urea 36.7 mmol/l) when calcium was 2.26 mmol/l. On development of hypocalcaemia her renal dysfunction had actually improved with a creatinine of 165 mmol/l and urea 3.5 mmol/l. Parathyroid hormone was 7.7 pmol/l (1.0–7.2) and 25 hydroxycalciferol levels 24 mcg/l (7–30). She was treated with intravenous calcium gluconate and oral supplementation. She was seen in clinic a month later with calcium 2.3 mmol/l and her supplements were discontinued. Her calcium remained normal off treatment.

Discussion: Hypocalcaemia in malaria occurs as part of acute renal failure. However, it is also recognised in cases with inappropriate PTH response (i.e. not substantially raised levels), hypophosphataemia and absence of significant renal dysfunction, as in our patient. The mechanism is unknown but it has been postulated that in acute malaria there is a lower serum calcium set-point for PTH secretion. The limited available literature looking at PTH and calcium levels in malaria patients with and without renal impairment supports this hypothesis. Although in our patient a lower free 1,25 hydroxycalciferol may have contributed, the above mechanism is a possible explanation.

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