Dr Manjri Raval1, Dr Christopher Yates1,2, Dr I-Lynn Lee1,2, Dr Joanne Said3,2, Dr Dev Kevat1,2
1Endocrinology and Diabetes Unit, Western Health, Melbourne, Australia, 2Department of Medicine, University of Melbourne, Melbourne, Australia, 3Maternal Fetal Medicine, Western Health, Melbourne, Australia
Biography:
Endocrinology Advanced Trainee with an interest in Obstetric Medicine & Endocrinology.
Abstract:
Introduction: Hypercalcemia occurs in approximately 0.03% of pregnancies and increases risks of morbidity and mortality due to maternal, fetal and neonatal complications. Determining aetiology and management is often challenging.
Case: A 33-year old woman, G2P1, 32+4weeks was reviewed in clinic with migraines, polyuria, polydipsia, and fatigue. She experienced no nausea or constipation. There was no family history of hypercalcemia, osteoporosis or renal calculi. Investigations showed corrected calcium (cCa) 2.95mmol/L (2.15–2.65), ionised calcium 1.40mmol/L (1.15–1.30), parathyroid hormone level 9.6pmol/L (2.0–8.5), vitamin D 59nmol/L (>50), and 24-hour urine creatinine 6.6mmol/24h (6.0–25.0) and calcium 5.1mmol/24h (2.0–7.5). 24-hour urine calcium/creatinine clearance ratio (CCR) was 0.0121, above the recognised threshold of 0.01 to exclude familial hypocalciuric hypocalcaemia (FHH). Ultrasound showed a hyperechoic structure suspicious for a parathyroid adenoma. Despite oral hydration of 3L/day, the patient was hospitalised for worsening hypercalcemia (cCa 3.05) at 34+1 and managed with intravenous fluids until delivery at 36+3weeks by elective caesarean section. The newborn had asymptomatic hypercalcemia requiring intravenous fluids; with calcium persistently elevated at three weeks of age. Maternal genetic testing for mutations causing FHH are underway.
Discussion: The treatment and management of hypercalcemia in pregnancy is challenging. Primary hyperparathyroidism needs prompt diagnosis as the incidence of clinically significant complications is high in both the fetus and the mother.(1-3) Surgical parathyroidectomy is the only definitive cure and intervention in the second trimester is preferable. Urinary CCRs may be inadequate to screen for FHH in pregnancy due to changes in calcium physiology. However, in our case the persistent asymptomatic hypercalcemia, negative imaging studies and neonatal hypercalcemia raises the possibility of FHH.
Conclusion: Management of hypercalcemia should aim to minimise pregnancy, fetal and neonatal complications. Early diagnosis and treatment is necessary and further studies are required to optimise outcomes.
Keywords
hypercalcemia, pregnancy, familial hypocalciuric hypercalcemia, primary hyperparathyroidism
References
1) Murthy A, Murthy N, Ashawesh K, Kulambil Padinjakara RN, Anwar A. Familial hypocalciuric hypercalcaemia and pregnancy outcome. Endocr Abst. 2009;19:16.
2) Abood A, Vestergaard P. Pregnancy outcomes in women with primary hyperparathyroidism. Eur J Endocrinol. 2014;171(1):69–76. 13.
3) Rodrigo N, Learoyd D, Glastras SJ. Complexities surrounding the diagnosis and management of hypercalcemia in pregnancy. Endocrinology, Diabetes & Metabolism Case Reports 2021;20-0163