Introduction: Pregnancy is characterized by increased intestinal calcium absorption, normal ionized or albumin-corrected calcium, high calcitriol, low PTH, gradually increasing PTHrP, and hypercalciuria. These differing hormonal changes can lead to nonclassic presentations of disorders of bone and mineral metabolism.
Case report: First-trimester 34-year-old multigravida patient presented with hyperemesis, abdominal pain, polyuria, polydipsia, leg cramps and constipation. Hypercalcaemia (4.13 mmol/l) with suppressed PTH was found while she was not taking any calcium. 25OH-VitD was low (40 nmol/l) and ACE level normal. 24 h urinary calcium and serum1, 25OH-VitD were elevated. PTHrP was not consistently elevated which may be related to the reliability of the assay itself. Imaging of breast, trunk revealed no evidence of maternal malignancy. BMD scan Hip T score was −1.7 and Z score −1.5 but Lumbar spine was normal. I.v. fluid therapy led to brief symptomatic improvement. Course of prednisolone failed to suppress calcium. Safety of bisphosphonates in pregnancy not established. Decision was made for medical termination of pregnancy (TOP) at 17 weeks from lack of symptomatic control of hypercalcaemia and the concern of its effect on the foetus. Calcium, PTHrP and 1,25OH-VitD levels normalised post termination. Foetal autopsy revealed no abnormalities apart from placental membrane calcification. The risks of gestational hypercalcaemia in future pregnancies discussed. She conceived again and developed uncontrolled hypercalcaemia with elevated 1,25OH-VitD and PTHrp requiring termination at 12 weeks with normalisation of calcium. Placental analysis failed to show abnormal PTHrP staining. Extensive counselling undertaken regarding future pregnancies. There was no documented hypercalcaemia in previous pregnancies with former partner. She conceived twice again with a resultant miscarriage at 8 weeks and TOP at 7 weeks.
Discussion: The usual causes of hypercalcaemia were excluded. This appears to be a pregnancy-related phenomenon, and postulated mechanisms are either excessive calcium gut absorption due to increased sensitivity to 1,25 Vitamin D or an occult source. Could this be related to aberrant prolactin receptors with resultant high PTH and altered gene transcription. There were limited studies in 2009 assessing the role of bisphosphonates or other drugs in pregnancy.
27 Apr - 01 May 2013
European Society of Endocrinology