Symptomatic hypocalcaemia in hypermagnesaemia-induced hypoparathyroidism, during magnesium tocolytic therapy--possible involvement of the calcium-sensing receptor.

5.3 mg/dl (1.32 mmol/l ); ionized calcium, 0.71 mmol/l; Introduction albumin, 3.3 g/dl (33 g/l ); and phosphorus, 4 mg/dl (1.29 mmol/l ). Twenty four hour urinary calcium excreHigh dose magnesium therapy, which causes profound tion was 300 mg. A day later plasma PTH (intact PTH hypermagnesaemia, is an established therapy for immunoassay kit, Nichols Institute Diagnostics, San eclampsia and premature labour. Usually the hyperJuan Capistrano, CA, USA) level was <8.5 pg/ml magnesaemia is tolerated well. More than two decades (normal range 10–65 pg/ml ). Intravenous calcium was ago hypocalcaemia was described in two obstetric given but due to continued labour and symptomatic patients receiving magnesium [1,2]. hypocalcaemia, magnesium therapy was stopped Cholst et al. [3] studied a group of seven pregnant (Figure 1). The symptoms of hypocalcaemia resolved women and showed that hypermagnesaemia-induced with the rise of serum calcium and the decline of serum hypocalcaemia was associated with transient hypoparamagnesium. Plasma PTH level increased to 26 pg/ml on thyroidism. Of note is the lack of symptoms in the day 3. She gave birth on the 25th week of her pregnancy. women who had hypocalcaemia. We present two patients who had magnesium tocolytic therapy, and during hypermagnesaemia developed prolonged symptomatic Case 2 hypocalcemia and undetectable PTH concentrations. We propose the involvement of the calcium-sensing receptor A 27-year-old woman on the 19th week of her pregin hypermagnesaemia-induced hypocalcaemia. nancy was admitted due to suspected twin to twin transfusion. During her stay in the ward premature labour occurred. As she did not respond to b-adreCase 1 nergic agonists and indomethacin, she was started on intravenous magnesium sulfate (a loading dose of 5 g A 28-year-old woman after in vitro fertilization procedand a maintenance dose of 2 g/h). On the second day ure was pregnant with twins. On the 24th week of a routine blood chemistry analysis showed a calcium pregnancy she had vaginal bleeding and premature level of 6.5 mg/dl (1.62 mmol/l ). On the third day of labour. She was started on oral b-adrenergic agonists magnesium treatment she complained of hoarseness, and 4 days later intravenous magnesium sulfate was muscle spasms, and was found to have tetany. Physical administered. Twelve hours after a loading dose of 5 g examination showed a positive Chvostek sign and of magnesium sulfate and a maintenance dose of 2 g/h, tendon hyperreflexia. Initial laboratory tests on admisshe complained of diplopia, general malaise, and paression including renal function were within normal limits. thesia especially over the face and extremities. On When symptoms occurred laboratory results showed examination a prominent Chvostek sign with marked the following serum biochemical values: magnesium, hyperreflexia were noticed. There were no signs of 6.1 mg/dl (2.51 mmol/l ); calcium, 6.3 mg/dl toxaemia. EKG showed a prolonged Q-T interval. (1.57 mmol/l ); ionized calcium, 0.84 mmol/l; albumin, Initial laboratory tests done on admission were within 3.4 g/dl (34 g/l ); and phosphorus, 3 mg/dl (1 mmol/l ). normal limits. When symptoms appeared, laboratory Plasma PTH level was <8.5 pg/ml. Intravenous and results showed the following serum concentrations: oral calcium were given with concomitant intravenous magnesium, 6.5 mg/dl (2.67 mmol/l ); total calcium, magnesium sulfate for another 8 days. She was intermittently symptomatic due to on going hypocalcaemia. Correspondence and offprint requests to: Haim Mayan MD, Since premature contractions persisted, the magnesium Department of Medicine E, Sheba Medical Center, Tel-Hashomer 52621, Israel. therapy was stopped with a prompt resolution of